Betsy Bates

LOS ANGELES—The list of purely idiopathic causes of pancreatitis is shrinking, Stephen J. Pandol, M.D., said at the 12th International Symposium on Pancreatic and Biliary Endoscopy sponsored by the Cedars-Sinai Medical Center.

Alcohol use remains the most common etiology, but an enhanced understanding of genetic and autoimmune contributors has demystified the cause of pancreatitis in many patients whose alcohol intake does not appear to put them at risk for the disorder.

No blood markers exist to pinpoint the cause of pancreatitis, and histologic evaluation of the pancreas is difficult, Dr. Pandol noted. Imaging is helpful in diagnosing structural etiologies but is most often nonspecific in terms of identifying a cause.

Alcohol intake directly relates to the relative risk of pancreatitis, and may interact with other factors, such as a hereditary predisposition or virus, to cause pancreatitis. Risk is elevated slightly at 50 g/day, equivalent to four beers, three-quarters of a bottle of wine, or a fifth of a fifth of hard liquor. At three times that intake level, the relative risk of pancreatitis reaches 15.

But automatically attributing pancreatitis to alcohol intake can be a mistake, said Dr. Pandol, professor of medicine at the University of California, Los Angeles.

“You could have gallstones causing pancreatitis in someone who drinks a lot,” he explained.

Certain drugs, cancer, toxins, and vascular abnormalities can trigger acute pancreatitis, and in some cases it can be iatrogenic, occurring after procedures to remove gallstones, for example.

Other potential etiologies that should not be overlooked include:

▸ Gallstones. Calculi are an obvious potential cause of pancreatitis, but they nonetheless are missed, sometimes with catastrophic results. Dr. Pandol said he is familiar with cases in which patients died of acute pancreatitis that was caused by unrecognized gallstones.

“You need good imaging studies to make sure you haven't missed this, because it's very treatable,” he said.

▸ Infectious etiologies. Salmonella can contribute to pancreatitis through a toxic mechanism. Parasitic infections can obstruct the pancreatic duct. In some cases, viruses may be to blame for pancreatitis, although the mechanism remains unclear. In mice, certain strains of coxsackievirus are benign until mice are fed alcohol, after which they develop “severe, rip-roaring, and lethal pancreatitis,” Dr. Pandol said.

▸ Trauma. Even distant trauma should not be ruled out as a possible etiology for pancreatitis. Dr. Pandol recalled a case of a female patient who had been kicked in the abdomen during a sexual assault several years prior to presenting with pancreatitis. Imaging revealed a stricture in the pancreatic duct.

Steering wheel injuries from motor vehicle accidents can rupture the pancreatic duct, he added.

▸ Autoimmune disease. Dr. Pandol isn't certain whether autoimmune pancreatitis is increasingly common, or just better recognized than in the past. Typically, symptoms are subacute, and imaging studies reveal an irregular, narrowed duct.

IgG4 markers are transient but may be seen early in the disease. IgE and autoimmune markers may also be positive, the latter in severe cases. Histology may reveal periductal lymphocytic-plasmacytic inflammation and fibrosis, but features may closely resemble pancreatic cancer. A large amount of tissue may be required at biopsy for a firm diagnosis.

If a patient has preexisting autoimmune disease such as Sjögren's syndrome or systemic lupus erythematosus, autoimmune pancreatitis is a likely diagnosis.

“But if there's a mass, one still has to rule out the possibility of cancer,” Dr. Pandol said.

Autoimmune dysfunction is one of the rare treatable causes of pancreatitis, since it is steroid responsive.

▸ Hereditary causes. Many trypsinogen mutations, mutations in the cystic fibrosis transmembrane regulator genes, and familial hypertriglyceridemia can cause pancreatitis.

Genetic testing—offered by companies such as Ambry Genetics, Irvine, Calif.—can detect relevant abnormalities in trypsin and trypsin inhibitor genes and cystic fibrosis genes, although some families don't want to be tested because of insurance concerns, he noted.

LOS ANGELES—The list of purely idiopathic causes of pancreatitis is shrinking, Stephen J. Pandol, M.D., said at the 12th International Symposium on Pancreatic and Biliary Endoscopy sponsored by the Cedars-Sinai Medical Center.

Alcohol use remains the most common etiology, but an enhanced understanding of genetic and autoimmune contributors has demystified the cause of pancreatitis in many patients whose alcohol intake does not appear to put them at risk for the disorder.

No blood markers exist to pinpoint the cause of pancreatitis, and histologic evaluation of the pancreas is difficult, Dr. Pandol noted. Imaging is helpful in diagnosing structural etiologies but is most often nonspecific in terms of identifying a cause.

Alcohol intake directly relates to the relative risk of pancreatitis, and may interact with other factors, such as a hereditary predisposition or virus, to cause pancreatitis. Risk is elevated slightly at 50 g/day, equivalent to four beers, three-quarters of a bottle of wine, or a fifth of a fifth of hard liquor. At three times that intake level, the relative risk of pancreatitis reaches 15.

But automatically attributing pancreatitis to alcohol intake can be a mistake, said Dr. Pandol, professor of medicine at the University of California, Los Angeles.

“You could have gallstones causing pancreatitis in someone who drinks a lot,” he explained.

Certain drugs, cancer, toxins, and vascular abnormalities can trigger acute pancreatitis, and in some cases it can be iatrogenic, occurring after procedures to remove gallstones, for example.

Other potential etiologies that should not be overlooked include:

▸ Gallstones. Calculi are an obvious potential cause of pancreatitis, but they nonetheless are missed, sometimes with catastrophic results. Dr. Pandol said he is familiar with cases in which patients died of acute pancreatitis that was caused by unrecognized gallstones.

“You need good imaging studies to make sure you haven't missed this, because it's very treatable,” he said.

▸ Infectious etiologies. Salmonella can contribute to pancreatitis through a toxic mechanism. Parasitic infections can obstruct the pancreatic duct. In some cases, viruses may be to blame for pancreatitis, although the mechanism remains unclear. In mice, certain strains of coxsackievirus are benign until mice are fed alcohol, after which they develop “severe, rip-roaring, and lethal pancreatitis,” Dr. Pandol said.

▸ Trauma. Even distant trauma should not be ruled out as a possible etiology for pancreatitis. Dr. Pandol recalled a case of a female patient who had been kicked in the abdomen during a sexual assault several years prior to presenting with pancreatitis. Imaging revealed a stricture in the pancreatic duct.

Steering wheel injuries from motor vehicle accidents can rupture the pancreatic duct, he added.

▸ Autoimmune disease. Dr. Pandol isn't certain whether autoimmune pancreatitis is increasingly common, or just better recognized than in the past. Typically, symptoms are subacute, and imaging studies reveal an irregular, narrowed duct.

IgG4 markers are transient but may be seen early in the disease. IgE and autoimmune markers may also be positive, the latter in severe cases. Histology may reveal periductal lymphocytic-plasmacytic inflammation and fibrosis, but features may closely resemble pancreatic cancer. A large amount of tissue may be required at biopsy for a firm diagnosis.

If a patient has preexisting autoimmune disease such as Sjögren's syndrome or systemic lupus erythematosus, autoimmune pancreatitis is a likely diagnosis.

“But if there's a mass, one still has to rule out the possibility of cancer,” Dr. Pandol said.

Autoimmune dysfunction is one of the rare treatable causes of pancreatitis, since it is steroid responsive.

▸ Hereditary causes. Many trypsinogen mutations, mutations in the cystic fibrosis transmembrane regulator genes, and familial hypertriglyceridemia can cause pancreatitis.

Genetic testing—offered by companies such as Ambry Genetics, Irvine, Calif.—can detect relevant abnormalities in trypsin and trypsin inhibitor genes and cystic fibrosis genes, although some families don't want to be tested because of insurance concerns, he noted.

LOS ANGELES—The list of purely idiopathic causes of pancreatitis is shrinking, Stephen J. Pandol, M.D., said at the 12th International Symposium on Pancreatic and Biliary Endoscopy sponsored by the Cedars-Sinai Medical Center.

Alcohol use remains the most common etiology, but an enhanced understanding of genetic and autoimmune contributors has demystified the cause of pancreatitis in many patients whose alcohol intake does not appear to put them at risk for the disorder.

No blood markers exist to pinpoint the cause of pancreatitis, and histologic evaluation of the pancreas is difficult, Dr. Pandol noted. Imaging is helpful in diagnosing structural etiologies but is most often nonspecific in terms of identifying a cause.

