CCR 11

The burden of pain among older patients is great, and its consequences can be "serious and significant," according to Dr. Perry G. Fine.

The prevalence of pain ranges from 25% to 50% in the older population and increases with age, he said.

In fact, among older nursing home residents, the prevalence is estimated at 45%-80%. In one study, 20% of individuals aged 65 and older admitted to having a day-long bout of pain in the past month, and about 60% said they had experienced pain for a year or more, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

The sources of pain in these patients are many and varied, and the consequences can include mood disorders, sleep disturbances, decreased socialization, increased health care utilization and costs, limitations in activities of daily living, comorbidities, and polypharmacy, all of which can lead to diminished function and quality of life.

Further complicating the problem is the fact that studies have repeatedly shown that pain in older adults is frequently undertreated, Dr. Fine said.

This may be the result of one or more of the numerous identified barriers to the management of pain in older patients, including language and cultural barriers, fear of judgment, fear of addiction, cognitive impairment, sensory impairment, and adverse effects such as fear of falling, constipation, sedation, and drug-drug interactions. Barriers for clinicians can include the lack of objective measures of pain and pain response, concerns regarding addiction and/or drug seeking, fear of causing harm from medication-related adverse effects, lack of time in the office setting, and lack of pain management training, according to findings from two studies on the topic (Clin. J. Pain. 2007;23[suppl. 1]:S1-43; J. Adv. Nurs. 2009;65:2-10).

Following a list of 10 "universal precautions" in pain management can help with overcoming some of these barriers, Dr. Fine said (Pain. Med. 2005;6:107-12). These include the following:

• Making a diagnosis with appropriate differential diagnoses.

• Performing psychological assessments, including evaluation for risk of addictive disorders.

• Obtaining informed consent.

• Developing treatment agreements.

• Performing pain and function assessments.

• Using pain medication – and particularly opioids – on a trial basis.

• Reassessing pain, function, and behavior.

• Regularly reassessing the "Four As" (analgesia, activities of daily living, adverse events, and aberrant drug-taking behaviors).

• Periodically reviewing diagnosis and comorbidities.

• Documenting thoroughly.

Also, keep in mind that aging results in a number of physiological changes that will influence both pharmacokinetics and pharmacodynamics, including changes in body composition; decreases in gastrointestinal motility, hepatic metabolism, renal clearance, and protein binding; and increased central nervous system sensitivity to noxious stimuli and medication effects, Dr. Fine said (Neurobiol. Aging 2010;31:494-503; Clin. J. Pain. 2004;20:220-6).

While speaking at the Congress of Clinical Rheumatology, Dr. Fine listed the following general principles to follow when it comes to pharmacotherapy in light of these changes and the needs of older adults:

• Titrate according to individual circumstances.

• Anticipate and monitor for adverse effects, prevent them when possible, and treat them when necessary.

• Practice synergy by combining lower doses of drugs that mediate analgesia via different mechanisms.

• Know and understand the distinctions among tolerance, dependence, addiction, and pseudoaddiction.

In those with cognitive impairment, in whom pain assessment can be particularly challenging, consider alternatives to standard numeric rating scales for pain assessment. Patients who have difficulty reporting pain based on these types of scales may do better with the Iowa Pain Thermometer, which allows a patient to rate pain using increments on a picture of a thermometer (Pain Med. 2007;8:585-600) or with the Brief Pain Inventory. Reports from caregivers may also be useful, Dr. Fine said.

Dr. Fine reported having no conflicts of interest that were relevant to his presentation.

The burden of pain among older patients is great, and its consequences can be "serious and significant," according to Dr. Perry G. Fine.

The prevalence of pain ranges from 25% to 50% in the older population and increases with age, he said.

In fact, among older nursing home residents, the prevalence is estimated at 45%-80%. In one study, 20% of individuals aged 65 and older admitted to having a day-long bout of pain in the past month, and about 60% said they had experienced pain for a year or more, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

The sources of pain in these patients are many and varied, and the consequences can include mood disorders, sleep disturbances, decreased socialization, increased health care utilization and costs, limitations in activities of daily living, comorbidities, and polypharmacy, all of which can lead to diminished function and quality of life.

Further complicating the problem is the fact that studies have repeatedly shown that pain in older adults is frequently undertreated, Dr. Fine said.

This may be the result of one or more of the numerous identified barriers to the management of pain in older patients, including language and cultural barriers, fear of judgment, fear of addiction, cognitive impairment, sensory impairment, and adverse effects such as fear of falling, constipation, sedation, and drug-drug interactions. Barriers for clinicians can include the lack of objective measures of pain and pain response, concerns regarding addiction and/or drug seeking, fear of causing harm from medication-related adverse effects, lack of time in the office setting, and lack of pain management training, according to findings from two studies on the topic (Clin. J. Pain. 2007;23[suppl. 1]:S1-43; J. Adv. Nurs. 2009;65:2-10).

Following a list of 10 "universal precautions" in pain management can help with overcoming some of these barriers, Dr. Fine said (Pain. Med. 2005;6:107-12). These include the following:

• Making a diagnosis with appropriate differential diagnoses.

• Performing psychological assessments, including evaluation for risk of addictive disorders.

• Obtaining informed consent.

• Developing treatment agreements.

• Performing pain and function assessments.

• Using pain medication – and particularly opioids – on a trial basis.

• Reassessing pain, function, and behavior.

• Regularly reassessing the "Four As" (analgesia, activities of daily living, adverse events, and aberrant drug-taking behaviors).

• Periodically reviewing diagnosis and comorbidities.

• Documenting thoroughly.

Also, keep in mind that aging results in a number of physiological changes that will influence both pharmacokinetics and pharmacodynamics, including changes in body composition; decreases in gastrointestinal motility, hepatic metabolism, renal clearance, and protein binding; and increased central nervous system sensitivity to noxious stimuli and medication effects, Dr. Fine said (Neurobiol. Aging 2010;31:494-503; Clin. J. Pain. 2004;20:220-6).

While speaking at the Congress of Clinical Rheumatology, Dr. Fine listed the following general principles to follow when it comes to pharmacotherapy in light of these changes and the needs of older adults:

• Titrate according to individual circumstances.

• Anticipate and monitor for adverse effects, prevent them when possible, and treat them when necessary.

• Practice synergy by combining lower doses of drugs that mediate analgesia via different mechanisms.

• Know and understand the distinctions among tolerance, dependence, addiction, and pseudoaddiction.

In those with cognitive impairment, in whom pain assessment can be particularly challenging, consider alternatives to standard numeric rating scales for pain assessment. Patients who have difficulty reporting pain based on these types of scales may do better with the Iowa Pain Thermometer, which allows a patient to rate pain using increments on a picture of a thermometer (Pain Med. 2007;8:585-600) or with the Brief Pain Inventory. Reports from caregivers may also be useful, Dr. Fine said.

Dr. Fine reported having no conflicts of interest that were relevant to his presentation.

The burden of pain among older patients is great, and its consequences can be "serious and significant," according to Dr. Perry G. Fine.

The prevalence of pain ranges from 25% to 50% in the older population and increases with age, he said.

In fact, among older nursing home residents, the prevalence is estimated at 45%-80%. In one study, 20% of individuals aged 65 and older admitted to having a day-long bout of pain in the past month, and about 60% said they had experienced pain for a year or more, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

The sources of pain in these patients are many and varied, and the consequences can include mood disorders, sleep disturbances, decreased socialization, increased health care utilization and costs, limitations in activities of daily living, comorbidities, and polypharmacy, all of which can lead to diminished function and quality of life.

Further complicating the problem is the fact that studies have repeatedly shown that pain in older adults is frequently undertreated, Dr. Fine said.

This may be the result of one or more of the numerous identified barriers to the management of pain in older patients, including language and cultural barriers, fear of judgment, fear of addiction, cognitive impairment, sensory impairment, and adverse effects such as fear of falling, constipation, sedation, and drug-drug interactions. Barriers for clinicians can include the lack of objective measures of pain and pain response, concerns regarding addiction and/or drug seeking, fear of causing harm from medication-related adverse effects, lack of time in the office setting, and lack of pain management training, according to findings from two studies on the topic (Clin. J. Pain. 2007;23[suppl. 1]:S1-43; J. Adv. Nurs. 2009;65:2-10).

Following a list of 10 "universal precautions" in pain management can help with overcoming some of these barriers, Dr. Fine said (Pain. Med. 2005;6:107-12). These include the following:

• Making a diagnosis with appropriate differential diagnoses.

• Performing psychological assessments, including evaluation for risk of addictive disorders.

• Obtaining informed consent.

• Developing treatment agreements.

• Performing pain and function assessments.

• Using pain medication – and particularly opioids – on a trial basis.

• Reassessing pain, function, and behavior.

• Regularly reassessing the "Four As" (analgesia, activities of daily living, adverse events, and aberrant drug-taking behaviors).

• Periodically reviewing diagnosis and comorbidities.

• Documenting thoroughly.

Also, keep in mind that aging results in a number of physiological changes that will influence both pharmacokinetics and pharmacodynamics, including changes in body composition; decreases in gastrointestinal motility, hepatic metabolism, renal clearance, and protein binding; and increased central nervous system sensitivity to noxious stimuli and medication effects, Dr. Fine said (Neurobiol. Aging 2010;31:494-503; Clin. J. Pain. 2004;20:220-6).

