Robert Finn

SANTA BARBARA, CALIF. — About half of patients using glucocorticoids for long periods will suffer compression fractures of the vertebrae if nothing is done to intervene, Barbara P. Lukert, M.D., said at a symposium sponsored by the American College of Rheumatology.

Bisphosphonate therapy is clearly effective in reducing fractures, whether started when initiating glucocorticoids or after a patient has been on them for a while. But bisphosphonates aren't enough, and other steps should be taken to manage these patients, said Dr. Lukert of the University of Kansas Medical Center in Kansas City.

Other opportunities to intervene include:

▸ Diet is critical. Since glucocorticoids are catabolic, patients need adequate protein intake, not just calcium and phosphorus.

▸ Heavily encourage patients to exercise, not only because of its benefits on bone. Glucocorticoids often cause myopathy, ranging from mild to severe, and exercise can stave this off. Strengthening the quadriceps and related muscle groups has been shown to prevent falls.

▸ Control urinary calcium. A very large percentage of patients on glucocorticoids will develop hypercalciuria, and restricting sodium in the diet will go a long way toward resolving this.

▸ Replace hormones as appropriate. Glucocorticoids inhibit pituitary gonadotropin, and men taking steroids often have low testosterone levels. If there's no contraindication, this testosterone should be replaced, Dr. Lukert said.

Women taking steroids often have low estrogen levels. If premenopausal women become amenorrheic on glucocorticoids, consider prescribing estrogen or progesterone. Dr. Lukert noted that estrogen replacement in postmenopausal women remains controversial.

Patients who have a bone mineral density (BMD) T score of less than −1.5 or are taking more than 10 mg/day of prednisone or the equivalent should receive bisphosphonate therapy as soon as corticosteroids are started.

Patients with a higher BMD taking lower doses of prednisone may hold off on starting bisphosphonate therapy at first and retest BMD after 6 months.

Another reasonable strategy is simply to give a bisphosphonate to all patients who anticipate taking steroids for several weeks or longer.

This strategy is certain to prevent fractures, but at the cost of treating 40%–50% of patients who would not have suffered a fracture even without the bisphosphonate prescription, Dr. Lukert said.

SANTA BARBARA, CALIF. — About half of patients using glucocorticoids for long periods will suffer compression fractures of the vertebrae if nothing is done to intervene, Barbara P. Lukert, M.D., said at a symposium sponsored by the American College of Rheumatology.

Bisphosphonate therapy is clearly effective in reducing fractures, whether started when initiating glucocorticoids or after a patient has been on them for a while. But bisphosphonates aren't enough, and other steps should be taken to manage these patients, said Dr. Lukert of the University of Kansas Medical Center in Kansas City.

Other opportunities to intervene include:

▸ Diet is critical. Since glucocorticoids are catabolic, patients need adequate protein intake, not just calcium and phosphorus.

▸ Heavily encourage patients to exercise, not only because of its benefits on bone. Glucocorticoids often cause myopathy, ranging from mild to severe, and exercise can stave this off. Strengthening the quadriceps and related muscle groups has been shown to prevent falls.

▸ Control urinary calcium. A very large percentage of patients on glucocorticoids will develop hypercalciuria, and restricting sodium in the diet will go a long way toward resolving this.

▸ Replace hormones as appropriate. Glucocorticoids inhibit pituitary gonadotropin, and men taking steroids often have low testosterone levels. If there's no contraindication, this testosterone should be replaced, Dr. Lukert said.

Women taking steroids often have low estrogen levels. If premenopausal women become amenorrheic on glucocorticoids, consider prescribing estrogen or progesterone. Dr. Lukert noted that estrogen replacement in postmenopausal women remains controversial.

Patients who have a bone mineral density (BMD) T score of less than −1.5 or are taking more than 10 mg/day of prednisone or the equivalent should receive bisphosphonate therapy as soon as corticosteroids are started.

Patients with a higher BMD taking lower doses of prednisone may hold off on starting bisphosphonate therapy at first and retest BMD after 6 months.

Another reasonable strategy is simply to give a bisphosphonate to all patients who anticipate taking steroids for several weeks or longer.

This strategy is certain to prevent fractures, but at the cost of treating 40%–50% of patients who would not have suffered a fracture even without the bisphosphonate prescription, Dr. Lukert said.

SANTA BARBARA, CALIF. — About half of patients using glucocorticoids for long periods will suffer compression fractures of the vertebrae if nothing is done to intervene, Barbara P. Lukert, M.D., said at a symposium sponsored by the American College of Rheumatology.

Bisphosphonate therapy is clearly effective in reducing fractures, whether started when initiating glucocorticoids or after a patient has been on them for a while. But bisphosphonates aren't enough, and other steps should be taken to manage these patients, said Dr. Lukert of the University of Kansas Medical Center in Kansas City.

Other opportunities to intervene include:

▸ Diet is critical. Since glucocorticoids are catabolic, patients need adequate protein intake, not just calcium and phosphorus.

▸ Heavily encourage patients to exercise, not only because of its benefits on bone. Glucocorticoids often cause myopathy, ranging from mild to severe, and exercise can stave this off. Strengthening the quadriceps and related muscle groups has been shown to prevent falls.

▸ Control urinary calcium. A very large percentage of patients on glucocorticoids will develop hypercalciuria, and restricting sodium in the diet will go a long way toward resolving this.

▸ Replace hormones as appropriate. Glucocorticoids inhibit pituitary gonadotropin, and men taking steroids often have low testosterone levels. If there's no contraindication, this testosterone should be replaced, Dr. Lukert said.

Women taking steroids often have low estrogen levels. If premenopausal women become amenorrheic on glucocorticoids, consider prescribing estrogen or progesterone. Dr. Lukert noted that estrogen replacement in postmenopausal women remains controversial.

Patients who have a bone mineral density (BMD) T score of less than −1.5 or are taking more than 10 mg/day of prednisone or the equivalent should receive bisphosphonate therapy as soon as corticosteroids are started.

Patients with a higher BMD taking lower doses of prednisone may hold off on starting bisphosphonate therapy at first and retest BMD after 6 months.

Another reasonable strategy is simply to give a bisphosphonate to all patients who anticipate taking steroids for several weeks or longer.

This strategy is certain to prevent fractures, but at the cost of treating 40%–50% of patients who would not have suffered a fracture even without the bisphosphonate prescription, Dr. Lukert said.

SANTA BARBARA, CALIF. — Deposition of calcium pyrophosphate dihydrate into joints can mimic several other conditions, including osteoarthritis, rheumatoid arthritis, and gout, and making a definitive diagnosis can be quite a challenge, Ann K. Rosenthal, M.D., said at a symposium sponsored by the American College of Rheumatology.

A definitive diagnosis of calcium pyrophosphate dihydrate (CPPD) deposition disease can be made only by identifying the crystals directly, using complex techniques such as x-ray diffraction or Fourier transform infrared spectroscopy, techniques that are unavailable in most clinical labs.

“Most of us diagnose CPPD deposition by synovial analysis,” said Dr. Rosenthal of the Medical College of Wisconsin, Milwaukee. “We look under polarizing light microscopy and see the positively birefringent crystals. This really remains the gold standard clinically.”

Unfortunately, CPPD crystals are often only weakly birefringent, with one study indicating that just 17%–40% of the crystals glow under polarizing light (Ann. Rheum. Dis. 1999;58:582–4). In contrast, practically all gout crystals are birefringent. For this reason, nonpolarizing light microscopy may be useful in diagnosing CPPD deposition disease.

The disease is such an excellent imitator of other rheumatic conditions that many physicians never suspect calcium crystals as a cause. In all likelihood, many cases are missed because of poor diagnostic techniques.

An analysis of a patient's risk factors for CPPD deposition disease provides little ammunition to increase the index of suspicion.

The condition is rare in people under the age of 60 but rapidly increases in incidence in older patients. About 50% of patients over the age of 90 have radiographic evidence of CPPD deposition. Women are slightly more likely than men to have CPPD deposition. And prior injury to the joint increases the risk of CPPD deposition.

A variety of metabolic disorders are associated with the formation of CPPD crystals. The most significant are hyperparathyroidism, hemochromatosis, hypomagnesemia, and gout, but case reports have implicated a number of other conditions.

The clinical presentation of CPPD-induced pseudogout, pseudo-rheumatoid arthritis, or pseudoosteoarthritis can differ in subtle ways from the true conditions. For example, pseudoosteoarthritis (the most common CPPD deposition disease) can appear identical to true osteoarthritis, although it may affect unusual joints.