Alcohol intake directly relates to the relative risk of pancreatitis, and may interact with other factors, such as a hereditary predisposition or virus, to cause pancreatitis. Risk is elevated slightly at 50 g/day, equivalent to four beers, three-quarters of a bottle of wine, or a fifth of a fifth of hard liquor. At three times that intake level, the relative risk of pancreatitis reaches 15.

But automatically attributing pancreatitis to alcohol intake can be a mistake, said Dr. Pandol, professor of medicine at the University of California, Los Angeles.

“You could have gallstones causing pancreatitis in someone who drinks a lot,” he explained.

Certain drugs, cancer, toxins, and vascular abnormalities can trigger acute pancreatitis, and in some cases it can be iatrogenic, occurring after procedures to remove gallstones, for example.

Other potential etiologies that should not be overlooked include:

▸ Gallstones. Calculi are an obvious potential cause of pancreatitis, but they nonetheless are missed, sometimes with catastrophic results. Dr. Pandol said he is familiar with cases in which patients died of acute pancreatitis that was caused by unrecognized gallstones.

“You need good imaging studies to make sure you haven't missed this, because it's very treatable,” he said.

▸ Infectious etiologies. Salmonella can contribute to pancreatitis through a toxic mechanism. Parasitic infections can obstruct the pancreatic duct. In some cases, viruses may be to blame for pancreatitis, although the mechanism remains unclear. In mice, certain strains of coxsackievirus are benign until mice are fed alcohol, after which they develop “severe, rip-roaring, and lethal pancreatitis,” Dr. Pandol said.

▸ Trauma. Even distant trauma should not be ruled out as a possible etiology for pancreatitis. Dr. Pandol recalled a case of a female patient who had been kicked in the abdomen during a sexual assault several years prior to presenting with pancreatitis. Imaging revealed a stricture in the pancreatic duct.

Steering wheel injuries from motor vehicle accidents can rupture the pancreatic duct, he added.

▸ Autoimmune disease. Dr. Pandol isn't certain whether autoimmune pancreatitis is increasingly common, or just better recognized than in the past. Typically, symptoms are subacute, and imaging studies reveal an irregular, narrowed duct.

IgG4 markers are transient but may be seen early in the disease. IgE and autoimmune markers may also be positive, the latter in severe cases. Histology may reveal periductal lymphocytic-plasmacytic inflammation and fibrosis, but features may closely resemble pancreatic cancer. A large amount of tissue may be required at biopsy for a firm diagnosis.

If a patient has preexisting autoimmune disease such as Sjögren's syndrome or systemic lupus erythematosus, autoimmune pancreatitis is a likely diagnosis.

“But if there's a mass, one still has to rule out the possibility of cancer,” Dr. Pandol said.

Autoimmune dysfunction is one of the rare treatable causes of pancreatitis, since it is steroid responsive.

▸ Hereditary causes. Many trypsinogen mutations, mutations in the cystic fibrosis transmembrane regulator genes, and familial hypertriglyceridemia can cause pancreatitis.

Genetic testing—offered by companies such as Ambry Genetics, Irvine, Calif.—can detect relevant abnormalities in trypsin and trypsin inhibitor genes and cystic fibrosis genes, although some families don't want to be tested because of insurance concerns, he noted.

LOS ANGELES—Timely diagnosis and treatment are essential in cases of gallstone pancreatitis, a tricky ailment that assumes a severe, necrotizing form in up to 25% of patients.

“This is a very serious disease, particularly in [those] patients who generally have a normal pancreas,” Kenneth F. Binmoeller, M.D., said at the 12th International Symposium on Pancreatic and Biliary Endoscopy sponsored by the Cedars-Sinai Medical Center.

Physicians should suspect gallstones in every acute pancreatitis patient with risk factors for gallstone disease, advised Dr. Binmoeller, director of interventional endoscopy at California Pacific Medical Center in San Francisco.

Many drugs heighten the risk of gallstone formation, including clofibrate, octreotide, ceftriaxone, and estrogens. Furthermore, laparoscopic cholecystectomy can cause stones to be milked from the cystic duct or the neck of the gallbladder into the common bile duct.

“If a patient develops pancreatitis a few days after [laparoscopic gallbladder surgery], you definitely want to think about gallstone pancreatitis,” he said.

Studies have shown that only one laboratory parameter—alanine aminotransferase greater than three times normal limits—has more than 95% sensitivity for diagnosing acute biliary pancreatitis. Bilirubin and alkaline phosphatase may rise because of extrinsic bile duct compression secondary to pancreatitis, so abnormal laboratory values are not diagnostic.

Because very small stones, especially at the ampulla of Vater, are most likely to cause biliary pancreatitis, the best diagnostic imaging modality for this indication is endoscopic ultrasound (EUS). “Here we get marvelous images of the bile duct,” Dr. Binmoeller said, pointing out tiny stones that could be missed on transabdominal ultrasound, computed tomography, or magnetic resonance cholangiopancreatography (MRCP).

Another advantage of EUS is its ability to image the ampulla both ultrasonographically and endoscopically.

Studies have shown that MRCP has 100% sensitivity with stones larger than 1 cm, he noted. But it has a much lower sensitivity in detecting small stones: 89% for stones 5-10 mm, and 71% for those smaller than 5 mm. Artifacts can make MRCP images milky, obscuring visualization of small stones and sludge shown clearly on EUS.

Unfortunately, neither EUS nor MRCP is widely available on an urgent basis, so some stones may go undetected when a patient presents with possible gallbladder pancreatitis. Nor is the best management strategy always clear.

A series of trials in the United Kingdom, Hong Kong, and Germany reached conflicting conclusions about the benefits and risks of urgent endoscopic retrograde cholangiopancreatography (ERCP) with or without sphincterotomy. A multicenter study in Germany found no outcome benefit and higher mortality in patients who underwent early ERCP compared with those managed conservatively, a conclusion that was “a real jolt to the whole endoscopic community,” Dr. Binmoeller said (N. Engl. J. Med. 1997;336:237-42).

Several methodologic problems plagued that study and the others, however, so the salient question remains: Is sphincterotomy more efficacious than conservative management in patients with severe pancreatitis without jaundice?

Until a well-designed study answers that question, Dr. Binmoeller proposes the following management algorithm, which he uses in his practice:

▸ Patients presenting with acute pancreatitis associated with a bilirubin value of more than 3 mg/dL or cholangiosepsis should undergo urgent ERCP with sphincterotomy and sweeping of the bile duct, regardless of whether a stone is seen on cholangiography.

▸ In the absence of the above criteria, patients should undergo at least a duodenoscopy for visualization of the ampulla and, if possible, EUS. An ERCP and sphincterotomy should be performed if pus or a bulging, edematous papilla is seen on duodenoscopy or if EUS reveals an impacted stone.n

A small impacted stone has been freed from the ampulla after sphincterotomy.

Endoscopic ultrasound detects stones too small to see with other techniques.

LOS ANGELES—Timely diagnosis and treatment are essential in cases of gallstone pancreatitis, a tricky ailment that assumes a severe, necrotizing form in up to 25% of patients.

“This is a very serious disease, particularly in [those] patients who generally have a normal pancreas,” Kenneth F. Binmoeller, M.D., said at the 12th International Symposium on Pancreatic and Biliary Endoscopy sponsored by the Cedars-Sinai Medical Center.

Physicians should suspect gallstones in every acute pancreatitis patient with risk factors for gallstone disease, advised Dr. Binmoeller, director of interventional endoscopy at California Pacific Medical Center in San Francisco.

Many drugs heighten the risk of gallstone formation, including clofibrate, octreotide, ceftriaxone, and estrogens. Furthermore, laparoscopic cholecystectomy can cause stones to be milked from the cystic duct or the neck of the gallbladder into the common bile duct.

“If a patient develops pancreatitis a few days after [laparoscopic gallbladder surgery], you definitely want to think about gallstone pancreatitis,” he said.

Studies have shown that only one laboratory parameter—alanine aminotransferase greater than three times normal limits—has more than 95% sensitivity for diagnosing acute biliary pancreatitis. Bilirubin and alkaline phosphatase may rise because of extrinsic bile duct compression secondary to pancreatitis, so abnormal laboratory values are not diagnostic.

Because very small stones, especially at the ampulla of Vater, are most likely to cause biliary pancreatitis, the best diagnostic imaging modality for this indication is endoscopic ultrasound (EUS). “Here we get marvelous images of the bile duct,” Dr. Binmoeller said, pointing out tiny stones that could be missed on transabdominal ultrasound, computed tomography, or magnetic resonance cholangiopancreatography (MRCP).

Another advantage of EUS is its ability to image the ampulla both ultrasonographically and endoscopically.

