Bruce K. Dixon

Selected patients with colorectal cancer metastasized to the liver can undergo a single procedure to remove lesions at both locations, according to a multicenter study presented at the Society of Surgical Oncology in Washington.

The traditional approach has been to remove the primary tumor and then place the patient on chemotherapy prior to doing a hepatic resection, said Dr. Bryan Clary, chief of hepatobiliary surgery Duke University, Durham, N.C.

“The rationale for that approach has been the perception that simultaneous hepatic and colorectal surgery is excessively morbid, but a growing body of evidence has called this strategy into question,” Dr. Clary said in an interview.

In about a third of patients newly diagnosed with colorectal cancer, disease already has spread to the liver, he added.

The Duke University researchers teamed with investigators from Johns Hopkins Medical Institutions in Baltimore and the University of Texas M.D. Anderson Cancer Center in Houston to conduct a retrospective outcomes study of 610 patients who had undergone either simultaneous (135) or separate (475) procedures for removal of synchronous colorectal and liver cancer.

Data for the years 1985 through 2006 were drawn from three large-volume hepatobiliary centers.

“We found that for patients who require a minor hepatectomy in conjunction with their colorectal operations, the risk does not seem to be increased in comparison with those undergoing staged liver resection,” Dr. Clary said.

In the minor hepatectomy cohort, defined as the removal of fewer than three liver segments, 99 were done simultaneously with colorectal surgery and 184 were staged procedures. Measures of intraoperative red blood cell transfusion, blood loss, positive resection margins, mortality, and morbidity were statistically similar. However, in the major hepatectomy group, mortality, overall morbidity, and severe morbidity were significantly higher for the simultaneous procedure, compared with the staged approach (8% vs. 1%, 44% vs. 27%, and 36% vs. 15%, respectively).

Simultaneous resection resulted in a significantly shorter median length of hospital stay (8.5 vs. 14 days) at the single institution where hospital time was calculated for both procedures, Dr. Clary explained.

Survival data were similar for simultaneous and staged resection. However, posthepatectomy chemotherapy significantly prolonged survival for patients with synchronous hepatic metastases, regardless of whether the resection was done simultaneously with or separate from colorectal procedure.

The 1-, 3-, and 5-year survival rates following posthepatectomy chemotherapy were 98%, 75%, and 55%, respectively. When no chemotherapy was given, those rates fell to 95%, 60%, and 41%.

“There is no compelling evidence that giving chemotherapy beforehand makes a difference, so in general, patients whose disease is resectable should have a resection, whereas marginal medical patients with a lot of comorbidities should be given chemotherapy prior to a complex operation,” Dr. Clary said in an interview, adding that these complex cases need to be much more carefully selected because in general, severe morbidity rates are increased with the simultaneous approach.

Chemotherapy is appropriate in patients whose liver disease is not resectable, in cases where hepatic resection has a low likelihood of achieving a negative margin, and where disease is suspected elsewhere in the body, he said.

Dr. Clary stressed the importance of early patient evaluation by a multidisciplinary team that includes a surgeon experienced in doing hepatic surgery.

Patients with obstructing colon cancers in urgent need of removal and those with significant bleeding from their primary tumors should not undergo this procedure, he said.

“The bottom line is that a single surgery should be considered in the patient who likely would require a minor hepatectomy for extirpation of their liver disease following early evaluation by a competent hepatic surgeon,” Dr. Clary said.

Selected patients with colorectal cancer metastasized to the liver can undergo a single procedure to remove lesions at both locations, according to a multicenter study presented at the Society of Surgical Oncology in Washington.

The traditional approach has been to remove the primary tumor and then place the patient on chemotherapy prior to doing a hepatic resection, said Dr. Bryan Clary, chief of hepatobiliary surgery Duke University, Durham, N.C.

“The rationale for that approach has been the perception that simultaneous hepatic and colorectal surgery is excessively morbid, but a growing body of evidence has called this strategy into question,” Dr. Clary said in an interview.

In about a third of patients newly diagnosed with colorectal cancer, disease already has spread to the liver, he added.

The Duke University researchers teamed with investigators from Johns Hopkins Medical Institutions in Baltimore and the University of Texas M.D. Anderson Cancer Center in Houston to conduct a retrospective outcomes study of 610 patients who had undergone either simultaneous (135) or separate (475) procedures for removal of synchronous colorectal and liver cancer.

Data for the years 1985 through 2006 were drawn from three large-volume hepatobiliary centers.

“We found that for patients who require a minor hepatectomy in conjunction with their colorectal operations, the risk does not seem to be increased in comparison with those undergoing staged liver resection,” Dr. Clary said.

In the minor hepatectomy cohort, defined as the removal of fewer than three liver segments, 99 were done simultaneously with colorectal surgery and 184 were staged procedures. Measures of intraoperative red blood cell transfusion, blood loss, positive resection margins, mortality, and morbidity were statistically similar. However, in the major hepatectomy group, mortality, overall morbidity, and severe morbidity were significantly higher for the simultaneous procedure, compared with the staged approach (8% vs. 1%, 44% vs. 27%, and 36% vs. 15%, respectively).

Simultaneous resection resulted in a significantly shorter median length of hospital stay (8.5 vs. 14 days) at the single institution where hospital time was calculated for both procedures, Dr. Clary explained.

Survival data were similar for simultaneous and staged resection. However, posthepatectomy chemotherapy significantly prolonged survival for patients with synchronous hepatic metastases, regardless of whether the resection was done simultaneously with or separate from colorectal procedure.

The 1-, 3-, and 5-year survival rates following posthepatectomy chemotherapy were 98%, 75%, and 55%, respectively. When no chemotherapy was given, those rates fell to 95%, 60%, and 41%.

“There is no compelling evidence that giving chemotherapy beforehand makes a difference, so in general, patients whose disease is resectable should have a resection, whereas marginal medical patients with a lot of comorbidities should be given chemotherapy prior to a complex operation,” Dr. Clary said in an interview, adding that these complex cases need to be much more carefully selected because in general, severe morbidity rates are increased with the simultaneous approach.

Chemotherapy is appropriate in patients whose liver disease is not resectable, in cases where hepatic resection has a low likelihood of achieving a negative margin, and where disease is suspected elsewhere in the body, he said.

Dr. Clary stressed the importance of early patient evaluation by a multidisciplinary team that includes a surgeon experienced in doing hepatic surgery.

Patients with obstructing colon cancers in urgent need of removal and those with significant bleeding from their primary tumors should not undergo this procedure, he said.

“The bottom line is that a single surgery should be considered in the patient who likely would require a minor hepatectomy for extirpation of their liver disease following early evaluation by a competent hepatic surgeon,” Dr. Clary said.

Selected patients with colorectal cancer metastasized to the liver can undergo a single procedure to remove lesions at both locations, according to a multicenter study presented at the Society of Surgical Oncology in Washington.

The traditional approach has been to remove the primary tumor and then place the patient on chemotherapy prior to doing a hepatic resection, said Dr. Bryan Clary, chief of hepatobiliary surgery Duke University, Durham, N.C.

“The rationale for that approach has been the perception that simultaneous hepatic and colorectal surgery is excessively morbid, but a growing body of evidence has called this strategy into question,” Dr. Clary said in an interview.

In about a third of patients newly diagnosed with colorectal cancer, disease already has spread to the liver, he added.

The Duke University researchers teamed with investigators from Johns Hopkins Medical Institutions in Baltimore and the University of Texas M.D. Anderson Cancer Center in Houston to conduct a retrospective outcomes study of 610 patients who had undergone either simultaneous (135) or separate (475) procedures for removal of synchronous colorectal and liver cancer.

Data for the years 1985 through 2006 were drawn from three large-volume hepatobiliary centers.

“We found that for patients who require a minor hepatectomy in conjunction with their colorectal operations, the risk does not seem to be increased in comparison with those undergoing staged liver resection,” Dr. Clary said.

In the minor hepatectomy cohort, defined as the removal of fewer than three liver segments, 99 were done simultaneously with colorectal surgery and 184 were staged procedures. Measures of intraoperative red blood cell transfusion, blood loss, positive resection margins, mortality, and morbidity were statistically similar. However, in the major hepatectomy group, mortality, overall morbidity, and severe morbidity were significantly higher for the simultaneous procedure, compared with the staged approach (8% vs. 1%, 44% vs. 27%, and 36% vs. 15%, respectively).

Simultaneous resection resulted in a significantly shorter median length of hospital stay (8.5 vs. 14 days) at the single institution where hospital time was calculated for both procedures, Dr. Clary explained.

Survival data were similar for simultaneous and staged resection. However, posthepatectomy chemotherapy significantly prolonged survival for patients with synchronous hepatic metastases, regardless of whether the resection was done simultaneously with or separate from colorectal procedure.

The 1-, 3-, and 5-year survival rates following posthepatectomy chemotherapy were 98%, 75%, and 55%, respectively. When no chemotherapy was given, those rates fell to 95%, 60%, and 41%.

“There is no compelling evidence that giving chemotherapy beforehand makes a difference, so in general, patients whose disease is resectable should have a resection, whereas marginal medical patients with a lot of comorbidities should be given chemotherapy prior to a complex operation,” Dr. Clary said in an interview, adding that these complex cases need to be much more carefully selected because in general, severe morbidity rates are increased with the simultaneous approach.

Chemotherapy is appropriate in patients whose liver disease is not resectable, in cases where hepatic resection has a low likelihood of achieving a negative margin, and where disease is suspected elsewhere in the body, he said.

Dr. Clary stressed the importance of early patient evaluation by a multidisciplinary team that includes a surgeon experienced in doing hepatic surgery.

Patients with obstructing colon cancers in urgent need of removal and those with significant bleeding from their primary tumors should not undergo this procedure, he said.

“The bottom line is that a single surgery should be considered in the patient who likely would require a minor hepatectomy for extirpation of their liver disease following early evaluation by a competent hepatic surgeon,” Dr. Clary said.

Patients with type 1 diabetes may be better protected from diabetic macular edema by improved control of glycemia, LDL cholesterol levels, and blood pressure, according to a 15-year follow-up study.

The prospective study was launched in 1990 with a cohort of 112 consecutive type 1 diabetes patients who did not have diabetic retinopathy or nephropathy at the time, according to Dr. Pedro Romero and colleagues at the Hospital Universitario Sant Joan de Reus, Universidad Rovira y Virgili, Spain.

“Our objective was to determine the epidemiological risk factors that influence the development of diabetic macular edema, in particular renal diabetic lesion (microalbuminuria or overt nephropathy),” according to Dr. Romero and colleagues.