“Perhaps a lot of what we're calling osteoarthritis is actually CPPD deposition disease,” Dr. Rosenthal said. One study demonstrated a 60% prevalence of either CPPD or basic calcium phosphate crystals (called BCP crystals or hydroxyapatite) in knee joints of patients with a preoperative diagnosis of osteoarthritis (J. Rheumatol. 2002;29:570–4).

Chondrocalcinosis is the radiographic hallmark of CPPD deposition disease, but it can be risky to diagnose the condition based on radiographic findings alone, Dr. Rosenthal said. Chondrocalcinosis appears as a linear deposition of calcium, often in the fibrocartilage or lining of the articular cartilage. It is most likely to be found in the symphysis pubis and the triangular cartilage of the wrist.

Ultrasound is the most promising new technique for CPPD diagnosis, with a recent study identifying three patterns that appear highly specific for CPPD deposition disease. The first is a punctate pattern with several thin hyperechoic spots in fibrocartilage and tendons. The second is characterized by homogeneous hyperechoic or oval deposits localized in bursae and articular recesses. The third pattern shows thin hyperechoic bands parallel to the articular surfaces (Ann. Rheum. Dis. 2005;64:638–40).

MRI adds little to a diagnosis, since calcification in cartilage can appear as high or low signal intensity.

On the other hand, CT scans can be quite sensitive and may be particularly useful for cases with spinal involvement. One advantage of CT scanning is that the technique can detect—and in some cases differentiate between—both BCP and CPPD crystals.

CPPD crystals are weakly birefringent under polarizing light microscopy (as shown). Only 17%–40% of CPPD crystals glow using such means.

SANTA BARBARA, CALIF. — Deposition of calcium pyrophosphate dihydrate into joints can mimic several other conditions, including osteoarthritis, rheumatoid arthritis, and gout, and making a definitive diagnosis can be quite a challenge, Ann K. Rosenthal, M.D., said at a symposium sponsored by the American College of Rheumatology.

A definitive diagnosis of calcium pyrophosphate dihydrate (CPPD) deposition disease can be made only by identifying the crystals directly, using complex techniques such as x-ray diffraction or Fourier transform infrared spectroscopy, techniques that are unavailable in most clinical labs.

“Most of us diagnose CPPD deposition by synovial analysis,” said Dr. Rosenthal of the Medical College of Wisconsin, Milwaukee. “We look under polarizing light microscopy and see the positively birefringent crystals. This really remains the gold standard clinically.”

Unfortunately, CPPD crystals are often only weakly birefringent, with one study indicating that just 17%–40% of the crystals glow under polarizing light (Ann. Rheum. Dis. 1999;58:582–4). In contrast, practically all gout crystals are birefringent. For this reason, nonpolarizing light microscopy may be useful in diagnosing CPPD deposition disease.

The disease is such an excellent imitator of other rheumatic conditions that many physicians never suspect calcium crystals as a cause. In all likelihood, many cases are missed because of poor diagnostic techniques.

An analysis of a patient's risk factors for CPPD deposition disease provides little ammunition to increase the index of suspicion.

The condition is rare in people under the age of 60 but rapidly increases in incidence in older patients. About 50% of patients over the age of 90 have radiographic evidence of CPPD deposition. Women are slightly more likely than men to have CPPD deposition. And prior injury to the joint increases the risk of CPPD deposition.

A variety of metabolic disorders are associated with the formation of CPPD crystals. The most significant are hyperparathyroidism, hemochromatosis, hypomagnesemia, and gout, but case reports have implicated a number of other conditions.

The clinical presentation of CPPD-induced pseudogout, pseudo-rheumatoid arthritis, or pseudoosteoarthritis can differ in subtle ways from the true conditions. For example, pseudoosteoarthritis (the most common CPPD deposition disease) can appear identical to true osteoarthritis, although it may affect unusual joints.

“Perhaps a lot of what we're calling osteoarthritis is actually CPPD deposition disease,” Dr. Rosenthal said. One study demonstrated a 60% prevalence of either CPPD or basic calcium phosphate crystals (called BCP crystals or hydroxyapatite) in knee joints of patients with a preoperative diagnosis of osteoarthritis (J. Rheumatol. 2002;29:570–4).

Chondrocalcinosis is the radiographic hallmark of CPPD deposition disease, but it can be risky to diagnose the condition based on radiographic findings alone, Dr. Rosenthal said. Chondrocalcinosis appears as a linear deposition of calcium, often in the fibrocartilage or lining of the articular cartilage. It is most likely to be found in the symphysis pubis and the triangular cartilage of the wrist.

Ultrasound is the most promising new technique for CPPD diagnosis, with a recent study identifying three patterns that appear highly specific for CPPD deposition disease. The first is a punctate pattern with several thin hyperechoic spots in fibrocartilage and tendons. The second is characterized by homogeneous hyperechoic or oval deposits localized in bursae and articular recesses. The third pattern shows thin hyperechoic bands parallel to the articular surfaces (Ann. Rheum. Dis. 2005;64:638–40).

MRI adds little to a diagnosis, since calcification in cartilage can appear as high or low signal intensity.

On the other hand, CT scans can be quite sensitive and may be particularly useful for cases with spinal involvement. One advantage of CT scanning is that the technique can detect—and in some cases differentiate between—both BCP and CPPD crystals.

CPPD crystals are weakly birefringent under polarizing light microscopy (as shown). Only 17%–40% of CPPD crystals glow using such means.

SANTA BARBARA, CALIF. — Deposition of calcium pyrophosphate dihydrate into joints can mimic several other conditions, including osteoarthritis, rheumatoid arthritis, and gout, and making a definitive diagnosis can be quite a challenge, Ann K. Rosenthal, M.D., said at a symposium sponsored by the American College of Rheumatology.

A definitive diagnosis of calcium pyrophosphate dihydrate (CPPD) deposition disease can be made only by identifying the crystals directly, using complex techniques such as x-ray diffraction or Fourier transform infrared spectroscopy, techniques that are unavailable in most clinical labs.

“Most of us diagnose CPPD deposition by synovial analysis,” said Dr. Rosenthal of the Medical College of Wisconsin, Milwaukee. “We look under polarizing light microscopy and see the positively birefringent crystals. This really remains the gold standard clinically.”

Unfortunately, CPPD crystals are often only weakly birefringent, with one study indicating that just 17%–40% of the crystals glow under polarizing light (Ann. Rheum. Dis. 1999;58:582–4). In contrast, practically all gout crystals are birefringent. For this reason, nonpolarizing light microscopy may be useful in diagnosing CPPD deposition disease.

The disease is such an excellent imitator of other rheumatic conditions that many physicians never suspect calcium crystals as a cause. In all likelihood, many cases are missed because of poor diagnostic techniques.

An analysis of a patient's risk factors for CPPD deposition disease provides little ammunition to increase the index of suspicion.

The condition is rare in people under the age of 60 but rapidly increases in incidence in older patients. About 50% of patients over the age of 90 have radiographic evidence of CPPD deposition. Women are slightly more likely than men to have CPPD deposition. And prior injury to the joint increases the risk of CPPD deposition.

A variety of metabolic disorders are associated with the formation of CPPD crystals. The most significant are hyperparathyroidism, hemochromatosis, hypomagnesemia, and gout, but case reports have implicated a number of other conditions.

The clinical presentation of CPPD-induced pseudogout, pseudo-rheumatoid arthritis, or pseudoosteoarthritis can differ in subtle ways from the true conditions. For example, pseudoosteoarthritis (the most common CPPD deposition disease) can appear identical to true osteoarthritis, although it may affect unusual joints.

“Perhaps a lot of what we're calling osteoarthritis is actually CPPD deposition disease,” Dr. Rosenthal said. One study demonstrated a 60% prevalence of either CPPD or basic calcium phosphate crystals (called BCP crystals or hydroxyapatite) in knee joints of patients with a preoperative diagnosis of osteoarthritis (J. Rheumatol. 2002;29:570–4).

Chondrocalcinosis is the radiographic hallmark of CPPD deposition disease, but it can be risky to diagnose the condition based on radiographic findings alone, Dr. Rosenthal said. Chondrocalcinosis appears as a linear deposition of calcium, often in the fibrocartilage or lining of the articular cartilage. It is most likely to be found in the symphysis pubis and the triangular cartilage of the wrist.