Studies have shown that MRCP has 100% sensitivity with stones larger than 1 cm, he noted. But it has a much lower sensitivity in detecting small stones: 89% for stones 5-10 mm, and 71% for those smaller than 5 mm. Artifacts can make MRCP images milky, obscuring visualization of small stones and sludge shown clearly on EUS.

Unfortunately, neither EUS nor MRCP is widely available on an urgent basis, so some stones may go undetected when a patient presents with possible gallbladder pancreatitis. Nor is the best management strategy always clear.

A series of trials in the United Kingdom, Hong Kong, and Germany reached conflicting conclusions about the benefits and risks of urgent endoscopic retrograde cholangiopancreatography (ERCP) with or without sphincterotomy. A multicenter study in Germany found no outcome benefit and higher mortality in patients who underwent early ERCP compared with those managed conservatively, a conclusion that was “a real jolt to the whole endoscopic community,” Dr. Binmoeller said (N. Engl. J. Med. 1997;336:237-42).

Several methodologic problems plagued that study and the others, however, so the salient question remains: Is sphincterotomy more efficacious than conservative management in patients with severe pancreatitis without jaundice?

Until a well-designed study answers that question, Dr. Binmoeller proposes the following management algorithm, which he uses in his practice:

▸ Patients presenting with acute pancreatitis associated with a bilirubin value of more than 3 mg/dL or cholangiosepsis should undergo urgent ERCP with sphincterotomy and sweeping of the bile duct, regardless of whether a stone is seen on cholangiography.

▸ In the absence of the above criteria, patients should undergo at least a duodenoscopy for visualization of the ampulla and, if possible, EUS. An ERCP and sphincterotomy should be performed if pus or a bulging, edematous papilla is seen on duodenoscopy or if EUS reveals an impacted stone.n

A small impacted stone has been freed from the ampulla after sphincterotomy.

Endoscopic ultrasound detects stones too small to see with other techniques.

LOS ANGELES—Timely diagnosis and treatment are essential in cases of gallstone pancreatitis, a tricky ailment that assumes a severe, necrotizing form in up to 25% of patients.

“This is a very serious disease, particularly in [those] patients who generally have a normal pancreas,” Kenneth F. Binmoeller, M.D., said at the 12th International Symposium on Pancreatic and Biliary Endoscopy sponsored by the Cedars-Sinai Medical Center.

Physicians should suspect gallstones in every acute pancreatitis patient with risk factors for gallstone disease, advised Dr. Binmoeller, director of interventional endoscopy at California Pacific Medical Center in San Francisco.

Many drugs heighten the risk of gallstone formation, including clofibrate, octreotide, ceftriaxone, and estrogens. Furthermore, laparoscopic cholecystectomy can cause stones to be milked from the cystic duct or the neck of the gallbladder into the common bile duct.

“If a patient develops pancreatitis a few days after [laparoscopic gallbladder surgery], you definitely want to think about gallstone pancreatitis,” he said.

Studies have shown that only one laboratory parameter—alanine aminotransferase greater than three times normal limits—has more than 95% sensitivity for diagnosing acute biliary pancreatitis. Bilirubin and alkaline phosphatase may rise because of extrinsic bile duct compression secondary to pancreatitis, so abnormal laboratory values are not diagnostic.

Because very small stones, especially at the ampulla of Vater, are most likely to cause biliary pancreatitis, the best diagnostic imaging modality for this indication is endoscopic ultrasound (EUS). “Here we get marvelous images of the bile duct,” Dr. Binmoeller said, pointing out tiny stones that could be missed on transabdominal ultrasound, computed tomography, or magnetic resonance cholangiopancreatography (MRCP).

Another advantage of EUS is its ability to image the ampulla both ultrasonographically and endoscopically.

Studies have shown that MRCP has 100% sensitivity with stones larger than 1 cm, he noted. But it has a much lower sensitivity in detecting small stones: 89% for stones 5-10 mm, and 71% for those smaller than 5 mm. Artifacts can make MRCP images milky, obscuring visualization of small stones and sludge shown clearly on EUS.

Unfortunately, neither EUS nor MRCP is widely available on an urgent basis, so some stones may go undetected when a patient presents with possible gallbladder pancreatitis. Nor is the best management strategy always clear.

A series of trials in the United Kingdom, Hong Kong, and Germany reached conflicting conclusions about the benefits and risks of urgent endoscopic retrograde cholangiopancreatography (ERCP) with or without sphincterotomy. A multicenter study in Germany found no outcome benefit and higher mortality in patients who underwent early ERCP compared with those managed conservatively, a conclusion that was “a real jolt to the whole endoscopic community,” Dr. Binmoeller said (N. Engl. J. Med. 1997;336:237-42).

Several methodologic problems plagued that study and the others, however, so the salient question remains: Is sphincterotomy more efficacious than conservative management in patients with severe pancreatitis without jaundice?

Until a well-designed study answers that question, Dr. Binmoeller proposes the following management algorithm, which he uses in his practice:

▸ Patients presenting with acute pancreatitis associated with a bilirubin value of more than 3 mg/dL or cholangiosepsis should undergo urgent ERCP with sphincterotomy and sweeping of the bile duct, regardless of whether a stone is seen on cholangiography.

▸ In the absence of the above criteria, patients should undergo at least a duodenoscopy for visualization of the ampulla and, if possible, EUS. An ERCP and sphincterotomy should be performed if pus or a bulging, edematous papilla is seen on duodenoscopy or if EUS reveals an impacted stone.n

A small impacted stone has been freed from the ampulla after sphincterotomy.

Endoscopic ultrasound detects stones too small to see with other techniques.

LOS ANGELES — The first human case of West Nile virus infection this year was diagnosed in Los Angeles in early February, perhaps setting the stage for an early and virulent season for the far western United States.

“Since West Nile virus was [first] detected in 1999, we've seen a lengthening period of transmission,” said Ned Hayes, M.D., of the Centers for Disease Control and Prevention's Division of Vector-Borne Infectious Diseases in Fort Collins, Colo.

As the virus has spread south and west across the United States, new “ecological dynamics” have influenced transmission patterns, he explained.

A wetter than normal winter in California and the Southwest may suit mosquitoes well, meaning physicians will need to be especially alert to possible cases of the now reportable disease.

The Los Angeles County Department of Health Services announced an infection in an older man in east Los Angeles County on Feb. 8. As of mid-February, state and federal health officials had not completed confirmatory tests on the case.

Symptoms of West Nile infection include fever, headache, fatigue, body aches, skin rash, and swollen lymph nodes.

More serious manifestations of West Nile encephalitis or meningitis include neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and a paralysis that can resemble polio.

“It doesn't matter whether we've had one case or five; if you see encephalitis or meningitis, you look for West Nile virus,” said Laurene Mascola, M.D., chief of the acute communicable disease control unit of Los Angeles County.

The first bird carrying the virus was found in mid-January, whereas no bird evidence was confirmed in California until the end of March in 2004. Twelve birds in eight counties had been found to have the virus by mid-February. “It's pretty much all up and down the state,” said Robert Miller, a spokesman for the California Department of Health Services in Sacramento.

Birds are an important player in the transmission cycle of West Nile virus and are carefully tracked, although mosquitoes are the direct vectors infecting humans.

California and the Southwest, where the disease struck hardest in 2004, have warmer climates than the northeastern states, where the virus first took hold in the United States. Mosquito vectors also differ, with Culex pipiens most common in the Northeast and C. tarsalis and C. quinquefasciatus often the culprits in the West.

C. tarsalis was a common vector in Colorado, where West Nile virus infected almost 3,000 people in 2003, killing 63. “It's a very efficient vector. It avidly bites humans and also bites birds, and it seems to transmit the virus very well.”

Dr. Hayes urged physicians to test for West Nile virus and report cases to their state health departments, which notify the CDC. “We have no way of knowing what's happening [in terms of transmission patterns] unless practicing physicians report their cases,” he said in an interview.

A special online registry for physicians reporting pregnant patients infected with the virus has been established by the CDC at its Web site, http://www.cdc.gov

West Nile virus infected 2,470 people in 40 states in 2004, resulting in 88 deaths. The highest number of cases was in 2003, when 9,862 infections and 264 deaths were reported. States have been variably affected over time. For example, Nebraska had 1,942 cases in 2003 but just 49 in 2004.

Though some have speculated that disease patterns may reflect herd immunity, Dr. Hayes discounted that theory. He said that even in the most concentrated “hot zones,” antibodies have been detected in just 3%-5% of the population.