The half-male, half-female cohort had a mean age of 40 years and a mean diabetes duration of 23.4 years. Arterial hypertension was present in 39% of patients.

Diabetic retinopathy was evaluated by photographs, through dilated pupils, of two 50-degree fields of each eye centered. The results were then classified as mild nonproliferative, moderate proliferative, severe proliferative, and proliferative (J. Diabetes Complications 2007;21:172–80).

Macular edema was considered present when retinal thickening involved or was within 500 mcm of the center of the macula; when hard exudates were at or within 500 mcm of the macula, if it was associated with a thickening of the adjacent retina (but no hard exudates remained after retinal thickening disappeared); and when the zone(s) of retinal thickening was (were) one disc area (or larger) in size, any part of which was within one disc diameter of the center of the macula.

The clinical classification used was the International Clinical Diabetic Retinopathy Disease Severity Scale, the investigators wrote.

After 15 years, one-half of the cohort had diabetic retinopathy (DR) and one-fifth of the cohort had diabetic macular edema (DME). More than half of those with DME had the focal type, a third were the diffuse form, and two patients had diffuse associated form to cystoid form (which is associated with diffuse form).

The mean visual acuity in patients with DME after 15 years was 0.31 in the Snellen chart test and 1.26 in the LogMAR test. The mean macular thickness was 356.21 mcm.

Factors found to be significant to the development of DME included:

▸ High levels of glycated hemoglobin. Glycemic control was classified into two groups: hemoglobin A_1c greater than 7.5% or less than 7.5% in concordance with the European Diabetes Policy Group. The value included in statistical analyses was the mean of all values obtained over the trial period.

▸ High levels of LDL cholesterol as defined by the American Diabetes Association categories (3.35 mmol/L or higher). In contrast to previously published research, no lipid parameters were associated with the progression of diabetic retinopathy or with proliferative diabetic retinopathy after adjustment for glycated hemoglobin and other risk factors, the investigators explained.

▸ The presence of macroangiopathy. For this, one or more of the following had to be present: symptoms of angina pectoris, history of myocardial infarction, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty, symptoms of or operation for intermittent claudication, history of amputation, transient ischemic attack, and stroke.

The authors maintained that this relationship between macroangiopathy and DME “may be explained, in part, by the increased incidence of macular edema with increased levels of lipids, which was strongly associated with the development of macroangiopathic lesions in” previous studies (Br. J. Ophthalmol. 2002;86:84–90; Ophthalmology 2002;109:1225–34).

▸ The presence of arterial hypertension, defined as a systolic measurement of 140 mm Hg or higher and a diastolic measurement of 90 mm Hg or higher.

This result contradicted an earlier finding from a 10-year study showing that the level of diastolic blood pressure was not a predictor in type 1 diabetes patients (Arch. Ophthalmol. 1995;113:601–6).

“However, a precedent study of that same group, at four years, found a positive relationship between diastolic blood pressure and the incidence of macular edema,” Dr. Romero and colleagues wrote.

▸ The severity of diabetic retinopathy, a finding which confirms previous studies.

The researchers expressed surprise that the study found no association with cigarette smoking, although an earlier study also failed to link cigarette smoking with DME (Ophthalmology 1996;103:1438–42). The current investigators hypothesize that cigarette smoking, through its deleterious effects on the retinal vasculature, may affect diabetic maculopathy.

“We did not demonstrate this effect, but if we had studied the angiographic findings in patients with diabetic macular edema, we may not have associated cigarette smoking with an increase in the development of areas of macular ischemia,” the investigators said.

“Our data suggest that better control of glycemia, LDL cholesterol levels, and blood pressure in type 1 diabetes patients may be beneficial in reducing the incidence of diabetic macular edema,” the researchers concluded, adding that their results validate the current guidelines for ophthalmologic care for the detection of diabetic macular edema over the long-term course of diabetes.

Patients with type 1 diabetes may be better protected from diabetic macular edema by improved control of glycemia, LDL cholesterol levels, and blood pressure, according to a 15-year follow-up study.

The prospective study was launched in 1990 with a cohort of 112 consecutive type 1 diabetes patients who did not have diabetic retinopathy or nephropathy at the time, according to Dr. Pedro Romero and colleagues at the Hospital Universitario Sant Joan de Reus, Universidad Rovira y Virgili, Spain.

“Our objective was to determine the epidemiological risk factors that influence the development of diabetic macular edema, in particular renal diabetic lesion (microalbuminuria or overt nephropathy),” according to Dr. Romero and colleagues.

The half-male, half-female cohort had a mean age of 40 years and a mean diabetes duration of 23.4 years. Arterial hypertension was present in 39% of patients.

Diabetic retinopathy was evaluated by photographs, through dilated pupils, of two 50-degree fields of each eye centered. The results were then classified as mild nonproliferative, moderate proliferative, severe proliferative, and proliferative (J. Diabetes Complications 2007;21:172–80).

Macular edema was considered present when retinal thickening involved or was within 500 mcm of the center of the macula; when hard exudates were at or within 500 mcm of the macula, if it was associated with a thickening of the adjacent retina (but no hard exudates remained after retinal thickening disappeared); and when the zone(s) of retinal thickening was (were) one disc area (or larger) in size, any part of which was within one disc diameter of the center of the macula.

The clinical classification used was the International Clinical Diabetic Retinopathy Disease Severity Scale, the investigators wrote.

After 15 years, one-half of the cohort had diabetic retinopathy (DR) and one-fifth of the cohort had diabetic macular edema (DME). More than half of those with DME had the focal type, a third were the diffuse form, and two patients had diffuse associated form to cystoid form (which is associated with diffuse form).

The mean visual acuity in patients with DME after 15 years was 0.31 in the Snellen chart test and 1.26 in the LogMAR test. The mean macular thickness was 356.21 mcm.

Factors found to be significant to the development of DME included:

▸ High levels of glycated hemoglobin. Glycemic control was classified into two groups: hemoglobin A_1c greater than 7.5% or less than 7.5% in concordance with the European Diabetes Policy Group. The value included in statistical analyses was the mean of all values obtained over the trial period.

▸ High levels of LDL cholesterol as defined by the American Diabetes Association categories (3.35 mmol/L or higher). In contrast to previously published research, no lipid parameters were associated with the progression of diabetic retinopathy or with proliferative diabetic retinopathy after adjustment for glycated hemoglobin and other risk factors, the investigators explained.

▸ The presence of macroangiopathy. For this, one or more of the following had to be present: symptoms of angina pectoris, history of myocardial infarction, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty, symptoms of or operation for intermittent claudication, history of amputation, transient ischemic attack, and stroke.

The authors maintained that this relationship between macroangiopathy and DME “may be explained, in part, by the increased incidence of macular edema with increased levels of lipids, which was strongly associated with the development of macroangiopathic lesions in” previous studies (Br. J. Ophthalmol. 2002;86:84–90; Ophthalmology 2002;109:1225–34).

▸ The presence of arterial hypertension, defined as a systolic measurement of 140 mm Hg or higher and a diastolic measurement of 90 mm Hg or higher.

This result contradicted an earlier finding from a 10-year study showing that the level of diastolic blood pressure was not a predictor in type 1 diabetes patients (Arch. Ophthalmol. 1995;113:601–6).

“However, a precedent study of that same group, at four years, found a positive relationship between diastolic blood pressure and the incidence of macular edema,” Dr. Romero and colleagues wrote.

▸ The severity of diabetic retinopathy, a finding which confirms previous studies.

The researchers expressed surprise that the study found no association with cigarette smoking, although an earlier study also failed to link cigarette smoking with DME (Ophthalmology 1996;103:1438–42). The current investigators hypothesize that cigarette smoking, through its deleterious effects on the retinal vasculature, may affect diabetic maculopathy.

“We did not demonstrate this effect, but if we had studied the angiographic findings in patients with diabetic macular edema, we may not have associated cigarette smoking with an increase in the development of areas of macular ischemia,” the investigators said.

“Our data suggest that better control of glycemia, LDL cholesterol levels, and blood pressure in type 1 diabetes patients may be beneficial in reducing the incidence of diabetic macular edema,” the researchers concluded, adding that their results validate the current guidelines for ophthalmologic care for the detection of diabetic macular edema over the long-term course of diabetes.

Patients with type 1 diabetes may be better protected from diabetic macular edema by improved control of glycemia, LDL cholesterol levels, and blood pressure, according to a 15-year follow-up study.

The prospective study was launched in 1990 with a cohort of 112 consecutive type 1 diabetes patients who did not have diabetic retinopathy or nephropathy at the time, according to Dr. Pedro Romero and colleagues at the Hospital Universitario Sant Joan de Reus, Universidad Rovira y Virgili, Spain.

“Our objective was to determine the epidemiological risk factors that influence the development of diabetic macular edema, in particular renal diabetic lesion (microalbuminuria or overt nephropathy),” according to Dr. Romero and colleagues.

The half-male, half-female cohort had a mean age of 40 years and a mean diabetes duration of 23.4 years. Arterial hypertension was present in 39% of patients.

Diabetic retinopathy was evaluated by photographs, through dilated pupils, of two 50-degree fields of each eye centered. The results were then classified as mild nonproliferative, moderate proliferative, severe proliferative, and proliferative (J. Diabetes Complications 2007;21:172–80).

Macular edema was considered present when retinal thickening involved or was within 500 mcm of the center of the macula; when hard exudates were at or within 500 mcm of the macula, if it was associated with a thickening of the adjacent retina (but no hard exudates remained after retinal thickening disappeared); and when the zone(s) of retinal thickening was (were) one disc area (or larger) in size, any part of which was within one disc diameter of the center of the macula.

The clinical classification used was the International Clinical Diabetic Retinopathy Disease Severity Scale, the investigators wrote.

After 15 years, one-half of the cohort had diabetic retinopathy (DR) and one-fifth of the cohort had diabetic macular edema (DME). More than half of those with DME had the focal type, a third were the diffuse form, and two patients had diffuse associated form to cystoid form (which is associated with diffuse form).

The mean visual acuity in patients with DME after 15 years was 0.31 in the Snellen chart test and 1.26 in the LogMAR test. The mean macular thickness was 356.21 mcm.

Factors found to be significant to the development of DME included:

▸ High levels of glycated hemoglobin. Glycemic control was classified into two groups: hemoglobin A_1c greater than 7.5% or less than 7.5% in concordance with the European Diabetes Policy Group. The value included in statistical analyses was the mean of all values obtained over the trial period.