Ultrasound is the most promising new technique for CPPD diagnosis, with a recent study identifying three patterns that appear highly specific for CPPD deposition disease. The first is a punctate pattern with several thin hyperechoic spots in fibrocartilage and tendons. The second is characterized by homogeneous hyperechoic or oval deposits localized in bursae and articular recesses. The third pattern shows thin hyperechoic bands parallel to the articular surfaces (Ann. Rheum. Dis. 2005;64:638–40).

MRI adds little to a diagnosis, since calcification in cartilage can appear as high or low signal intensity.

On the other hand, CT scans can be quite sensitive and may be particularly useful for cases with spinal involvement. One advantage of CT scanning is that the technique can detect—and in some cases differentiate between—both BCP and CPPD crystals.

CPPD crystals are weakly birefringent under polarizing light microscopy (as shown). Only 17%–40% of CPPD crystals glow using such means.

SAN FRANCISCO — Cat scratch disease is a surprisingly common cause of prolonged, alarming fever in children, Sheldon L. Kaplan, M.D., said at a meeting on clinical pediatrics sponsored by the University of California, San Francisco.

Typically presenting with a fever of unknown origin along with abdominal pain, children with cat scratch disease (CSD) typically go for 3–6 weeks before being referred to an infectious disease specialist and receiving a proper diagnosis, said Dr. Kaplan, of Baylor College of Medicine, Houston.

He described the case of a 12-year-old girl who was admitted to Texas Children's Hospital following a 3-week history of intermittent fevers between 38.3°C and 40.6° C and 2 days of right upper quadrant pain. She also reported a weight loss of 4.5 kg.

The patient had a history of dog and kitten scratches, and a physical exam revealed enlarged and tender left and right inguinal lymph nodes. Her erythrocyte sedimentation rate was very high at 93 mm/hr, but two blood cultures and a urine culture were sterile, and a stool culture for routine pathogens also was negative.

An ultrasound exam found two mildly enlarged lymph nodes in the right lower quadrant, but an abdominal CT scan was normal.

Serologies for toxoplasmosis, cytomegalo virus, and Epstein-Barr virus were all negative, and no antinuclear antibody was detected. Transaminase and bilirubin concentrations were normal. Serum markers for inflammatory bowel disease were normal, but the child underwent a colonoscopy on the seventh hospital day that was essentially normal as well.

Finally her physicians ordered a Bartonella henselae titer, and she proved to be positive for the causative organism of CSD.

Dr. Kaplan offered a few tips for making a CSD diagnosis in a somewhat more timely fashion, and for treating the disease:

▸ Children with CSD almost always have exposure to cats. Kittens are more likely to be infected, and fleas provide the most common mode of transmission. There's no good evidence that fleas can transmit B. henselae directly to humans, however.

▸ Patients typically present with a prolonged but intermittent fever and abdominal pain. They feel well between bouts of fever.

▸ “If you're lucky and very observant, you may see a papule at the site where the cat scratched,” Dr. Kaplan said. These papules may last for 2 weeks, and there also may be some lymphadenopathy.

▸ Often there will be hepatosplenomegaly, and the liver will be tender to palpation.

▸ An ultrasound of the liver or spleen will show characteristic granulomas.

▸ Children with CSD typically respond within 48 hours to rifampin (20 mg/kg per day in two divided doses for 14 days), sometimes with the addition of an aminoglycoside.

SAN FRANCISCO — Cat scratch disease is a surprisingly common cause of prolonged, alarming fever in children, Sheldon L. Kaplan, M.D., said at a meeting on clinical pediatrics sponsored by the University of California, San Francisco.

Typically presenting with a fever of unknown origin along with abdominal pain, children with cat scratch disease (CSD) typically go for 3–6 weeks before being referred to an infectious disease specialist and receiving a proper diagnosis, said Dr. Kaplan, of Baylor College of Medicine, Houston.

He described the case of a 12-year-old girl who was admitted to Texas Children's Hospital following a 3-week history of intermittent fevers between 38.3°C and 40.6° C and 2 days of right upper quadrant pain. She also reported a weight loss of 4.5 kg.

The patient had a history of dog and kitten scratches, and a physical exam revealed enlarged and tender left and right inguinal lymph nodes. Her erythrocyte sedimentation rate was very high at 93 mm/hr, but two blood cultures and a urine culture were sterile, and a stool culture for routine pathogens also was negative.

An ultrasound exam found two mildly enlarged lymph nodes in the right lower quadrant, but an abdominal CT scan was normal.

Serologies for toxoplasmosis, cytomegalo virus, and Epstein-Barr virus were all negative, and no antinuclear antibody was detected. Transaminase and bilirubin concentrations were normal. Serum markers for inflammatory bowel disease were normal, but the child underwent a colonoscopy on the seventh hospital day that was essentially normal as well.

Finally her physicians ordered a Bartonella henselae titer, and she proved to be positive for the causative organism of CSD.

Dr. Kaplan offered a few tips for making a CSD diagnosis in a somewhat more timely fashion, and for treating the disease:

▸ Children with CSD almost always have exposure to cats. Kittens are more likely to be infected, and fleas provide the most common mode of transmission. There's no good evidence that fleas can transmit B. henselae directly to humans, however.

▸ Patients typically present with a prolonged but intermittent fever and abdominal pain. They feel well between bouts of fever.

▸ “If you're lucky and very observant, you may see a papule at the site where the cat scratched,” Dr. Kaplan said. These papules may last for 2 weeks, and there also may be some lymphadenopathy.

▸ Often there will be hepatosplenomegaly, and the liver will be tender to palpation.

▸ An ultrasound of the liver or spleen will show characteristic granulomas.

▸ Children with CSD typically respond within 48 hours to rifampin (20 mg/kg per day in two divided doses for 14 days), sometimes with the addition of an aminoglycoside.

SAN FRANCISCO — Cat scratch disease is a surprisingly common cause of prolonged, alarming fever in children, Sheldon L. Kaplan, M.D., said at a meeting on clinical pediatrics sponsored by the University of California, San Francisco.

Typically presenting with a fever of unknown origin along with abdominal pain, children with cat scratch disease (CSD) typically go for 3–6 weeks before being referred to an infectious disease specialist and receiving a proper diagnosis, said Dr. Kaplan, of Baylor College of Medicine, Houston.

He described the case of a 12-year-old girl who was admitted to Texas Children's Hospital following a 3-week history of intermittent fevers between 38.3°C and 40.6° C and 2 days of right upper quadrant pain. She also reported a weight loss of 4.5 kg.

The patient had a history of dog and kitten scratches, and a physical exam revealed enlarged and tender left and right inguinal lymph nodes. Her erythrocyte sedimentation rate was very high at 93 mm/hr, but two blood cultures and a urine culture were sterile, and a stool culture for routine pathogens also was negative.

An ultrasound exam found two mildly enlarged lymph nodes in the right lower quadrant, but an abdominal CT scan was normal.

Serologies for toxoplasmosis, cytomegalo virus, and Epstein-Barr virus were all negative, and no antinuclear antibody was detected. Transaminase and bilirubin concentrations were normal. Serum markers for inflammatory bowel disease were normal, but the child underwent a colonoscopy on the seventh hospital day that was essentially normal as well.

Finally her physicians ordered a Bartonella henselae titer, and she proved to be positive for the causative organism of CSD.

Dr. Kaplan offered a few tips for making a CSD diagnosis in a somewhat more timely fashion, and for treating the disease:

▸ Children with CSD almost always have exposure to cats. Kittens are more likely to be infected, and fleas provide the most common mode of transmission. There's no good evidence that fleas can transmit B. henselae directly to humans, however.

▸ Patients typically present with a prolonged but intermittent fever and abdominal pain. They feel well between bouts of fever.

▸ “If you're lucky and very observant, you may see a papule at the site where the cat scratched,” Dr. Kaplan said. These papules may last for 2 weeks, and there also may be some lymphadenopathy.

▸ Often there will be hepatosplenomegaly, and the liver will be tender to palpation.

▸ An ultrasound of the liver or spleen will show characteristic granulomas.

▸ Children with CSD typically respond within 48 hours to rifampin (20 mg/kg per day in two divided doses for 14 days), sometimes with the addition of an aminoglycoside.

RENO, NEV. — A retrospective study examining 473 pregnancies complicated by preeclampsia has uncovered several significant racial and ethnic differences in the expression of the disorder.