While speaking at the Congress of Clinical Rheumatology, Dr. Fine listed the following general principles to follow when it comes to pharmacotherapy in light of these changes and the needs of older adults:

• Titrate according to individual circumstances.

• Anticipate and monitor for adverse effects, prevent them when possible, and treat them when necessary.

• Practice synergy by combining lower doses of drugs that mediate analgesia via different mechanisms.

• Know and understand the distinctions among tolerance, dependence, addiction, and pseudoaddiction.

In those with cognitive impairment, in whom pain assessment can be particularly challenging, consider alternatives to standard numeric rating scales for pain assessment. Patients who have difficulty reporting pain based on these types of scales may do better with the Iowa Pain Thermometer, which allows a patient to rate pain using increments on a picture of a thermometer (Pain Med. 2007;8:585-600) or with the Brief Pain Inventory. Reports from caregivers may also be useful, Dr. Fine said.

Dr. Fine reported having no conflicts of interest that were relevant to his presentation.

The jury is still out on just how cardiovascular risk should be screened and managed in rheumatoid arthritis patients, but it is clear that the risk is increased and must be addressed.

Patients with RA are known to have a lower probability of survival than do controls, and a major cause of excess death is from cardiovascular disease. In one study, silent myocardial infarction was shown to occur more often in RA patients than controls, and sudden death was also more likely in the RA patients (Arthritis Rheum. 2005;52:402-11). In another study, survival among patients with acute cardiac syndrome was substantially reduced in RA vs. non-RA patients (Ann. Rheum. Dis. 2006;65:348-53).

In fact, RA is now considered by some experts to be equivalent to diabetes mellitus in terms of the extent to which it confers cardiovascular risk, according to Dr. Joan Bathon, director of the division of rheumatology at Columbia University, New York.

The European League Against Rheumatism (EULAR) has proposed that conventional cardiovascular risk models be multiplied by 1.5 when risk is assessed in RA patients, said Dr. Bathon (Ann. Rheum. Dis. 2010;69:325-31).

This approach is not well validated and may not be widely used at this point, according to Dr. Bathon. But the proposal illustrates the importance of focusing on cardiovascular risk in RA patients. Furthermore, it suggests that considering RA as a risk factor equivalent to diabetes mellitus – at least for making decisions about LDL cholesterol goals – is a reasonable strategy, she said.

She also said that a potential screening strategy involves yearly cardiovascular risk screening. The benefits of using imaging and biomarkers for screening are unclear, and no guidelines are currently in place. Some data suggest that the use of carotid ultrasound scans to look for plaques and to assess intima-media thickness – and the calculation of a coronary artery calcium score using CT – may be useful in patients older than 40 years.

As for potential management strategies, aspirin therapy might be useful but should be considered in the context of other medications the patient is taking.

Statins are also a potential management tool, but questions remain about whether all RA patients should be treated regardless of LDL cholesterol level, Dr. Bathon said.

Definite treatment strategies for RA patients include weight management for overweight patients – which will help reduce inflammation – as well as exercise for all RA patients, because good quality muscle building will help restore insulin sensitivity and reduce fat depots that are the most inflammatory. Tight blood pressure control and tight RA control are also imperative, Dr. Bathon said.

She noted that conventional cardiovascular risk factors do not fully explain the excess risk in RA patients, and that inflammation probably plays an important role.

"We also have to think about ourselves," she said, referring to whether rheumatologists are aggressive enough in their management of cardiovascular risk in RA patients.

There is some question as to whether the increased risk in RA patients, compared with controls, is a result of less-aggressive treatment, she said.

Dr. Bathon had no disclosures relevant to her presentation.

The jury is still out on just how cardiovascular risk should be screened and managed in rheumatoid arthritis patients, but it is clear that the risk is increased and must be addressed.

Patients with RA are known to have a lower probability of survival than do controls, and a major cause of excess death is from cardiovascular disease. In one study, silent myocardial infarction was shown to occur more often in RA patients than controls, and sudden death was also more likely in the RA patients (Arthritis Rheum. 2005;52:402-11). In another study, survival among patients with acute cardiac syndrome was substantially reduced in RA vs. non-RA patients (Ann. Rheum. Dis. 2006;65:348-53).

In fact, RA is now considered by some experts to be equivalent to diabetes mellitus in terms of the extent to which it confers cardiovascular risk, according to Dr. Joan Bathon, director of the division of rheumatology at Columbia University, New York.

The European League Against Rheumatism (EULAR) has proposed that conventional cardiovascular risk models be multiplied by 1.5 when risk is assessed in RA patients, said Dr. Bathon (Ann. Rheum. Dis. 2010;69:325-31).

This approach is not well validated and may not be widely used at this point, according to Dr. Bathon. But the proposal illustrates the importance of focusing on cardiovascular risk in RA patients. Furthermore, it suggests that considering RA as a risk factor equivalent to diabetes mellitus – at least for making decisions about LDL cholesterol goals – is a reasonable strategy, she said.

She also said that a potential screening strategy involves yearly cardiovascular risk screening. The benefits of using imaging and biomarkers for screening are unclear, and no guidelines are currently in place. Some data suggest that the use of carotid ultrasound scans to look for plaques and to assess intima-media thickness – and the calculation of a coronary artery calcium score using CT – may be useful in patients older than 40 years.

As for potential management strategies, aspirin therapy might be useful but should be considered in the context of other medications the patient is taking.

Statins are also a potential management tool, but questions remain about whether all RA patients should be treated regardless of LDL cholesterol level, Dr. Bathon said.

Definite treatment strategies for RA patients include weight management for overweight patients – which will help reduce inflammation – as well as exercise for all RA patients, because good quality muscle building will help restore insulin sensitivity and reduce fat depots that are the most inflammatory. Tight blood pressure control and tight RA control are also imperative, Dr. Bathon said.

She noted that conventional cardiovascular risk factors do not fully explain the excess risk in RA patients, and that inflammation probably plays an important role.

"We also have to think about ourselves," she said, referring to whether rheumatologists are aggressive enough in their management of cardiovascular risk in RA patients.

There is some question as to whether the increased risk in RA patients, compared with controls, is a result of less-aggressive treatment, she said.

Dr. Bathon had no disclosures relevant to her presentation.

The jury is still out on just how cardiovascular risk should be screened and managed in rheumatoid arthritis patients, but it is clear that the risk is increased and must be addressed.

Patients with RA are known to have a lower probability of survival than do controls, and a major cause of excess death is from cardiovascular disease. In one study, silent myocardial infarction was shown to occur more often in RA patients than controls, and sudden death was also more likely in the RA patients (Arthritis Rheum. 2005;52:402-11). In another study, survival among patients with acute cardiac syndrome was substantially reduced in RA vs. non-RA patients (Ann. Rheum. Dis. 2006;65:348-53).

In fact, RA is now considered by some experts to be equivalent to diabetes mellitus in terms of the extent to which it confers cardiovascular risk, according to Dr. Joan Bathon, director of the division of rheumatology at Columbia University, New York.

The European League Against Rheumatism (EULAR) has proposed that conventional cardiovascular risk models be multiplied by 1.5 when risk is assessed in RA patients, said Dr. Bathon (Ann. Rheum. Dis. 2010;69:325-31).

This approach is not well validated and may not be widely used at this point, according to Dr. Bathon. But the proposal illustrates the importance of focusing on cardiovascular risk in RA patients. Furthermore, it suggests that considering RA as a risk factor equivalent to diabetes mellitus – at least for making decisions about LDL cholesterol goals – is a reasonable strategy, she said.

She also said that a potential screening strategy involves yearly cardiovascular risk screening. The benefits of using imaging and biomarkers for screening are unclear, and no guidelines are currently in place. Some data suggest that the use of carotid ultrasound scans to look for plaques and to assess intima-media thickness – and the calculation of a coronary artery calcium score using CT – may be useful in patients older than 40 years.

As for potential management strategies, aspirin therapy might be useful but should be considered in the context of other medications the patient is taking.

Statins are also a potential management tool, but questions remain about whether all RA patients should be treated regardless of LDL cholesterol level, Dr. Bathon said.

Definite treatment strategies for RA patients include weight management for overweight patients – which will help reduce inflammation – as well as exercise for all RA patients, because good quality muscle building will help restore insulin sensitivity and reduce fat depots that are the most inflammatory. Tight blood pressure control and tight RA control are also imperative, Dr. Bathon said.

She noted that conventional cardiovascular risk factors do not fully explain the excess risk in RA patients, and that inflammation probably plays an important role.

"We also have to think about ourselves," she said, referring to whether rheumatologists are aggressive enough in their management of cardiovascular risk in RA patients.

There is some question as to whether the increased risk in RA patients, compared with controls, is a result of less-aggressive treatment, she said.

Dr. Bathon had no disclosures relevant to her presentation.

Patients presenting with hyperuricemia or gout should be evaluated for metabolic syndrome, and any recommendations regarding dietary changes and medical treatment for gout should take into consideration the potential benefits of urate reduction, according to Dr. N. Lawrence Edwards.