▸ High levels of LDL cholesterol as defined by the American Diabetes Association categories (3.35 mmol/L or higher). In contrast to previously published research, no lipid parameters were associated with the progression of diabetic retinopathy or with proliferative diabetic retinopathy after adjustment for glycated hemoglobin and other risk factors, the investigators explained.

▸ The presence of macroangiopathy. For this, one or more of the following had to be present: symptoms of angina pectoris, history of myocardial infarction, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty, symptoms of or operation for intermittent claudication, history of amputation, transient ischemic attack, and stroke.

The authors maintained that this relationship between macroangiopathy and DME “may be explained, in part, by the increased incidence of macular edema with increased levels of lipids, which was strongly associated with the development of macroangiopathic lesions in” previous studies (Br. J. Ophthalmol. 2002;86:84–90; Ophthalmology 2002;109:1225–34).

▸ The presence of arterial hypertension, defined as a systolic measurement of 140 mm Hg or higher and a diastolic measurement of 90 mm Hg or higher.

This result contradicted an earlier finding from a 10-year study showing that the level of diastolic blood pressure was not a predictor in type 1 diabetes patients (Arch. Ophthalmol. 1995;113:601–6).

“However, a precedent study of that same group, at four years, found a positive relationship between diastolic blood pressure and the incidence of macular edema,” Dr. Romero and colleagues wrote.

▸ The severity of diabetic retinopathy, a finding which confirms previous studies.

The researchers expressed surprise that the study found no association with cigarette smoking, although an earlier study also failed to link cigarette smoking with DME (Ophthalmology 1996;103:1438–42). The current investigators hypothesize that cigarette smoking, through its deleterious effects on the retinal vasculature, may affect diabetic maculopathy.

“We did not demonstrate this effect, but if we had studied the angiographic findings in patients with diabetic macular edema, we may not have associated cigarette smoking with an increase in the development of areas of macular ischemia,” the investigators said.

“Our data suggest that better control of glycemia, LDL cholesterol levels, and blood pressure in type 1 diabetes patients may be beneficial in reducing the incidence of diabetic macular edema,” the researchers concluded, adding that their results validate the current guidelines for ophthalmologic care for the detection of diabetic macular edema over the long-term course of diabetes.

CHICAGO — An enzyme found in brain cells may become the first bedside biomarker for assessing the severity of traumatic brain injury, according to Dr. Linda Papa.

In a multicenter trial, levels of the enzyme ubiquitin C-terminal hydrolase (UCH-L1) rose significantly in severely injured brains, an increase that paralleled the rise in cerebral spinal fluid and correlated with the Glasgow Coma Scale (GCS) score, Dr. Papa told the annual meeting of the Society for Academic Emergency Medicine.

If further study confirms the value of UCH-L1 as the first clinical biomarker in traumatic brain injury (TBI), physicians will be better able to identify targets for drug therapy and guide the timing of treatment with such agents as tissue plasminogen activator, explained Dr. Papa, director of academic clinical research at Orlando Regional Medical Center.

This prospective case-control study enrolled consecutive adult patients presenting to two tertiary care teaching hospitals following severe TBIs, defined by a GCS score of less than 8 and requiring invasive intracerebral monitoring. Fourteen patients with severe TBI were enrolled over 16 months. Their mean age was 38 years, and four-fifths were men. Patients were excluded if they did not have ventriculostomy, which is necessary to obtain cerebrospinal fluid (CSF). Ventricular CSF was drained from each patient at 6, 12, 24, 48, 72, and 96 hours following TBI, and was measured by enzyme-linked immunosorbent assay for UCH-L1 levels.

Mean 12-hour UCH-L1 levels in the control group of uninjured patients with other indications for CSF drainage were 145 ng/mL for patients with GCS scores of 3–5, and 38.5 ng/mL in those with GCS scores of 6–8. Similarly, 24-hour levels were 76 and 36 ng/mL for those with GCS scores of 3–5 and 6–8, respectively. The largest increase in the experimental biomarker occurred during the first 48 hours after injury, Dr. Papa said, noting: “Then we found that patients with evolving lesions had significantly higher levels of the biomarker” than did patients with nonevolving lesions at both 48 and 72 hours.”

“There is a significant increase in CSF UCH-L1 following severe human TBI compared to uninjured controls, and there is a significant association with severity of injury as measured by GCS and the presence of evolving lesions on CT,” Dr. Papa concluded, adding that these data suggest that UCH-L1 is a potential TBI biomarker.

Levels of the enzyme in the CSF corresponded to severity of injury and to CT evidence of evolving lesions. DR. PAPA

CHICAGO — An enzyme found in brain cells may become the first bedside biomarker for assessing the severity of traumatic brain injury, according to Dr. Linda Papa.

In a multicenter trial, levels of the enzyme ubiquitin C-terminal hydrolase (UCH-L1) rose significantly in severely injured brains, an increase that paralleled the rise in cerebral spinal fluid and correlated with the Glasgow Coma Scale (GCS) score, Dr. Papa told the annual meeting of the Society for Academic Emergency Medicine.

If further study confirms the value of UCH-L1 as the first clinical biomarker in traumatic brain injury (TBI), physicians will be better able to identify targets for drug therapy and guide the timing of treatment with such agents as tissue plasminogen activator, explained Dr. Papa, director of academic clinical research at Orlando Regional Medical Center.

This prospective case-control study enrolled consecutive adult patients presenting to two tertiary care teaching hospitals following severe TBIs, defined by a GCS score of less than 8 and requiring invasive intracerebral monitoring. Fourteen patients with severe TBI were enrolled over 16 months. Their mean age was 38 years, and four-fifths were men. Patients were excluded if they did not have ventriculostomy, which is necessary to obtain cerebrospinal fluid (CSF). Ventricular CSF was drained from each patient at 6, 12, 24, 48, 72, and 96 hours following TBI, and was measured by enzyme-linked immunosorbent assay for UCH-L1 levels.

Mean 12-hour UCH-L1 levels in the control group of uninjured patients with other indications for CSF drainage were 145 ng/mL for patients with GCS scores of 3–5, and 38.5 ng/mL in those with GCS scores of 6–8. Similarly, 24-hour levels were 76 and 36 ng/mL for those with GCS scores of 3–5 and 6–8, respectively. The largest increase in the experimental biomarker occurred during the first 48 hours after injury, Dr. Papa said, noting: “Then we found that patients with evolving lesions had significantly higher levels of the biomarker” than did patients with nonevolving lesions at both 48 and 72 hours.”

“There is a significant increase in CSF UCH-L1 following severe human TBI compared to uninjured controls, and there is a significant association with severity of injury as measured by GCS and the presence of evolving lesions on CT,” Dr. Papa concluded, adding that these data suggest that UCH-L1 is a potential TBI biomarker.

Levels of the enzyme in the CSF corresponded to severity of injury and to CT evidence of evolving lesions. DR. PAPA

CHICAGO — An enzyme found in brain cells may become the first bedside biomarker for assessing the severity of traumatic brain injury, according to Dr. Linda Papa.

In a multicenter trial, levels of the enzyme ubiquitin C-terminal hydrolase (UCH-L1) rose significantly in severely injured brains, an increase that paralleled the rise in cerebral spinal fluid and correlated with the Glasgow Coma Scale (GCS) score, Dr. Papa told the annual meeting of the Society for Academic Emergency Medicine.

If further study confirms the value of UCH-L1 as the first clinical biomarker in traumatic brain injury (TBI), physicians will be better able to identify targets for drug therapy and guide the timing of treatment with such agents as tissue plasminogen activator, explained Dr. Papa, director of academic clinical research at Orlando Regional Medical Center.

This prospective case-control study enrolled consecutive adult patients presenting to two tertiary care teaching hospitals following severe TBIs, defined by a GCS score of less than 8 and requiring invasive intracerebral monitoring. Fourteen patients with severe TBI were enrolled over 16 months. Their mean age was 38 years, and four-fifths were men. Patients were excluded if they did not have ventriculostomy, which is necessary to obtain cerebrospinal fluid (CSF). Ventricular CSF was drained from each patient at 6, 12, 24, 48, 72, and 96 hours following TBI, and was measured by enzyme-linked immunosorbent assay for UCH-L1 levels.

Mean 12-hour UCH-L1 levels in the control group of uninjured patients with other indications for CSF drainage were 145 ng/mL for patients with GCS scores of 3–5, and 38.5 ng/mL in those with GCS scores of 6–8. Similarly, 24-hour levels were 76 and 36 ng/mL for those with GCS scores of 3–5 and 6–8, respectively. The largest increase in the experimental biomarker occurred during the first 48 hours after injury, Dr. Papa said, noting: “Then we found that patients with evolving lesions had significantly higher levels of the biomarker” than did patients with nonevolving lesions at both 48 and 72 hours.”

“There is a significant increase in CSF UCH-L1 following severe human TBI compared to uninjured controls, and there is a significant association with severity of injury as measured by GCS and the presence of evolving lesions on CT,” Dr. Papa concluded, adding that these data suggest that UCH-L1 is a potential TBI biomarker.

Levels of the enzyme in the CSF corresponded to severity of injury and to CT evidence of evolving lesions. DR. PAPA

Patient phone calls are a necessity, and a potential liability, but Dr. S. Germain Cassiere said keeping track of calls is no longer a nightmare.

He has created software, called MessageTracker, to make this process easier.

The receptionist application initiates patient call records. When a call comes in, a receptionist fills out a template that pops up on his or her monitor. The record is sent to the physician, who sends it to a server computer that houses the database tables.

The nurse application contains a call record grid that resembles a spreadsheet showing calls that need responses. A nurse or physician documents the responses in the record. Once completed, the record is marked “done” and is automatically eliminated, said Dr. Cassiere, an internist in group practice in Shreveport, La.

Unless one wants printed records, the process is electronic. It cuts liability risk associated with missed and unreturned calls.

Calls can be searched by date or by the name of the patient or physician. “Our practice of six general internists handles 40,000–50,000 calls each year,” he said.

MessageTracker can be run without Microsoft's SQL Server as the database engine, so instead of the approximately $15,000 cost of the SQL Server and client licenses, Dr. Cassiere's cost for using the Nexus Database System was about $1,000.

MessageTracker is not currently for sale, but Dr. Cassiere said he's working on an improved version that will be available for purchase.

Patient phone calls are a necessity, and a potential liability, but Dr. S. Germain Cassiere said keeping track of calls is no longer a nightmare.

He has created software, called MessageTracker, to make this process easier.