African American women with preeclampsia tend to have more severe hypertension and more often require antihypertensive medication than the population at large, according to a poster presentation by Amy Goodwin, M.D., of Case Western Reserve University, Cleveland, and her associates at the annual meeting of the Society for Maternal-Fetal Medicine.

While 37% of the full sample had severe hypertension at diagnosis, 45% of African American women had severe hypertension.

African American women were also significantly more likely to require antihypertensive medication intrapartum (12% vs. 8.8%), postpartum (18% vs. 13%), and at discharge (35% vs. 27%).

Non-Hispanic white women more frequently manifest severe hypertension with hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. While 24% of the full sample exhibited HELLP, the rate among white women was 30%.

Hispanic women tend to present with preeclampsia later in gestation and with less severe disease than the rest of the population. They presented at a mean of 36 weeks of gestation vs. 34.4 weeks for the rest of the population, and a smaller proportion of them exhibited severe hypertension at diagnosis (27% vs. 37%).

The study found no significant differences by race or ethnicity in a number of other factors including proteinuria, eclampsia, intrauterine fetal distress, intrauterine growth retardation, abruption, and recurrent preeclampsia, they said.

RENO, NEV. — A retrospective study examining 473 pregnancies complicated by preeclampsia has uncovered several significant racial and ethnic differences in the expression of the disorder.

African American women with preeclampsia tend to have more severe hypertension and more often require antihypertensive medication than the population at large, according to a poster presentation by Amy Goodwin, M.D., of Case Western Reserve University, Cleveland, and her associates at the annual meeting of the Society for Maternal-Fetal Medicine.

While 37% of the full sample had severe hypertension at diagnosis, 45% of African American women had severe hypertension.

African American women were also significantly more likely to require antihypertensive medication intrapartum (12% vs. 8.8%), postpartum (18% vs. 13%), and at discharge (35% vs. 27%).

Non-Hispanic white women more frequently manifest severe hypertension with hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. While 24% of the full sample exhibited HELLP, the rate among white women was 30%.

Hispanic women tend to present with preeclampsia later in gestation and with less severe disease than the rest of the population. They presented at a mean of 36 weeks of gestation vs. 34.4 weeks for the rest of the population, and a smaller proportion of them exhibited severe hypertension at diagnosis (27% vs. 37%).

The study found no significant differences by race or ethnicity in a number of other factors including proteinuria, eclampsia, intrauterine fetal distress, intrauterine growth retardation, abruption, and recurrent preeclampsia, they said.

RENO, NEV. — A retrospective study examining 473 pregnancies complicated by preeclampsia has uncovered several significant racial and ethnic differences in the expression of the disorder.

African American women with preeclampsia tend to have more severe hypertension and more often require antihypertensive medication than the population at large, according to a poster presentation by Amy Goodwin, M.D., of Case Western Reserve University, Cleveland, and her associates at the annual meeting of the Society for Maternal-Fetal Medicine.

While 37% of the full sample had severe hypertension at diagnosis, 45% of African American women had severe hypertension.

African American women were also significantly more likely to require antihypertensive medication intrapartum (12% vs. 8.8%), postpartum (18% vs. 13%), and at discharge (35% vs. 27%).

Non-Hispanic white women more frequently manifest severe hypertension with hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. While 24% of the full sample exhibited HELLP, the rate among white women was 30%.

Hispanic women tend to present with preeclampsia later in gestation and with less severe disease than the rest of the population. They presented at a mean of 36 weeks of gestation vs. 34.4 weeks for the rest of the population, and a smaller proportion of them exhibited severe hypertension at diagnosis (27% vs. 37%).

The study found no significant differences by race or ethnicity in a number of other factors including proteinuria, eclampsia, intrauterine fetal distress, intrauterine growth retardation, abruption, and recurrent preeclampsia, they said.

SAN FRANCISCO — Lack of treatment efficacy is only one of the reasons that acne therapy often fails in teenagers, Lee T. Zane, M.D., reported at a meeting on clinical pediatrics sponsored by the University of California, San Francisco.

Poor adherence is also a factor, said Dr. Zane of the university. And poor adherence can stem from several things. The treatment regimen may be too complex, or patients may stop treatment prematurely when they don't see quick results. Adverse effects of therapy often lead to poor adherence too. In some cases, the patient may have conceptual opposition to certain modes of therapy.

Dr. Zane offered these tips to optimize adherence:

▸ Simplify the treatment regimen. Use fewer agents or combination agents. Combinations of clindamycin and benzoyl peroxide are available now. Coming soon there may be retinoids plus antibiotics and retinoids plus benzoyl peroxide.

▸ Minimize the adverse effects. Because benzoyl peroxide can be especially irritating, maximize retinoid therapy before maximizing benzoyl peroxide.

With retinoids and benzoyl peroxide, advise patients that a pea-sized dollop should be enough to cover the face. Using more will not improve the result, but will increase irritation.

Advise them to apply topical agents to dry skin, waiting 20–30 minutes after washing.

▸ Set realistic expectations. Tell patients to try a therapy for at least 2 full months before deciding whether it's effective.

“I'm going for a slow and steady course of therapy followed by long-term maintenance,” Dr. Zane said. “It's not a quick cure. It's really about management of a chronic condition and prevention.

▸ Remember that your clinical assessment of disease severity may differ dramatically from the patient's assessment. A single pustule on otherwise porcelain skin may be more damaging psychologically than widespread disease.

▸ Peer opinion is often far more compelling than scientific data. The physician may be focusing on the patient's face, but if his friends are making fun of the acne on his back, he'll be more concerned about that.

▸ Warn patients about behaviors that worsen acne. Physicians have long advised against picking or squeezing, but they also should point out that scrubbing or exfoliating can promote the formation of comedones. Rubbing the skin during sports or other activities also can promote acne.

Finally, some medications can exacerbate symptoms. These include lithium, topical and oral corticosteroids, and androgenic steroids.

SAN FRANCISCO — Lack of treatment efficacy is only one of the reasons that acne therapy often fails in teenagers, Lee T. Zane, M.D., reported at a meeting on clinical pediatrics sponsored by the University of California, San Francisco.

Poor adherence is also a factor, said Dr. Zane of the university. And poor adherence can stem from several things. The treatment regimen may be too complex, or patients may stop treatment prematurely when they don't see quick results. Adverse effects of therapy often lead to poor adherence too. In some cases, the patient may have conceptual opposition to certain modes of therapy.

Dr. Zane offered these tips to optimize adherence:

▸ Simplify the treatment regimen. Use fewer agents or combination agents. Combinations of clindamycin and benzoyl peroxide are available now. Coming soon there may be retinoids plus antibiotics and retinoids plus benzoyl peroxide.

▸ Minimize the adverse effects. Because benzoyl peroxide can be especially irritating, maximize retinoid therapy before maximizing benzoyl peroxide.

With retinoids and benzoyl peroxide, advise patients that a pea-sized dollop should be enough to cover the face. Using more will not improve the result, but will increase irritation.

Advise them to apply topical agents to dry skin, waiting 20–30 minutes after washing.

▸ Set realistic expectations. Tell patients to try a therapy for at least 2 full months before deciding whether it's effective.

“I'm going for a slow and steady course of therapy followed by long-term maintenance,” Dr. Zane said. “It's not a quick cure. It's really about management of a chronic condition and prevention.

▸ Remember that your clinical assessment of disease severity may differ dramatically from the patient's assessment. A single pustule on otherwise porcelain skin may be more damaging psychologically than widespread disease.

▸ Peer opinion is often far more compelling than scientific data. The physician may be focusing on the patient's face, but if his friends are making fun of the acne on his back, he'll be more concerned about that.

▸ Warn patients about behaviors that worsen acne. Physicians have long advised against picking or squeezing, but they also should point out that scrubbing or exfoliating can promote the formation of comedones. Rubbing the skin during sports or other activities also can promote acne.

Finally, some medications can exacerbate symptoms. These include lithium, topical and oral corticosteroids, and androgenic steroids.

SAN FRANCISCO — Lack of treatment efficacy is only one of the reasons that acne therapy often fails in teenagers, Lee T. Zane, M.D., reported at a meeting on clinical pediatrics sponsored by the University of California, San Francisco.