Both hyperuricemia and gout are independent risk factors for metabolic syndrome and its individual components, said Dr. Edwards, professor of medicine at the University of Florida, Gainesville.

In a 2007 study looking at the prevalence of metabolic syndrome in nearly 8,700 patients with hyperuricemia from the NHANES (National Health and Nutrition Examination Survey) III database, the prevalence of metabolic syndrome increased in tandem with increasing levels of serum urate, and the increase persisted across subgroups stratified by age, sex, alcohol intake, body mass index, hypertension, and diabetes (Am. J. Med. 2007;120:442-7).

The investigators found that the prevalence of metabolic syndrome (defined using both original and revised National Cholesterol Education Program Adult Treatment Panel III criteria) was 19% in those with uric acid levels less than 6 mg/dL, 36% in those with 8.0-8.9 mg/dL, 62% for 9.0-9.9 mg/dL, and 71% for levels of 10 mg/dL or greater.

Physicians should recognize that metabolic syndrome occurs frequently in patients with hyperuricemia, and should be treated to prevent serious complications, they concluded.

In a related study, the prevalence of metabolic syndrome in patients with doctor-diagnosed gout from the same NHANES population was high (nearly 63%) when compared with 25% in those without a gout diagnosis. The prevalence was even higher (83%) among those with a more stringently defined gout diagnosis (specifically, those on urate-lower therapy), Dr. Edwards noted (Arthritis Rheum. 2007;57:109-15).

As with hyperuricemia, the investigators concluded that the prevalence of metabolic syndrome is high in individuals with gout, and that, given the serious complications that can be associated with metabolic syndrome, the condition should be recognized and taken into account when clinicians plan the long-term treatment of patients with gout.

Evaluating Gout Patients for Metabolic Syndrome

The findings of these two studies support a pathogenic overlap between metabolic syndrome and gout, and underscore the importance of evaluating gout patients for the syndrome, Dr. Edwards said.

"You see a lot of patients coming in, and they haven’t had fasting glucoses performed, blood pressures may be a little out of control, and weight is certainly out of control," he noted. "We need to look at these patients much more seriously than if they only have gout; they need a full-court press on all of their metabolic problems and not just their uric acid."

Dietary recommendations that consist of the standard advice to avoid foods high in purines are not sufficient. Patients will often cut out meat and shellfish but replace those with foods high in carbohydrates and fat, which can increase insulin resistance. Therefore, it is important to advise patients to reduce intake of high-purine foods and also to avoid high-fat foods and the wrong kinds of carbohydrates.

About 40% of their diet should be complex carbohydrates, no more than 30% should be proteins, and no more than 30% should be mono- or polyunsaturated fats, he said.

As for medical treatment considerations, it is important to keep in mind the mechanisms of hyperuricemia as it relates to insulin resistance, he added.

In patients who are hypertriglyceridemic, for example, niacin is a commonly used drug. However, niacin can elevate uric acid levels "by quite a margin" of 1.5-2.5 mg/dL. Conversely, fenofibrate can also be used to treat hypertriglyceridemia, and can lower the levels by a similar margin.

"So just making that switch might make a pretty substantial difference," Dr. Edwards said.

In patients who are being treated for hypertension, keep in mind that hydroclorothiazide is associated with elevated uric acid levels and consider switching to the angiotensin receptor blocker losartan in those in whom hydrochlorothiazide is used solely for hypertension control and not for fluid control, as losartan has uric acid lowering effects, he said.

Dr. Edwards had no disclosures relevant to his presentation.

Patients presenting with hyperuricemia or gout should be evaluated for metabolic syndrome, and any recommendations regarding dietary changes and medical treatment for gout should take into consideration the potential benefits of urate reduction, according to Dr. N. Lawrence Edwards.

Both hyperuricemia and gout are independent risk factors for metabolic syndrome and its individual components, said Dr. Edwards, professor of medicine at the University of Florida, Gainesville.

In a 2007 study looking at the prevalence of metabolic syndrome in nearly 8,700 patients with hyperuricemia from the NHANES (National Health and Nutrition Examination Survey) III database, the prevalence of metabolic syndrome increased in tandem with increasing levels of serum urate, and the increase persisted across subgroups stratified by age, sex, alcohol intake, body mass index, hypertension, and diabetes (Am. J. Med. 2007;120:442-7).

The investigators found that the prevalence of metabolic syndrome (defined using both original and revised National Cholesterol Education Program Adult Treatment Panel III criteria) was 19% in those with uric acid levels less than 6 mg/dL, 36% in those with 8.0-8.9 mg/dL, 62% for 9.0-9.9 mg/dL, and 71% for levels of 10 mg/dL or greater.

Physicians should recognize that metabolic syndrome occurs frequently in patients with hyperuricemia, and should be treated to prevent serious complications, they concluded.

In a related study, the prevalence of metabolic syndrome in patients with doctor-diagnosed gout from the same NHANES population was high (nearly 63%) when compared with 25% in those without a gout diagnosis. The prevalence was even higher (83%) among those with a more stringently defined gout diagnosis (specifically, those on urate-lower therapy), Dr. Edwards noted (Arthritis Rheum. 2007;57:109-15).

As with hyperuricemia, the investigators concluded that the prevalence of metabolic syndrome is high in individuals with gout, and that, given the serious complications that can be associated with metabolic syndrome, the condition should be recognized and taken into account when clinicians plan the long-term treatment of patients with gout.

Evaluating Gout Patients for Metabolic Syndrome

The findings of these two studies support a pathogenic overlap between metabolic syndrome and gout, and underscore the importance of evaluating gout patients for the syndrome, Dr. Edwards said.

"You see a lot of patients coming in, and they haven’t had fasting glucoses performed, blood pressures may be a little out of control, and weight is certainly out of control," he noted. "We need to look at these patients much more seriously than if they only have gout; they need a full-court press on all of their metabolic problems and not just their uric acid."

Dietary recommendations that consist of the standard advice to avoid foods high in purines are not sufficient. Patients will often cut out meat and shellfish but replace those with foods high in carbohydrates and fat, which can increase insulin resistance. Therefore, it is important to advise patients to reduce intake of high-purine foods and also to avoid high-fat foods and the wrong kinds of carbohydrates.

About 40% of their diet should be complex carbohydrates, no more than 30% should be proteins, and no more than 30% should be mono- or polyunsaturated fats, he said.

As for medical treatment considerations, it is important to keep in mind the mechanisms of hyperuricemia as it relates to insulin resistance, he added.

In patients who are hypertriglyceridemic, for example, niacin is a commonly used drug. However, niacin can elevate uric acid levels "by quite a margin" of 1.5-2.5 mg/dL. Conversely, fenofibrate can also be used to treat hypertriglyceridemia, and can lower the levels by a similar margin.

"So just making that switch might make a pretty substantial difference," Dr. Edwards said.

In patients who are being treated for hypertension, keep in mind that hydroclorothiazide is associated with elevated uric acid levels and consider switching to the angiotensin receptor blocker losartan in those in whom hydrochlorothiazide is used solely for hypertension control and not for fluid control, as losartan has uric acid lowering effects, he said.

Dr. Edwards had no disclosures relevant to his presentation.

Patients presenting with hyperuricemia or gout should be evaluated for metabolic syndrome, and any recommendations regarding dietary changes and medical treatment for gout should take into consideration the potential benefits of urate reduction, according to Dr. N. Lawrence Edwards.

Both hyperuricemia and gout are independent risk factors for metabolic syndrome and its individual components, said Dr. Edwards, professor of medicine at the University of Florida, Gainesville.

In a 2007 study looking at the prevalence of metabolic syndrome in nearly 8,700 patients with hyperuricemia from the NHANES (National Health and Nutrition Examination Survey) III database, the prevalence of metabolic syndrome increased in tandem with increasing levels of serum urate, and the increase persisted across subgroups stratified by age, sex, alcohol intake, body mass index, hypertension, and diabetes (Am. J. Med. 2007;120:442-7).

The investigators found that the prevalence of metabolic syndrome (defined using both original and revised National Cholesterol Education Program Adult Treatment Panel III criteria) was 19% in those with uric acid levels less than 6 mg/dL, 36% in those with 8.0-8.9 mg/dL, 62% for 9.0-9.9 mg/dL, and 71% for levels of 10 mg/dL or greater.

Physicians should recognize that metabolic syndrome occurs frequently in patients with hyperuricemia, and should be treated to prevent serious complications, they concluded.

In a related study, the prevalence of metabolic syndrome in patients with doctor-diagnosed gout from the same NHANES population was high (nearly 63%) when compared with 25% in those without a gout diagnosis. The prevalence was even higher (83%) among those with a more stringently defined gout diagnosis (specifically, those on urate-lower therapy), Dr. Edwards noted (Arthritis Rheum. 2007;57:109-15).

As with hyperuricemia, the investigators concluded that the prevalence of metabolic syndrome is high in individuals with gout, and that, given the serious complications that can be associated with metabolic syndrome, the condition should be recognized and taken into account when clinicians plan the long-term treatment of patients with gout.

Evaluating Gout Patients for Metabolic Syndrome

The findings of these two studies support a pathogenic overlap between metabolic syndrome and gout, and underscore the importance of evaluating gout patients for the syndrome, Dr. Edwards said.

