Susan E. Meadows, MLS

Evidence summary

The influence of cigarette smoking on the development of CHD has been well documented.^1,2 RR ranges from 1.5 to 3, depending on variables such as age, sex, and quantity of tobacco used.³ Quitting smoking reduces overall mortality more than other forms of secondary prevention, including aspirin, β-blockers, angiotensin-converting enzyme inhibitors, and cholesterol-lowering statins.³ In the wake of such evidence-based findings, the American Heart Association and American College of Cardiology Task Force developed clinical practice guidelines that recommend complete smoking cessation for secondary prevention of CHD in cardiac patients.⁴

0 cigarettes=lower mortality and morbidity

A Cochrane Heart Group meta-analysis examining all-cause CHD mortality in 20 cohort studies (n=12,603 patients), found a 36% reduction in mortality risk for CHD patients who quit smoking compared with those who didn’t (RR=0.64; 95% confidence interval [CI], 0.58-0.71).³ The review also noted a reduction in risk for nonfatal myocardial infarctions (RR=0.68; 95% CI, 0.57-0.82).³ The authors didn’t report how soon after smoking cessation mortality risk declined.

The authors acknowledge several limitations of the review, including the use of observational data and crude estimates, as well as potential publication bias and the misclassification of smoking status. Notably, however, their findings are consistent with the landmark prospective, community-based cohort Framingham Heart Study (N=1422), which indicates that smoking status predicts overall and morbidity-free survival at age 85.⁵

Smoking cessation has also been found to significantly affect morbidity among cardiac patients. Short-term benefits have been demonstrated in CHD patients after a myocardial infarction or coronary artery revascularization.⁶ Smoking status at 1-year follow-up was associated with a significant reduction in subsequent cardiac events (myocardial infarction, ischemic cerebrovascular event, revascularization, or death from CHD) when smokers who quit after an initial CHD event were compared with continuing smokers (odds ratio=0.71; 95% CI, 0.38-1.33).⁶

Going the distance is worth it

Regarding the role of extended abstinence on subsequent cardiac events, long-term quit status in post-coronary artery bypass graft (CABG) surgery patients has been found to predict decreased morbidity and lower rates of repeat revascularization surgery. Findings from the Coronary Artery Surgery Study show that, at 10-year follow-up, nonsmokers were more likely to be free of angina (54% of nonsmokers vs 42% of smokers; P=.02, NNT=8.3) and less likely to experience moderate to severe physical limitations (13% of non-smokers vs 24% of smokers; P=.0004; NNT=9.1). Nonsmokers also had fewer CHD-related admissions than smokers (2.6 vs 3.8; P<.0001).⁷

Another study found similar results at 20-year follow-up: Patients who had quit smoking underwent fewer repeat CABGs than smokers (RR=1.41; 95% CI, 1.02-1.94).⁸ The difference between post-CABG survival curves for quitters versus smokers increased from 3% at 5 years (98% vs 95%) to 15% at 15 years (70% vs 55%; P<.0001; NNT=6.7).⁸

Recommendations

The US Department of Health and Human Services recommends smoking cessation as an integral part of both primary and secondary prevention of CHD. Quitting reduces development of atherosclerosis and lowers the incidence of initial and recurrent myocardial infarction, thrombosis, cardiac arrhythmia, and death from cardiovascular causes.²

Evidence summary

The influence of cigarette smoking on the development of CHD has been well documented.^1,2 RR ranges from 1.5 to 3, depending on variables such as age, sex, and quantity of tobacco used.³ Quitting smoking reduces overall mortality more than other forms of secondary prevention, including aspirin, β-blockers, angiotensin-converting enzyme inhibitors, and cholesterol-lowering statins.³ In the wake of such evidence-based findings, the American Heart Association and American College of Cardiology Task Force developed clinical practice guidelines that recommend complete smoking cessation for secondary prevention of CHD in cardiac patients.⁴

0 cigarettes=lower mortality and morbidity

A Cochrane Heart Group meta-analysis examining all-cause CHD mortality in 20 cohort studies (n=12,603 patients), found a 36% reduction in mortality risk for CHD patients who quit smoking compared with those who didn’t (RR=0.64; 95% confidence interval [CI], 0.58-0.71).³ The review also noted a reduction in risk for nonfatal myocardial infarctions (RR=0.68; 95% CI, 0.57-0.82).³ The authors didn’t report how soon after smoking cessation mortality risk declined.

The authors acknowledge several limitations of the review, including the use of observational data and crude estimates, as well as potential publication bias and the misclassification of smoking status. Notably, however, their findings are consistent with the landmark prospective, community-based cohort Framingham Heart Study (N=1422), which indicates that smoking status predicts overall and morbidity-free survival at age 85.⁵

Smoking cessation has also been found to significantly affect morbidity among cardiac patients. Short-term benefits have been demonstrated in CHD patients after a myocardial infarction or coronary artery revascularization.⁶ Smoking status at 1-year follow-up was associated with a significant reduction in subsequent cardiac events (myocardial infarction, ischemic cerebrovascular event, revascularization, or death from CHD) when smokers who quit after an initial CHD event were compared with continuing smokers (odds ratio=0.71; 95% CI, 0.38-1.33).⁶

Going the distance is worth it

Regarding the role of extended abstinence on subsequent cardiac events, long-term quit status in post-coronary artery bypass graft (CABG) surgery patients has been found to predict decreased morbidity and lower rates of repeat revascularization surgery. Findings from the Coronary Artery Surgery Study show that, at 10-year follow-up, nonsmokers were more likely to be free of angina (54% of nonsmokers vs 42% of smokers; P=.02, NNT=8.3) and less likely to experience moderate to severe physical limitations (13% of non-smokers vs 24% of smokers; P=.0004; NNT=9.1). Nonsmokers also had fewer CHD-related admissions than smokers (2.6 vs 3.8; P<.0001).⁷

Another study found similar results at 20-year follow-up: Patients who had quit smoking underwent fewer repeat CABGs than smokers (RR=1.41; 95% CI, 1.02-1.94).⁸ The difference between post-CABG survival curves for quitters versus smokers increased from 3% at 5 years (98% vs 95%) to 15% at 15 years (70% vs 55%; P<.0001; NNT=6.7).⁸

Recommendations

The US Department of Health and Human Services recommends smoking cessation as an integral part of both primary and secondary prevention of CHD. Quitting reduces development of atherosclerosis and lowers the incidence of initial and recurrent myocardial infarction, thrombosis, cardiac arrhythmia, and death from cardiovascular causes.²

Evidence summary

The influence of cigarette smoking on the development of CHD has been well documented.^1,2 RR ranges from 1.5 to 3, depending on variables such as age, sex, and quantity of tobacco used.³ Quitting smoking reduces overall mortality more than other forms of secondary prevention, including aspirin, β-blockers, angiotensin-converting enzyme inhibitors, and cholesterol-lowering statins.³ In the wake of such evidence-based findings, the American Heart Association and American College of Cardiology Task Force developed clinical practice guidelines that recommend complete smoking cessation for secondary prevention of CHD in cardiac patients.⁴

0 cigarettes=lower mortality and morbidity

A Cochrane Heart Group meta-analysis examining all-cause CHD mortality in 20 cohort studies (n=12,603 patients), found a 36% reduction in mortality risk for CHD patients who quit smoking compared with those who didn’t (RR=0.64; 95% confidence interval [CI], 0.58-0.71).³ The review also noted a reduction in risk for nonfatal myocardial infarctions (RR=0.68; 95% CI, 0.57-0.82).³ The authors didn’t report how soon after smoking cessation mortality risk declined.