On the other hand, changes in weather, bird migration and infection patterns, mosquito abatement, and basic prevention strategies such as wearing mosquito repellant, may change human infection rates over time.

LOS ANGELES — The first human case of West Nile virus infection this year was diagnosed in Los Angeles in early February, perhaps setting the stage for an early and virulent season for the far western United States.

“Since West Nile virus was [first] detected in 1999, we've seen a lengthening period of transmission,” said Ned Hayes, M.D., of the Centers for Disease Control and Prevention's Division of Vector-Borne Infectious Diseases in Fort Collins, Colo.

As the virus has spread south and west across the United States, new “ecological dynamics” have influenced transmission patterns, he explained.

A wetter than normal winter in California and the Southwest may suit mosquitoes well, meaning physicians will need to be especially alert to possible cases of the now reportable disease.

The Los Angeles County Department of Health Services announced an infection in an older man in east Los Angeles County on Feb. 8. As of mid-February, state and federal health officials had not completed confirmatory tests on the case.

Symptoms of West Nile infection include fever, headache, fatigue, body aches, skin rash, and swollen lymph nodes.

More serious manifestations of West Nile encephalitis or meningitis include neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and a paralysis that can resemble polio.

“It doesn't matter whether we've had one case or five; if you see encephalitis or meningitis, you look for West Nile virus,” said Laurene Mascola, M.D., chief of the acute communicable disease control unit of Los Angeles County.

The first bird carrying the virus was found in mid-January, whereas no bird evidence was confirmed in California until the end of March in 2004. Twelve birds in eight counties had been found to have the virus by mid-February. “It's pretty much all up and down the state,” said Robert Miller, a spokesman for the California Department of Health Services in Sacramento.

Birds are an important player in the transmission cycle of West Nile virus and are carefully tracked, although mosquitoes are the direct vectors infecting humans.

California and the Southwest, where the disease struck hardest in 2004, have warmer climates than the northeastern states, where the virus first took hold in the United States. Mosquito vectors also differ, with Culex pipiens most common in the Northeast and C. tarsalis and C. quinquefasciatus often the culprits in the West.

C. tarsalis was a common vector in Colorado, where West Nile virus infected almost 3,000 people in 2003, killing 63. “It's a very efficient vector. It avidly bites humans and also bites birds, and it seems to transmit the virus very well.”

Dr. Hayes urged physicians to test for West Nile virus and report cases to their state health departments, which notify the CDC. “We have no way of knowing what's happening [in terms of transmission patterns] unless practicing physicians report their cases,” he said in an interview.

A special online registry for physicians reporting pregnant patients infected with the virus has been established by the CDC at its Web site, http://www.cdc.gov

West Nile virus infected 2,470 people in 40 states in 2004, resulting in 88 deaths. The highest number of cases was in 2003, when 9,862 infections and 264 deaths were reported. States have been variably affected over time. For example, Nebraska had 1,942 cases in 2003 but just 49 in 2004.

Though some have speculated that disease patterns may reflect herd immunity, Dr. Hayes discounted that theory. He said that even in the most concentrated “hot zones,” antibodies have been detected in just 3%-5% of the population.

On the other hand, changes in weather, bird migration and infection patterns, mosquito abatement, and basic prevention strategies such as wearing mosquito repellant, may change human infection rates over time.

LOS ANGELES — The first human case of West Nile virus infection this year was diagnosed in Los Angeles in early February, perhaps setting the stage for an early and virulent season for the far western United States.

“Since West Nile virus was [first] detected in 1999, we've seen a lengthening period of transmission,” said Ned Hayes, M.D., of the Centers for Disease Control and Prevention's Division of Vector-Borne Infectious Diseases in Fort Collins, Colo.

As the virus has spread south and west across the United States, new “ecological dynamics” have influenced transmission patterns, he explained.

A wetter than normal winter in California and the Southwest may suit mosquitoes well, meaning physicians will need to be especially alert to possible cases of the now reportable disease.

The Los Angeles County Department of Health Services announced an infection in an older man in east Los Angeles County on Feb. 8. As of mid-February, state and federal health officials had not completed confirmatory tests on the case.

Symptoms of West Nile infection include fever, headache, fatigue, body aches, skin rash, and swollen lymph nodes.

More serious manifestations of West Nile encephalitis or meningitis include neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and a paralysis that can resemble polio.

“It doesn't matter whether we've had one case or five; if you see encephalitis or meningitis, you look for West Nile virus,” said Laurene Mascola, M.D., chief of the acute communicable disease control unit of Los Angeles County.

The first bird carrying the virus was found in mid-January, whereas no bird evidence was confirmed in California until the end of March in 2004. Twelve birds in eight counties had been found to have the virus by mid-February. “It's pretty much all up and down the state,” said Robert Miller, a spokesman for the California Department of Health Services in Sacramento.

Birds are an important player in the transmission cycle of West Nile virus and are carefully tracked, although mosquitoes are the direct vectors infecting humans.

California and the Southwest, where the disease struck hardest in 2004, have warmer climates than the northeastern states, where the virus first took hold in the United States. Mosquito vectors also differ, with Culex pipiens most common in the Northeast and C. tarsalis and C. quinquefasciatus often the culprits in the West.

C. tarsalis was a common vector in Colorado, where West Nile virus infected almost 3,000 people in 2003, killing 63. “It's a very efficient vector. It avidly bites humans and also bites birds, and it seems to transmit the virus very well.”

Dr. Hayes urged physicians to test for West Nile virus and report cases to their state health departments, which notify the CDC. “We have no way of knowing what's happening [in terms of transmission patterns] unless practicing physicians report their cases,” he said in an interview.

A special online registry for physicians reporting pregnant patients infected with the virus has been established by the CDC at its Web site, http://www.cdc.gov

West Nile virus infected 2,470 people in 40 states in 2004, resulting in 88 deaths. The highest number of cases was in 2003, when 9,862 infections and 264 deaths were reported. States have been variably affected over time. For example, Nebraska had 1,942 cases in 2003 but just 49 in 2004.

Though some have speculated that disease patterns may reflect herd immunity, Dr. Hayes discounted that theory. He said that even in the most concentrated “hot zones,” antibodies have been detected in just 3%-5% of the population.

On the other hand, changes in weather, bird migration and infection patterns, mosquito abatement, and basic prevention strategies such as wearing mosquito repellant, may change human infection rates over time.

FLORENCE, ITALY — A case-control study conducted in Greece lends support to the theory that a “superclean” environment during infancy and early childhood may predispose children to atopic dermatitis.

Penny Emmanouil, M.D., and associates in the department of dermatology at Pentelis Children's Hospital in Athens, Greece, studied home hygiene, standards of living, exposure to infections, and vaccination rates among 150 children aged 28 days to 3 years who were seen for atopic dermatitis (AD) symptoms at an outpatient clinic.

These results were compared with data from a group of 150 children aged 35 days to 3 years who had no atopic symptoms during the same period.

Findings were released at the 13th Congress of the European Academy of Dermatology and Venereology.

A strong association was found between superclean environments and the presence of AD. The cleaner the household and the higher the family standard of living, the more likely it was that children had AD.

Significant differences were seen in the two groups of children. For instance, nearly half of children with AD had their own bedrooms, while those without AD symptoms tended to share living space with parents and siblings. Those with AD were more likely to live in larger, cleaner, more well-to-do households with fewer children.

No relationships were seen between vaccinations or infections and AD.

More work must be done to tease out risk factors that may be responsible for the development of AD in early childhood, Dr. Emmanouil said.

However, she hypothesized that exposure to microbes might be restricted in those households that practice meticulous hygiene

“As a result, the immune system in infancy and early childhood is restricted, and the switch from the TH2- to TH1-mediated immune response is impaired,” she said.

FLORENCE, ITALY — A case-control study conducted in Greece lends support to the theory that a “superclean” environment during infancy and early childhood may predispose children to atopic dermatitis.

Penny Emmanouil, M.D., and associates in the department of dermatology at Pentelis Children's Hospital in Athens, Greece, studied home hygiene, standards of living, exposure to infections, and vaccination rates among 150 children aged 28 days to 3 years who were seen for atopic dermatitis (AD) symptoms at an outpatient clinic.

These results were compared with data from a group of 150 children aged 35 days to 3 years who had no atopic symptoms during the same period.

Findings were released at the 13th Congress of the European Academy of Dermatology and Venereology.

A strong association was found between superclean environments and the presence of AD. The cleaner the household and the higher the family standard of living, the more likely it was that children had AD.