"You see a lot of patients coming in, and they haven’t had fasting glucoses performed, blood pressures may be a little out of control, and weight is certainly out of control," he noted. "We need to look at these patients much more seriously than if they only have gout; they need a full-court press on all of their metabolic problems and not just their uric acid."

Dietary recommendations that consist of the standard advice to avoid foods high in purines are not sufficient. Patients will often cut out meat and shellfish but replace those with foods high in carbohydrates and fat, which can increase insulin resistance. Therefore, it is important to advise patients to reduce intake of high-purine foods and also to avoid high-fat foods and the wrong kinds of carbohydrates.

About 40% of their diet should be complex carbohydrates, no more than 30% should be proteins, and no more than 30% should be mono- or polyunsaturated fats, he said.

As for medical treatment considerations, it is important to keep in mind the mechanisms of hyperuricemia as it relates to insulin resistance, he added.

In patients who are hypertriglyceridemic, for example, niacin is a commonly used drug. However, niacin can elevate uric acid levels "by quite a margin" of 1.5-2.5 mg/dL. Conversely, fenofibrate can also be used to treat hypertriglyceridemia, and can lower the levels by a similar margin.

"So just making that switch might make a pretty substantial difference," Dr. Edwards said.

In patients who are being treated for hypertension, keep in mind that hydroclorothiazide is associated with elevated uric acid levels and consider switching to the angiotensin receptor blocker losartan in those in whom hydrochlorothiazide is used solely for hypertension control and not for fluid control, as losartan has uric acid lowering effects, he said.

Dr. Edwards had no disclosures relevant to his presentation.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Opioid rotation is a common and potentially beneficial practice for helping to relieve chronic pain in patients who require ongoing opioid therapy, but there is very little data to guide best practice.

The recommended approach, therefore, is one that focuses on safety, Dr. Perry Fine said at the Congress of Clinical Rheumatology.

Clinicians should consider opioid rotation when patients on chronic opioid therapy experience intolerable adverse effects, or when benefits are inadequate despite dose increases, according to recently published clinical guidelines (J. Pain 2009;10:113-30).

However, it is important to consider a number of factors before making changes in treatment, including demographic, disease-related, and treatment-related factors, as well as comorbidities, concomitant pharmacotherapy, drug sensitivities, and social situation, said Dr. Fine, professor of anesthesiology at the University of Utah, Salt Lake City.

If a decision is made to convert a patient’s treatment, a two-step, safety-focused approach is needed, he said.

Step 1 involves an "automatic safety factor" calculation. That is, the equianalgesic dose of the new opioid should be calculated via an equianalgesic table such as a mu-agonist dose chart, and, with a few exceptions, an automatic dose reduction of 25%-50% should be made, except if the new drug is methadone or transdermal fentanyl.

A 25% reduction for opioids (other than methadone or fentanyl) is adequate in patients with no risk factors and/or if the switch is to a different route of administration of the same drug. A 50% reduction is needed in those receiving a relatively high dose of the current opioid, those who are elderly or frail, and those of Chinese lineage, as the Chinese population has been shown to be at increased risk of poor metabolism of opioid drugs, Dr. Fine said.

If the switch is to methadone, a 75%-90% dose reduction is needed, and if the switch is to transdermal fentanyl, use the reduction that is built into the conversion charts provided in the prescribing information, he advised.

If an oral transmucosal fentanyl citrate formulation is used, start with the lowest dose, he added.

The second safety-focused conversion step involves patient-specific adjustments. The patient should be assessed for pain severity and other medical or psychosocial characteristics, and appropriate additional adjustments should be made to the initial dose of the new opioid. For severe pain, consider a dose increase. If pain is under control, but the patient is experiencing adverse effects, any adjustments to the dose should be minimal.

In patients with specific vulnerabilities such as advanced age, renal insufficiency, or cognitive impairment, an additional 10%-30% dose reduction should be considered, Dr. Fine said.

He used as an example a case involving a patient with mild renal insufficiency who was undergoing a switch from morphine to hydromorphone. The patient had moderate pain, mild confusion, and was on multiple other medications. According to step 1, an automatic 25% reduction in the equianalgesic hydromorphone dose would be calculated. According to step 2, an additional 25% reduction would be taken because of the patient’s decreased renal clearance, cognitive problems, and potential drug-drug interactions. Dosage would then be titrated based on the patient’s response.

It is important that a strategy for frequent assessment of initial response be in place, Dr. Fine said, noting that this may involve regular phone calls to the patient or scheduled office visits. This will allow for improved safety and appropriate titration, he said.

Dr. Fine offered the following examples of initial dose calculation in three common analgesic conversions:

• To convert controlled-release oxycodone (60 mg oral dose twice daily) to controlled-release morphine:

1. Calculate the total oxycodone 24-hour dose (120 mg).

2. Determine the morphine dose equivalency (20 mg oxycodone = 30 mg morphine).

3. Convert the 24-hour oxycodone dose to the morphine dose (120 mg oxycodone = 180 mg morphine).

4. Reduce the morphine dose by 25% (135 mg morphine).

5. Split the total morphine dose to the twice-daily dose (67.5 mg). Because the controlled-release (extended-release) morphine is not provided in this exact dose, give the closest available dose (60 mg, twice daily).

• To convert controlled-release morphine (30 mg oral dose twice daily) to transdermal fentanyl:

1. Calculate the total morphine 24-hour dose (60 mg).

2. Use the prescribing information to determine the oral equivalent dose of transdermal fentanyl (60 mg oral morphine = 25 mcg/hr transdermal fentanyl patch).

3. Prescribe 25 mcg/hr transdermal fentanyl patch to be changed every 3 days. Supply patient with five patches (a 15-day supply); instruct patient on application, and follow-up by phone or in office within 2-3 days.

• To convert methadone (20 mg oral dose three times daily) to extended-release oxymorphone:

1. Calculate the total methadone 24-hour dose (60 mg daily).

2. Use mu-agonist dose chart to calculate oxymorphone dose equivalency to methadone (5 mg methadone = 10 mg oxymorphone).

3. Convert the 24-hour methadone dose to oxymorphone dose (60 mg methadone = 120 mg oxymorphone).

4. Reduce the dose by 50% and split the 50% total calculated oxymorphone dosage to a twice-daily dose. Prescribe oxymorphone ER (30 mg oral dose every 12 hours).

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King (now Pfizer), Meda, and Purdue-Pharma. He also is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Methadone can be an effective treatment for chronic pain, but there are a number of concerns that must be considered when prescribing this opioid, Dr. Perry G. Fine said at the Congress of Clinical Rheumatology.

Among the benefits of the effective mu-opioid analgesic with N-methyl-d-aspartate receptor antagonist properties are its low cost, dosing formulation versatility, long duration of action, and favorable metabolic profile. However, it also has highly variable pharmacokinetics, a very long half-life compared with its analgesic duration of action, and nonlinear dose conversion.

While prescribing has increased dramatically over the last several years, especially compared with other opioids, so has the number of methadone-related deaths relative to deaths associated with other opioids, according to a 2007 report from the National Drug Intelligence Center.

Prescribing this drug requires methadone-specific knowledge and vigilance on the part of the prescriber, as well as a highly responsible patient and/or caregiver who will monitor use and side effects, particularly during titration, according to Dr. Fine, professor of anesthesiology at the Pain Research Center, University of Utah, Salt Lake City.

Potential problems with methadone include drug-drug interactions and cardiac toxicity. Sudden death, even at therapeutic levels, can occur.

Drug-drug interactions can include adverse reactions in patients on monoamine-increasing drugs. Also, serum levels are increased by CYP3A4 and CYP2B6 inhibitors (such as certain antiretrovirals, clarithromycin, itraconazole, erythromycin, fluconazole, grapefruit juice, and more), and this has been associated with multiple overdose deaths, prompting a black-box warning advisory in 2006, Dr. Fine said.

Potential cardiac toxicity is the newest concern; treatment has been shown in some patients to prolong the corrected QT (QTc) interval, and while prescribing guidelines do not yet reflect this, a baseline electrocardiogram is advisable, Dr. Fine said.

According to current guidelines from the American Pain Society–American Academy of Pain Medicine, a reasonable starting dose in most opioid-naive patients is 2.5 mg every 8 hours. Dose increases can begin after a minimum of 10 days. Older patients, or those with renal or hepatic comorbidities, require less frequent dosing, and more cautious dose titration. Methadone treatment is not advisable for breakthrough pain because of its long half-life and variable pharmacokinetics (J. Pain. 2009;10:113-20).

Titration, according to Dr. Fine, should include dose increases of 1-2.5 mg every 8 hours in frail, older patients or patients with a history of sleep apnea, and 2.5-5 mg every 8 hours in robust younger patients. Increases should be made every 5-7 days if needed.

Advise patients or caregivers that:

– Adequate pain relief from methadone may not occur for several days or weeks.

– Methadone should be taken exactly as directed.

– Short-acting rescue medications can be used until sufficient baseline analgesia is achieved.

– Any signs of increased sedations, mental clouding, snoring, or periodic apnea should be called in (supply an emergency phone number).

– No alcohol, benzodiazepines, or other CNS depressants should be used – especially at night – unless specifically prescribed or approved by the physician who prescribed the methadone.