The authors acknowledge several limitations of the review, including the use of observational data and crude estimates, as well as potential publication bias and the misclassification of smoking status. Notably, however, their findings are consistent with the landmark prospective, community-based cohort Framingham Heart Study (N=1422), which indicates that smoking status predicts overall and morbidity-free survival at age 85.⁵

Smoking cessation has also been found to significantly affect morbidity among cardiac patients. Short-term benefits have been demonstrated in CHD patients after a myocardial infarction or coronary artery revascularization.⁶ Smoking status at 1-year follow-up was associated with a significant reduction in subsequent cardiac events (myocardial infarction, ischemic cerebrovascular event, revascularization, or death from CHD) when smokers who quit after an initial CHD event were compared with continuing smokers (odds ratio=0.71; 95% CI, 0.38-1.33).⁶

Going the distance is worth it

Regarding the role of extended abstinence on subsequent cardiac events, long-term quit status in post-coronary artery bypass graft (CABG) surgery patients has been found to predict decreased morbidity and lower rates of repeat revascularization surgery. Findings from the Coronary Artery Surgery Study show that, at 10-year follow-up, nonsmokers were more likely to be free of angina (54% of nonsmokers vs 42% of smokers; P=.02, NNT=8.3) and less likely to experience moderate to severe physical limitations (13% of non-smokers vs 24% of smokers; P=.0004; NNT=9.1). Nonsmokers also had fewer CHD-related admissions than smokers (2.6 vs 3.8; P<.0001).⁷

Another study found similar results at 20-year follow-up: Patients who had quit smoking underwent fewer repeat CABGs than smokers (RR=1.41; 95% CI, 1.02-1.94).⁸ The difference between post-CABG survival curves for quitters versus smokers increased from 3% at 5 years (98% vs 95%) to 15% at 15 years (70% vs 55%; P<.0001; NNT=6.7).⁸

Recommendations

The US Department of Health and Human Services recommends smoking cessation as an integral part of both primary and secondary prevention of CHD. Quitting reduces development of atherosclerosis and lowers the incidence of initial and recurrent myocardial infarction, thrombosis, cardiac arrhythmia, and death from cardiovascular causes.²

Evidence summary

Prevalence and types

In areas where iodine supplementation is routine, the prevalence of goiter is estimated to be 4% to 7%; however, autopsy studies show a 50% prevalence of nodules, most of which are multinodular goiter.¹ Multinodular goiter is diagnosed in up to 5% of the general population and can be classified as euthyroid (“nontoxic”), hypothyroid, or hyperthyroid (“toxic”).¹ Multinodular goiter is the most common diagnosis in cases of euthyroid goiter, but other conditions such as diffuse goiter (often idiopathic), thyroiditis, and neoplasms can also present in a euthyroid state.

Diagnosis: Exam and imaging

Studies show variable correlation between physical exam findings and findings on imaging studies. In a retrospective chart review, ultrasound findings differed from clinical exam findings in 63% of cases.² Thyroid ultrasound is less expensive and less invasive than other imaging modalities, provides excellent visualization of thyroid structure and the nature of cysts and nodules, and allows for estimation of thyroid size.

Computed tomography and magnetic resonance imaging perform better for visualization of extension of thyroid tissue substernally and are also preferred for evaluation of the neck in cases of severe local complications of goiter, such as compressive symptoms.³

The malignant potential in multinodular goiter (2%–4%) is similar to that of solitary nodules (4%–6%).³ Therefore, any dominant nodule in a multinodular goiter should be evaluated the same way one would evaluate a solitary nodule.

Treatment and follow-up

Patients with a reassuring initial work-up can be followed clinically and should be assessed with serial clinical evaluations. No evidence could be found regarding optimal intervals for examination and testing; yearly exams and TSH testing are considered adequate by some experts.⁴

Because a few non-benign conditions such as thyroiditis and neoplasm can sometimes present in a euthyroid state, the clinician should be alert for any physical exam or laboratory changes. If any changes occur, then further workup is indicated.

Suppressive therapy with thyroxine is an option for decreasing thyroid size in euthyroid goiter, but this therapy remains controversial. One placebo-controlled trial of thyroid suppression in nontoxic multinodular goiter showed regression of thyroid size with suppressive therapy (58% reduction in size in treatment group vs 5% reduction in control group). However, not all goiters responded to this therapy, and the thyroid size returned to pretreatment size within 9 months of discontinuation of suppressive therapy.⁵

Many experts argue against the use of suppressive therapy in long-standing goiters, citing less response from these patients, along with concern about side effects and possible oversuppression, but the evidence in this area is limited. Patients who are treated with thyroxine should be followed for possible side effects of the medication, including arrhythmia and osteopenia, particularly in elderly patients and those who take the medication for long periods.

Recommendations of others

Guidelines from the American Association of Clinical Endocrinology’s Task Force on Thyroid Nodules, released in 2006, recommends ultrasound be used routinely in the case of multinodular goiter to assist with diagnosis, detect suspicious nodules that may require biopsy, and to serve as an objective baseline measure. This group recommends against use of suppression therapy in long-standing goiters.⁶

Evidence summary

Prevalence and types

In areas where iodine supplementation is routine, the prevalence of goiter is estimated to be 4% to 7%; however, autopsy studies show a 50% prevalence of nodules, most of which are multinodular goiter.¹ Multinodular goiter is diagnosed in up to 5% of the general population and can be classified as euthyroid (“nontoxic”), hypothyroid, or hyperthyroid (“toxic”).¹ Multinodular goiter is the most common diagnosis in cases of euthyroid goiter, but other conditions such as diffuse goiter (often idiopathic), thyroiditis, and neoplasms can also present in a euthyroid state.

Diagnosis: Exam and imaging

Studies show variable correlation between physical exam findings and findings on imaging studies. In a retrospective chart review, ultrasound findings differed from clinical exam findings in 63% of cases.² Thyroid ultrasound is less expensive and less invasive than other imaging modalities, provides excellent visualization of thyroid structure and the nature of cysts and nodules, and allows for estimation of thyroid size.

Computed tomography and magnetic resonance imaging perform better for visualization of extension of thyroid tissue substernally and are also preferred for evaluation of the neck in cases of severe local complications of goiter, such as compressive symptoms.³

The malignant potential in multinodular goiter (2%–4%) is similar to that of solitary nodules (4%–6%).³ Therefore, any dominant nodule in a multinodular goiter should be evaluated the same way one would evaluate a solitary nodule.

Treatment and follow-up

Patients with a reassuring initial work-up can be followed clinically and should be assessed with serial clinical evaluations. No evidence could be found regarding optimal intervals for examination and testing; yearly exams and TSH testing are considered adequate by some experts.⁴

Because a few non-benign conditions such as thyroiditis and neoplasm can sometimes present in a euthyroid state, the clinician should be alert for any physical exam or laboratory changes. If any changes occur, then further workup is indicated.

Suppressive therapy with thyroxine is an option for decreasing thyroid size in euthyroid goiter, but this therapy remains controversial. One placebo-controlled trial of thyroid suppression in nontoxic multinodular goiter showed regression of thyroid size with suppressive therapy (58% reduction in size in treatment group vs 5% reduction in control group). However, not all goiters responded to this therapy, and the thyroid size returned to pretreatment size within 9 months of discontinuation of suppressive therapy.⁵

Many experts argue against the use of suppressive therapy in long-standing goiters, citing less response from these patients, along with concern about side effects and possible oversuppression, but the evidence in this area is limited. Patients who are treated with thyroxine should be followed for possible side effects of the medication, including arrhythmia and osteopenia, particularly in elderly patients and those who take the medication for long periods.