The receptionist application initiates patient call records. When a call comes in, a receptionist fills out a template that pops up on his or her monitor. The record is sent to the physician, who sends it to a server computer that houses the database tables.

The nurse application contains a call record grid that resembles a spreadsheet showing calls that need responses. A nurse or physician documents the responses in the record. Once completed, the record is marked “done” and is automatically eliminated, said Dr. Cassiere, an internist in group practice in Shreveport, La.

Unless one wants printed records, the process is electronic. It cuts liability risk associated with missed and unreturned calls.

Calls can be searched by date or by the name of the patient or physician. “Our practice of six general internists handles 40,000–50,000 calls each year,” he said.

MessageTracker can be run without Microsoft's SQL Server as the database engine, so instead of the approximately $15,000 cost of the SQL Server and client licenses, Dr. Cassiere's cost for using the Nexus Database System was about $1,000.

MessageTracker is not currently for sale, but Dr. Cassiere said he's working on an improved version that will be available for purchase.

Patient phone calls are a necessity, and a potential liability, but Dr. S. Germain Cassiere said keeping track of calls is no longer a nightmare.

He has created software, called MessageTracker, to make this process easier.

The receptionist application initiates patient call records. When a call comes in, a receptionist fills out a template that pops up on his or her monitor. The record is sent to the physician, who sends it to a server computer that houses the database tables.

The nurse application contains a call record grid that resembles a spreadsheet showing calls that need responses. A nurse or physician documents the responses in the record. Once completed, the record is marked “done” and is automatically eliminated, said Dr. Cassiere, an internist in group practice in Shreveport, La.

Unless one wants printed records, the process is electronic. It cuts liability risk associated with missed and unreturned calls.

Calls can be searched by date or by the name of the patient or physician. “Our practice of six general internists handles 40,000–50,000 calls each year,” he said.

MessageTracker can be run without Microsoft's SQL Server as the database engine, so instead of the approximately $15,000 cost of the SQL Server and client licenses, Dr. Cassiere's cost for using the Nexus Database System was about $1,000.

MessageTracker is not currently for sale, but Dr. Cassiere said he's working on an improved version that will be available for purchase.

The incidence of invasive pneumococcal disease among children younger than 5 years with sickle cell disease plummeted during 2001–2004, according to a new study which suggests that credit belongs to the 7-valent pneumococcal conjugate vaccine introduced in 2000.

“Our study clearly demonstrates that the incidence of invasive pneumococcal disease dramatically decreased after the introduction of pneumococcal conjugate vaccine into the routine childhood immunization schedule,” Dr. Natasha B. Halasa and colleagues wrote.

The data were derived from the follow-up of 2,026 individuals with sickle cell disease (SCD) enrolled in Tennessee Medicaid (TennCare) from Jan. 1, 1995, through Dec. 31, 2004 (Clin. Infect. Dis. 2007;44:1428–33).

During the study period, 37 individuals (0.6–44 years) with SCD had invasive pneumococcal disease (IPD), and no individuals with SCD had more than one episode of IPD during the study period.

In a comparison of the pre-PCV period (1995–1999) with the post-PCV period (2001–2004), the IPD rate decreased 91% in children aged less than 2 years (from 3,600 to 335 cases per 100,000 person-years) and by 93% in children under 5 years (from 2,044 to 134 cases per 100,000 person-years). In the post-PCV era, a mean 69% of children less than 2 years had evidence of receiving one or more doses of PCV during the prior year.

Although penicillin prophylaxis and pneumococcal polysaccharide vaccine have decreased the rate of invasive pneumococcal disease (IPD) in this high-risk population, breakthrough disease still occurs—most commonly among children younger than 3 years—and IPD continues to be a leading cause of death in children with SCD, the researchers explained.

This study, which showed a mean 92% drop in infection after 2000 among children younger than 5 years, raises important questions about the continued use of penicillin, according to Dr. Martin H. Steinberg, whose accompanying editorial poses the question, “Is prophylactic penicillin needed if conjugate vaccination is so effective?”

“Widespread penicillin use is not risk free. Penicillin-resistant strains of S. pneumoniae are increasing in number, and about 40% of isolates associated with sickle cell disease have some measure of resistance,” said Dr. Steinberg, with the departments of medicine, pediatrics, and pathology and laboratory medicine at Boston University (Clin. Infect. Dis. 2007;44:1434–5).

Dr. Steinberg believes that the susceptibility of S. pneumoniae to penicillin might be decreasing, and he points out that prophylaxis is less effective in carriers of intermediate-resistant and resistant serotypes.

In North America, the 7-valent conjugate vaccine protects against greater than 70% of the serotypes isolated from patients in the preconjugate vaccine era, he said. “However, two-thirds of the serotypes not included in the vaccine were susceptible to penicillin, and the use of this vaccine appeared to decrease the number of antibiotic-resistant, pneumococcal infections (N. Engl. J. Med. 2006;354:1455–63).”

Pending the arrival of a more efficacious 13-valent vaccine, antibiotic prophylaxis could be useful, Dr. Steinberg explained, adding that suboptimal compliance with preventive treatment limits penicillin's effectiveness.

In the Tennessee cohort, only 25% to 30% of the children with SCD who were younger than 5 years had their penicillin prescriptions filled for more than 270 days of a 1-year period. These numbers are similar to those found in an earlier study (JAMA 2003;290:1057–61), Dr. Halasa and colleagues said.

Because ongoing penicillin prophylaxis is difficult to sustain, the effectiveness of this approach in practice appears to be less than that demonstrated in the landmark randomized, clinical trial in which the antibiotic produced an 84% reduction in the rate of IPD among children with SCD the researchers said (N. Engl. J. Med. 1986;314:1593–9).

This study has several limitations, according to Dr. Halasa and her team: The number of individuals with SCD and IPD was small and consisted of patients who lived in surveillance counties in Tennessee and who were enrolled in the Tennessee Medicaid program.

“The pre-PCV era IPD rates in individuals with SCD in this study, however, were nearly identical to those reported from other locations, suggesting that these results are generalizable to others with SCD in the United States,” they argue.

A second limitation was that vaccination records, especially from the period prior to the introduction of PCV, may not have captured receipt of all pneumococcal vaccines by persons enrolled in TennCare.

With the universal administration of PCV to all children, both with and without SCD, it is expected that the rates of IPD will continue to decrease among all children, the authors wrote.

“However, ongoing monitoring of these rates and serotyping of all invasive pneumococcal isolates must remain an important priority to monitor whether serotype replacement will occur under continued vaccine pressure. Despite this caution, our data indicate that PCV is effective for reducing the rate of IPD, especially among vulnerable populations,” they concluded.

The incidence of invasive pneumococcal disease among children younger than 5 years with sickle cell disease plummeted during 2001–2004, according to a new study which suggests that credit belongs to the 7-valent pneumococcal conjugate vaccine introduced in 2000.

“Our study clearly demonstrates that the incidence of invasive pneumococcal disease dramatically decreased after the introduction of pneumococcal conjugate vaccine into the routine childhood immunization schedule,” Dr. Natasha B. Halasa and colleagues wrote.

The data were derived from the follow-up of 2,026 individuals with sickle cell disease (SCD) enrolled in Tennessee Medicaid (TennCare) from Jan. 1, 1995, through Dec. 31, 2004 (Clin. Infect. Dis. 2007;44:1428–33).

During the study period, 37 individuals (0.6–44 years) with SCD had invasive pneumococcal disease (IPD), and no individuals with SCD had more than one episode of IPD during the study period.

In a comparison of the pre-PCV period (1995–1999) with the post-PCV period (2001–2004), the IPD rate decreased 91% in children aged less than 2 years (from 3,600 to 335 cases per 100,000 person-years) and by 93% in children under 5 years (from 2,044 to 134 cases per 100,000 person-years). In the post-PCV era, a mean 69% of children less than 2 years had evidence of receiving one or more doses of PCV during the prior year.

Although penicillin prophylaxis and pneumococcal polysaccharide vaccine have decreased the rate of invasive pneumococcal disease (IPD) in this high-risk population, breakthrough disease still occurs—most commonly among children younger than 3 years—and IPD continues to be a leading cause of death in children with SCD, the researchers explained.

This study, which showed a mean 92% drop in infection after 2000 among children younger than 5 years, raises important questions about the continued use of penicillin, according to Dr. Martin H. Steinberg, whose accompanying editorial poses the question, “Is prophylactic penicillin needed if conjugate vaccination is so effective?”

“Widespread penicillin use is not risk free. Penicillin-resistant strains of S. pneumoniae are increasing in number, and about 40% of isolates associated with sickle cell disease have some measure of resistance,” said Dr. Steinberg, with the departments of medicine, pediatrics, and pathology and laboratory medicine at Boston University (Clin. Infect. Dis. 2007;44:1434–5).

Dr. Steinberg believes that the susceptibility of S. pneumoniae to penicillin might be decreasing, and he points out that prophylaxis is less effective in carriers of intermediate-resistant and resistant serotypes.

In North America, the 7-valent conjugate vaccine protects against greater than 70% of the serotypes isolated from patients in the preconjugate vaccine era, he said. “However, two-thirds of the serotypes not included in the vaccine were susceptible to penicillin, and the use of this vaccine appeared to decrease the number of antibiotic-resistant, pneumococcal infections (N. Engl. J. Med. 2006;354:1455–63).”

Pending the arrival of a more efficacious 13-valent vaccine, antibiotic prophylaxis could be useful, Dr. Steinberg explained, adding that suboptimal compliance with preventive treatment limits penicillin's effectiveness.

In the Tennessee cohort, only 25% to 30% of the children with SCD who were younger than 5 years had their penicillin prescriptions filled for more than 270 days of a 1-year period. These numbers are similar to those found in an earlier study (JAMA 2003;290:1057–61), Dr. Halasa and colleagues said.

Because ongoing penicillin prophylaxis is difficult to sustain, the effectiveness of this approach in practice appears to be less than that demonstrated in the landmark randomized, clinical trial in which the antibiotic produced an 84% reduction in the rate of IPD among children with SCD the researchers said (N. Engl. J. Med. 1986;314:1593–9).

This study has several limitations, according to Dr. Halasa and her team: The number of individuals with SCD and IPD was small and consisted of patients who lived in surveillance counties in Tennessee and who were enrolled in the Tennessee Medicaid program.

“The pre-PCV era IPD rates in individuals with SCD in this study, however, were nearly identical to those reported from other locations, suggesting that these results are generalizable to others with SCD in the United States,” they argue.

A second limitation was that vaccination records, especially from the period prior to the introduction of PCV, may not have captured receipt of all pneumococcal vaccines by persons enrolled in TennCare.