Also, follow up every day during dose titration by a telephone call, through home nursing, or by an office visit, and perform an in-person evaluation weekly until dose stabilization and then monthly thereafter if there are no major ongoing changes in health status, Dr. Fine said.

In-person evaluations should be performed every 3 months once the patient is fully stable, he added.

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King Pharmaceuticals (now Pfizer), Meda Pharmaceuticals, and Purdue Pharma. He is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Methadone can be an effective treatment for chronic pain, but there are a number of concerns that must be considered when prescribing this opioid, Dr. Perry G. Fine said at the Congress of Clinical Rheumatology.

Among the benefits of the effective mu-opioid analgesic with N-methyl-d-aspartate receptor antagonist properties are its low cost, dosing formulation versatility, long duration of action, and favorable metabolic profile. However, it also has highly variable pharmacokinetics, a very long half-life compared with its analgesic duration of action, and nonlinear dose conversion.

While prescribing has increased dramatically over the last several years, especially compared with other opioids, so has the number of methadone-related deaths relative to deaths associated with other opioids, according to a 2007 report from the National Drug Intelligence Center.

Prescribing this drug requires methadone-specific knowledge and vigilance on the part of the prescriber, as well as a highly responsible patient and/or caregiver who will monitor use and side effects, particularly during titration, according to Dr. Fine, professor of anesthesiology at the Pain Research Center, University of Utah, Salt Lake City.

Potential problems with methadone include drug-drug interactions and cardiac toxicity. Sudden death, even at therapeutic levels, can occur.

Drug-drug interactions can include adverse reactions in patients on monoamine-increasing drugs. Also, serum levels are increased by CYP3A4 and CYP2B6 inhibitors (such as certain antiretrovirals, clarithromycin, itraconazole, erythromycin, fluconazole, grapefruit juice, and more), and this has been associated with multiple overdose deaths, prompting a black-box warning advisory in 2006, Dr. Fine said.

Potential cardiac toxicity is the newest concern; treatment has been shown in some patients to prolong the corrected QT (QTc) interval, and while prescribing guidelines do not yet reflect this, a baseline electrocardiogram is advisable, Dr. Fine said.

According to current guidelines from the American Pain Society–American Academy of Pain Medicine, a reasonable starting dose in most opioid-naive patients is 2.5 mg every 8 hours. Dose increases can begin after a minimum of 10 days. Older patients, or those with renal or hepatic comorbidities, require less frequent dosing, and more cautious dose titration. Methadone treatment is not advisable for breakthrough pain because of its long half-life and variable pharmacokinetics (J. Pain. 2009;10:113-20).

Titration, according to Dr. Fine, should include dose increases of 1-2.5 mg every 8 hours in frail, older patients or patients with a history of sleep apnea, and 2.5-5 mg every 8 hours in robust younger patients. Increases should be made every 5-7 days if needed.

Advise patients or caregivers that:

– Adequate pain relief from methadone may not occur for several days or weeks.

– Methadone should be taken exactly as directed.

– Short-acting rescue medications can be used until sufficient baseline analgesia is achieved.

– Any signs of increased sedations, mental clouding, snoring, or periodic apnea should be called in (supply an emergency phone number).

– No alcohol, benzodiazepines, or other CNS depressants should be used – especially at night – unless specifically prescribed or approved by the physician who prescribed the methadone.

Also, follow up every day during dose titration by a telephone call, through home nursing, or by an office visit, and perform an in-person evaluation weekly until dose stabilization and then monthly thereafter if there are no major ongoing changes in health status, Dr. Fine said.

In-person evaluations should be performed every 3 months once the patient is fully stable, he added.

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King Pharmaceuticals (now Pfizer), Meda Pharmaceuticals, and Purdue Pharma. He is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Methadone can be an effective treatment for chronic pain, but there are a number of concerns that must be considered when prescribing this opioid, Dr. Perry G. Fine said at the Congress of Clinical Rheumatology.

Among the benefits of the effective mu-opioid analgesic with N-methyl-d-aspartate receptor antagonist properties are its low cost, dosing formulation versatility, long duration of action, and favorable metabolic profile. However, it also has highly variable pharmacokinetics, a very long half-life compared with its analgesic duration of action, and nonlinear dose conversion.

While prescribing has increased dramatically over the last several years, especially compared with other opioids, so has the number of methadone-related deaths relative to deaths associated with other opioids, according to a 2007 report from the National Drug Intelligence Center.

Prescribing this drug requires methadone-specific knowledge and vigilance on the part of the prescriber, as well as a highly responsible patient and/or caregiver who will monitor use and side effects, particularly during titration, according to Dr. Fine, professor of anesthesiology at the Pain Research Center, University of Utah, Salt Lake City.

Potential problems with methadone include drug-drug interactions and cardiac toxicity. Sudden death, even at therapeutic levels, can occur.

Drug-drug interactions can include adverse reactions in patients on monoamine-increasing drugs. Also, serum levels are increased by CYP3A4 and CYP2B6 inhibitors (such as certain antiretrovirals, clarithromycin, itraconazole, erythromycin, fluconazole, grapefruit juice, and more), and this has been associated with multiple overdose deaths, prompting a black-box warning advisory in 2006, Dr. Fine said.

Potential cardiac toxicity is the newest concern; treatment has been shown in some patients to prolong the corrected QT (QTc) interval, and while prescribing guidelines do not yet reflect this, a baseline electrocardiogram is advisable, Dr. Fine said.

According to current guidelines from the American Pain Society–American Academy of Pain Medicine, a reasonable starting dose in most opioid-naive patients is 2.5 mg every 8 hours. Dose increases can begin after a minimum of 10 days. Older patients, or those with renal or hepatic comorbidities, require less frequent dosing, and more cautious dose titration. Methadone treatment is not advisable for breakthrough pain because of its long half-life and variable pharmacokinetics (J. Pain. 2009;10:113-20).

Titration, according to Dr. Fine, should include dose increases of 1-2.5 mg every 8 hours in frail, older patients or patients with a history of sleep apnea, and 2.5-5 mg every 8 hours in robust younger patients. Increases should be made every 5-7 days if needed.

Advise patients or caregivers that:

– Adequate pain relief from methadone may not occur for several days or weeks.

– Methadone should be taken exactly as directed.

– Short-acting rescue medications can be used until sufficient baseline analgesia is achieved.

– Any signs of increased sedations, mental clouding, snoring, or periodic apnea should be called in (supply an emergency phone number).

– No alcohol, benzodiazepines, or other CNS depressants should be used – especially at night – unless specifically prescribed or approved by the physician who prescribed the methadone.

Also, follow up every day during dose titration by a telephone call, through home nursing, or by an office visit, and perform an in-person evaluation weekly until dose stabilization and then monthly thereafter if there are no major ongoing changes in health status, Dr. Fine said.

In-person evaluations should be performed every 3 months once the patient is fully stable, he added.

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King Pharmaceuticals (now Pfizer), Meda Pharmaceuticals, and Purdue Pharma. He is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Methadone can be an effective treatment for chronic pain, but there are a number of concerns that must be considered when prescribing this opioid, Dr. Perry G. Fine said at the Congress of Clinical Rheumatology.

Among the benefits of the effective mu-opioid analgesic with N-methyl-d-aspartate receptor antagonist properties are its low cost, dosing formulation versatility, long duration of action, and favorable metabolic profile. However, it also has highly variable pharmacokinetics, a very long half-life compared with its analgesic duration of action, and nonlinear dose conversion.

While prescribing has increased dramatically over the last several years, especially compared with other opioids, so has the number of methadone-related deaths relative to deaths associated with other opioids, according to a 2007 report from the National Drug Intelligence Center.

Prescribing this drug requires methadone-specific knowledge and vigilance on the part of the prescriber, as well as a highly responsible patient and/or caregiver who will monitor use and side effects, particularly during titration, according to Dr. Fine, professor of anesthesiology at the Pain Research Center, University of Utah, Salt Lake City.

Potential problems with methadone include drug-drug interactions and cardiac toxicity. Sudden death, even at therapeutic levels, can occur.

Drug-drug interactions can include adverse reactions in patients on monoamine-increasing drugs. Also, serum levels are increased by CYP3A4 and CYP2B6 inhibitors (such as certain antiretrovirals, clarithromycin, itraconazole, erythromycin, fluconazole, grapefruit juice, and more), and this has been associated with multiple overdose deaths, prompting a black-box warning advisory in 2006, Dr. Fine said.

Potential cardiac toxicity is the newest concern; treatment has been shown in some patients to prolong the corrected QT (QTc) interval, and while prescribing guidelines do not yet reflect this, a baseline electrocardiogram is advisable, Dr. Fine said.

According to current guidelines from the American Pain Society–American Academy of Pain Medicine, a reasonable starting dose in most opioid-naive patients is 2.5 mg every 8 hours. Dose increases can begin after a minimum of 10 days. Older patients, or those with renal or hepatic comorbidities, require less frequent dosing, and more cautious dose titration. Methadone treatment is not advisable for breakthrough pain because of its long half-life and variable pharmacokinetics (J. Pain. 2009;10:113-20).

Titration, according to Dr. Fine, should include dose increases of 1-2.5 mg every 8 hours in frail, older patients or patients with a history of sleep apnea, and 2.5-5 mg every 8 hours in robust younger patients. Increases should be made every 5-7 days if needed.