Poor adherence is also a factor, said Dr. Zane of the university. And poor adherence can stem from several things. The treatment regimen may be too complex, or patients may stop treatment prematurely when they don't see quick results. Adverse effects of therapy often lead to poor adherence too. In some cases, the patient may have conceptual opposition to certain modes of therapy.

Dr. Zane offered these tips to optimize adherence:

▸ Simplify the treatment regimen. Use fewer agents or combination agents. Combinations of clindamycin and benzoyl peroxide are available now. Coming soon there may be retinoids plus antibiotics and retinoids plus benzoyl peroxide.

▸ Minimize the adverse effects. Because benzoyl peroxide can be especially irritating, maximize retinoid therapy before maximizing benzoyl peroxide.

With retinoids and benzoyl peroxide, advise patients that a pea-sized dollop should be enough to cover the face. Using more will not improve the result, but will increase irritation.

Advise them to apply topical agents to dry skin, waiting 20–30 minutes after washing.

▸ Set realistic expectations. Tell patients to try a therapy for at least 2 full months before deciding whether it's effective.

“I'm going for a slow and steady course of therapy followed by long-term maintenance,” Dr. Zane said. “It's not a quick cure. It's really about management of a chronic condition and prevention.

▸ Remember that your clinical assessment of disease severity may differ dramatically from the patient's assessment. A single pustule on otherwise porcelain skin may be more damaging psychologically than widespread disease.

▸ Peer opinion is often far more compelling than scientific data. The physician may be focusing on the patient's face, but if his friends are making fun of the acne on his back, he'll be more concerned about that.

▸ Warn patients about behaviors that worsen acne. Physicians have long advised against picking or squeezing, but they also should point out that scrubbing or exfoliating can promote the formation of comedones. Rubbing the skin during sports or other activities also can promote acne.

Finally, some medications can exacerbate symptoms. These include lithium, topical and oral corticosteroids, and androgenic steroids.

SANTA FE, N.M. – A study of children's autonomic responses to reward and negative mood induction suggests that when conduct disorder and depression are comorbid, depression is the primary disorder.

In a poster presentation at the annual meeting of the Society for Psychophysiological Research, Hilary K. Mead, a graduate student working in the Child and Adolescent Adjustment Project at the University of Washington (Seattle), noted that previous studies have suggested that comorbidity rates for the two conditions may be as high as 82%, but that it's unclear whether conduct disorder (CD) arises from depression or whether depression arises from CD.

A third possibility is that neither condition is primary and that both are driven by a common etiological substrate, with each representing an alternative manifestation of a single biological disposition. This hypothesis found no support in the experimental results, Ms. Mead noted.

The experiment involved 116 children, aged 8–12 years. Eighteen of those children had conduct disorder and/or oppositional defiant disorder, 15 had depression and/or dysthymia, 37 had comorbid depression and conduct disorder, and 46 had no psychiatric condition.

All children had their electrodermal responses (EDR), their respiratory sinus arrhythmia (RSA), and their cardiac pre-ejection period (PEP) measured during three successive experimental conditions: a 5-minute baseline, a monetary incentive task, and negative mood induction via an emotionally evocative film clip.

If CD were the primary disorder, groups with CD alone and with comorbid CD and depression would be expected to have a similar pattern of autonomic responses.

On the other hand, if depression were primary, groups with depression alone and comorbid CD and depression would show similar autonomic responses. If neither condition were primary, all three groups of children with psychiatric disorders would be expected to be similar, Ms. Mead said in her poster.

As it turned out, children with CD had a pattern of autonomic responses that differed significantly from the other groups. The EDR of children with CD did not change across trials of the reward incentive task, while all other groups showed decreases in EDR. During negative mood induction, children with CD had decreasing PEP and increasing RSA, while the other groups showed no change from baseline.

The investigators concluded that depression is the primary disorder in children with comorbid internalizing and externalizing psychopathologic symptoms.

The National Institutes of Health funded the study.

SANTA FE, N.M. – A study of children's autonomic responses to reward and negative mood induction suggests that when conduct disorder and depression are comorbid, depression is the primary disorder.

In a poster presentation at the annual meeting of the Society for Psychophysiological Research, Hilary K. Mead, a graduate student working in the Child and Adolescent Adjustment Project at the University of Washington (Seattle), noted that previous studies have suggested that comorbidity rates for the two conditions may be as high as 82%, but that it's unclear whether conduct disorder (CD) arises from depression or whether depression arises from CD.

A third possibility is that neither condition is primary and that both are driven by a common etiological substrate, with each representing an alternative manifestation of a single biological disposition. This hypothesis found no support in the experimental results, Ms. Mead noted.

The experiment involved 116 children, aged 8–12 years. Eighteen of those children had conduct disorder and/or oppositional defiant disorder, 15 had depression and/or dysthymia, 37 had comorbid depression and conduct disorder, and 46 had no psychiatric condition.

All children had their electrodermal responses (EDR), their respiratory sinus arrhythmia (RSA), and their cardiac pre-ejection period (PEP) measured during three successive experimental conditions: a 5-minute baseline, a monetary incentive task, and negative mood induction via an emotionally evocative film clip.

If CD were the primary disorder, groups with CD alone and with comorbid CD and depression would be expected to have a similar pattern of autonomic responses.

On the other hand, if depression were primary, groups with depression alone and comorbid CD and depression would show similar autonomic responses. If neither condition were primary, all three groups of children with psychiatric disorders would be expected to be similar, Ms. Mead said in her poster.

As it turned out, children with CD had a pattern of autonomic responses that differed significantly from the other groups. The EDR of children with CD did not change across trials of the reward incentive task, while all other groups showed decreases in EDR. During negative mood induction, children with CD had decreasing PEP and increasing RSA, while the other groups showed no change from baseline.

The investigators concluded that depression is the primary disorder in children with comorbid internalizing and externalizing psychopathologic symptoms.

The National Institutes of Health funded the study.

SANTA FE, N.M. – A study of children's autonomic responses to reward and negative mood induction suggests that when conduct disorder and depression are comorbid, depression is the primary disorder.

In a poster presentation at the annual meeting of the Society for Psychophysiological Research, Hilary K. Mead, a graduate student working in the Child and Adolescent Adjustment Project at the University of Washington (Seattle), noted that previous studies have suggested that comorbidity rates for the two conditions may be as high as 82%, but that it's unclear whether conduct disorder (CD) arises from depression or whether depression arises from CD.

A third possibility is that neither condition is primary and that both are driven by a common etiological substrate, with each representing an alternative manifestation of a single biological disposition. This hypothesis found no support in the experimental results, Ms. Mead noted.

The experiment involved 116 children, aged 8–12 years. Eighteen of those children had conduct disorder and/or oppositional defiant disorder, 15 had depression and/or dysthymia, 37 had comorbid depression and conduct disorder, and 46 had no psychiatric condition.

All children had their electrodermal responses (EDR), their respiratory sinus arrhythmia (RSA), and their cardiac pre-ejection period (PEP) measured during three successive experimental conditions: a 5-minute baseline, a monetary incentive task, and negative mood induction via an emotionally evocative film clip.

If CD were the primary disorder, groups with CD alone and with comorbid CD and depression would be expected to have a similar pattern of autonomic responses.

On the other hand, if depression were primary, groups with depression alone and comorbid CD and depression would show similar autonomic responses. If neither condition were primary, all three groups of children with psychiatric disorders would be expected to be similar, Ms. Mead said in her poster.

As it turned out, children with CD had a pattern of autonomic responses that differed significantly from the other groups. The EDR of children with CD did not change across trials of the reward incentive task, while all other groups showed decreases in EDR. During negative mood induction, children with CD had decreasing PEP and increasing RSA, while the other groups showed no change from baseline.

The investigators concluded that depression is the primary disorder in children with comorbid internalizing and externalizing psychopathologic symptoms.

The National Institutes of Health funded the study.

SAN FRANCISCO — The epidemic of childhood obesity shows no signs of abating, and studies have demonstrated only modest results from diet and exercise, unless an intensive boot-camp approach is used, Robert H. Lustig, M.D., said at a meeting on clinical pediatrics, sponsored by the University of California, San Francisco.

Intensive treatment—that is, pharmacotherapy or surgery—is indicated in an adolescent whose BMI is greater than two standard deviations from the norm for his or her age, and who has at least one significant comorbidity, said Dr. Lustig of UCSF.

Such comorbidities include metabolic, orthopedic, and cardiopulmonary complications as well as psychological distress, he said, and the majority of obese adolescents have at least one of these.