With the universal administration of PCV to all children, both with and without SCD, it is expected that the rates of IPD will continue to decrease among all children, the authors wrote.

“However, ongoing monitoring of these rates and serotyping of all invasive pneumococcal isolates must remain an important priority to monitor whether serotype replacement will occur under continued vaccine pressure. Despite this caution, our data indicate that PCV is effective for reducing the rate of IPD, especially among vulnerable populations,” they concluded.

The incidence of invasive pneumococcal disease among children younger than 5 years with sickle cell disease plummeted during 2001–2004, according to a new study which suggests that credit belongs to the 7-valent pneumococcal conjugate vaccine introduced in 2000.

“Our study clearly demonstrates that the incidence of invasive pneumococcal disease dramatically decreased after the introduction of pneumococcal conjugate vaccine into the routine childhood immunization schedule,” Dr. Natasha B. Halasa and colleagues wrote.

The data were derived from the follow-up of 2,026 individuals with sickle cell disease (SCD) enrolled in Tennessee Medicaid (TennCare) from Jan. 1, 1995, through Dec. 31, 2004 (Clin. Infect. Dis. 2007;44:1428–33).

During the study period, 37 individuals (0.6–44 years) with SCD had invasive pneumococcal disease (IPD), and no individuals with SCD had more than one episode of IPD during the study period.

In a comparison of the pre-PCV period (1995–1999) with the post-PCV period (2001–2004), the IPD rate decreased 91% in children aged less than 2 years (from 3,600 to 335 cases per 100,000 person-years) and by 93% in children under 5 years (from 2,044 to 134 cases per 100,000 person-years). In the post-PCV era, a mean 69% of children less than 2 years had evidence of receiving one or more doses of PCV during the prior year.

Although penicillin prophylaxis and pneumococcal polysaccharide vaccine have decreased the rate of invasive pneumococcal disease (IPD) in this high-risk population, breakthrough disease still occurs—most commonly among children younger than 3 years—and IPD continues to be a leading cause of death in children with SCD, the researchers explained.

This study, which showed a mean 92% drop in infection after 2000 among children younger than 5 years, raises important questions about the continued use of penicillin, according to Dr. Martin H. Steinberg, whose accompanying editorial poses the question, “Is prophylactic penicillin needed if conjugate vaccination is so effective?”

“Widespread penicillin use is not risk free. Penicillin-resistant strains of S. pneumoniae are increasing in number, and about 40% of isolates associated with sickle cell disease have some measure of resistance,” said Dr. Steinberg, with the departments of medicine, pediatrics, and pathology and laboratory medicine at Boston University (Clin. Infect. Dis. 2007;44:1434–5).

Dr. Steinberg believes that the susceptibility of S. pneumoniae to penicillin might be decreasing, and he points out that prophylaxis is less effective in carriers of intermediate-resistant and resistant serotypes.

In North America, the 7-valent conjugate vaccine protects against greater than 70% of the serotypes isolated from patients in the preconjugate vaccine era, he said. “However, two-thirds of the serotypes not included in the vaccine were susceptible to penicillin, and the use of this vaccine appeared to decrease the number of antibiotic-resistant, pneumococcal infections (N. Engl. J. Med. 2006;354:1455–63).”

Pending the arrival of a more efficacious 13-valent vaccine, antibiotic prophylaxis could be useful, Dr. Steinberg explained, adding that suboptimal compliance with preventive treatment limits penicillin's effectiveness.

In the Tennessee cohort, only 25% to 30% of the children with SCD who were younger than 5 years had their penicillin prescriptions filled for more than 270 days of a 1-year period. These numbers are similar to those found in an earlier study (JAMA 2003;290:1057–61), Dr. Halasa and colleagues said.

Because ongoing penicillin prophylaxis is difficult to sustain, the effectiveness of this approach in practice appears to be less than that demonstrated in the landmark randomized, clinical trial in which the antibiotic produced an 84% reduction in the rate of IPD among children with SCD the researchers said (N. Engl. J. Med. 1986;314:1593–9).

This study has several limitations, according to Dr. Halasa and her team: The number of individuals with SCD and IPD was small and consisted of patients who lived in surveillance counties in Tennessee and who were enrolled in the Tennessee Medicaid program.

“The pre-PCV era IPD rates in individuals with SCD in this study, however, were nearly identical to those reported from other locations, suggesting that these results are generalizable to others with SCD in the United States,” they argue.

A second limitation was that vaccination records, especially from the period prior to the introduction of PCV, may not have captured receipt of all pneumococcal vaccines by persons enrolled in TennCare.

With the universal administration of PCV to all children, both with and without SCD, it is expected that the rates of IPD will continue to decrease among all children, the authors wrote.

“However, ongoing monitoring of these rates and serotyping of all invasive pneumococcal isolates must remain an important priority to monitor whether serotype replacement will occur under continued vaccine pressure. Despite this caution, our data indicate that PCV is effective for reducing the rate of IPD, especially among vulnerable populations,” they concluded.

KEYSTONE, COLO. — Nasal corticosteroids remain the first line of treatment for most patients with seasonal allergic rhinitis, according to Dr. Harold S. Nelson.

“Nasal steroids started before the beginning of the season [work well],” Dr. Nelson said at a meeting on allergy/clinical immunology, asthma, and pulmonary medicine. “If people come in during the season and are symptomatic, using 20 mg prednisone three times a day to depress the inflammation greatly enhances the effectiveness of the nasal steroid.”

The use of antihistamines as a first line of treatment for seasonal allergic rhinitis is an antiquated approach, said Dr. Nelson, professor in the division of allergy and clinical immunology at National Jewish Medical and Research Center in Denver, which sponsored the meeting. “[They] are something you use for the person who has intermittent symptoms.”

Antihistamine-decongestant combinations, and cromolyn sodium nasal solution started 9 weeks before the onset of symptoms, each provide moderate relief, though cromolyn sodium is short acting and has to be taken six times a day, Dr. Nelson said.

Intranasal corticosteroids also outperform antihistamines when the two are compared on an as-needed (PRN) basis for the reduction of allergic inflammation, Dr. Nelson said (Arch. Intern. Med. 2001;161:2581–7).

Recent findings have shown that seasonal treatment that combined antihistamine and a nasal steroid (levocetirizine as an add-on to fluticasone) was of marginal value and led the authors to deem the practice “inappropriate” (Clin. Exp. Allergy 2006;36:676–84).

There is nothing in the drug pipeline that is better than current therapy for allergic rhinitis, Dr. Nelson said. The Food and Drug Administration is considering a request to approve the combination of montelukast and loratadine, which has been shown to be superior to either drug alone for alleviating nasal obstruction and itchy, sneezy, and runny symptoms (J. Allergy Clin. Immunol. 2000;105:917–27).

According to Dr. Nelson, the choices, from least to most effective, are:

▸ Leukotriene-receptor antagonists (less than 10% relief, compared with placebo).

▸ Antihistamines, anticholinergics (rhinorrhea only), decongestants (obstruction only), and nasal corticosteroids started during season (less than 20% relief).

▸ Cromolyn (six times per day) started before season, antihistamine/decongestant combinations (20%–40% relief).

▸ Nasal corticosteroids started before season or after 4 weeks, allergen immunotherapy (greater than 40% relief).

The use of antihistaminesas a first line of therapy for seasonal allergies is an antiquated approach. DR. NELSON

KEYSTONE, COLO. — Nasal corticosteroids remain the first line of treatment for most patients with seasonal allergic rhinitis, according to Dr. Harold S. Nelson.

“Nasal steroids started before the beginning of the season [work well],” Dr. Nelson said at a meeting on allergy/clinical immunology, asthma, and pulmonary medicine. “If people come in during the season and are symptomatic, using 20 mg prednisone three times a day to depress the inflammation greatly enhances the effectiveness of the nasal steroid.”

The use of antihistamines as a first line of treatment for seasonal allergic rhinitis is an antiquated approach, said Dr. Nelson, professor in the division of allergy and clinical immunology at National Jewish Medical and Research Center in Denver, which sponsored the meeting. “[They] are something you use for the person who has intermittent symptoms.”

Antihistamine-decongestant combinations, and cromolyn sodium nasal solution started 9 weeks before the onset of symptoms, each provide moderate relief, though cromolyn sodium is short acting and has to be taken six times a day, Dr. Nelson said.

Intranasal corticosteroids also outperform antihistamines when the two are compared on an as-needed (PRN) basis for the reduction of allergic inflammation, Dr. Nelson said (Arch. Intern. Med. 2001;161:2581–7).

Recent findings have shown that seasonal treatment that combined antihistamine and a nasal steroid (levocetirizine as an add-on to fluticasone) was of marginal value and led the authors to deem the practice “inappropriate” (Clin. Exp. Allergy 2006;36:676–84).

There is nothing in the drug pipeline that is better than current therapy for allergic rhinitis, Dr. Nelson said. The Food and Drug Administration is considering a request to approve the combination of montelukast and loratadine, which has been shown to be superior to either drug alone for alleviating nasal obstruction and itchy, sneezy, and runny symptoms (J. Allergy Clin. Immunol. 2000;105:917–27).

According to Dr. Nelson, the choices, from least to most effective, are:

▸ Leukotriene-receptor antagonists (less than 10% relief, compared with placebo).

▸ Antihistamines, anticholinergics (rhinorrhea only), decongestants (obstruction only), and nasal corticosteroids started during season (less than 20% relief).

▸ Cromolyn (six times per day) started before season, antihistamine/decongestant combinations (20%–40% relief).

▸ Nasal corticosteroids started before season or after 4 weeks, allergen immunotherapy (greater than 40% relief).

The use of antihistaminesas a first line of therapy for seasonal allergies is an antiquated approach. DR. NELSON

KEYSTONE, COLO. — Nasal corticosteroids remain the first line of treatment for most patients with seasonal allergic rhinitis, according to Dr. Harold S. Nelson.

“Nasal steroids started before the beginning of the season [work well],” Dr. Nelson said at a meeting on allergy/clinical immunology, asthma, and pulmonary medicine. “If people come in during the season and are symptomatic, using 20 mg prednisone three times a day to depress the inflammation greatly enhances the effectiveness of the nasal steroid.”

The use of antihistamines as a first line of treatment for seasonal allergic rhinitis is an antiquated approach, said Dr. Nelson, professor in the division of allergy and clinical immunology at National Jewish Medical and Research Center in Denver, which sponsored the meeting. “[They] are something you use for the person who has intermittent symptoms.”