Recommendations of others

Guidelines from the American Association of Clinical Endocrinology’s Task Force on Thyroid Nodules, released in 2006, recommends ultrasound be used routinely in the case of multinodular goiter to assist with diagnosis, detect suspicious nodules that may require biopsy, and to serve as an objective baseline measure. This group recommends against use of suppression therapy in long-standing goiters.⁶

Evidence summary

Prevalence and types

In areas where iodine supplementation is routine, the prevalence of goiter is estimated to be 4% to 7%; however, autopsy studies show a 50% prevalence of nodules, most of which are multinodular goiter.¹ Multinodular goiter is diagnosed in up to 5% of the general population and can be classified as euthyroid (“nontoxic”), hypothyroid, or hyperthyroid (“toxic”).¹ Multinodular goiter is the most common diagnosis in cases of euthyroid goiter, but other conditions such as diffuse goiter (often idiopathic), thyroiditis, and neoplasms can also present in a euthyroid state.

Diagnosis: Exam and imaging

Studies show variable correlation between physical exam findings and findings on imaging studies. In a retrospective chart review, ultrasound findings differed from clinical exam findings in 63% of cases.² Thyroid ultrasound is less expensive and less invasive than other imaging modalities, provides excellent visualization of thyroid structure and the nature of cysts and nodules, and allows for estimation of thyroid size.

Computed tomography and magnetic resonance imaging perform better for visualization of extension of thyroid tissue substernally and are also preferred for evaluation of the neck in cases of severe local complications of goiter, such as compressive symptoms.³

The malignant potential in multinodular goiter (2%–4%) is similar to that of solitary nodules (4%–6%).³ Therefore, any dominant nodule in a multinodular goiter should be evaluated the same way one would evaluate a solitary nodule.

Treatment and follow-up

Patients with a reassuring initial work-up can be followed clinically and should be assessed with serial clinical evaluations. No evidence could be found regarding optimal intervals for examination and testing; yearly exams and TSH testing are considered adequate by some experts.⁴

Because a few non-benign conditions such as thyroiditis and neoplasm can sometimes present in a euthyroid state, the clinician should be alert for any physical exam or laboratory changes. If any changes occur, then further workup is indicated.

Suppressive therapy with thyroxine is an option for decreasing thyroid size in euthyroid goiter, but this therapy remains controversial. One placebo-controlled trial of thyroid suppression in nontoxic multinodular goiter showed regression of thyroid size with suppressive therapy (58% reduction in size in treatment group vs 5% reduction in control group). However, not all goiters responded to this therapy, and the thyroid size returned to pretreatment size within 9 months of discontinuation of suppressive therapy.⁵

Many experts argue against the use of suppressive therapy in long-standing goiters, citing less response from these patients, along with concern about side effects and possible oversuppression, but the evidence in this area is limited. Patients who are treated with thyroxine should be followed for possible side effects of the medication, including arrhythmia and osteopenia, particularly in elderly patients and those who take the medication for long periods.

Recommendations of others

Guidelines from the American Association of Clinical Endocrinology’s Task Force on Thyroid Nodules, released in 2006, recommends ultrasound be used routinely in the case of multinodular goiter to assist with diagnosis, detect suspicious nodules that may require biopsy, and to serve as an objective baseline measure. This group recommends against use of suppression therapy in long-standing goiters.⁶

Evidence summary

No published studies compare varying durations of treatment with steroids for contact dermatitis due to plants, including rhus. Many review articles refer to rebound dermatitis when using courses of oral steroids (such as Medrol dosepaks) for fewer than 14 days. One case report noted failure of a tapering dose over 5 days of oral methylprednisolone for treatment of poison ivy contact dermatitis.²

Most review articles recommend systemic steroids for severe poison ivy contact dermatitis, but these articles do not define “severe,” describe the taper, or give a definite length of treatment.^3-5 One review recommends a tapering dose of oral prednisone to prevent rebound recurrence if the rash affects >25% of the body surface area, has severe blistering or itching, or significantly involves the face, hands, or genital area. That review suggests starting with oral prednisone 60 mg/d for 4 days, followed by a 10-day taper (50 mg/d for 2 days, 40 mg/d for 2 days, 30 mg/d for 2 days, 20 mg/d for 2 days, then 10 mg/d for 2 days).³

Another review recommends using systemic steroids for severe cases, defined as involvement of greater than 20% of total body surface area, bullae formation, or extensive facial involvement. That review recommends a starting dose of 1 mg/kg/d, or 40 to 60 mg/d in adults, followed by a 2- to 3-week taper of oral prednisone.⁴ A third review recommends using prednisone for children with allergic contact dermatitis involving more than 10% of the total body surface area.⁵

Recommendations from others

Guidelines for treatment of contact dermatitis published by the American Academy of Dermatology recommend topical treatment alone for mild cases of contact dermatitis, defined as “limited site of involvement, acute contact dermatitis when the offending agent has been removed, or chronic contact dermatitis with limited symptoms.” The guideline states that systemic treatment may be indicated to control itching or edema, or for moderate to severe cases. The systemic treatments listed include oral or intramuscular corticosteroids, but no discussion of duration is mentioned.⁶

UpToDate discusses avoidance of the offending substance for 2 to 4 weeks, use of topical corticosteroids of medium to strong potency for a limited time (without defining the duration), and use of systemic corticosteroids in severe cases, prescribing a course of prednisone at 40 mg daily for 4 to 6 days followed by 20 mg for 4 to 6 days.⁷

eMedicine states that although oral systemic steroids, with a taper of prednisone over 10 to 14 days, are the standard for severe toxicodendron dermatitis, some authors suggest high-potency steroid creams twice daily for a week, then daily for a week.⁸

ACP Medicine states that most cases of allergic contact dermatitis are “effectively managed without use of systemic corticosteroids,” but that “short courses of systemic corticosteroids are indicated for patients with severe vesiculobullous eruptions of the hands and feet or face,” without describing duration or dose.⁹

Evidence summary

No published studies compare varying durations of treatment with steroids for contact dermatitis due to plants, including rhus. Many review articles refer to rebound dermatitis when using courses of oral steroids (such as Medrol dosepaks) for fewer than 14 days. One case report noted failure of a tapering dose over 5 days of oral methylprednisolone for treatment of poison ivy contact dermatitis.²

Most review articles recommend systemic steroids for severe poison ivy contact dermatitis, but these articles do not define “severe,” describe the taper, or give a definite length of treatment.^3-5 One review recommends a tapering dose of oral prednisone to prevent rebound recurrence if the rash affects >25% of the body surface area, has severe blistering or itching, or significantly involves the face, hands, or genital area. That review suggests starting with oral prednisone 60 mg/d for 4 days, followed by a 10-day taper (50 mg/d for 2 days, 40 mg/d for 2 days, 30 mg/d for 2 days, 20 mg/d for 2 days, then 10 mg/d for 2 days).³

Another review recommends using systemic steroids for severe cases, defined as involvement of greater than 20% of total body surface area, bullae formation, or extensive facial involvement. That review recommends a starting dose of 1 mg/kg/d, or 40 to 60 mg/d in adults, followed by a 2- to 3-week taper of oral prednisone.⁴ A third review recommends using prednisone for children with allergic contact dermatitis involving more than 10% of the total body surface area.⁵

Recommendations from others

Guidelines for treatment of contact dermatitis published by the American Academy of Dermatology recommend topical treatment alone for mild cases of contact dermatitis, defined as “limited site of involvement, acute contact dermatitis when the offending agent has been removed, or chronic contact dermatitis with limited symptoms.” The guideline states that systemic treatment may be indicated to control itching or edema, or for moderate to severe cases. The systemic treatments listed include oral or intramuscular corticosteroids, but no discussion of duration is mentioned.⁶

UpToDate discusses avoidance of the offending substance for 2 to 4 weeks, use of topical corticosteroids of medium to strong potency for a limited time (without defining the duration), and use of systemic corticosteroids in severe cases, prescribing a course of prednisone at 40 mg daily for 4 to 6 days followed by 20 mg for 4 to 6 days.⁷

eMedicine states that although oral systemic steroids, with a taper of prednisone over 10 to 14 days, are the standard for severe toxicodendron dermatitis, some authors suggest high-potency steroid creams twice daily for a week, then daily for a week.⁸