Advise patients or caregivers that:

– Adequate pain relief from methadone may not occur for several days or weeks.

– Methadone should be taken exactly as directed.

– Short-acting rescue medications can be used until sufficient baseline analgesia is achieved.

– Any signs of increased sedations, mental clouding, snoring, or periodic apnea should be called in (supply an emergency phone number).

– No alcohol, benzodiazepines, or other CNS depressants should be used – especially at night – unless specifically prescribed or approved by the physician who prescribed the methadone.

Also, follow up every day during dose titration by a telephone call, through home nursing, or by an office visit, and perform an in-person evaluation weekly until dose stabilization and then monthly thereafter if there are no major ongoing changes in health status, Dr. Fine said.

In-person evaluations should be performed every 3 months once the patient is fully stable, he added.

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King Pharmaceuticals (now Pfizer), Meda Pharmaceuticals, and Purdue Pharma. He is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Methadone can be an effective treatment for chronic pain, but there are a number of concerns that must be considered when prescribing this opioid, Dr. Perry G. Fine said at the Congress of Clinical Rheumatology.

Among the benefits of the effective mu-opioid analgesic with N-methyl-d-aspartate receptor antagonist properties are its low cost, dosing formulation versatility, long duration of action, and favorable metabolic profile. However, it also has highly variable pharmacokinetics, a very long half-life compared with its analgesic duration of action, and nonlinear dose conversion.

While prescribing has increased dramatically over the last several years, especially compared with other opioids, so has the number of methadone-related deaths relative to deaths associated with other opioids, according to a 2007 report from the National Drug Intelligence Center.

Prescribing this drug requires methadone-specific knowledge and vigilance on the part of the prescriber, as well as a highly responsible patient and/or caregiver who will monitor use and side effects, particularly during titration, according to Dr. Fine, professor of anesthesiology at the Pain Research Center, University of Utah, Salt Lake City.

Potential problems with methadone include drug-drug interactions and cardiac toxicity. Sudden death, even at therapeutic levels, can occur.

Drug-drug interactions can include adverse reactions in patients on monoamine-increasing drugs. Also, serum levels are increased by CYP3A4 and CYP2B6 inhibitors (such as certain antiretrovirals, clarithromycin, itraconazole, erythromycin, fluconazole, grapefruit juice, and more), and this has been associated with multiple overdose deaths, prompting a black-box warning advisory in 2006, Dr. Fine said.

Potential cardiac toxicity is the newest concern; treatment has been shown in some patients to prolong the corrected QT (QTc) interval, and while prescribing guidelines do not yet reflect this, a baseline electrocardiogram is advisable, Dr. Fine said.

According to current guidelines from the American Pain Society–American Academy of Pain Medicine, a reasonable starting dose in most opioid-naive patients is 2.5 mg every 8 hours. Dose increases can begin after a minimum of 10 days. Older patients, or those with renal or hepatic comorbidities, require less frequent dosing, and more cautious dose titration. Methadone treatment is not advisable for breakthrough pain because of its long half-life and variable pharmacokinetics (J. Pain. 2009;10:113-20).

Titration, according to Dr. Fine, should include dose increases of 1-2.5 mg every 8 hours in frail, older patients or patients with a history of sleep apnea, and 2.5-5 mg every 8 hours in robust younger patients. Increases should be made every 5-7 days if needed.

Advise patients or caregivers that:

– Adequate pain relief from methadone may not occur for several days or weeks.

– Methadone should be taken exactly as directed.

– Short-acting rescue medications can be used until sufficient baseline analgesia is achieved.

– Any signs of increased sedations, mental clouding, snoring, or periodic apnea should be called in (supply an emergency phone number).

– No alcohol, benzodiazepines, or other CNS depressants should be used – especially at night – unless specifically prescribed or approved by the physician who prescribed the methadone.

Also, follow up every day during dose titration by a telephone call, through home nursing, or by an office visit, and perform an in-person evaluation weekly until dose stabilization and then monthly thereafter if there are no major ongoing changes in health status, Dr. Fine said.

In-person evaluations should be performed every 3 months once the patient is fully stable, he added.

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King Pharmaceuticals (now Pfizer), Meda Pharmaceuticals, and Purdue Pharma. He is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – Methadone can be an effective treatment for chronic pain, but there are a number of concerns that must be considered when prescribing this opioid, Dr. Perry G. Fine said at the Congress of Clinical Rheumatology.

Among the benefits of the effective mu-opioid analgesic with N-methyl-d-aspartate receptor antagonist properties are its low cost, dosing formulation versatility, long duration of action, and favorable metabolic profile. However, it also has highly variable pharmacokinetics, a very long half-life compared with its analgesic duration of action, and nonlinear dose conversion.

While prescribing has increased dramatically over the last several years, especially compared with other opioids, so has the number of methadone-related deaths relative to deaths associated with other opioids, according to a 2007 report from the National Drug Intelligence Center.

Prescribing this drug requires methadone-specific knowledge and vigilance on the part of the prescriber, as well as a highly responsible patient and/or caregiver who will monitor use and side effects, particularly during titration, according to Dr. Fine, professor of anesthesiology at the Pain Research Center, University of Utah, Salt Lake City.

Potential problems with methadone include drug-drug interactions and cardiac toxicity. Sudden death, even at therapeutic levels, can occur.

Drug-drug interactions can include adverse reactions in patients on monoamine-increasing drugs. Also, serum levels are increased by CYP3A4 and CYP2B6 inhibitors (such as certain antiretrovirals, clarithromycin, itraconazole, erythromycin, fluconazole, grapefruit juice, and more), and this has been associated with multiple overdose deaths, prompting a black-box warning advisory in 2006, Dr. Fine said.

Potential cardiac toxicity is the newest concern; treatment has been shown in some patients to prolong the corrected QT (QTc) interval, and while prescribing guidelines do not yet reflect this, a baseline electrocardiogram is advisable, Dr. Fine said.

According to current guidelines from the American Pain Society–American Academy of Pain Medicine, a reasonable starting dose in most opioid-naive patients is 2.5 mg every 8 hours. Dose increases can begin after a minimum of 10 days. Older patients, or those with renal or hepatic comorbidities, require less frequent dosing, and more cautious dose titration. Methadone treatment is not advisable for breakthrough pain because of its long half-life and variable pharmacokinetics (J. Pain. 2009;10:113-20).

Titration, according to Dr. Fine, should include dose increases of 1-2.5 mg every 8 hours in frail, older patients or patients with a history of sleep apnea, and 2.5-5 mg every 8 hours in robust younger patients. Increases should be made every 5-7 days if needed.

Advise patients or caregivers that:

– Adequate pain relief from methadone may not occur for several days or weeks.

– Methadone should be taken exactly as directed.

– Short-acting rescue medications can be used until sufficient baseline analgesia is achieved.

– Any signs of increased sedations, mental clouding, snoring, or periodic apnea should be called in (supply an emergency phone number).

– No alcohol, benzodiazepines, or other CNS depressants should be used – especially at night – unless specifically prescribed or approved by the physician who prescribed the methadone.

Also, follow up every day during dose titration by a telephone call, through home nursing, or by an office visit, and perform an in-person evaluation weekly until dose stabilization and then monthly thereafter if there are no major ongoing changes in health status, Dr. Fine said.

In-person evaluations should be performed every 3 months once the patient is fully stable, he added.

Dr. Fine has served as an advisory board member for Ameritox, Covidien, King Pharmaceuticals (now Pfizer), Meda Pharmaceuticals, and Purdue Pharma. He is a consultant for Cephalon and Johnson & Johnson.

DESTIN, FLA. – A conservative approach is best when it comes to making a diagnosis of Behçet’s disease, Dr. Kenneth Calamia said at the Congress of Clinical Rheumatology.

Although oral and genital ulcers are common in the disease, they also are a common manifestation of many other conditions, and it is important to consider the other possible causes first.

The importance of a Behçet’s diagnosis doesn’t have anything to do with ulcers – it has to do with the risk or presence of serious manifestations, including vascular disease, central nervous system manifestations, and uveitis, said Dr. Calamia of the department of medicine at the Mayo Clinic in Jacksonville, Fla.

"You don’t want to [needlessly] give a patient the baggage of that diagnosis," he said, noting that in patients diagnosed with Behçet’s, everything will be attributed to the disease for the rest of their lives.

In the United States and Europe, true Behçet’s is quite rare (about 0.3-7.5 cases/100,000 population), compared with places like Turkey and other "Silk Road" areas, which have a very high prevalence (100-370 cases/100,000 population). In those areas, more severe forms are much more prevalent, and the benign mucocutaneous symptoms that comprise most of the cases in America are referred to as American Behçet’s disease, Dr. Calamia said.

The term "Behçet’s syndrome" also can be used to describe the types of cases typically seen in the United States, but in many cases, the diagnosis is actually "complex aphthosis," he said, adding that Behçet’s treatment principles can nonetheless be used to help patients with this condition.

Complex aphthosis is a term used by oral dermatologists to help classify types of recurrent aphthous stomatitis. As opposed to simple aphthosis, which is characterized by episodic, short-lived lesions that are few in number, recur three to six times per year, and tend to affect nonkeratinized mucosa, complex aphthosis lesions can be continuous, numerous, large, slow-healing, and debilitating.