Antihistamine-decongestant combinations, and cromolyn sodium nasal solution started 9 weeks before the onset of symptoms, each provide moderate relief, though cromolyn sodium is short acting and has to be taken six times a day, Dr. Nelson said.

Intranasal corticosteroids also outperform antihistamines when the two are compared on an as-needed (PRN) basis for the reduction of allergic inflammation, Dr. Nelson said (Arch. Intern. Med. 2001;161:2581–7).

Recent findings have shown that seasonal treatment that combined antihistamine and a nasal steroid (levocetirizine as an add-on to fluticasone) was of marginal value and led the authors to deem the practice “inappropriate” (Clin. Exp. Allergy 2006;36:676–84).

There is nothing in the drug pipeline that is better than current therapy for allergic rhinitis, Dr. Nelson said. The Food and Drug Administration is considering a request to approve the combination of montelukast and loratadine, which has been shown to be superior to either drug alone for alleviating nasal obstruction and itchy, sneezy, and runny symptoms (J. Allergy Clin. Immunol. 2000;105:917–27).

According to Dr. Nelson, the choices, from least to most effective, are:

▸ Leukotriene-receptor antagonists (less than 10% relief, compared with placebo).

▸ Antihistamines, anticholinergics (rhinorrhea only), decongestants (obstruction only), and nasal corticosteroids started during season (less than 20% relief).

▸ Cromolyn (six times per day) started before season, antihistamine/decongestant combinations (20%–40% relief).

▸ Nasal corticosteroids started before season or after 4 weeks, allergen immunotherapy (greater than 40% relief).

The use of antihistaminesas a first line of therapy for seasonal allergies is an antiquated approach. DR. NELSON

If you're not ready to invest thousands of dollars in an electronic medical records system, a desktop label writer may be just what the doctor ordered.

“This is a very cost-effective alternative for anyone who doesn't have an EMR system,” said Dr. Stephanie Lucas, who equipped her two-physician Detroit practice with several Dymo Twin Turbo label makers at a cost of about $150 apiece.

“I have all my prescriptions on the attached software, so all I have to do to print a label is go to the list on my computer, click on the prescription, and it comes out of the machine,” Dr. Lucas said.

She puts one label into the patient's chart and gives a second, signed, copy to the patient to take to the pharmacy. “Or I stick the label or labels on a sheet of paper and fax it to the pharmacy,” she said.

The internist and endocrinologist take an extra step to ensure that patients know what their medications are for. For example, in addition to printing “Statin 20 mg #90,” the label also says “cholesterol med.”

“Patients love it, and pharmacists appreciate being able to read the prescriptions without ever having to call and ask me what I wrote,” said Dr. Lucas, whose poor handwriting in grammar school drew a few knuckle raps from a ruler-wielding teacher.

The desktop labeling system also integrates with many software programs such as Outlook and Quickbooks to produce individual labels. “It's nice because it has an optional mailing bar code to facilitate mailing,” she added.

The label maker also prints individual postage stamps using the Web site www.stamps.com

“In addition, the data management software that comes with the machine contains our entire Rolodex file of physicians, so that patients referred to another facility get a legible copy of the name, address, and phone number on a printed label that can be affixed to the lab sheets or tickler file,” she said.

Dr. Lucas uses the label maker to print legible, customized instructions for each patient, and puts a second copy into each chart.

'Pharmacists appreciate being able to read the prescriptions without ever having to call.' DR. LUCAS

If you're not ready to invest thousands of dollars in an electronic medical records system, a desktop label writer may be just what the doctor ordered.

“This is a very cost-effective alternative for anyone who doesn't have an EMR system,” said Dr. Stephanie Lucas, who equipped her two-physician Detroit practice with several Dymo Twin Turbo label makers at a cost of about $150 apiece.

“I have all my prescriptions on the attached software, so all I have to do to print a label is go to the list on my computer, click on the prescription, and it comes out of the machine,” Dr. Lucas said.

She puts one label into the patient's chart and gives a second, signed, copy to the patient to take to the pharmacy. “Or I stick the label or labels on a sheet of paper and fax it to the pharmacy,” she said.

The internist and endocrinologist take an extra step to ensure that patients know what their medications are for. For example, in addition to printing “Statin 20 mg #90,” the label also says “cholesterol med.”

“Patients love it, and pharmacists appreciate being able to read the prescriptions without ever having to call and ask me what I wrote,” said Dr. Lucas, whose poor handwriting in grammar school drew a few knuckle raps from a ruler-wielding teacher.

The desktop labeling system also integrates with many software programs such as Outlook and Quickbooks to produce individual labels. “It's nice because it has an optional mailing bar code to facilitate mailing,” she added.

The label maker also prints individual postage stamps using the Web site www.stamps.com

“In addition, the data management software that comes with the machine contains our entire Rolodex file of physicians, so that patients referred to another facility get a legible copy of the name, address, and phone number on a printed label that can be affixed to the lab sheets or tickler file,” she said.

Dr. Lucas uses the label maker to print legible, customized instructions for each patient, and puts a second copy into each chart.

'Pharmacists appreciate being able to read the prescriptions without ever having to call.' DR. LUCAS

If you're not ready to invest thousands of dollars in an electronic medical records system, a desktop label writer may be just what the doctor ordered.

“This is a very cost-effective alternative for anyone who doesn't have an EMR system,” said Dr. Stephanie Lucas, who equipped her two-physician Detroit practice with several Dymo Twin Turbo label makers at a cost of about $150 apiece.

“I have all my prescriptions on the attached software, so all I have to do to print a label is go to the list on my computer, click on the prescription, and it comes out of the machine,” Dr. Lucas said.

She puts one label into the patient's chart and gives a second, signed, copy to the patient to take to the pharmacy. “Or I stick the label or labels on a sheet of paper and fax it to the pharmacy,” she said.

The internist and endocrinologist take an extra step to ensure that patients know what their medications are for. For example, in addition to printing “Statin 20 mg #90,” the label also says “cholesterol med.”

“Patients love it, and pharmacists appreciate being able to read the prescriptions without ever having to call and ask me what I wrote,” said Dr. Lucas, whose poor handwriting in grammar school drew a few knuckle raps from a ruler-wielding teacher.

The desktop labeling system also integrates with many software programs such as Outlook and Quickbooks to produce individual labels. “It's nice because it has an optional mailing bar code to facilitate mailing,” she added.

The label maker also prints individual postage stamps using the Web site www.stamps.com

“In addition, the data management software that comes with the machine contains our entire Rolodex file of physicians, so that patients referred to another facility get a legible copy of the name, address, and phone number on a printed label that can be affixed to the lab sheets or tickler file,” she said.

Dr. Lucas uses the label maker to print legible, customized instructions for each patient, and puts a second copy into each chart.

'Pharmacists appreciate being able to read the prescriptions without ever having to call.' DR. LUCAS

ST. LOUIS – Anxiety disorders may be transmitted from one generation to the next by specific family environmental factors such as parental modeling, overcontrolling parental behavior, and family conflict, according to a study presented at the annual conference of the Anxiety Disorders Association of America.

The role of genetics in anxiety is not clear, though it's thought that heredity is a minor player, said Kelly L. Drake, Ph.D., who is among several investigators trying to find answers to this complicated disorder.

A key factor in this parent-to-child psychopathology is anxiety sensitivity (AS), which is based on the belief that internal symptoms of anxiety will have harmful consequences socially, physically, or mentally. “Basically, anxiety sensitivity is the fear of fear,” said Dr. Drake in an interview.

Anxious parents may transmit, verbally or nonverbally, misinformation to their children that can put them at risk for becoming hypersensitive to symptoms of anxiety–racing heart, sweaty palms, and feeling faint–and ultimately for developing full-blown anxiety disorders, said Dr. Drake, senior research program coordinator in the department of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore.

Child anxiety disorders occur in about 10% of youth and are associated with significant impairment in functioning, she explained.

“These children often are misdiagnosed and therefore undertreated, and they tend to overutilize medical services,” Dr. Drake said.

Known risk factors for childhood anxiety disorders include parent psychopathology; increased rates of anxiety disorders and somatic symptoms in children of anxious or depressed parents; a moderate genetic heritability; and parent anxiety sensitivity, Dr. Drake said.

Potential mediators of childhood anxiety include child anxiety sensitivity, which is predicted by parental anxiety sensitivity; and family environment, including threatening, hostile, or rejecting parenting styles, she said, adding that parents of anxious children often are described as anxious, controlling, overprotective, affectionless, and demanding.

Also, child anxiety is related to family environments with greater conflict, less cohesion, and poor communication.

Dr. Drake set out to test two hypotheses:

▸ Child anxiety will be influenced by parental AS and anxiety-based psychopathology, depending on the level of the child's AS.

▸ Child anxiety will be influenced by parental AS and anxiety-based psychopathology, depending on the levels of family expressiveness, conflict, independence, and control.

The study involved a multiethnic community sample of 157 youth-parent dyads. The youths ranged in age from 7 to 18 years and 60% were female. More than three-quarters of the parents were women. Mean family income was $53,000. Three-quarters of the study group were European American.

Child and parent measures were derived using the Child Anxiety Sensitivity Index, the Multidimensional Anxiety Scale for Children, the Anxiety Sensitivity Index, the Symptom Checklist-90-Revised, and the Family Environment Scale.

Participants were asked to complete questionnaires independently and return them to the investigators. The response rate was 10.2%.

The results suggested that child AS mediates the relationship between parent psychopathology and child anxiety but does not mediate the relation between parental AS and child anxiety. Second, family conflict and control mediate the relationship between parental psychopathology and child anxiety and also between parental AS and child anxiety, Dr. Drake said.

She proposes that information transmission and parental modeling are the primary ways anxiety disorders are passed from parent to child.

“It's possible that parents might transmit information to a child verbally or nonverbally indicating the dangerousness of anxiety symptoms. Children may internalize that and begin to fear their own symptoms of anxiety and that can put them at risk for developing excessive levels of anxiety,” she said.

In addition, a parent may model anxious behavior; for example, refusing to go to work because of a report that has to be presented to the boss. “It's demonstrating avoidance behavior in front of the child and teaching the child to avoid frightening, challenging, or stressful situations,” Dr. Drake said.

One approach to interrupting this anxiety cycle is to educate parents about the nature of AS to eliminate the erroneous assumption that symptoms of anxiety will have harmful consequences, she explained.

“Clinicians can intervene with anxious parents to limit transmission of maladaptive beliefs and ineffective coping strategies,” she said, adding that parents can be taught adaptive coping skills to enhance modeling of successful coping and approach behavior.