ACP Medicine states that most cases of allergic contact dermatitis are “effectively managed without use of systemic corticosteroids,” but that “short courses of systemic corticosteroids are indicated for patients with severe vesiculobullous eruptions of the hands and feet or face,” without describing duration or dose.⁹

Evidence summary

No published studies compare varying durations of treatment with steroids for contact dermatitis due to plants, including rhus. Many review articles refer to rebound dermatitis when using courses of oral steroids (such as Medrol dosepaks) for fewer than 14 days. One case report noted failure of a tapering dose over 5 days of oral methylprednisolone for treatment of poison ivy contact dermatitis.²

Most review articles recommend systemic steroids for severe poison ivy contact dermatitis, but these articles do not define “severe,” describe the taper, or give a definite length of treatment.^3-5 One review recommends a tapering dose of oral prednisone to prevent rebound recurrence if the rash affects >25% of the body surface area, has severe blistering or itching, or significantly involves the face, hands, or genital area. That review suggests starting with oral prednisone 60 mg/d for 4 days, followed by a 10-day taper (50 mg/d for 2 days, 40 mg/d for 2 days, 30 mg/d for 2 days, 20 mg/d for 2 days, then 10 mg/d for 2 days).³

Another review recommends using systemic steroids for severe cases, defined as involvement of greater than 20% of total body surface area, bullae formation, or extensive facial involvement. That review recommends a starting dose of 1 mg/kg/d, or 40 to 60 mg/d in adults, followed by a 2- to 3-week taper of oral prednisone.⁴ A third review recommends using prednisone for children with allergic contact dermatitis involving more than 10% of the total body surface area.⁵

Recommendations from others

Guidelines for treatment of contact dermatitis published by the American Academy of Dermatology recommend topical treatment alone for mild cases of contact dermatitis, defined as “limited site of involvement, acute contact dermatitis when the offending agent has been removed, or chronic contact dermatitis with limited symptoms.” The guideline states that systemic treatment may be indicated to control itching or edema, or for moderate to severe cases. The systemic treatments listed include oral or intramuscular corticosteroids, but no discussion of duration is mentioned.⁶

UpToDate discusses avoidance of the offending substance for 2 to 4 weeks, use of topical corticosteroids of medium to strong potency for a limited time (without defining the duration), and use of systemic corticosteroids in severe cases, prescribing a course of prednisone at 40 mg daily for 4 to 6 days followed by 20 mg for 4 to 6 days.⁷

eMedicine states that although oral systemic steroids, with a taper of prednisone over 10 to 14 days, are the standard for severe toxicodendron dermatitis, some authors suggest high-potency steroid creams twice daily for a week, then daily for a week.⁸

ACP Medicine states that most cases of allergic contact dermatitis are “effectively managed without use of systemic corticosteroids,” but that “short courses of systemic corticosteroids are indicated for patients with severe vesiculobullous eruptions of the hands and feet or face,” without describing duration or dose.⁹

Evidence summary

The primary role of colposcopy is to identify cervical lesions, allowing directed biopsies to identify invasive cancer or its precursors. Although colposcopy has been studied as a primary screening technique, issues of cost, accessibility, invasiveness, and low specificity severely limit its usefulness in this role.¹ Using histology as the gold standard, the sensitivity of colposcopy for cervical abnormalities is high (96%; 95% confidence interval [CI], 95%–97%), but the specificity is much lower (48%; 95% CI, 47%–49%).² This low specificity means that more than half of women with no cervical pathology will have an abnormal colposcopy result. The corresponding positive and negative likelihood ratios are 2 and 0.1, respectively. Consequently, a normal colposcopy result can effectively rule out cervical pathology, thus supporting its role as a diagnostic rather than a screening tool.

While most lesions are found by abnormal cytology, the sensitivity of the Papanicolaou smear ranges from 30% to 89%.³ Therefore, colposcopy is also indicated for patients with symptoms suggestive of cervical dysplasia or cancer (abnormal appearance of the cervix, or persistent and undiagnosed vaginal discharge or bleeding), even in the setting of normal cytology.⁴

Colposcopy is also indicated for follow-up after treatment of cervical dysplasia. One study⁵ identified 3 risk factors for recurrence of dysplasia after a loop electrocautery excision procedure (LEEP): residual disease at either the endocervical or ectocervical margins, and involvement of endocervical glands. The presence of these risk factors predicted a recurrence rate of almost 70%.⁵ Because 8% of the recurrences were missed on cytology, the authors recommended colposcopy 6 months after LEEP for patients with these risk factors.

Recommendations from others

The place of colposcopy in the work-up of patients with abnormal cytology is well supported. With the recent revision of the Bethesda System by the National Cancer Institute,⁶ the American Society for Colposcopy and Cervical Pathology (ASCCP) held a consensus conference to review the literature and provide evidence-based guidelines for management of abnormal cervical cytology.⁷ Its recommendations on colposcopy are summarized in the Table.

The U.S. Preventive Services Task Force’s 1996 recommendations found insufficient evidence to recommend either for or against the use of colposcopy as a screening tool for cervical cancer. Based on high cost and low specificity, it recommends against screening colposcopy.⁸

TABLE
Recommendations for colposcopy, American Society for Colposcopy and Cervical Pathology⁷

Evidence summary

The primary role of colposcopy is to identify cervical lesions, allowing directed biopsies to identify invasive cancer or its precursors. Although colposcopy has been studied as a primary screening technique, issues of cost, accessibility, invasiveness, and low specificity severely limit its usefulness in this role.¹ Using histology as the gold standard, the sensitivity of colposcopy for cervical abnormalities is high (96%; 95% confidence interval [CI], 95%–97%), but the specificity is much lower (48%; 95% CI, 47%–49%).² This low specificity means that more than half of women with no cervical pathology will have an abnormal colposcopy result. The corresponding positive and negative likelihood ratios are 2 and 0.1, respectively. Consequently, a normal colposcopy result can effectively rule out cervical pathology, thus supporting its role as a diagnostic rather than a screening tool.

While most lesions are found by abnormal cytology, the sensitivity of the Papanicolaou smear ranges from 30% to 89%.³ Therefore, colposcopy is also indicated for patients with symptoms suggestive of cervical dysplasia or cancer (abnormal appearance of the cervix, or persistent and undiagnosed vaginal discharge or bleeding), even in the setting of normal cytology.⁴

Colposcopy is also indicated for follow-up after treatment of cervical dysplasia. One study⁵ identified 3 risk factors for recurrence of dysplasia after a loop electrocautery excision procedure (LEEP): residual disease at either the endocervical or ectocervical margins, and involvement of endocervical glands. The presence of these risk factors predicted a recurrence rate of almost 70%.⁵ Because 8% of the recurrences were missed on cytology, the authors recommended colposcopy 6 months after LEEP for patients with these risk factors.

Recommendations from others

The place of colposcopy in the work-up of patients with abnormal cytology is well supported. With the recent revision of the Bethesda System by the National Cancer Institute,⁶ the American Society for Colposcopy and Cervical Pathology (ASCCP) held a consensus conference to review the literature and provide evidence-based guidelines for management of abnormal cervical cytology.⁷ Its recommendations on colposcopy are summarized in the Table.