Significant differences were seen in the two groups of children. For instance, nearly half of children with AD had their own bedrooms, while those without AD symptoms tended to share living space with parents and siblings. Those with AD were more likely to live in larger, cleaner, more well-to-do households with fewer children.

No relationships were seen between vaccinations or infections and AD.

More work must be done to tease out risk factors that may be responsible for the development of AD in early childhood, Dr. Emmanouil said.

However, she hypothesized that exposure to microbes might be restricted in those households that practice meticulous hygiene

“As a result, the immune system in infancy and early childhood is restricted, and the switch from the TH2- to TH1-mediated immune response is impaired,” she said.

FLORENCE, ITALY — A case-control study conducted in Greece lends support to the theory that a “superclean” environment during infancy and early childhood may predispose children to atopic dermatitis.

Penny Emmanouil, M.D., and associates in the department of dermatology at Pentelis Children's Hospital in Athens, Greece, studied home hygiene, standards of living, exposure to infections, and vaccination rates among 150 children aged 28 days to 3 years who were seen for atopic dermatitis (AD) symptoms at an outpatient clinic.

These results were compared with data from a group of 150 children aged 35 days to 3 years who had no atopic symptoms during the same period.

Findings were released at the 13th Congress of the European Academy of Dermatology and Venereology.

A strong association was found between superclean environments and the presence of AD. The cleaner the household and the higher the family standard of living, the more likely it was that children had AD.

Significant differences were seen in the two groups of children. For instance, nearly half of children with AD had their own bedrooms, while those without AD symptoms tended to share living space with parents and siblings. Those with AD were more likely to live in larger, cleaner, more well-to-do households with fewer children.

No relationships were seen between vaccinations or infections and AD.

More work must be done to tease out risk factors that may be responsible for the development of AD in early childhood, Dr. Emmanouil said.

However, she hypothesized that exposure to microbes might be restricted in those households that practice meticulous hygiene

“As a result, the immune system in infancy and early childhood is restricted, and the switch from the TH2- to TH1-mediated immune response is impaired,” she said.

RANCHO MIRAGE, CALIF. – Healthy young adults who are chronic “short sleepers”–getting an average of about 5 hours of sleep a night–must secrete 30% more insulin than other adults to achieve a normal glucose curve.

The finding, which points to a potentially important connection between sleep, diabetes risk, and obesity, was just one of a series of observations made during detailed sleep studies conducted at the University of Chicago in recent years and presented by Eve Van Cauter, Ph.D., a professor of medicine at the university.

Sleep deprivation leads to decreased levels of the satiety hormone leptin, increases in the hunger hormone ghrelin, and impaired glucose tolerance, Dr. Van Cauter and associates discovered when they created a “sleep debt” in healthy adults by restricting the number of hours they slept, she said at a conference on sleep in infancy and childhood sponsored by the Annenberg Center for Health Sciences.

“In 1 week of sleep restriction, we brought volunteers to a prediabetic state. That was kind of a frightening thought,” she said in describing one of her early studies into the metabolic and endocrine consequences of too little sleep (Lancet 1999;354:1435–9).

One of the first consequences of sleeplessness is appetite dysregulation, the study showed. “Essentially, the accelerator for hunger [ghrelin] was pushed and the brake for satiety [leptin] was released,” she explained. “The leptin levels are screaming 'More food! More food!'”

Sleep-deprived volunteers–even those receiving consistent and adequate amounts of energy via intravenous glucose–become famished, particularly craving high-carbohydrate foods such as candy, cookies, potato chips, and pasta.

“We have two studies suggesting that if you have a sleep debt, you might be less able to control hunger,” she said at the meeting.

To study glucose tolerance and sleep, Dr. Van Cauter and her associates recently recruited 44 lean, healthy young adults, half of whom were chronic short sleepers who averaged 5 hours, 16 minutes of sleep a night, and half of whom averaged 7 hours, 52 minutes of sleep per night. The subjects were stratified by diabetes risk according to their ethnicity and family history of the disease.

“We found a clear relationship between sleep duration and insulin sensitivity. The short sleepers had lowered insulin sensitivity and the longer sleepers had higher insulin sensitivity, but the relationship was really only significant in those with a low ethnicity-based diabetes risk,” she said.

Further statistical tests revealed significant differences in insulin sensitivity associated with both ethnicity-based diabetes risk and sleep duration. For young healthy subjects in their 20s who were considered to be at low risk for diabetes, the impact of sleep deprivation on insulin sensitivity was profound, placing them in a risk category similar to that of Mexican Americans or 61- to 80-year-olds.

Dr. Van Cauter noted that sharply rising curves in the prevalence of obesity in the United States since the 1960s mirror reverse curves in the amount of sleep Americans get–the smallest amount in the industrialized world.

“I'm not saying that sleep curtailment, which is an increasingly prevalent behavior, is the cause of rising rates of obesity, but certainly, it hasn't helped,” she said.

An ongoing study is attempting to determine whether sleep recovery can improve glucose tolerance among chronically sleep-deprived patients who already have impaired insulin sensitivity. Chronic short sleepers between 35 and 41 years old spend 10 hours per night in a darkened sleep laboratory for 8–10 nights.

“You have to pay them,” she observed, noting that for many Americans, shortened sleep is a way of life.

Early results suggest that a longstanding sleep debt cannot be recovered in some short sleepers, who remain awake most of the hours they spend in laboratory-imposed darkness.

However, chronically sleep-deprived subjects who do extend their sleeping time show a rapid and impressive improvement in glucose tolerance, particularly at the 90-minute mark in glucose tolerance tests.

The average improvement of 25 mg/dL “is about what you can get with an antidiabetic drug like Metformin,” she said. “We're pursuing this vigorously.

RANCHO MIRAGE, CALIF. – Healthy young adults who are chronic “short sleepers”–getting an average of about 5 hours of sleep a night–must secrete 30% more insulin than other adults to achieve a normal glucose curve.

The finding, which points to a potentially important connection between sleep, diabetes risk, and obesity, was just one of a series of observations made during detailed sleep studies conducted at the University of Chicago in recent years and presented by Eve Van Cauter, Ph.D., a professor of medicine at the university.

Sleep deprivation leads to decreased levels of the satiety hormone leptin, increases in the hunger hormone ghrelin, and impaired glucose tolerance, Dr. Van Cauter and associates discovered when they created a “sleep debt” in healthy adults by restricting the number of hours they slept, she said at a conference on sleep in infancy and childhood sponsored by the Annenberg Center for Health Sciences.

“In 1 week of sleep restriction, we brought volunteers to a prediabetic state. That was kind of a frightening thought,” she said in describing one of her early studies into the metabolic and endocrine consequences of too little sleep (Lancet 1999;354:1435–9).

One of the first consequences of sleeplessness is appetite dysregulation, the study showed. “Essentially, the accelerator for hunger [ghrelin] was pushed and the brake for satiety [leptin] was released,” she explained. “The leptin levels are screaming 'More food! More food!'”

Sleep-deprived volunteers–even those receiving consistent and adequate amounts of energy via intravenous glucose–become famished, particularly craving high-carbohydrate foods such as candy, cookies, potato chips, and pasta.

“We have two studies suggesting that if you have a sleep debt, you might be less able to control hunger,” she said at the meeting.

To study glucose tolerance and sleep, Dr. Van Cauter and her associates recently recruited 44 lean, healthy young adults, half of whom were chronic short sleepers who averaged 5 hours, 16 minutes of sleep a night, and half of whom averaged 7 hours, 52 minutes of sleep per night. The subjects were stratified by diabetes risk according to their ethnicity and family history of the disease.

“We found a clear relationship between sleep duration and insulin sensitivity. The short sleepers had lowered insulin sensitivity and the longer sleepers had higher insulin sensitivity, but the relationship was really only significant in those with a low ethnicity-based diabetes risk,” she said.

Further statistical tests revealed significant differences in insulin sensitivity associated with both ethnicity-based diabetes risk and sleep duration. For young healthy subjects in their 20s who were considered to be at low risk for diabetes, the impact of sleep deprivation on insulin sensitivity was profound, placing them in a risk category similar to that of Mexican Americans or 61- to 80-year-olds.

Dr. Van Cauter noted that sharply rising curves in the prevalence of obesity in the United States since the 1960s mirror reverse curves in the amount of sleep Americans get–the smallest amount in the industrialized world.

“I'm not saying that sleep curtailment, which is an increasingly prevalent behavior, is the cause of rising rates of obesity, but certainly, it hasn't helped,” she said.

An ongoing study is attempting to determine whether sleep recovery can improve glucose tolerance among chronically sleep-deprived patients who already have impaired insulin sensitivity. Chronic short sleepers between 35 and 41 years old spend 10 hours per night in a darkened sleep laboratory for 8–10 nights.