Finally, the study suggests that certain family factors, such as conflict and control, also are associated with anxiety.

“So clinicians would be well served to target those family factors; to teach parents that being overcontrolling and overprotective only limits their child's opportunities and shelters the child from challenging situations,” Dr. Drake said in an interview.

Anxious parents may transmit misinformation to their children that can make them hypersensitive to anxiety symptoms. DR. DRAKE

ST. LOUIS – Anxiety disorders may be transmitted from one generation to the next by specific family environmental factors such as parental modeling, overcontrolling parental behavior, and family conflict, according to a study presented at the annual conference of the Anxiety Disorders Association of America.

The role of genetics in anxiety is not clear, though it's thought that heredity is a minor player, said Kelly L. Drake, Ph.D., who is among several investigators trying to find answers to this complicated disorder.

A key factor in this parent-to-child psychopathology is anxiety sensitivity (AS), which is based on the belief that internal symptoms of anxiety will have harmful consequences socially, physically, or mentally. “Basically, anxiety sensitivity is the fear of fear,” said Dr. Drake in an interview.

Anxious parents may transmit, verbally or nonverbally, misinformation to their children that can put them at risk for becoming hypersensitive to symptoms of anxiety–racing heart, sweaty palms, and feeling faint–and ultimately for developing full-blown anxiety disorders, said Dr. Drake, senior research program coordinator in the department of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore.

Child anxiety disorders occur in about 10% of youth and are associated with significant impairment in functioning, she explained.

“These children often are misdiagnosed and therefore undertreated, and they tend to overutilize medical services,” Dr. Drake said.

Known risk factors for childhood anxiety disorders include parent psychopathology; increased rates of anxiety disorders and somatic symptoms in children of anxious or depressed parents; a moderate genetic heritability; and parent anxiety sensitivity, Dr. Drake said.

Potential mediators of childhood anxiety include child anxiety sensitivity, which is predicted by parental anxiety sensitivity; and family environment, including threatening, hostile, or rejecting parenting styles, she said, adding that parents of anxious children often are described as anxious, controlling, overprotective, affectionless, and demanding.

Also, child anxiety is related to family environments with greater conflict, less cohesion, and poor communication.

Dr. Drake set out to test two hypotheses:

▸ Child anxiety will be influenced by parental AS and anxiety-based psychopathology, depending on the level of the child's AS.

▸ Child anxiety will be influenced by parental AS and anxiety-based psychopathology, depending on the levels of family expressiveness, conflict, independence, and control.

The study involved a multiethnic community sample of 157 youth-parent dyads. The youths ranged in age from 7 to 18 years and 60% were female. More than three-quarters of the parents were women. Mean family income was $53,000. Three-quarters of the study group were European American.

Child and parent measures were derived using the Child Anxiety Sensitivity Index, the Multidimensional Anxiety Scale for Children, the Anxiety Sensitivity Index, the Symptom Checklist-90-Revised, and the Family Environment Scale.

Participants were asked to complete questionnaires independently and return them to the investigators. The response rate was 10.2%.

The results suggested that child AS mediates the relationship between parent psychopathology and child anxiety but does not mediate the relation between parental AS and child anxiety. Second, family conflict and control mediate the relationship between parental psychopathology and child anxiety and also between parental AS and child anxiety, Dr. Drake said.

She proposes that information transmission and parental modeling are the primary ways anxiety disorders are passed from parent to child.

“It's possible that parents might transmit information to a child verbally or nonverbally indicating the dangerousness of anxiety symptoms. Children may internalize that and begin to fear their own symptoms of anxiety and that can put them at risk for developing excessive levels of anxiety,” she said.

In addition, a parent may model anxious behavior; for example, refusing to go to work because of a report that has to be presented to the boss. “It's demonstrating avoidance behavior in front of the child and teaching the child to avoid frightening, challenging, or stressful situations,” Dr. Drake said.

One approach to interrupting this anxiety cycle is to educate parents about the nature of AS to eliminate the erroneous assumption that symptoms of anxiety will have harmful consequences, she explained.

“Clinicians can intervene with anxious parents to limit transmission of maladaptive beliefs and ineffective coping strategies,” she said, adding that parents can be taught adaptive coping skills to enhance modeling of successful coping and approach behavior.

Finally, the study suggests that certain family factors, such as conflict and control, also are associated with anxiety.

“So clinicians would be well served to target those family factors; to teach parents that being overcontrolling and overprotective only limits their child's opportunities and shelters the child from challenging situations,” Dr. Drake said in an interview.

Anxious parents may transmit misinformation to their children that can make them hypersensitive to anxiety symptoms. DR. DRAKE

ST. LOUIS – Anxiety disorders may be transmitted from one generation to the next by specific family environmental factors such as parental modeling, overcontrolling parental behavior, and family conflict, according to a study presented at the annual conference of the Anxiety Disorders Association of America.

The role of genetics in anxiety is not clear, though it's thought that heredity is a minor player, said Kelly L. Drake, Ph.D., who is among several investigators trying to find answers to this complicated disorder.

A key factor in this parent-to-child psychopathology is anxiety sensitivity (AS), which is based on the belief that internal symptoms of anxiety will have harmful consequences socially, physically, or mentally. “Basically, anxiety sensitivity is the fear of fear,” said Dr. Drake in an interview.

Anxious parents may transmit, verbally or nonverbally, misinformation to their children that can put them at risk for becoming hypersensitive to symptoms of anxiety–racing heart, sweaty palms, and feeling faint–and ultimately for developing full-blown anxiety disorders, said Dr. Drake, senior research program coordinator in the department of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore.

Child anxiety disorders occur in about 10% of youth and are associated with significant impairment in functioning, she explained.

“These children often are misdiagnosed and therefore undertreated, and they tend to overutilize medical services,” Dr. Drake said.

Known risk factors for childhood anxiety disorders include parent psychopathology; increased rates of anxiety disorders and somatic symptoms in children of anxious or depressed parents; a moderate genetic heritability; and parent anxiety sensitivity, Dr. Drake said.

Potential mediators of childhood anxiety include child anxiety sensitivity, which is predicted by parental anxiety sensitivity; and family environment, including threatening, hostile, or rejecting parenting styles, she said, adding that parents of anxious children often are described as anxious, controlling, overprotective, affectionless, and demanding.

Also, child anxiety is related to family environments with greater conflict, less cohesion, and poor communication.

Dr. Drake set out to test two hypotheses:

▸ Child anxiety will be influenced by parental AS and anxiety-based psychopathology, depending on the level of the child's AS.

▸ Child anxiety will be influenced by parental AS and anxiety-based psychopathology, depending on the levels of family expressiveness, conflict, independence, and control.

The study involved a multiethnic community sample of 157 youth-parent dyads. The youths ranged in age from 7 to 18 years and 60% were female. More than three-quarters of the parents were women. Mean family income was $53,000. Three-quarters of the study group were European American.

Child and parent measures were derived using the Child Anxiety Sensitivity Index, the Multidimensional Anxiety Scale for Children, the Anxiety Sensitivity Index, the Symptom Checklist-90-Revised, and the Family Environment Scale.

Participants were asked to complete questionnaires independently and return them to the investigators. The response rate was 10.2%.

The results suggested that child AS mediates the relationship between parent psychopathology and child anxiety but does not mediate the relation between parental AS and child anxiety. Second, family conflict and control mediate the relationship between parental psychopathology and child anxiety and also between parental AS and child anxiety, Dr. Drake said.

She proposes that information transmission and parental modeling are the primary ways anxiety disorders are passed from parent to child.

“It's possible that parents might transmit information to a child verbally or nonverbally indicating the dangerousness of anxiety symptoms. Children may internalize that and begin to fear their own symptoms of anxiety and that can put them at risk for developing excessive levels of anxiety,” she said.

In addition, a parent may model anxious behavior; for example, refusing to go to work because of a report that has to be presented to the boss. “It's demonstrating avoidance behavior in front of the child and teaching the child to avoid frightening, challenging, or stressful situations,” Dr. Drake said.

One approach to interrupting this anxiety cycle is to educate parents about the nature of AS to eliminate the erroneous assumption that symptoms of anxiety will have harmful consequences, she explained.

“Clinicians can intervene with anxious parents to limit transmission of maladaptive beliefs and ineffective coping strategies,” she said, adding that parents can be taught adaptive coping skills to enhance modeling of successful coping and approach behavior.

Finally, the study suggests that certain family factors, such as conflict and control, also are associated with anxiety.

“So clinicians would be well served to target those family factors; to teach parents that being overcontrolling and overprotective only limits their child's opportunities and shelters the child from challenging situations,” Dr. Drake said in an interview.

Anxious parents may transmit misinformation to their children that can make them hypersensitive to anxiety symptoms. DR. DRAKE

Patient phone calls are a necessity, and a potential liability, which every practice must deal with, but Dr. S. Germain Cassiere said keeping track of calls is no longer a nightmare.

He has created software, called MessageTracker, to make this process easier.

The receptionist application initiates patient call records. When a call comes in, a receptionist fills out a template that appears on her desktop monitor. The call record is then sent to the respective physician, who sends it to the server computer that houses the database tables.

The nurse application contains a call record grid that resembles a spreadsheet, showing calls waiting for responses. A nurse or physician documents the responses in the call record.

Once completed, the call record is marked “done” and is automatically eliminated from the grid, said Dr. Cassiere, an internist who is in group practice in Shreveport, La.

With the exception of those physicians who still want their call records printed out, the entire process is electronic, Dr. Cassiere explained.

“I don't have to worry about lost phone calls, illegible handwriting, delays in getting calls to a nurse, undocumented responses to calls, and not knowing which calls have or have not been answered,” he said.

The system also reduces liability risk associated with missed and unreturned calls.

In addition, any calls logged in a given year or past years can be searched by date or by the name of the patient or physician. “Our practice of six general internists handles 40,000–50,000 calls each year,” he said.

And because MessageTracker can be run without using Microsoft's SQL Server as the database engine, the tracking software adds relatively little to an office's overhead. Instead of the approximately $15,000 cost of the SQL Server and client licenses for his office, Dr. Cassiere's cost for using the Nexus Database System was about $1,000.

“The beauty of it is that I can deploy the software and the server without incurring any license fees, [which] would be the case if I wrote this in Microsoft SQL Server, which would have required that we purchase a separate license for each of the 25 people in our practice,” he explained.

MessageTracker is not currently for sale, but Dr. Cassiere said he's working on an improved version that will be available for purchase.