The U.S. Preventive Services Task Force’s 1996 recommendations found insufficient evidence to recommend either for or against the use of colposcopy as a screening tool for cervical cancer. Based on high cost and low specificity, it recommends against screening colposcopy.⁸

TABLE
Recommendations for colposcopy, American Society for Colposcopy and Cervical Pathology⁷

Evidence summary

The primary role of colposcopy is to identify cervical lesions, allowing directed biopsies to identify invasive cancer or its precursors. Although colposcopy has been studied as a primary screening technique, issues of cost, accessibility, invasiveness, and low specificity severely limit its usefulness in this role.¹ Using histology as the gold standard, the sensitivity of colposcopy for cervical abnormalities is high (96%; 95% confidence interval [CI], 95%–97%), but the specificity is much lower (48%; 95% CI, 47%–49%).² This low specificity means that more than half of women with no cervical pathology will have an abnormal colposcopy result. The corresponding positive and negative likelihood ratios are 2 and 0.1, respectively. Consequently, a normal colposcopy result can effectively rule out cervical pathology, thus supporting its role as a diagnostic rather than a screening tool.

While most lesions are found by abnormal cytology, the sensitivity of the Papanicolaou smear ranges from 30% to 89%.³ Therefore, colposcopy is also indicated for patients with symptoms suggestive of cervical dysplasia or cancer (abnormal appearance of the cervix, or persistent and undiagnosed vaginal discharge or bleeding), even in the setting of normal cytology.⁴

Colposcopy is also indicated for follow-up after treatment of cervical dysplasia. One study⁵ identified 3 risk factors for recurrence of dysplasia after a loop electrocautery excision procedure (LEEP): residual disease at either the endocervical or ectocervical margins, and involvement of endocervical glands. The presence of these risk factors predicted a recurrence rate of almost 70%.⁵ Because 8% of the recurrences were missed on cytology, the authors recommended colposcopy 6 months after LEEP for patients with these risk factors.

Recommendations from others

The place of colposcopy in the work-up of patients with abnormal cytology is well supported. With the recent revision of the Bethesda System by the National Cancer Institute,⁶ the American Society for Colposcopy and Cervical Pathology (ASCCP) held a consensus conference to review the literature and provide evidence-based guidelines for management of abnormal cervical cytology.⁷ Its recommendations on colposcopy are summarized in the Table.

The U.S. Preventive Services Task Force’s 1996 recommendations found insufficient evidence to recommend either for or against the use of colposcopy as a screening tool for cervical cancer. Based on high cost and low specificity, it recommends against screening colposcopy.⁸

TABLE
Recommendations for colposcopy, American Society for Colposcopy and Cervical Pathology⁷

EVIDENCE-BASED ANSWER

Most recent randomized controlled clinical trials have not found a benefit in antioxidants (vitamin C, vitamin E, and/or beta-carotene) for preventing cardiovascular disease, including stroke. These recent clinical studies have not confirmed earlier observational studies that suggested a benefit. No studies have assessed only stroke patients and stroke outcomes. (Grade of recommendation: A, based on randomized controlled clinical trials and a systematic review of antioxidants and cardiovascular disease.)

Evidence summary

The Heart Outcomes Prevention Evaluation (HOPE) trial was a 4.5-year randomized controlled clinical trial of vitamin E or placebo in 9541 patients aged 55 years or older with a history of coronary artery disease, stroke, peripheral vascular disease, or diabetes and other cardiovascular disease risk factors. No difference was noted between vitamin E and placebo for the outcomes of stroke, death, or other cardiac outcomes for these high-risk patients.¹ In a randomized controlled clinical trial of 29,133 Finnish male smokers, the overall net stroke morbidity and mortality with antioxidants was not significantly different from placebo. However, a trend toward higher rates of subarachnoid hemorrhages was found (relative risk [RR] = 1.5; 95% confidence interval [CI], 0.97–2.32; numbers needed to harm [NNH] = 833), while the cerebral infarction rate was decreased (RR = 0.86; 95% CI, 0.75–0.99; numbers needed to treat = 239) by vitamin E. Beta-carotene increased intracerebral hemorrhage (RR = 1.61; 95% CI, 1.10–2.36; NNH = 546).² Subsequent subgroup analysis showed a significant decrease in cerebral infarction (RR = 0.33; 95% CI, 0.14–0.78) without increasing subarachnoid hemorrhage in hypertensive, diabetic men taking vitamin E.³ Given the inherent methodological perils of subgroup analysis, this association requires further study before clinical implementation.

The Italian GISSI study of 11,324 patients with a recent myocardial infarction showed no effect of vitamin E on the combined outcomes of death, myocardial infarction, and stroke.⁴ In the Heart Protection Study, 20,536 adults between the ages of 40 and 80 years with cardiovascular disease, stroke, or diabetes were given vitamin E, vitamin C, beta-carotene, or placebo for 5 years. No significant differences were noted between vitamins and placebo in fatal or nonfatal stroke (RR = 0.99; 95% CI, 0.87–1.12).⁵

Although prior observational studies have hinted at a link between antioxidants and improved cardiovascular outcomes, the recently published Health Professionals Follow-up Study found no benefit to vitamin C or E in preventing strokes, based on the dietary assessment of 43,738 men, aged 40 to 75 years, who were not known to have cardiovascular disease or diabetes.⁶

Recommendations from others

The American Heart Association Science Advisory and Coordinating Committee commented on antioxidant use in 1999. While their emphasis was on coronary heart disease, they concluded that the general population should “consume a balanced diet with emphasis on antioxidant-rich fruits and vegetables and whole grains,” noting that “the absence of efficacy and safety data from randomized trials precludes the establishment of population-wide recommendations regarding vitamin E supplementation.”⁷ Some authors argue that the failure to demonstrate a benefit from antioxidants is due to inadequate antioxidant dosing, treatment length, or type of antioxidant.⁸

Read a Clinical Commentary by Dan Sontheimer, MD, MBA, online at http://www.FPIN.org.

EVIDENCE-BASED ANSWER

Most recent randomized controlled clinical trials have not found a benefit in antioxidants (vitamin C, vitamin E, and/or beta-carotene) for preventing cardiovascular disease, including stroke. These recent clinical studies have not confirmed earlier observational studies that suggested a benefit. No studies have assessed only stroke patients and stroke outcomes. (Grade of recommendation: A, based on randomized controlled clinical trials and a systematic review of antioxidants and cardiovascular disease.)

Evidence summary

The Heart Outcomes Prevention Evaluation (HOPE) trial was a 4.5-year randomized controlled clinical trial of vitamin E or placebo in 9541 patients aged 55 years or older with a history of coronary artery disease, stroke, peripheral vascular disease, or diabetes and other cardiovascular disease risk factors. No difference was noted between vitamin E and placebo for the outcomes of stroke, death, or other cardiac outcomes for these high-risk patients.¹ In a randomized controlled clinical trial of 29,133 Finnish male smokers, the overall net stroke morbidity and mortality with antioxidants was not significantly different from placebo. However, a trend toward higher rates of subarachnoid hemorrhages was found (relative risk [RR] = 1.5; 95% confidence interval [CI], 0.97–2.32; numbers needed to harm [NNH] = 833), while the cerebral infarction rate was decreased (RR = 0.86; 95% CI, 0.75–0.99; numbers needed to treat = 239) by vitamin E. Beta-carotene increased intracerebral hemorrhage (RR = 1.61; 95% CI, 1.10–2.36; NNH = 546).² Subsequent subgroup analysis showed a significant decrease in cerebral infarction (RR = 0.33; 95% CI, 0.14–0.78) without increasing subarachnoid hemorrhage in hypertensive, diabetic men taking vitamin E.³ Given the inherent methodological perils of subgroup analysis, this association requires further study before clinical implementation.