Unfortunately, pharmacotherapy for obesity has a dubious history. Drugs used in the past, such as thyroid hormone, dinitrophenol, amphetamine, fenfluramine, phenylpropanolamine, and ephedra are well known for significant complications, including death. In addition, many clinicians are hesitant to prescribe drugs to children or adolescents when their long-term effects remain unknown.

Given that obesity can result from a number of underlying conditions and the variable results of many pharmacotherapies, the trick is to pick a drug that matches the patient's characteristics, said Dr. Lustig. He discussed four available drugs, two of which are approved by the Food and Drug Administration for use in children:

▸ Sibutramine (Meridia) is an anorectic agent. Sibutramine should complement a program of diet and exercise. Studies of adolescents who were given sibutramine have shown that they had significant weight loss, especially in the first 6 months. The FDA has approved the drug for use in patients over age 16 years.

Responses to sibutramine are highly variable, however, and few predictors of response have been identified. Moreover, side effects can be significant. In one study, 19 of 43 adolescents had mild hypertension and tachycardia in response to sibutramine, and 5 required discontinuation of the drug.

Other side effects include insomnia, anxiety, headache, depression, and the risk of serotonin syndrome when used in combination with certain other drugs. Sibutramine should not be routinely used in adolescents, said Dr. Lustig.

▸ Orlistat (Xenical) is a pancreatic lipase inhibitor. This drug decreases intestinal fat absorption, and is approved for use in children above age 12 years. Orlistat, in combination with behavioral intervention, results in significant weight loss over 4 months, according to a study of 534 subjects. However, children taking orlistat regained lost weight within a year, although they still remained significantly lighter than the children taking placebo, who gained weight.

Unless fat restrictions can be maintained, side effects include flatulence, diarrhea, and anal leakage.

▸ Metformin (Glucophage) is another drug approved for use in children. It reduces hepatic gluconeogenesis, increases hepatic insulin sensitivity, and lowers fasting insulin levels.

This drug is approved for use in type 2 diabetes mellitus, but not specifically for obesity. Nevertheless, studies have shown that metformin decreases food intake, reduces fat stores, improves lipid profiles, inhibits progression from impaired glucose tolerance to type 2 diabetes, and reduces cardiovascular morbidity and mortality in adults with diabetes.

In obese adolescents with impaired insulin sensitivity, studies have demonstrated significant decreases in BMI even when metformin is administered without dietary restrictions. The drug may be especially useful in adolescents taking psychotropic medications such as olanzapine, risperidone, quetiapine, or valproate.

The drug is most useful in adolescents who have severe insulin resistance, but not those who are insulin sensitive, Dr. Lustig said. Another group that may benefit may be obese girls with polycystic ovarian syndrome.

Metformin's side effects include abdominal discomfort that lasts for about 1 month, rare lactic acidosis, and urinary losses of B vitamins. Dr. Lustig said that all patients taking metformin should also take a daily multivitamin.

▸ Octreotide (Sandostatin) inhibits the opening of calcium channels in beta cells and reduces glucose-dependent insulin secretion.

Not approved for use in obese adolescents, octreotide seems especially effective in children with “hypothalamic obesity” arising from insults to the central nervous system.

Side effects include transient GI distress and gallstones, which can be prevented by ursodiol. Other limitations include its high cost and the requirement for parenteral administration.

SAN FRANCISCO — The epidemic of childhood obesity shows no signs of abating, and studies have demonstrated only modest results from diet and exercise, unless an intensive boot-camp approach is used, Robert H. Lustig, M.D., said at a meeting on clinical pediatrics, sponsored by the University of California, San Francisco.

Intensive treatment—that is, pharmacotherapy or surgery—is indicated in an adolescent whose BMI is greater than two standard deviations from the norm for his or her age, and who has at least one significant comorbidity, said Dr. Lustig of UCSF.

Such comorbidities include metabolic, orthopedic, and cardiopulmonary complications as well as psychological distress, he said, and the majority of obese adolescents have at least one of these.

Unfortunately, pharmacotherapy for obesity has a dubious history. Drugs used in the past, such as thyroid hormone, dinitrophenol, amphetamine, fenfluramine, phenylpropanolamine, and ephedra are well known for significant complications, including death. In addition, many clinicians are hesitant to prescribe drugs to children or adolescents when their long-term effects remain unknown.

Given that obesity can result from a number of underlying conditions and the variable results of many pharmacotherapies, the trick is to pick a drug that matches the patient's characteristics, said Dr. Lustig. He discussed four available drugs, two of which are approved by the Food and Drug Administration for use in children:

▸ Sibutramine (Meridia) is an anorectic agent. Sibutramine should complement a program of diet and exercise. Studies of adolescents who were given sibutramine have shown that they had significant weight loss, especially in the first 6 months. The FDA has approved the drug for use in patients over age 16 years.

Responses to sibutramine are highly variable, however, and few predictors of response have been identified. Moreover, side effects can be significant. In one study, 19 of 43 adolescents had mild hypertension and tachycardia in response to sibutramine, and 5 required discontinuation of the drug.

Other side effects include insomnia, anxiety, headache, depression, and the risk of serotonin syndrome when used in combination with certain other drugs. Sibutramine should not be routinely used in adolescents, said Dr. Lustig.

▸ Orlistat (Xenical) is a pancreatic lipase inhibitor. This drug decreases intestinal fat absorption, and is approved for use in children above age 12 years. Orlistat, in combination with behavioral intervention, results in significant weight loss over 4 months, according to a study of 534 subjects. However, children taking orlistat regained lost weight within a year, although they still remained significantly lighter than the children taking placebo, who gained weight.

Unless fat restrictions can be maintained, side effects include flatulence, diarrhea, and anal leakage.

▸ Metformin (Glucophage) is another drug approved for use in children. It reduces hepatic gluconeogenesis, increases hepatic insulin sensitivity, and lowers fasting insulin levels.

This drug is approved for use in type 2 diabetes mellitus, but not specifically for obesity. Nevertheless, studies have shown that metformin decreases food intake, reduces fat stores, improves lipid profiles, inhibits progression from impaired glucose tolerance to type 2 diabetes, and reduces cardiovascular morbidity and mortality in adults with diabetes.

In obese adolescents with impaired insulin sensitivity, studies have demonstrated significant decreases in BMI even when metformin is administered without dietary restrictions. The drug may be especially useful in adolescents taking psychotropic medications such as olanzapine, risperidone, quetiapine, or valproate.

The drug is most useful in adolescents who have severe insulin resistance, but not those who are insulin sensitive, Dr. Lustig said. Another group that may benefit may be obese girls with polycystic ovarian syndrome.

Metformin's side effects include abdominal discomfort that lasts for about 1 month, rare lactic acidosis, and urinary losses of B vitamins. Dr. Lustig said that all patients taking metformin should also take a daily multivitamin.

▸ Octreotide (Sandostatin) inhibits the opening of calcium channels in beta cells and reduces glucose-dependent insulin secretion.

Not approved for use in obese adolescents, octreotide seems especially effective in children with “hypothalamic obesity” arising from insults to the central nervous system.

Side effects include transient GI distress and gallstones, which can be prevented by ursodiol. Other limitations include its high cost and the requirement for parenteral administration.

SAN FRANCISCO — The epidemic of childhood obesity shows no signs of abating, and studies have demonstrated only modest results from diet and exercise, unless an intensive boot-camp approach is used, Robert H. Lustig, M.D., said at a meeting on clinical pediatrics, sponsored by the University of California, San Francisco.

Intensive treatment—that is, pharmacotherapy or surgery—is indicated in an adolescent whose BMI is greater than two standard deviations from the norm for his or her age, and who has at least one significant comorbidity, said Dr. Lustig of UCSF.

Such comorbidities include metabolic, orthopedic, and cardiopulmonary complications as well as psychological distress, he said, and the majority of obese adolescents have at least one of these.

Unfortunately, pharmacotherapy for obesity has a dubious history. Drugs used in the past, such as thyroid hormone, dinitrophenol, amphetamine, fenfluramine, phenylpropanolamine, and ephedra are well known for significant complications, including death. In addition, many clinicians are hesitant to prescribe drugs to children or adolescents when their long-term effects remain unknown.