Patient phone calls are a necessity, and a potential liability, which every practice must deal with, but Dr. S. Germain Cassiere said keeping track of calls is no longer a nightmare.

He has created software, called MessageTracker, to make this process easier.

The receptionist application initiates patient call records. When a call comes in, a receptionist fills out a template that appears on her desktop monitor. The call record is then sent to the respective physician, who sends it to the server computer that houses the database tables.

The nurse application contains a call record grid that resembles a spreadsheet, showing calls waiting for responses. A nurse or physician documents the responses in the call record.

Once completed, the call record is marked “done” and is automatically eliminated from the grid, said Dr. Cassiere, an internist who is in group practice in Shreveport, La.

With the exception of those physicians who still want their call records printed out, the entire process is electronic, Dr. Cassiere explained.

“I don't have to worry about lost phone calls, illegible handwriting, delays in getting calls to a nurse, undocumented responses to calls, and not knowing which calls have or have not been answered,” he said.

The system also reduces liability risk associated with missed and unreturned calls.

In addition, any calls logged in a given year or past years can be searched by date or by the name of the patient or physician. “Our practice of six general internists handles 40,000–50,000 calls each year,” he said.

And because MessageTracker can be run without using Microsoft's SQL Server as the database engine, the tracking software adds relatively little to an office's overhead. Instead of the approximately $15,000 cost of the SQL Server and client licenses for his office, Dr. Cassiere's cost for using the Nexus Database System was about $1,000.

“The beauty of it is that I can deploy the software and the server without incurring any license fees, [which] would be the case if I wrote this in Microsoft SQL Server, which would have required that we purchase a separate license for each of the 25 people in our practice,” he explained.

MessageTracker is not currently for sale, but Dr. Cassiere said he's working on an improved version that will be available for purchase.

Patient phone calls are a necessity, and a potential liability, which every practice must deal with, but Dr. S. Germain Cassiere said keeping track of calls is no longer a nightmare.

He has created software, called MessageTracker, to make this process easier.

The receptionist application initiates patient call records. When a call comes in, a receptionist fills out a template that appears on her desktop monitor. The call record is then sent to the respective physician, who sends it to the server computer that houses the database tables.

The nurse application contains a call record grid that resembles a spreadsheet, showing calls waiting for responses. A nurse or physician documents the responses in the call record.

Once completed, the call record is marked “done” and is automatically eliminated from the grid, said Dr. Cassiere, an internist who is in group practice in Shreveport, La.

With the exception of those physicians who still want their call records printed out, the entire process is electronic, Dr. Cassiere explained.

“I don't have to worry about lost phone calls, illegible handwriting, delays in getting calls to a nurse, undocumented responses to calls, and not knowing which calls have or have not been answered,” he said.

The system also reduces liability risk associated with missed and unreturned calls.

In addition, any calls logged in a given year or past years can be searched by date or by the name of the patient or physician. “Our practice of six general internists handles 40,000–50,000 calls each year,” he said.

And because MessageTracker can be run without using Microsoft's SQL Server as the database engine, the tracking software adds relatively little to an office's overhead. Instead of the approximately $15,000 cost of the SQL Server and client licenses for his office, Dr. Cassiere's cost for using the Nexus Database System was about $1,000.

“The beauty of it is that I can deploy the software and the server without incurring any license fees, [which] would be the case if I wrote this in Microsoft SQL Server, which would have required that we purchase a separate license for each of the 25 people in our practice,” he explained.

MessageTracker is not currently for sale, but Dr. Cassiere said he's working on an improved version that will be available for purchase.

KEYSTONE, COLO. — Physicians treating patients with asthma and other airway symptoms should not rely solely on gastroenterologists' interpretations of pH probe tests, because they might miss laryngeal-pharyngeal reflux that threatens the upper airway, Dr. Donna Bratton said at a meeting on allergy/clinical immunology, asthma, and pulmonary medicine.

“Gastroenterologists may not be familiar with patients with asthma, chronic cough, or laryngitis, and pH probe patterns may look unfamiliar in the context of what they usually see,” said Dr. Bratton, an allergist with the National Jewish Medical and Research Center in Denver. “If they don't find something significant in the lower esophagus, they may miss something significant in the larynx or pharynx.”

Asthma patients with suspected gastroesophageal reflux (GER) or laryngeal-pharyngeal reflux (LPR) are a heterogeneous population in terms of esophageal acidification. Some patients have short episodes of reflux and others show prolonged episodes associated with esophageal injury, she said at the meeting, which was sponsored by the National Jewish Medical and Research Center.

“GI doctors are very good at treating GER with proton pump inhibition therapy, which appears to work best in the most severe cases. But when patients have short periods of acid reflux that are full column to the top probe and don't result in prolonged acid exposure, they don't know what it means, and we see this same pattern in LPR,” the allergist said.

Some of the patterns and parameters that are known to injure the esophagus are not necessarily seen in airway dysfunction patients, but that doesn't mean they aren't having significant reflux that might go into the esophagus or even higher into the pharyngeal area, Dr. Bratton said in an interview.

Standard pH probe monitoring is unable to detect nonacid GER, which doesn't concern GI doctors because it doesn't injure the esophagus. Although the esophagus has many defense mechanisms against acid, other compounds in reflux might damage the airway, Dr. Bratton said.

“Bile and enzymes from the duodenum do not show up on a pH probe, and when you get all the way up out of the esophagus into the LP area, those tissues do not have some of the defenses that the esophagus does,” she said. Symptoms might be generated merely from those protective mechanisms being repeatedly triggered by nonacidic material, she added.

Dr. Bratton's message to doctors treating airway disease is simple: “Either have a close relationship with your GI doc if he or she shows an interest in airway disease, or look at these probe studies yourself and see if the patterns are posing significant problems that are correlated with patients' symptoms or disease,” she said.

The esophagus has many defense mechanisms against acid, but other compounds in reflux might damage the airway. DR. BRATTON

KEYSTONE, COLO. — Physicians treating patients with asthma and other airway symptoms should not rely solely on gastroenterologists' interpretations of pH probe tests, because they might miss laryngeal-pharyngeal reflux that threatens the upper airway, Dr. Donna Bratton said at a meeting on allergy/clinical immunology, asthma, and pulmonary medicine.

“Gastroenterologists may not be familiar with patients with asthma, chronic cough, or laryngitis, and pH probe patterns may look unfamiliar in the context of what they usually see,” said Dr. Bratton, an allergist with the National Jewish Medical and Research Center in Denver. “If they don't find something significant in the lower esophagus, they may miss something significant in the larynx or pharynx.”

Asthma patients with suspected gastroesophageal reflux (GER) or laryngeal-pharyngeal reflux (LPR) are a heterogeneous population in terms of esophageal acidification. Some patients have short episodes of reflux and others show prolonged episodes associated with esophageal injury, she said at the meeting, which was sponsored by the National Jewish Medical and Research Center.

“GI doctors are very good at treating GER with proton pump inhibition therapy, which appears to work best in the most severe cases. But when patients have short periods of acid reflux that are full column to the top probe and don't result in prolonged acid exposure, they don't know what it means, and we see this same pattern in LPR,” the allergist said.

Some of the patterns and parameters that are known to injure the esophagus are not necessarily seen in airway dysfunction patients, but that doesn't mean they aren't having significant reflux that might go into the esophagus or even higher into the pharyngeal area, Dr. Bratton said in an interview.

Standard pH probe monitoring is unable to detect nonacid GER, which doesn't concern GI doctors because it doesn't injure the esophagus. Although the esophagus has many defense mechanisms against acid, other compounds in reflux might damage the airway, Dr. Bratton said.

“Bile and enzymes from the duodenum do not show up on a pH probe, and when you get all the way up out of the esophagus into the LP area, those tissues do not have some of the defenses that the esophagus does,” she said. Symptoms might be generated merely from those protective mechanisms being repeatedly triggered by nonacidic material, she added.

Dr. Bratton's message to doctors treating airway disease is simple: “Either have a close relationship with your GI doc if he or she shows an interest in airway disease, or look at these probe studies yourself and see if the patterns are posing significant problems that are correlated with patients' symptoms or disease,” she said.

The esophagus has many defense mechanisms against acid, but other compounds in reflux might damage the airway. DR. BRATTON

KEYSTONE, COLO. — Physicians treating patients with asthma and other airway symptoms should not rely solely on gastroenterologists' interpretations of pH probe tests, because they might miss laryngeal-pharyngeal reflux that threatens the upper airway, Dr. Donna Bratton said at a meeting on allergy/clinical immunology, asthma, and pulmonary medicine.

“Gastroenterologists may not be familiar with patients with asthma, chronic cough, or laryngitis, and pH probe patterns may look unfamiliar in the context of what they usually see,” said Dr. Bratton, an allergist with the National Jewish Medical and Research Center in Denver. “If they don't find something significant in the lower esophagus, they may miss something significant in the larynx or pharynx.”

Asthma patients with suspected gastroesophageal reflux (GER) or laryngeal-pharyngeal reflux (LPR) are a heterogeneous population in terms of esophageal acidification. Some patients have short episodes of reflux and others show prolonged episodes associated with esophageal injury, she said at the meeting, which was sponsored by the National Jewish Medical and Research Center.

“GI doctors are very good at treating GER with proton pump inhibition therapy, which appears to work best in the most severe cases. But when patients have short periods of acid reflux that are full column to the top probe and don't result in prolonged acid exposure, they don't know what it means, and we see this same pattern in LPR,” the allergist said.

Some of the patterns and parameters that are known to injure the esophagus are not necessarily seen in airway dysfunction patients, but that doesn't mean they aren't having significant reflux that might go into the esophagus or even higher into the pharyngeal area, Dr. Bratton said in an interview.

Standard pH probe monitoring is unable to detect nonacid GER, which doesn't concern GI doctors because it doesn't injure the esophagus. Although the esophagus has many defense mechanisms against acid, other compounds in reflux might damage the airway, Dr. Bratton said.

“Bile and enzymes from the duodenum do not show up on a pH probe, and when you get all the way up out of the esophagus into the LP area, those tissues do not have some of the defenses that the esophagus does,” she said. Symptoms might be generated merely from those protective mechanisms being repeatedly triggered by nonacidic material, she added.

Dr. Bratton's message to doctors treating airway disease is simple: “Either have a close relationship with your GI doc if he or she shows an interest in airway disease, or look at these probe studies yourself and see if the patterns are posing significant problems that are correlated with patients' symptoms or disease,” she said.

The esophagus has many defense mechanisms against acid, but other compounds in reflux might damage the airway. DR. BRATTON