The Italian GISSI study of 11,324 patients with a recent myocardial infarction showed no effect of vitamin E on the combined outcomes of death, myocardial infarction, and stroke.⁴ In the Heart Protection Study, 20,536 adults between the ages of 40 and 80 years with cardiovascular disease, stroke, or diabetes were given vitamin E, vitamin C, beta-carotene, or placebo for 5 years. No significant differences were noted between vitamins and placebo in fatal or nonfatal stroke (RR = 0.99; 95% CI, 0.87–1.12).⁵

Although prior observational studies have hinted at a link between antioxidants and improved cardiovascular outcomes, the recently published Health Professionals Follow-up Study found no benefit to vitamin C or E in preventing strokes, based on the dietary assessment of 43,738 men, aged 40 to 75 years, who were not known to have cardiovascular disease or diabetes.⁶

Recommendations from others

The American Heart Association Science Advisory and Coordinating Committee commented on antioxidant use in 1999. While their emphasis was on coronary heart disease, they concluded that the general population should “consume a balanced diet with emphasis on antioxidant-rich fruits and vegetables and whole grains,” noting that “the absence of efficacy and safety data from randomized trials precludes the establishment of population-wide recommendations regarding vitamin E supplementation.”⁷ Some authors argue that the failure to demonstrate a benefit from antioxidants is due to inadequate antioxidant dosing, treatment length, or type of antioxidant.⁸

Read a Clinical Commentary by Dan Sontheimer, MD, MBA, online at http://www.FPIN.org.

EVIDENCE-BASED ANSWER

Most recent randomized controlled clinical trials have not found a benefit in antioxidants (vitamin C, vitamin E, and/or beta-carotene) for preventing cardiovascular disease, including stroke. These recent clinical studies have not confirmed earlier observational studies that suggested a benefit. No studies have assessed only stroke patients and stroke outcomes. (Grade of recommendation: A, based on randomized controlled clinical trials and a systematic review of antioxidants and cardiovascular disease.)

Evidence summary

The Heart Outcomes Prevention Evaluation (HOPE) trial was a 4.5-year randomized controlled clinical trial of vitamin E or placebo in 9541 patients aged 55 years or older with a history of coronary artery disease, stroke, peripheral vascular disease, or diabetes and other cardiovascular disease risk factors. No difference was noted between vitamin E and placebo for the outcomes of stroke, death, or other cardiac outcomes for these high-risk patients.¹ In a randomized controlled clinical trial of 29,133 Finnish male smokers, the overall net stroke morbidity and mortality with antioxidants was not significantly different from placebo. However, a trend toward higher rates of subarachnoid hemorrhages was found (relative risk [RR] = 1.5; 95% confidence interval [CI], 0.97–2.32; numbers needed to harm [NNH] = 833), while the cerebral infarction rate was decreased (RR = 0.86; 95% CI, 0.75–0.99; numbers needed to treat = 239) by vitamin E. Beta-carotene increased intracerebral hemorrhage (RR = 1.61; 95% CI, 1.10–2.36; NNH = 546).² Subsequent subgroup analysis showed a significant decrease in cerebral infarction (RR = 0.33; 95% CI, 0.14–0.78) without increasing subarachnoid hemorrhage in hypertensive, diabetic men taking vitamin E.³ Given the inherent methodological perils of subgroup analysis, this association requires further study before clinical implementation.

The Italian GISSI study of 11,324 patients with a recent myocardial infarction showed no effect of vitamin E on the combined outcomes of death, myocardial infarction, and stroke.⁴ In the Heart Protection Study, 20,536 adults between the ages of 40 and 80 years with cardiovascular disease, stroke, or diabetes were given vitamin E, vitamin C, beta-carotene, or placebo for 5 years. No significant differences were noted between vitamins and placebo in fatal or nonfatal stroke (RR = 0.99; 95% CI, 0.87–1.12).⁵

Although prior observational studies have hinted at a link between antioxidants and improved cardiovascular outcomes, the recently published Health Professionals Follow-up Study found no benefit to vitamin C or E in preventing strokes, based on the dietary assessment of 43,738 men, aged 40 to 75 years, who were not known to have cardiovascular disease or diabetes.⁶

Recommendations from others

The American Heart Association Science Advisory and Coordinating Committee commented on antioxidant use in 1999. While their emphasis was on coronary heart disease, they concluded that the general population should “consume a balanced diet with emphasis on antioxidant-rich fruits and vegetables and whole grains,” noting that “the absence of efficacy and safety data from randomized trials precludes the establishment of population-wide recommendations regarding vitamin E supplementation.”⁷ Some authors argue that the failure to demonstrate a benefit from antioxidants is due to inadequate antioxidant dosing, treatment length, or type of antioxidant.⁸

Read a Clinical Commentary by Dan Sontheimer, MD, MBA, online at http://www.FPIN.org.

EVIDENCE-BASED ANSWER

Efforts to increase physical activity or decrease sedentary activities have shown some short-term benefit, and adding dietary changes may be more effective. Aiming interventions at parents, intensive family therapy, comprehensive school-based programs, and selecting motivated children for subspecialty care may improve success. (Grade of recommendation: B, based on poor-quality randomized controlled trials [RCTs] and heterogeneous systematic reviews.) Other potentially effective short-term strategies include screening with body mass index (BMI) for age (grade of recommendation: C, extrapolation from cohort studies and ecological research) or dietary counseling (grade of recommendation: D, conflicting poor-quality RCTs). No drugs are currently approved for pediatric obesity therapy in the United States.

Evidence summary

Pediatric obesity increases the risk of adverse outcomes in adulthood, independent of adult BMI.¹ Trials aiming to reduce childhood obesity suffer from serious methodological constraints. No long-term (> 2 years) evidence is available. Many apparently efficacious interventions are beyond the scope of primary care physicians. A detailed summary is available online at http://www.FPIN.org.

Several studies have examined the value of isolated changes in either diet or activity level. Randomized controlled trials and retrospective cohort studies of dietary advice alone show short-term efficacy (weeks to months).¹ Most involve intensive subspecialty care for extremely obese children who are 120% to 140% over their ideal body weight. Trials without careful selection of motivated children had dropout rates up to 87%. One Italian RCT showed a 12% reduction in the number of obese children in schools receiving multimedia dietary advice compared with a 5% to 6% increase in those schools receiving only written or no advice.² Several RCTs reduced obesity by introducing or improving school-based physical activity.¹ Two RCTs that discouraged sedentary activity through counseling or school-based programs also reduced obesity.^3,4

Two larger trials integrated diet and exercise advice into school curricula. One study emphasized improving school menus, but no difference was observed because children compensated by overeating at home.⁵ The other emphasized reducing sedentary activities and found lower obesity rates in the intervention schools, but only for girls.⁶ A third trial provided family-based dietary and behavior counseling, but emphasized either increasing physical activity or decreasing sedentary activity.⁷ Both strategies resulted in reduced obesity compared with controls. A systematic review supported the combined approach of these trials, finding diet and exercise interventions superior to diet interventions alone.⁸

Some evidence supports focusing on the family rather than just the child. A systematic review found that family therapy prevented pediatric obesity.⁹ An RCT found that focusing on parents as the sole change agent was superior to targeting the child.¹⁰

Recommendations from others

Expert consensus promotes screening because of obesity’s increasing incidence and associated morbidity and mortality.¹¹ The Maternal and Child Health Bureau recommends a primary goal of healthy eating and activity. They recommend treating when the body mass index is >95th percentile, and assessing the child and family’s willingness to change. Primary strategies are to begin early, involve the family, promote parenting skills, and increase activity and reduce high-calorie food intake. They also recommend ongoing support to maintain weight loss.⁹

Clinical Commentary by Tess Bobo, MD, at http://www.fpin.org.

EVIDENCE-BASED ANSWER

Efforts to increase physical activity or decrease sedentary activities have shown some short-term benefit, and adding dietary changes may be more effective. Aiming interventions at parents, intensive family therapy, comprehensive school-based programs, and selecting motivated children for subspecialty care may improve success. (Grade of recommendation: B, based on poor-quality randomized controlled trials [RCTs] and heterogeneous systematic reviews.) Other potentially effective short-term strategies include screening with body mass index (BMI) for age (grade of recommendation: C, extrapolation from cohort studies and ecological research) or dietary counseling (grade of recommendation: D, conflicting poor-quality RCTs). No drugs are currently approved for pediatric obesity therapy in the United States.