“You have to pay them,” she observed, noting that for many Americans, shortened sleep is a way of life.

Early results suggest that a longstanding sleep debt cannot be recovered in some short sleepers, who remain awake most of the hours they spend in laboratory-imposed darkness.

However, chronically sleep-deprived subjects who do extend their sleeping time show a rapid and impressive improvement in glucose tolerance, particularly at the 90-minute mark in glucose tolerance tests.

The average improvement of 25 mg/dL “is about what you can get with an antidiabetic drug like Metformin,” she said. “We're pursuing this vigorously.

RANCHO MIRAGE, CALIF. – Healthy young adults who are chronic “short sleepers”–getting an average of about 5 hours of sleep a night–must secrete 30% more insulin than other adults to achieve a normal glucose curve.

The finding, which points to a potentially important connection between sleep, diabetes risk, and obesity, was just one of a series of observations made during detailed sleep studies conducted at the University of Chicago in recent years and presented by Eve Van Cauter, Ph.D., a professor of medicine at the university.

Sleep deprivation leads to decreased levels of the satiety hormone leptin, increases in the hunger hormone ghrelin, and impaired glucose tolerance, Dr. Van Cauter and associates discovered when they created a “sleep debt” in healthy adults by restricting the number of hours they slept, she said at a conference on sleep in infancy and childhood sponsored by the Annenberg Center for Health Sciences.

“In 1 week of sleep restriction, we brought volunteers to a prediabetic state. That was kind of a frightening thought,” she said in describing one of her early studies into the metabolic and endocrine consequences of too little sleep (Lancet 1999;354:1435–9).

One of the first consequences of sleeplessness is appetite dysregulation, the study showed. “Essentially, the accelerator for hunger [ghrelin] was pushed and the brake for satiety [leptin] was released,” she explained. “The leptin levels are screaming 'More food! More food!'”

Sleep-deprived volunteers–even those receiving consistent and adequate amounts of energy via intravenous glucose–become famished, particularly craving high-carbohydrate foods such as candy, cookies, potato chips, and pasta.

“We have two studies suggesting that if you have a sleep debt, you might be less able to control hunger,” she said at the meeting.

To study glucose tolerance and sleep, Dr. Van Cauter and her associates recently recruited 44 lean, healthy young adults, half of whom were chronic short sleepers who averaged 5 hours, 16 minutes of sleep a night, and half of whom averaged 7 hours, 52 minutes of sleep per night. The subjects were stratified by diabetes risk according to their ethnicity and family history of the disease.

“We found a clear relationship between sleep duration and insulin sensitivity. The short sleepers had lowered insulin sensitivity and the longer sleepers had higher insulin sensitivity, but the relationship was really only significant in those with a low ethnicity-based diabetes risk,” she said.

Further statistical tests revealed significant differences in insulin sensitivity associated with both ethnicity-based diabetes risk and sleep duration. For young healthy subjects in their 20s who were considered to be at low risk for diabetes, the impact of sleep deprivation on insulin sensitivity was profound, placing them in a risk category similar to that of Mexican Americans or 61- to 80-year-olds.

Dr. Van Cauter noted that sharply rising curves in the prevalence of obesity in the United States since the 1960s mirror reverse curves in the amount of sleep Americans get–the smallest amount in the industrialized world.

“I'm not saying that sleep curtailment, which is an increasingly prevalent behavior, is the cause of rising rates of obesity, but certainly, it hasn't helped,” she said.

An ongoing study is attempting to determine whether sleep recovery can improve glucose tolerance among chronically sleep-deprived patients who already have impaired insulin sensitivity. Chronic short sleepers between 35 and 41 years old spend 10 hours per night in a darkened sleep laboratory for 8–10 nights.

“You have to pay them,” she observed, noting that for many Americans, shortened sleep is a way of life.

Early results suggest that a longstanding sleep debt cannot be recovered in some short sleepers, who remain awake most of the hours they spend in laboratory-imposed darkness.

However, chronically sleep-deprived subjects who do extend their sleeping time show a rapid and impressive improvement in glucose tolerance, particularly at the 90-minute mark in glucose tolerance tests.

The average improvement of 25 mg/dL “is about what you can get with an antidiabetic drug like Metformin,” she said. “We're pursuing this vigorously.

FLORENCE, ITALY — Recalcitrant lichen amyloidosis can be safely and effectively treated with dermabrasion in an office setting using tumescent anesthesia, William Y.M. Tang, M.D., said at the 13th Congress of the European Academy of Dermatology and Venereology.

Lichen amyloidosis is a rare, chronic condition characterized by profoundly pruritic yellow to reddish-brown hyperkeratotic papules symmetrically dispersed over the extremities and (sometimes) the trunk. Pathology reveals insoluble fibrillar protein, or amyloid. The condition is seen more frequently in males than females and is believed to be more common in people of Asian descent.

Management is difficult, said Dr. Tang, a Sai Ying Pung-based dermatologist with the social hygiene service in the government department of health in Hong Kong.

Dermabrasion has been described as an effective, long-lasting treatment modality, and Dr. Tang concurs. However, he said pain control is a substantial problem when dermabrasion is performed over the large areas of skin affected by lichen amyloidosis. General anesthesia is usually required.

In an attempt to determine whether the procedure could be done in an office setting, Dr. Tang performed it on five male patients aged 43-73 years who had lichen amyloidosis for 3-20 years on their shins (four patients) and/or forearms (three patients). They were not responsive to potent topical steroids, emollients, or oral antihistamines. Dr. Tang infiltrated standard tumescent anesthesia solution into the subcutaneous compartment through a 22-gauge spinal cannula in a fan-shaped manner to his patients' most severely pruritic regions. Treated areas ranged from 72 cm2 to 150 cm2 and required 42-113 mL of tumescent solution.

After 30 minutes, he performed dermabrasion using an electric motor-driven dermabrader fitted with a stainless, olive-shaped head with spiral cutting edges rotating at 20,000 rpm. "The [dermabrader] head was moved with even, light pressure across the skin surface to remove the epidermis down to the papillary dermis," he said. A paraffin gauze dressing was applied and a mild analgesic prescribed. Dressings were changed daily for 2-3 weeks until reepithelialization occurred.

"Itch reduction was immediate in all patients," Dr. Tang said. Patients also experienced symptomatic relief for the duration of follow-up, which in some patients lasted 21 months. All patients rated their results as cosmetically improved. Although a few papules returned in two of five patients, they were less pruritic than in the initial cases. No procedure-related complications were reported. Adverse events included mild cellulitis and hypopigmentation; the latter improved with time.

Lichen amyloidosis is characterized by profoundly pruritic yellow to reddish-brown hyperkeratotic papules.

Dermabrasion using in-office tumescent anesthesia eased pain and resulted in immediate itch reduction. Photos courtesy Dr. William Y.M. Tang

FLORENCE, ITALY — Recalcitrant lichen amyloidosis can be safely and effectively treated with dermabrasion in an office setting using tumescent anesthesia, William Y.M. Tang, M.D., said at the 13th Congress of the European Academy of Dermatology and Venereology.

Lichen amyloidosis is a rare, chronic condition characterized by profoundly pruritic yellow to reddish-brown hyperkeratotic papules symmetrically dispersed over the extremities and (sometimes) the trunk. Pathology reveals insoluble fibrillar protein, or amyloid. The condition is seen more frequently in males than females and is believed to be more common in people of Asian descent.

Management is difficult, said Dr. Tang, a Sai Ying Pung-based dermatologist with the social hygiene service in the government department of health in Hong Kong.

Dermabrasion has been described as an effective, long-lasting treatment modality, and Dr. Tang concurs. However, he said pain control is a substantial problem when dermabrasion is performed over the large areas of skin affected by lichen amyloidosis. General anesthesia is usually required.

In an attempt to determine whether the procedure could be done in an office setting, Dr. Tang performed it on five male patients aged 43-73 years who had lichen amyloidosis for 3-20 years on their shins (four patients) and/or forearms (three patients). They were not responsive to potent topical steroids, emollients, or oral antihistamines. Dr. Tang infiltrated standard tumescent anesthesia solution into the subcutaneous compartment through a 22-gauge spinal cannula in a fan-shaped manner to his patients' most severely pruritic regions. Treated areas ranged from 72 cm2 to 150 cm2 and required 42-113 mL of tumescent solution.