Given that obesity can result from a number of underlying conditions and the variable results of many pharmacotherapies, the trick is to pick a drug that matches the patient's characteristics, said Dr. Lustig. He discussed four available drugs, two of which are approved by the Food and Drug Administration for use in children:

▸ Sibutramine (Meridia) is an anorectic agent. Sibutramine should complement a program of diet and exercise. Studies of adolescents who were given sibutramine have shown that they had significant weight loss, especially in the first 6 months. The FDA has approved the drug for use in patients over age 16 years.

Responses to sibutramine are highly variable, however, and few predictors of response have been identified. Moreover, side effects can be significant. In one study, 19 of 43 adolescents had mild hypertension and tachycardia in response to sibutramine, and 5 required discontinuation of the drug.

Other side effects include insomnia, anxiety, headache, depression, and the risk of serotonin syndrome when used in combination with certain other drugs. Sibutramine should not be routinely used in adolescents, said Dr. Lustig.

▸ Orlistat (Xenical) is a pancreatic lipase inhibitor. This drug decreases intestinal fat absorption, and is approved for use in children above age 12 years. Orlistat, in combination with behavioral intervention, results in significant weight loss over 4 months, according to a study of 534 subjects. However, children taking orlistat regained lost weight within a year, although they still remained significantly lighter than the children taking placebo, who gained weight.

Unless fat restrictions can be maintained, side effects include flatulence, diarrhea, and anal leakage.

▸ Metformin (Glucophage) is another drug approved for use in children. It reduces hepatic gluconeogenesis, increases hepatic insulin sensitivity, and lowers fasting insulin levels.

This drug is approved for use in type 2 diabetes mellitus, but not specifically for obesity. Nevertheless, studies have shown that metformin decreases food intake, reduces fat stores, improves lipid profiles, inhibits progression from impaired glucose tolerance to type 2 diabetes, and reduces cardiovascular morbidity and mortality in adults with diabetes.

In obese adolescents with impaired insulin sensitivity, studies have demonstrated significant decreases in BMI even when metformin is administered without dietary restrictions. The drug may be especially useful in adolescents taking psychotropic medications such as olanzapine, risperidone, quetiapine, or valproate.

The drug is most useful in adolescents who have severe insulin resistance, but not those who are insulin sensitive, Dr. Lustig said. Another group that may benefit may be obese girls with polycystic ovarian syndrome.

Metformin's side effects include abdominal discomfort that lasts for about 1 month, rare lactic acidosis, and urinary losses of B vitamins. Dr. Lustig said that all patients taking metformin should also take a daily multivitamin.

▸ Octreotide (Sandostatin) inhibits the opening of calcium channels in beta cells and reduces glucose-dependent insulin secretion.

Not approved for use in obese adolescents, octreotide seems especially effective in children with “hypothalamic obesity” arising from insults to the central nervous system.

Side effects include transient GI distress and gallstones, which can be prevented by ursodiol. Other limitations include its high cost and the requirement for parenteral administration.

SAN ANTONIO — Almost half of men who remain sexually potent after radical prostatectomy exhibit “climacturia”—leakage of urine at orgasm—according to a poster presented by Jason Lee, M.D., at the annual meeting of the American Urological Association.

In a consecutive cohort of 42 men who were at least 12 months post prostatectomy, 19 (45%) reported climacturia. Dr. Lee and his colleagues from Princess Margaret Hospital, Toronto, found no significant associations between climacturia and age, time since surgery, Gleason score, international prostate symptom score, urine flow rate, or the presence of incontinence.

Among the men experiencing climacturia, 4 (21%) said they experienced it rarely and 9 (47%) said they experienced it occasionally. Four others (21%) experienced climacturia most of the time or always.

Nine of the men (52%) said that the condition caused them significant bother, and 10 said it caused them nonsignificant bother. Four men (21%) said it caused their partners significant bother, and 15 (79%) said it caused their partners nonsignificant bother.

Leakage was only a few drops in 11 of the men, but 2 men said they leaked more than an ounce of urine, and a third man said he leaked more than 5 ounces.

Most of the men (16 of 19 [84%]) coped with their climacturia by voiding before intercourse. Two men additionally required a condom. Three men took no action.

The investigators concluded that climacturia is not uncommon following radical prostatectomy, and it should be discussed as a possible complication for men evaluating their treatment options.

SAN ANTONIO — Almost half of men who remain sexually potent after radical prostatectomy exhibit “climacturia”—leakage of urine at orgasm—according to a poster presented by Jason Lee, M.D., at the annual meeting of the American Urological Association.

In a consecutive cohort of 42 men who were at least 12 months post prostatectomy, 19 (45%) reported climacturia. Dr. Lee and his colleagues from Princess Margaret Hospital, Toronto, found no significant associations between climacturia and age, time since surgery, Gleason score, international prostate symptom score, urine flow rate, or the presence of incontinence.

Among the men experiencing climacturia, 4 (21%) said they experienced it rarely and 9 (47%) said they experienced it occasionally. Four others (21%) experienced climacturia most of the time or always.

Nine of the men (52%) said that the condition caused them significant bother, and 10 said it caused them nonsignificant bother. Four men (21%) said it caused their partners significant bother, and 15 (79%) said it caused their partners nonsignificant bother.

Leakage was only a few drops in 11 of the men, but 2 men said they leaked more than an ounce of urine, and a third man said he leaked more than 5 ounces.

Most of the men (16 of 19 [84%]) coped with their climacturia by voiding before intercourse. Two men additionally required a condom. Three men took no action.

The investigators concluded that climacturia is not uncommon following radical prostatectomy, and it should be discussed as a possible complication for men evaluating their treatment options.

SAN ANTONIO — Almost half of men who remain sexually potent after radical prostatectomy exhibit “climacturia”—leakage of urine at orgasm—according to a poster presented by Jason Lee, M.D., at the annual meeting of the American Urological Association.

In a consecutive cohort of 42 men who were at least 12 months post prostatectomy, 19 (45%) reported climacturia. Dr. Lee and his colleagues from Princess Margaret Hospital, Toronto, found no significant associations between climacturia and age, time since surgery, Gleason score, international prostate symptom score, urine flow rate, or the presence of incontinence.

Among the men experiencing climacturia, 4 (21%) said they experienced it rarely and 9 (47%) said they experienced it occasionally. Four others (21%) experienced climacturia most of the time or always.

Nine of the men (52%) said that the condition caused them significant bother, and 10 said it caused them nonsignificant bother. Four men (21%) said it caused their partners significant bother, and 15 (79%) said it caused their partners nonsignificant bother.

Leakage was only a few drops in 11 of the men, but 2 men said they leaked more than an ounce of urine, and a third man said he leaked more than 5 ounces.

Most of the men (16 of 19 [84%]) coped with their climacturia by voiding before intercourse. Two men additionally required a condom. Three men took no action.

The investigators concluded that climacturia is not uncommon following radical prostatectomy, and it should be discussed as a possible complication for men evaluating their treatment options.

ANAHEIM, CALIF. — An extract of the catechins found in green tea appears to be effective in preventing the progression of high-grade prostatic intraepithelial neoplasia to invasive prostate cancer, Saverio Bettuzzi, Ph.D., reported at the annual meeting of the American Association for Cancer Research.

In the placebo-controlled, double-blind study, 30 men with prostatic intraepithelial neoplasia (PIN) took 200 mg of green tea catechins (GTCs) three times daily for 6 months. Another 30 men with PIN took a placebo.

Catechins are antioxidants, and they belong to a class of polyphenols called flavanols. Epigallocatechin-3-gallate (EGCG) is the major catechin in green tea, and in tissue culture EGCG has been shown to induce apoptosis in cancer cells, but not normal cells.

All the participants underwent biopsies at study entry and 6 and 12 months later.

At 12 months, nine (30%) of the men who took placebo had progressed to prostate cancer. Only one (3.3%) of the men who took GTC had progression of PIN to invasive cancer, for an apparent efficacy rate of 90%. The difference between the groups was statistically significant.

The participants were aged 5–75 years. Men who drank green tea, who were vegetarians, or who were taking antioxidants or antiandrogenic therapy were excluded from the study.

Dr. Bettuzzi, of the University of Parma (Italy), said that previous studies have shown that about 30% of men with PIN will typically progress to invasive prostate cancer within a year, the same rate as in the placebo arm of his study.

No serious adverse events occurred among the men taking GTCs.

The investigators measured levels of prostate-specific antigen (PSA) every 3 months during the course of the study. They noted no significant differences in PSA levels between the two groups.