Evidence summary

Pediatric obesity increases the risk of adverse outcomes in adulthood, independent of adult BMI.¹ Trials aiming to reduce childhood obesity suffer from serious methodological constraints. No long-term (> 2 years) evidence is available. Many apparently efficacious interventions are beyond the scope of primary care physicians. A detailed summary is available online at http://www.FPIN.org.

Several studies have examined the value of isolated changes in either diet or activity level. Randomized controlled trials and retrospective cohort studies of dietary advice alone show short-term efficacy (weeks to months).¹ Most involve intensive subspecialty care for extremely obese children who are 120% to 140% over their ideal body weight. Trials without careful selection of motivated children had dropout rates up to 87%. One Italian RCT showed a 12% reduction in the number of obese children in schools receiving multimedia dietary advice compared with a 5% to 6% increase in those schools receiving only written or no advice.² Several RCTs reduced obesity by introducing or improving school-based physical activity.¹ Two RCTs that discouraged sedentary activity through counseling or school-based programs also reduced obesity.^3,4

Two larger trials integrated diet and exercise advice into school curricula. One study emphasized improving school menus, but no difference was observed because children compensated by overeating at home.⁵ The other emphasized reducing sedentary activities and found lower obesity rates in the intervention schools, but only for girls.⁶ A third trial provided family-based dietary and behavior counseling, but emphasized either increasing physical activity or decreasing sedentary activity.⁷ Both strategies resulted in reduced obesity compared with controls. A systematic review supported the combined approach of these trials, finding diet and exercise interventions superior to diet interventions alone.⁸

Some evidence supports focusing on the family rather than just the child. A systematic review found that family therapy prevented pediatric obesity.⁹ An RCT found that focusing on parents as the sole change agent was superior to targeting the child.¹⁰

Recommendations from others

Expert consensus promotes screening because of obesity’s increasing incidence and associated morbidity and mortality.¹¹ The Maternal and Child Health Bureau recommends a primary goal of healthy eating and activity. They recommend treating when the body mass index is >95th percentile, and assessing the child and family’s willingness to change. Primary strategies are to begin early, involve the family, promote parenting skills, and increase activity and reduce high-calorie food intake. They also recommend ongoing support to maintain weight loss.⁹

Clinical Commentary by Tess Bobo, MD, at http://www.fpin.org.

EVIDENCE-BASED ANSWER

Efforts to increase physical activity or decrease sedentary activities have shown some short-term benefit, and adding dietary changes may be more effective. Aiming interventions at parents, intensive family therapy, comprehensive school-based programs, and selecting motivated children for subspecialty care may improve success. (Grade of recommendation: B, based on poor-quality randomized controlled trials [RCTs] and heterogeneous systematic reviews.) Other potentially effective short-term strategies include screening with body mass index (BMI) for age (grade of recommendation: C, extrapolation from cohort studies and ecological research) or dietary counseling (grade of recommendation: D, conflicting poor-quality RCTs). No drugs are currently approved for pediatric obesity therapy in the United States.

Evidence summary

Pediatric obesity increases the risk of adverse outcomes in adulthood, independent of adult BMI.¹ Trials aiming to reduce childhood obesity suffer from serious methodological constraints. No long-term (> 2 years) evidence is available. Many apparently efficacious interventions are beyond the scope of primary care physicians. A detailed summary is available online at http://www.FPIN.org.

Several studies have examined the value of isolated changes in either diet or activity level. Randomized controlled trials and retrospective cohort studies of dietary advice alone show short-term efficacy (weeks to months).¹ Most involve intensive subspecialty care for extremely obese children who are 120% to 140% over their ideal body weight. Trials without careful selection of motivated children had dropout rates up to 87%. One Italian RCT showed a 12% reduction in the number of obese children in schools receiving multimedia dietary advice compared with a 5% to 6% increase in those schools receiving only written or no advice.² Several RCTs reduced obesity by introducing or improving school-based physical activity.¹ Two RCTs that discouraged sedentary activity through counseling or school-based programs also reduced obesity.^3,4

Two larger trials integrated diet and exercise advice into school curricula. One study emphasized improving school menus, but no difference was observed because children compensated by overeating at home.⁵ The other emphasized reducing sedentary activities and found lower obesity rates in the intervention schools, but only for girls.⁶ A third trial provided family-based dietary and behavior counseling, but emphasized either increasing physical activity or decreasing sedentary activity.⁷ Both strategies resulted in reduced obesity compared with controls. A systematic review supported the combined approach of these trials, finding diet and exercise interventions superior to diet interventions alone.⁸

Some evidence supports focusing on the family rather than just the child. A systematic review found that family therapy prevented pediatric obesity.⁹ An RCT found that focusing on parents as the sole change agent was superior to targeting the child.¹⁰

Recommendations from others

Expert consensus promotes screening because of obesity’s increasing incidence and associated morbidity and mortality.¹¹ The Maternal and Child Health Bureau recommends a primary goal of healthy eating and activity. They recommend treating when the body mass index is >95th percentile, and assessing the child and family’s willingness to change. Primary strategies are to begin early, involve the family, promote parenting skills, and increase activity and reduce high-calorie food intake. They also recommend ongoing support to maintain weight loss.⁹

Clinical Commentary by Tess Bobo, MD, at http://www.fpin.org.

EVIDENCE-BASED ANSWER

Large published randomized controlled trials (RCTs) show that pravastatin and simvastatin are well-tolerated and reduce major coronary events such as death, myocardial infarction, and revascularization by about 25%. The Heart Protection Study suggested this benefit is noted even among individuals with pretreatment low-density lipoprotein (LDL) cholesterol of less than 100 mg/dL. Fluvastatin reduces major coronary events, but current studies are too small to prove reduced overall mortality. The best evidence to date suggests that most patients at significant risk for major coronary events should be given pravastatin or simvastatin 40 mg daily, without concern for the initial or follow-up LDL levels. (Grade of recommendation: A, based on large randomized trials.)

Evidence summary

The evidence is solid to support the use of HMG–CoA reductase inhibitors (statins) for patients with coronary artery disease (CAD). The Scandinavian Simvastatin Survival study used simvastatin 20 mg daily unless total cholesterol levels did not decrease to less than 200 mg/dL.¹ The Long-Term Intervention with Pravastatin in Ischaemic Disease study randomized patients to pravastatin 40 mg daily or placebo, without titration.² The intervention arm in the Cholesterol and Recurrent Events trial was also pravastatin 40 mg daily, with cholestyramine added if the LDL level remained higher than 175 mg/dL.³ The Lescol Intervention Prevention study randomized patients after angioplasty to fluvastatin 40 mg twice daily or placebo.⁴ The Heart Protection Study used simvastatin 40 mg daily, without titration.⁵ No RCTs have evaluated the clinical benefit of adding medications to adequate doses of statins to lower LDL to less than 175 mg/dL. See Table of major RCTs with clinical outcomes.