After 30 minutes, he performed dermabrasion using an electric motor-driven dermabrader fitted with a stainless, olive-shaped head with spiral cutting edges rotating at 20,000 rpm. "The [dermabrader] head was moved with even, light pressure across the skin surface to remove the epidermis down to the papillary dermis," he said. A paraffin gauze dressing was applied and a mild analgesic prescribed. Dressings were changed daily for 2-3 weeks until reepithelialization occurred.

"Itch reduction was immediate in all patients," Dr. Tang said. Patients also experienced symptomatic relief for the duration of follow-up, which in some patients lasted 21 months. All patients rated their results as cosmetically improved. Although a few papules returned in two of five patients, they were less pruritic than in the initial cases. No procedure-related complications were reported. Adverse events included mild cellulitis and hypopigmentation; the latter improved with time.

Lichen amyloidosis is characterized by profoundly pruritic yellow to reddish-brown hyperkeratotic papules.

Dermabrasion using in-office tumescent anesthesia eased pain and resulted in immediate itch reduction. Photos courtesy Dr. William Y.M. Tang

FLORENCE, ITALY — Recalcitrant lichen amyloidosis can be safely and effectively treated with dermabrasion in an office setting using tumescent anesthesia, William Y.M. Tang, M.D., said at the 13th Congress of the European Academy of Dermatology and Venereology.

Lichen amyloidosis is a rare, chronic condition characterized by profoundly pruritic yellow to reddish-brown hyperkeratotic papules symmetrically dispersed over the extremities and (sometimes) the trunk. Pathology reveals insoluble fibrillar protein, or amyloid. The condition is seen more frequently in males than females and is believed to be more common in people of Asian descent.

Management is difficult, said Dr. Tang, a Sai Ying Pung-based dermatologist with the social hygiene service in the government department of health in Hong Kong.

Dermabrasion has been described as an effective, long-lasting treatment modality, and Dr. Tang concurs. However, he said pain control is a substantial problem when dermabrasion is performed over the large areas of skin affected by lichen amyloidosis. General anesthesia is usually required.

In an attempt to determine whether the procedure could be done in an office setting, Dr. Tang performed it on five male patients aged 43-73 years who had lichen amyloidosis for 3-20 years on their shins (four patients) and/or forearms (three patients). They were not responsive to potent topical steroids, emollients, or oral antihistamines. Dr. Tang infiltrated standard tumescent anesthesia solution into the subcutaneous compartment through a 22-gauge spinal cannula in a fan-shaped manner to his patients' most severely pruritic regions. Treated areas ranged from 72 cm2 to 150 cm2 and required 42-113 mL of tumescent solution.

After 30 minutes, he performed dermabrasion using an electric motor-driven dermabrader fitted with a stainless, olive-shaped head with spiral cutting edges rotating at 20,000 rpm. "The [dermabrader] head was moved with even, light pressure across the skin surface to remove the epidermis down to the papillary dermis," he said. A paraffin gauze dressing was applied and a mild analgesic prescribed. Dressings were changed daily for 2-3 weeks until reepithelialization occurred.

"Itch reduction was immediate in all patients," Dr. Tang said. Patients also experienced symptomatic relief for the duration of follow-up, which in some patients lasted 21 months. All patients rated their results as cosmetically improved. Although a few papules returned in two of five patients, they were less pruritic than in the initial cases. No procedure-related complications were reported. Adverse events included mild cellulitis and hypopigmentation; the latter improved with time.

Lichen amyloidosis is characterized by profoundly pruritic yellow to reddish-brown hyperkeratotic papules.

Dermabrasion using in-office tumescent anesthesia eased pain and resulted in immediate itch reduction. Photos courtesy Dr. William Y.M. Tang

RANCHO MIRAGE, CALIF. — Mothers who experience high levels of stress during early pregnancy appear to convey distress signals to their fetuses, prompting them to produce high levels of hormones that speed delivery.

The phenomenon suggests the presence of a “placental clock” for parturition that may be set months before the onset of labor, said Curt A. Sandman, Ph.D., professor and vice chair of psychiatry at the University of California, Irvine.

The pattern was seen in a prospective evaluation of pregnant California women who happened to be enrolled in a comprehensive study of pregnancy outcomes when the magnitude 6.7 Northridge earthquake struck on Jan. 17, 1994, killing dozens of people and leveling thousands of homes.

Those subjects who were in their first trimester showed highly elevated levels of stress hormones, but those in their third trimester had much lower levels of stress hormones, Dr. Sandman said at a conference on sleep in infancy and childhood sponsored by the Annenberg Center for Health Sciences. Months later, women who had been exposed to the stress of the earthquake early in pregnancy were significantly more likely than other mothers to deliver early.

“An early maternal message that it's a hostile world primes the placental clock for a CRH [corticotropin-releasing hormone] response later,” he said.

Subsequent studies in 550 consecutive pregnant subjects confirmed a consistent link between high levels of maternal cortisol early in pregnancy and elevated levels of placenta-derived CRH in the third trimester. Every 1 U of cortisol (μg/dL) measured at weeks 14–16 predicted 34 U of CRH (pg/dL) at 30–32 weeks' gestation.

Elevated CRH not only seems to speed delivery, but also appears to have profound consequences on the fetal response to stimuli and, later, a child's response to stress.

The complex interaction between maternal stress, fetal CRH, pregnancy outcomes, and infant and childhood behavior has been the target of studies conducted over more than 12 years as part of the women and children's health and well-being project at UCI, Dr. Sandman explained.

More than 1,000 women and 600–700 infants have been enrolled thus far in studies that begin with extensive prenatal assessment beginning at about 10 weeks' gestation. Neuroendocrine profiles assess the maternal stress axis, while ultrasound examinations and studies of fetal behavior continue throughout pregnancy.

Infant stress examinations begin with the routine first heel-stick test received in the nursery, when researchers take advantage of a naturally occurring opportunity to evaluate salivary cortisol. Babies' responses to the stress of immunizations are also measured and temperament analyses conducted at 6–8 weeks.

The children continue to be followed. Beginning at aged 5–7 years, they are assessed with cognitive tests and structural MRI.

A number of intriguing observations have emerged from the UCI studies, including evidence that suggests stress in the womb may have far-reaching consequences on health and behavior.

The metabolic story begins early in pregnancy, with an increase in neuropeptides from the maternal hypothalamic-pituitary-adrenal stress axis. Apparently in response, the placenta produces circulating CRH, which in turn downregulates the maternal stress system, blocking communication between the hypothalamus and pituitary.

Both the quantity and the timing of stress hormone production is important.

“Women, as pregnancy advances, become immunized to the effects of stress,” explained Dr. Sandman, who said the finding explains why stress hormones were not as high in subjects who experienced the earthquake late in pregnancy.

Further research by the UCI group suggests that the fetus is very much influenced by stress signals. Fetuses exposed to high levels of stress hormones show a diminished ability to respond to new and familiar auditory stimuli. After birth, babies exposed early to high levels of stress hormones exhibit altered fear responses.

Dr. Sandman said these preliminary findings are not altogether surprising. Animal studies show that drought or famine produces smaller offspring, born early. This represents adaptation, since those animals that survive are small, requiring less food than usual in an environment of scarce resources.

Preterm birth may be an attempt to escape an inhospitable environment, identified as such by an exquisitely sensitive placenta measuring signals suggesting malnourishment or high levels of stress.

RANCHO MIRAGE, CALIF. — Mothers who experience high levels of stress during early pregnancy appear to convey distress signals to their fetuses, prompting them to produce high levels of hormones that speed delivery.

The phenomenon suggests the presence of a “placental clock” for parturition that may be set months before the onset of labor, said Curt A. Sandman, Ph.D., professor and vice chair of psychiatry at the University of California, Irvine.

The pattern was seen in a prospective evaluation of pregnant California women who happened to be enrolled in a comprehensive study of pregnancy outcomes when the magnitude 6.7 Northridge earthquake struck on Jan. 17, 1994, killing dozens of people and leveling thousands of homes.

Those subjects who were in their first trimester showed highly elevated levels of stress hormones, but those in their third trimester had much lower levels of stress hormones, Dr. Sandman said at a conference on sleep in infancy and childhood sponsored by the Annenberg Center for Health Sciences. Months later, women who had been exposed to the stress of the earthquake early in pregnancy were significantly more likely than other mothers to deliver early.

“An early maternal message that it's a hostile world primes the placental clock for a CRH [corticotropin-releasing hormone] response later,” he said.

Subsequent studies in 550 consecutive pregnant subjects confirmed a consistent link between high levels of maternal cortisol early in pregnancy and elevated levels of placenta-derived CRH in the third trimester. Every 1 U of cortisol (μg/dL) measured at weeks 14–16 predicted 34 U of CRH (pg/dL) at 30–32 weeks' gestation.