GTCs were extracted in the laboratory, although Dr. Bettuzzi said that green tea extracts are also available commercially. The 600-mg daily dose of GTCs corresponds to about 12–15 cups of green tea daily. He said that 10–20 cups of green tea is the normal daily intake in China.

Dr. Bettuzzi said he had no financial conflicts related to the study, which was supported in part by Genprofiler GmbH, a company in Bolzano, Italy, that manufactures diagnostics for molecular biology.

ANAHEIM, CALIF. — An extract of the catechins found in green tea appears to be effective in preventing the progression of high-grade prostatic intraepithelial neoplasia to invasive prostate cancer, Saverio Bettuzzi, Ph.D., reported at the annual meeting of the American Association for Cancer Research.

In the placebo-controlled, double-blind study, 30 men with prostatic intraepithelial neoplasia (PIN) took 200 mg of green tea catechins (GTCs) three times daily for 6 months. Another 30 men with PIN took a placebo.

Catechins are antioxidants, and they belong to a class of polyphenols called flavanols. Epigallocatechin-3-gallate (EGCG) is the major catechin in green tea, and in tissue culture EGCG has been shown to induce apoptosis in cancer cells, but not normal cells.

All the participants underwent biopsies at study entry and 6 and 12 months later.

At 12 months, nine (30%) of the men who took placebo had progressed to prostate cancer. Only one (3.3%) of the men who took GTC had progression of PIN to invasive cancer, for an apparent efficacy rate of 90%. The difference between the groups was statistically significant.

The participants were aged 5–75 years. Men who drank green tea, who were vegetarians, or who were taking antioxidants or antiandrogenic therapy were excluded from the study.

Dr. Bettuzzi, of the University of Parma (Italy), said that previous studies have shown that about 30% of men with PIN will typically progress to invasive prostate cancer within a year, the same rate as in the placebo arm of his study.

No serious adverse events occurred among the men taking GTCs.

The investigators measured levels of prostate-specific antigen (PSA) every 3 months during the course of the study. They noted no significant differences in PSA levels between the two groups.

GTCs were extracted in the laboratory, although Dr. Bettuzzi said that green tea extracts are also available commercially. The 600-mg daily dose of GTCs corresponds to about 12–15 cups of green tea daily. He said that 10–20 cups of green tea is the normal daily intake in China.

Dr. Bettuzzi said he had no financial conflicts related to the study, which was supported in part by Genprofiler GmbH, a company in Bolzano, Italy, that manufactures diagnostics for molecular biology.

ANAHEIM, CALIF. — An extract of the catechins found in green tea appears to be effective in preventing the progression of high-grade prostatic intraepithelial neoplasia to invasive prostate cancer, Saverio Bettuzzi, Ph.D., reported at the annual meeting of the American Association for Cancer Research.

In the placebo-controlled, double-blind study, 30 men with prostatic intraepithelial neoplasia (PIN) took 200 mg of green tea catechins (GTCs) three times daily for 6 months. Another 30 men with PIN took a placebo.

Catechins are antioxidants, and they belong to a class of polyphenols called flavanols. Epigallocatechin-3-gallate (EGCG) is the major catechin in green tea, and in tissue culture EGCG has been shown to induce apoptosis in cancer cells, but not normal cells.

All the participants underwent biopsies at study entry and 6 and 12 months later.

At 12 months, nine (30%) of the men who took placebo had progressed to prostate cancer. Only one (3.3%) of the men who took GTC had progression of PIN to invasive cancer, for an apparent efficacy rate of 90%. The difference between the groups was statistically significant.

The participants were aged 5–75 years. Men who drank green tea, who were vegetarians, or who were taking antioxidants or antiandrogenic therapy were excluded from the study.

Dr. Bettuzzi, of the University of Parma (Italy), said that previous studies have shown that about 30% of men with PIN will typically progress to invasive prostate cancer within a year, the same rate as in the placebo arm of his study.

No serious adverse events occurred among the men taking GTCs.

The investigators measured levels of prostate-specific antigen (PSA) every 3 months during the course of the study. They noted no significant differences in PSA levels between the two groups.

GTCs were extracted in the laboratory, although Dr. Bettuzzi said that green tea extracts are also available commercially. The 600-mg daily dose of GTCs corresponds to about 12–15 cups of green tea daily. He said that 10–20 cups of green tea is the normal daily intake in China.

Dr. Bettuzzi said he had no financial conflicts related to the study, which was supported in part by Genprofiler GmbH, a company in Bolzano, Italy, that manufactures diagnostics for molecular biology.

SAN ANTONIO — The digital rectal exam continues to play a critical role in identifying men with prostate cancer, according to a poster presentation by Joel Slaton, M.D., and Cesar Ercole, M.D., at the annual meeting of the American Urological Association.

Twenty-seven of 85 men (32%) with low prostate-specific antigen (PSA) levels and an abnormal digital rectal examination (DRE) had positive biopsies, reported Dr. Slaton and Dr. Ercole of the University of Minnesota, Minneapolis. Of those, 9 men (33%) were found to have high-grade tumors. The cancers would have been missed if the screening had relied on PSA alone.

The investigators attributed the false-negative PSA findings to tumors that were so poorly differentiated they underproduced PSA.

The study was a retrospective review of 3,817 prostate cancer screening visits between 1990 and 2000 where both DRE and PSA were performed. Of those, 81% of men had both a normal DRE and a normal PSA (defined as less than 4 ng/L). Those men did not undergo biopsy.

The remaining 719 men all had an abnormal DRE, a high PSA, or both, and all underwent biopsy; 240 of them (33%) were found to have cancer.

Of the 359 men with high PSA and abnormal DRE, 139 (39%) had positive biopsies, and slightly more than 20% had high-grade tumors. Of the 275 men with high PSA and normal DRE, 74 (27%) had positive biopsies, and about 20% had high-grade tumors.

SAN ANTONIO — The digital rectal exam continues to play a critical role in identifying men with prostate cancer, according to a poster presentation by Joel Slaton, M.D., and Cesar Ercole, M.D., at the annual meeting of the American Urological Association.

Twenty-seven of 85 men (32%) with low prostate-specific antigen (PSA) levels and an abnormal digital rectal examination (DRE) had positive biopsies, reported Dr. Slaton and Dr. Ercole of the University of Minnesota, Minneapolis. Of those, 9 men (33%) were found to have high-grade tumors. The cancers would have been missed if the screening had relied on PSA alone.

The investigators attributed the false-negative PSA findings to tumors that were so poorly differentiated they underproduced PSA.

The study was a retrospective review of 3,817 prostate cancer screening visits between 1990 and 2000 where both DRE and PSA were performed. Of those, 81% of men had both a normal DRE and a normal PSA (defined as less than 4 ng/L). Those men did not undergo biopsy.

The remaining 719 men all had an abnormal DRE, a high PSA, or both, and all underwent biopsy; 240 of them (33%) were found to have cancer.

Of the 359 men with high PSA and abnormal DRE, 139 (39%) had positive biopsies, and slightly more than 20% had high-grade tumors. Of the 275 men with high PSA and normal DRE, 74 (27%) had positive biopsies, and about 20% had high-grade tumors.

SAN ANTONIO — The digital rectal exam continues to play a critical role in identifying men with prostate cancer, according to a poster presentation by Joel Slaton, M.D., and Cesar Ercole, M.D., at the annual meeting of the American Urological Association.

Twenty-seven of 85 men (32%) with low prostate-specific antigen (PSA) levels and an abnormal digital rectal examination (DRE) had positive biopsies, reported Dr. Slaton and Dr. Ercole of the University of Minnesota, Minneapolis. Of those, 9 men (33%) were found to have high-grade tumors. The cancers would have been missed if the screening had relied on PSA alone.

The investigators attributed the false-negative PSA findings to tumors that were so poorly differentiated they underproduced PSA.

The study was a retrospective review of 3,817 prostate cancer screening visits between 1990 and 2000 where both DRE and PSA were performed. Of those, 81% of men had both a normal DRE and a normal PSA (defined as less than 4 ng/L). Those men did not undergo biopsy.

The remaining 719 men all had an abnormal DRE, a high PSA, or both, and all underwent biopsy; 240 of them (33%) were found to have cancer.

Of the 359 men with high PSA and abnormal DRE, 139 (39%) had positive biopsies, and slightly more than 20% had high-grade tumors. Of the 275 men with high PSA and normal DRE, 74 (27%) had positive biopsies, and about 20% had high-grade tumors.