Keep in mind that both simple and complex aphthosis can be associated with menstruation, sprue, inflammatory bowel disease, HIV, hematologic disorders (such as cyclic neutropenia, IgA deficiency, myelodysplasia/myeloproliferation), various deficiencies (B vitamins, folate, iron, and zinc), and smoking cessation, Dr. Calamia said, explaining that smoking tends to increase keratinization, which protects against ulcers, and that protection is lost when a patient quits.

In a study conducted by an oral dermatologist several years ago, only 9% of 269 patients with severe complex aphthosis – 16% of whom also had genital ulcers – had a Behçet’s diagnosis, he noted.

Some other diagnoses in the cohort included anemia in 25%, gastrointestinal disease in 16%, hematologic disorders in 5%, mucosal disease in 6%, smoking discontinuation in 4%, and drug-related ulcers in 3%.

"[Complex aphthosis] is the diagnosis I prefer in those who have mouth and genital ulcers, but nothing else to support a diagnosis of Behçet’s," he said.

Consider the other possible causes of the ulcers, and also consider the differential diagnoses for recurrent aphthous stomatitis, which include recurrent intraoral herpes simplex virus, Wegener’s granulomatosis, oral Crohn’s disease, pyostomatitis vegetans, erythema multiforme, lichen planus, mucous membrane pemphigoid, and pemphigus vulgaris, he said.

A diffuse, widespread, and chronic presentation, which is not characteristic of recurrent aphthous stomatitis or Behçet’s, can help differentiate between those conditions and these differential diagnoses, he said.

Dr. Calamia disclosed that he has received research support from Genentech and Celgene, and has served on an advisory board for Centocor.

DESTIN, FLA. – A conservative approach is best when it comes to making a diagnosis of Behçet’s disease, Dr. Kenneth Calamia said at the Congress of Clinical Rheumatology.

Although oral and genital ulcers are common in the disease, they also are a common manifestation of many other conditions, and it is important to consider the other possible causes first.

The importance of a Behçet’s diagnosis doesn’t have anything to do with ulcers – it has to do with the risk or presence of serious manifestations, including vascular disease, central nervous system manifestations, and uveitis, said Dr. Calamia of the department of medicine at the Mayo Clinic in Jacksonville, Fla.

"You don’t want to [needlessly] give a patient the baggage of that diagnosis," he said, noting that in patients diagnosed with Behçet’s, everything will be attributed to the disease for the rest of their lives.

In the United States and Europe, true Behçet’s is quite rare (about 0.3-7.5 cases/100,000 population), compared with places like Turkey and other "Silk Road" areas, which have a very high prevalence (100-370 cases/100,000 population). In those areas, more severe forms are much more prevalent, and the benign mucocutaneous symptoms that comprise most of the cases in America are referred to as American Behçet’s disease, Dr. Calamia said.

The term "Behçet’s syndrome" also can be used to describe the types of cases typically seen in the United States, but in many cases, the diagnosis is actually "complex aphthosis," he said, adding that Behçet’s treatment principles can nonetheless be used to help patients with this condition.

Complex aphthosis is a term used by oral dermatologists to help classify types of recurrent aphthous stomatitis. As opposed to simple aphthosis, which is characterized by episodic, short-lived lesions that are few in number, recur three to six times per year, and tend to affect nonkeratinized mucosa, complex aphthosis lesions can be continuous, numerous, large, slow-healing, and debilitating.

Keep in mind that both simple and complex aphthosis can be associated with menstruation, sprue, inflammatory bowel disease, HIV, hematologic disorders (such as cyclic neutropenia, IgA deficiency, myelodysplasia/myeloproliferation), various deficiencies (B vitamins, folate, iron, and zinc), and smoking cessation, Dr. Calamia said, explaining that smoking tends to increase keratinization, which protects against ulcers, and that protection is lost when a patient quits.

In a study conducted by an oral dermatologist several years ago, only 9% of 269 patients with severe complex aphthosis – 16% of whom also had genital ulcers – had a Behçet’s diagnosis, he noted.

Some other diagnoses in the cohort included anemia in 25%, gastrointestinal disease in 16%, hematologic disorders in 5%, mucosal disease in 6%, smoking discontinuation in 4%, and drug-related ulcers in 3%.

"[Complex aphthosis] is the diagnosis I prefer in those who have mouth and genital ulcers, but nothing else to support a diagnosis of Behçet’s," he said.

Consider the other possible causes of the ulcers, and also consider the differential diagnoses for recurrent aphthous stomatitis, which include recurrent intraoral herpes simplex virus, Wegener’s granulomatosis, oral Crohn’s disease, pyostomatitis vegetans, erythema multiforme, lichen planus, mucous membrane pemphigoid, and pemphigus vulgaris, he said.

A diffuse, widespread, and chronic presentation, which is not characteristic of recurrent aphthous stomatitis or Behçet’s, can help differentiate between those conditions and these differential diagnoses, he said.

Dr. Calamia disclosed that he has received research support from Genentech and Celgene, and has served on an advisory board for Centocor.

DESTIN, FLA. – A conservative approach is best when it comes to making a diagnosis of Behçet’s disease, Dr. Kenneth Calamia said at the Congress of Clinical Rheumatology.

Although oral and genital ulcers are common in the disease, they also are a common manifestation of many other conditions, and it is important to consider the other possible causes first.

The importance of a Behçet’s diagnosis doesn’t have anything to do with ulcers – it has to do with the risk or presence of serious manifestations, including vascular disease, central nervous system manifestations, and uveitis, said Dr. Calamia of the department of medicine at the Mayo Clinic in Jacksonville, Fla.

"You don’t want to [needlessly] give a patient the baggage of that diagnosis," he said, noting that in patients diagnosed with Behçet’s, everything will be attributed to the disease for the rest of their lives.

In the United States and Europe, true Behçet’s is quite rare (about 0.3-7.5 cases/100,000 population), compared with places like Turkey and other "Silk Road" areas, which have a very high prevalence (100-370 cases/100,000 population). In those areas, more severe forms are much more prevalent, and the benign mucocutaneous symptoms that comprise most of the cases in America are referred to as American Behçet’s disease, Dr. Calamia said.

The term "Behçet’s syndrome" also can be used to describe the types of cases typically seen in the United States, but in many cases, the diagnosis is actually "complex aphthosis," he said, adding that Behçet’s treatment principles can nonetheless be used to help patients with this condition.

Complex aphthosis is a term used by oral dermatologists to help classify types of recurrent aphthous stomatitis. As opposed to simple aphthosis, which is characterized by episodic, short-lived lesions that are few in number, recur three to six times per year, and tend to affect nonkeratinized mucosa, complex aphthosis lesions can be continuous, numerous, large, slow-healing, and debilitating.

Keep in mind that both simple and complex aphthosis can be associated with menstruation, sprue, inflammatory bowel disease, HIV, hematologic disorders (such as cyclic neutropenia, IgA deficiency, myelodysplasia/myeloproliferation), various deficiencies (B vitamins, folate, iron, and zinc), and smoking cessation, Dr. Calamia said, explaining that smoking tends to increase keratinization, which protects against ulcers, and that protection is lost when a patient quits.

In a study conducted by an oral dermatologist several years ago, only 9% of 269 patients with severe complex aphthosis – 16% of whom also had genital ulcers – had a Behçet’s diagnosis, he noted.

Some other diagnoses in the cohort included anemia in 25%, gastrointestinal disease in 16%, hematologic disorders in 5%, mucosal disease in 6%, smoking discontinuation in 4%, and drug-related ulcers in 3%.

"[Complex aphthosis] is the diagnosis I prefer in those who have mouth and genital ulcers, but nothing else to support a diagnosis of Behçet’s," he said.

Consider the other possible causes of the ulcers, and also consider the differential diagnoses for recurrent aphthous stomatitis, which include recurrent intraoral herpes simplex virus, Wegener’s granulomatosis, oral Crohn’s disease, pyostomatitis vegetans, erythema multiforme, lichen planus, mucous membrane pemphigoid, and pemphigus vulgaris, he said.

A diffuse, widespread, and chronic presentation, which is not characteristic of recurrent aphthous stomatitis or Behçet’s, can help differentiate between those conditions and these differential diagnoses, he said.

Dr. Calamia disclosed that he has received research support from Genentech and Celgene, and has served on an advisory board for Centocor.

DESTIN, FLA. – A conservative approach is best when it comes to making a diagnosis of Behçet’s disease, Dr. Kenneth Calamia said at the Congress of Clinical Rheumatology.

Although oral and genital ulcers are common in the disease, they also are a common manifestation of many other conditions, and it is important to consider the other possible causes first.

The importance of a Behçet’s diagnosis doesn’t have anything to do with ulcers – it has to do with the risk or presence of serious manifestations, including vascular disease, central nervous system manifestations, and uveitis, said Dr. Calamia of the department of medicine at the Mayo Clinic in Jacksonville, Fla.

"You don’t want to [needlessly] give a patient the baggage of that diagnosis," he said, noting that in patients diagnosed with Behçet’s, everything will be attributed to the disease for the rest of their lives.