Subgroup analyses of earlier major RCTs had suggested that patients with CAD and low initial LDL levels (< 125 mg/dL) have little to gain from pravastatin.^2,3 However, the Heart Protection Study enrolled 20,000 people with CAD or equivalent (diabetes, peripheral vascular disease, stroke, etc).⁵ The study demonstrated a reduction of major coronary events with simvastatin, with numbers needed to treat (NNT) of 19 (P < .0001); the NNT for reduction in all-cause mortality was 55 (P = .0003). The benefit of simvastatin was noted in virtually every predefined subgroup, including individuals older than 70 years, women, and patients without known CAD (but with CAD equivalents). Notably, no difference in benefit was found between patients with different pretreatment LDL levels. A significant reduction in major vascular events was noted even for the 3400 subjects with pretreatment LDL levels of less than 100 mg/dL (NNT = 22, P = .0006). A greater percentage reduction in LDL with medication did not predict better clinical outcomes.⁵

TABLE

LDL levels and relative risk of major coronary events after treatment

Recommendations from others

The National Cholesterol Education Project (NCEP) recommends that patients with CAD and an LDL of more than 130 mg/dL adopt therapeutic lifestyle changes and start LDL-lowering medication, usually a statin. For patients with LDL between 100 and 130 mg/dL, the NCEP recommends therapeutic lifestyle changes, with the option of adding a statin. For patients with LDL less than 100 mg/dL, maintenance of LDL control is recommended with therapeutic lifestyle changes. For patients with high initial LDL levels that stay above 100 mg/dL on statin therapy, the NCEP recommends that additional medications, such as nicotinic acid or fibrates, as well as intensive therapeutic lifestyle changes, be considered.⁶

Clinical Commentary by William Chavey, MD, at http://www.fpin.org.

EVIDENCE-BASED ANSWER

Large published randomized controlled trials (RCTs) show that pravastatin and simvastatin are well-tolerated and reduce major coronary events such as death, myocardial infarction, and revascularization by about 25%. The Heart Protection Study suggested this benefit is noted even among individuals with pretreatment low-density lipoprotein (LDL) cholesterol of less than 100 mg/dL. Fluvastatin reduces major coronary events, but current studies are too small to prove reduced overall mortality. The best evidence to date suggests that most patients at significant risk for major coronary events should be given pravastatin or simvastatin 40 mg daily, without concern for the initial or follow-up LDL levels. (Grade of recommendation: A, based on large randomized trials.)

Evidence summary

The evidence is solid to support the use of HMG–CoA reductase inhibitors (statins) for patients with coronary artery disease (CAD). The Scandinavian Simvastatin Survival study used simvastatin 20 mg daily unless total cholesterol levels did not decrease to less than 200 mg/dL.¹ The Long-Term Intervention with Pravastatin in Ischaemic Disease study randomized patients to pravastatin 40 mg daily or placebo, without titration.² The intervention arm in the Cholesterol and Recurrent Events trial was also pravastatin 40 mg daily, with cholestyramine added if the LDL level remained higher than 175 mg/dL.³ The Lescol Intervention Prevention study randomized patients after angioplasty to fluvastatin 40 mg twice daily or placebo.⁴ The Heart Protection Study used simvastatin 40 mg daily, without titration.⁵ No RCTs have evaluated the clinical benefit of adding medications to adequate doses of statins to lower LDL to less than 175 mg/dL. See Table of major RCTs with clinical outcomes.

Subgroup analyses of earlier major RCTs had suggested that patients with CAD and low initial LDL levels (< 125 mg/dL) have little to gain from pravastatin.^2,3 However, the Heart Protection Study enrolled 20,000 people with CAD or equivalent (diabetes, peripheral vascular disease, stroke, etc).⁵ The study demonstrated a reduction of major coronary events with simvastatin, with numbers needed to treat (NNT) of 19 (P < .0001); the NNT for reduction in all-cause mortality was 55 (P = .0003). The benefit of simvastatin was noted in virtually every predefined subgroup, including individuals older than 70 years, women, and patients without known CAD (but with CAD equivalents). Notably, no difference in benefit was found between patients with different pretreatment LDL levels. A significant reduction in major vascular events was noted even for the 3400 subjects with pretreatment LDL levels of less than 100 mg/dL (NNT = 22, P = .0006). A greater percentage reduction in LDL with medication did not predict better clinical outcomes.⁵

TABLE

LDL levels and relative risk of major coronary events after treatment

Recommendations from others

The National Cholesterol Education Project (NCEP) recommends that patients with CAD and an LDL of more than 130 mg/dL adopt therapeutic lifestyle changes and start LDL-lowering medication, usually a statin. For patients with LDL between 100 and 130 mg/dL, the NCEP recommends therapeutic lifestyle changes, with the option of adding a statin. For patients with LDL less than 100 mg/dL, maintenance of LDL control is recommended with therapeutic lifestyle changes. For patients with high initial LDL levels that stay above 100 mg/dL on statin therapy, the NCEP recommends that additional medications, such as nicotinic acid or fibrates, as well as intensive therapeutic lifestyle changes, be considered.⁶

Clinical Commentary by William Chavey, MD, at http://www.fpin.org.

EVIDENCE-BASED ANSWER

Large published randomized controlled trials (RCTs) show that pravastatin and simvastatin are well-tolerated and reduce major coronary events such as death, myocardial infarction, and revascularization by about 25%. The Heart Protection Study suggested this benefit is noted even among individuals with pretreatment low-density lipoprotein (LDL) cholesterol of less than 100 mg/dL. Fluvastatin reduces major coronary events, but current studies are too small to prove reduced overall mortality. The best evidence to date suggests that most patients at significant risk for major coronary events should be given pravastatin or simvastatin 40 mg daily, without concern for the initial or follow-up LDL levels. (Grade of recommendation: A, based on large randomized trials.)

Evidence summary

The evidence is solid to support the use of HMG–CoA reductase inhibitors (statins) for patients with coronary artery disease (CAD). The Scandinavian Simvastatin Survival study used simvastatin 20 mg daily unless total cholesterol levels did not decrease to less than 200 mg/dL.¹ The Long-Term Intervention with Pravastatin in Ischaemic Disease study randomized patients to pravastatin 40 mg daily or placebo, without titration.² The intervention arm in the Cholesterol and Recurrent Events trial was also pravastatin 40 mg daily, with cholestyramine added if the LDL level remained higher than 175 mg/dL.³ The Lescol Intervention Prevention study randomized patients after angioplasty to fluvastatin 40 mg twice daily or placebo.⁴ The Heart Protection Study used simvastatin 40 mg daily, without titration.⁵ No RCTs have evaluated the clinical benefit of adding medications to adequate doses of statins to lower LDL to less than 175 mg/dL. See Table of major RCTs with clinical outcomes.

Subgroup analyses of earlier major RCTs had suggested that patients with CAD and low initial LDL levels (< 125 mg/dL) have little to gain from pravastatin.^2,3 However, the Heart Protection Study enrolled 20,000 people with CAD or equivalent (diabetes, peripheral vascular disease, stroke, etc).⁵ The study demonstrated a reduction of major coronary events with simvastatin, with numbers needed to treat (NNT) of 19 (P < .0001); the NNT for reduction in all-cause mortality was 55 (P = .0003). The benefit of simvastatin was noted in virtually every predefined subgroup, including individuals older than 70 years, women, and patients without known CAD (but with CAD equivalents). Notably, no difference in benefit was found between patients with different pretreatment LDL levels. A significant reduction in major vascular events was noted even for the 3400 subjects with pretreatment LDL levels of less than 100 mg/dL (NNT = 22, P = .0006). A greater percentage reduction in LDL with medication did not predict better clinical outcomes.⁵

TABLE

LDL levels and relative risk of major coronary events after treatment

Recommendations from others

The National Cholesterol Education Project (NCEP) recommends that patients with CAD and an LDL of more than 130 mg/dL adopt therapeutic lifestyle changes and start LDL-lowering medication, usually a statin. For patients with LDL between 100 and 130 mg/dL, the NCEP recommends therapeutic lifestyle changes, with the option of adding a statin. For patients with LDL less than 100 mg/dL, maintenance of LDL control is recommended with therapeutic lifestyle changes. For patients with high initial LDL levels that stay above 100 mg/dL on statin therapy, the NCEP recommends that additional medications, such as nicotinic acid or fibrates, as well as intensive therapeutic lifestyle changes, be considered.⁶

Clinical Commentary by William Chavey, MD, at http://www.fpin.org.