In the United States and Europe, true Behçet’s is quite rare (about 0.3-7.5 cases/100,000 population), compared with places like Turkey and other "Silk Road" areas, which have a very high prevalence (100-370 cases/100,000 population). In those areas, more severe forms are much more prevalent, and the benign mucocutaneous symptoms that comprise most of the cases in America are referred to as American Behçet’s disease, Dr. Calamia said.

The term "Behçet’s syndrome" also can be used to describe the types of cases typically seen in the United States, but in many cases, the diagnosis is actually "complex aphthosis," he said, adding that Behçet’s treatment principles can nonetheless be used to help patients with this condition.

Complex aphthosis is a term used by oral dermatologists to help classify types of recurrent aphthous stomatitis. As opposed to simple aphthosis, which is characterized by episodic, short-lived lesions that are few in number, recur three to six times per year, and tend to affect nonkeratinized mucosa, complex aphthosis lesions can be continuous, numerous, large, slow-healing, and debilitating.

Keep in mind that both simple and complex aphthosis can be associated with menstruation, sprue, inflammatory bowel disease, HIV, hematologic disorders (such as cyclic neutropenia, IgA deficiency, myelodysplasia/myeloproliferation), various deficiencies (B vitamins, folate, iron, and zinc), and smoking cessation, Dr. Calamia said, explaining that smoking tends to increase keratinization, which protects against ulcers, and that protection is lost when a patient quits.

In a study conducted by an oral dermatologist several years ago, only 9% of 269 patients with severe complex aphthosis – 16% of whom also had genital ulcers – had a Behçet’s diagnosis, he noted.

Some other diagnoses in the cohort included anemia in 25%, gastrointestinal disease in 16%, hematologic disorders in 5%, mucosal disease in 6%, smoking discontinuation in 4%, and drug-related ulcers in 3%.

"[Complex aphthosis] is the diagnosis I prefer in those who have mouth and genital ulcers, but nothing else to support a diagnosis of Behçet’s," he said.

Consider the other possible causes of the ulcers, and also consider the differential diagnoses for recurrent aphthous stomatitis, which include recurrent intraoral herpes simplex virus, Wegener’s granulomatosis, oral Crohn’s disease, pyostomatitis vegetans, erythema multiforme, lichen planus, mucous membrane pemphigoid, and pemphigus vulgaris, he said.

A diffuse, widespread, and chronic presentation, which is not characteristic of recurrent aphthous stomatitis or Behçet’s, can help differentiate between those conditions and these differential diagnoses, he said.

Dr. Calamia disclosed that he has received research support from Genentech and Celgene, and has served on an advisory board for Centocor.

DESTIN, FLA. – A conservative approach is best when it comes to making a diagnosis of Behçet’s disease, Dr. Kenneth Calamia said at the Congress of Clinical Rheumatology.

Although oral and genital ulcers are common in the disease, they also are a common manifestation of many other conditions, and it is important to consider the other possible causes first.

The importance of a Behçet’s diagnosis doesn’t have anything to do with ulcers – it has to do with the risk or presence of serious manifestations, including vascular disease, central nervous system manifestations, and uveitis, said Dr. Calamia of the department of medicine at the Mayo Clinic in Jacksonville, Fla.

"You don’t want to [needlessly] give a patient the baggage of that diagnosis," he said, noting that in patients diagnosed with Behçet’s, everything will be attributed to the disease for the rest of their lives.

In the United States and Europe, true Behçet’s is quite rare (about 0.3-7.5 cases/100,000 population), compared with places like Turkey and other "Silk Road" areas, which have a very high prevalence (100-370 cases/100,000 population). In those areas, more severe forms are much more prevalent, and the benign mucocutaneous symptoms that comprise most of the cases in America are referred to as American Behçet’s disease, Dr. Calamia said.

The term "Behçet’s syndrome" also can be used to describe the types of cases typically seen in the United States, but in many cases, the diagnosis is actually "complex aphthosis," he said, adding that Behçet’s treatment principles can nonetheless be used to help patients with this condition.

Complex aphthosis is a term used by oral dermatologists to help classify types of recurrent aphthous stomatitis. As opposed to simple aphthosis, which is characterized by episodic, short-lived lesions that are few in number, recur three to six times per year, and tend to affect nonkeratinized mucosa, complex aphthosis lesions can be continuous, numerous, large, slow-healing, and debilitating.

Keep in mind that both simple and complex aphthosis can be associated with menstruation, sprue, inflammatory bowel disease, HIV, hematologic disorders (such as cyclic neutropenia, IgA deficiency, myelodysplasia/myeloproliferation), various deficiencies (B vitamins, folate, iron, and zinc), and smoking cessation, Dr. Calamia said, explaining that smoking tends to increase keratinization, which protects against ulcers, and that protection is lost when a patient quits.

In a study conducted by an oral dermatologist several years ago, only 9% of 269 patients with severe complex aphthosis – 16% of whom also had genital ulcers – had a Behçet’s diagnosis, he noted.

Some other diagnoses in the cohort included anemia in 25%, gastrointestinal disease in 16%, hematologic disorders in 5%, mucosal disease in 6%, smoking discontinuation in 4%, and drug-related ulcers in 3%.

"[Complex aphthosis] is the diagnosis I prefer in those who have mouth and genital ulcers, but nothing else to support a diagnosis of Behçet’s," he said.

Consider the other possible causes of the ulcers, and also consider the differential diagnoses for recurrent aphthous stomatitis, which include recurrent intraoral herpes simplex virus, Wegener’s granulomatosis, oral Crohn’s disease, pyostomatitis vegetans, erythema multiforme, lichen planus, mucous membrane pemphigoid, and pemphigus vulgaris, he said.

A diffuse, widespread, and chronic presentation, which is not characteristic of recurrent aphthous stomatitis or Behçet’s, can help differentiate between those conditions and these differential diagnoses, he said.

Dr. Calamia disclosed that he has received research support from Genentech and Celgene, and has served on an advisory board for Centocor.

DESTIN, FLA. – A conservative approach is best when it comes to making a diagnosis of Behçet’s disease, Dr. Kenneth Calamia said at the Congress of Clinical Rheumatology.

Although oral and genital ulcers are common in the disease, they also are a common manifestation of many other conditions, and it is important to consider the other possible causes first.

The importance of a Behçet’s diagnosis doesn’t have anything to do with ulcers – it has to do with the risk or presence of serious manifestations, including vascular disease, central nervous system manifestations, and uveitis, said Dr. Calamia of the department of medicine at the Mayo Clinic in Jacksonville, Fla.

"You don’t want to [needlessly] give a patient the baggage of that diagnosis," he said, noting that in patients diagnosed with Behçet’s, everything will be attributed to the disease for the rest of their lives.

In the United States and Europe, true Behçet’s is quite rare (about 0.3-7.5 cases/100,000 population), compared with places like Turkey and other "Silk Road" areas, which have a very high prevalence (100-370 cases/100,000 population). In those areas, more severe forms are much more prevalent, and the benign mucocutaneous symptoms that comprise most of the cases in America are referred to as American Behçet’s disease, Dr. Calamia said.

The term "Behçet’s syndrome" also can be used to describe the types of cases typically seen in the United States, but in many cases, the diagnosis is actually "complex aphthosis," he said, adding that Behçet’s treatment principles can nonetheless be used to help patients with this condition.

Complex aphthosis is a term used by oral dermatologists to help classify types of recurrent aphthous stomatitis. As opposed to simple aphthosis, which is characterized by episodic, short-lived lesions that are few in number, recur three to six times per year, and tend to affect nonkeratinized mucosa, complex aphthosis lesions can be continuous, numerous, large, slow-healing, and debilitating.

Keep in mind that both simple and complex aphthosis can be associated with menstruation, sprue, inflammatory bowel disease, HIV, hematologic disorders (such as cyclic neutropenia, IgA deficiency, myelodysplasia/myeloproliferation), various deficiencies (B vitamins, folate, iron, and zinc), and smoking cessation, Dr. Calamia said, explaining that smoking tends to increase keratinization, which protects against ulcers, and that protection is lost when a patient quits.

In a study conducted by an oral dermatologist several years ago, only 9% of 269 patients with severe complex aphthosis – 16% of whom also had genital ulcers – had a Behçet’s diagnosis, he noted.

Some other diagnoses in the cohort included anemia in 25%, gastrointestinal disease in 16%, hematologic disorders in 5%, mucosal disease in 6%, smoking discontinuation in 4%, and drug-related ulcers in 3%.

"[Complex aphthosis] is the diagnosis I prefer in those who have mouth and genital ulcers, but nothing else to support a diagnosis of Behçet’s," he said.

Consider the other possible causes of the ulcers, and also consider the differential diagnoses for recurrent aphthous stomatitis, which include recurrent intraoral herpes simplex virus, Wegener’s granulomatosis, oral Crohn’s disease, pyostomatitis vegetans, erythema multiforme, lichen planus, mucous membrane pemphigoid, and pemphigus vulgaris, he said.

A diffuse, widespread, and chronic presentation, which is not characteristic of recurrent aphthous stomatitis or Behçet’s, can help differentiate between those conditions and these differential diagnoses, he said.

Dr. Calamia disclosed that he has received research support from Genentech and Celgene, and has served on an advisory board for Centocor.