Elevated CRH not only seems to speed delivery, but also appears to have profound consequences on the fetal response to stimuli and, later, a child's response to stress.

The complex interaction between maternal stress, fetal CRH, pregnancy outcomes, and infant and childhood behavior has been the target of studies conducted over more than 12 years as part of the women and children's health and well-being project at UCI, Dr. Sandman explained.

More than 1,000 women and 600–700 infants have been enrolled thus far in studies that begin with extensive prenatal assessment beginning at about 10 weeks' gestation. Neuroendocrine profiles assess the maternal stress axis, while ultrasound examinations and studies of fetal behavior continue throughout pregnancy.

Infant stress examinations begin with the routine first heel-stick test received in the nursery, when researchers take advantage of a naturally occurring opportunity to evaluate salivary cortisol. Babies' responses to the stress of immunizations are also measured and temperament analyses conducted at 6–8 weeks.

The children continue to be followed. Beginning at aged 5–7 years, they are assessed with cognitive tests and structural MRI.

A number of intriguing observations have emerged from the UCI studies, including evidence that suggests stress in the womb may have far-reaching consequences on health and behavior.

The metabolic story begins early in pregnancy, with an increase in neuropeptides from the maternal hypothalamic-pituitary-adrenal stress axis. Apparently in response, the placenta produces circulating CRH, which in turn downregulates the maternal stress system, blocking communication between the hypothalamus and pituitary.

Both the quantity and the timing of stress hormone production is important.

“Women, as pregnancy advances, become immunized to the effects of stress,” explained Dr. Sandman, who said the finding explains why stress hormones were not as high in subjects who experienced the earthquake late in pregnancy.

Further research by the UCI group suggests that the fetus is very much influenced by stress signals. Fetuses exposed to high levels of stress hormones show a diminished ability to respond to new and familiar auditory stimuli. After birth, babies exposed early to high levels of stress hormones exhibit altered fear responses.

Dr. Sandman said these preliminary findings are not altogether surprising. Animal studies show that drought or famine produces smaller offspring, born early. This represents adaptation, since those animals that survive are small, requiring less food than usual in an environment of scarce resources.

Preterm birth may be an attempt to escape an inhospitable environment, identified as such by an exquisitely sensitive placenta measuring signals suggesting malnourishment or high levels of stress.

RANCHO MIRAGE, CALIF. — Mothers who experience high levels of stress during early pregnancy appear to convey distress signals to their fetuses, prompting them to produce high levels of hormones that speed delivery.

The phenomenon suggests the presence of a “placental clock” for parturition that may be set months before the onset of labor, said Curt A. Sandman, Ph.D., professor and vice chair of psychiatry at the University of California, Irvine.

The pattern was seen in a prospective evaluation of pregnant California women who happened to be enrolled in a comprehensive study of pregnancy outcomes when the magnitude 6.7 Northridge earthquake struck on Jan. 17, 1994, killing dozens of people and leveling thousands of homes.

Those subjects who were in their first trimester showed highly elevated levels of stress hormones, but those in their third trimester had much lower levels of stress hormones, Dr. Sandman said at a conference on sleep in infancy and childhood sponsored by the Annenberg Center for Health Sciences. Months later, women who had been exposed to the stress of the earthquake early in pregnancy were significantly more likely than other mothers to deliver early.

“An early maternal message that it's a hostile world primes the placental clock for a CRH [corticotropin-releasing hormone] response later,” he said.

Subsequent studies in 550 consecutive pregnant subjects confirmed a consistent link between high levels of maternal cortisol early in pregnancy and elevated levels of placenta-derived CRH in the third trimester. Every 1 U of cortisol (μg/dL) measured at weeks 14–16 predicted 34 U of CRH (pg/dL) at 30–32 weeks' gestation.

Elevated CRH not only seems to speed delivery, but also appears to have profound consequences on the fetal response to stimuli and, later, a child's response to stress.

The complex interaction between maternal stress, fetal CRH, pregnancy outcomes, and infant and childhood behavior has been the target of studies conducted over more than 12 years as part of the women and children's health and well-being project at UCI, Dr. Sandman explained.

More than 1,000 women and 600–700 infants have been enrolled thus far in studies that begin with extensive prenatal assessment beginning at about 10 weeks' gestation. Neuroendocrine profiles assess the maternal stress axis, while ultrasound examinations and studies of fetal behavior continue throughout pregnancy.

Infant stress examinations begin with the routine first heel-stick test received in the nursery, when researchers take advantage of a naturally occurring opportunity to evaluate salivary cortisol. Babies' responses to the stress of immunizations are also measured and temperament analyses conducted at 6–8 weeks.

The children continue to be followed. Beginning at aged 5–7 years, they are assessed with cognitive tests and structural MRI.

A number of intriguing observations have emerged from the UCI studies, including evidence that suggests stress in the womb may have far-reaching consequences on health and behavior.

The metabolic story begins early in pregnancy, with an increase in neuropeptides from the maternal hypothalamic-pituitary-adrenal stress axis. Apparently in response, the placenta produces circulating CRH, which in turn downregulates the maternal stress system, blocking communication between the hypothalamus and pituitary.

Both the quantity and the timing of stress hormone production is important.

“Women, as pregnancy advances, become immunized to the effects of stress,” explained Dr. Sandman, who said the finding explains why stress hormones were not as high in subjects who experienced the earthquake late in pregnancy.

Further research by the UCI group suggests that the fetus is very much influenced by stress signals. Fetuses exposed to high levels of stress hormones show a diminished ability to respond to new and familiar auditory stimuli. After birth, babies exposed early to high levels of stress hormones exhibit altered fear responses.

Dr. Sandman said these preliminary findings are not altogether surprising. Animal studies show that drought or famine produces smaller offspring, born early. This represents adaptation, since those animals that survive are small, requiring less food than usual in an environment of scarce resources.

Preterm birth may be an attempt to escape an inhospitable environment, identified as such by an exquisitely sensitive placenta measuring signals suggesting malnourishment or high levels of stress.

FLORENCE, ITALY — An alternative to the classic, 150-year-old surgical technique for repairing ingrown toenails may be associated with fewer recurrences and a much-improved aesthetic result, two dermatologists reported at the 13th Congress of the European Academy of Dermatology and Venereology.

Bernard Noel, M.D., and his coauthor Renatto G. Panizzon, M.D., maintain that their technique is superior to Emmert plasty, a procedure that consists of a rather superficial wedge excision of granulation tissue, as well as the adjacent nail bed and the corresponding matrix.

To refine Emmert plasty, however, they first had to scrutinize its steps to understand why it has a recurrence rate as high as 10%–30%.

Dr. Noel and Dr. Panizzon, professor of dermatology at the University of Lausanne (Switzerland), theorized that recurrences may be related to the surgical target of Emmert plasty: the nail, which is narrowed by the radical surgery and sometimes left in a dystrophic state that may be vulnerable to the same pressure that led to the ingrown nail initially.

Moreover, when a significant portion of the nail bed is sacrificed and the nail width is permanently reduced, aesthetic results are often “unsatisfactory,” according to Dr. Noel, chief of dermatologic surgery and the wound healing clinic at Centre Hospitalier Universitaire Vaudois of the University of Lausanne.

By contrast, their approach preserves the nail apparatus while deeply targeting the granulation tissue and reducing the size of the toe itself. “The breadth of the toe extremity is clearly reduced in a way that radically reduces the lateral pressure exerted by the shoes,” Dr. Noel said.

“The great toe looks thinner, with a nail plate covering almost completely the distal phalange, reducing, therefore, the risk of recurrence,” he noted.

The procedure is performed using a digital block and tourniquet at the toe base. Large, deep excisions remove granulation tissue before the wounds are closed in standard fashion. Among 10 patients followed for a year or more, there has been a 100% success rate and no incidence of recurrence, Dr. Noel and Dr. Panizzon reported in their detailed poster presentation.

The authors believe their findings bode well for patients who are prone to develop ingrown toenails, which are the most common of all toenail disorders, believed to account for as many as 20% of foot-related physician visits.

Excessive pressure on the lateral toenail due to body weight, ill-fitting shoes, or improperly cut toenails all have been cited as contributors to the inflammation and the formation of granulation tissue that causes nails, usually of the great toe, to become ingrown.

When patient education and conservative therapy fail, repeated recurrences can lead to infections and extreme discomfort.

Granulation tissue is removed by using large and deep excisions.

The breadth of the toe is clearly reduced but the nail apparatus is preserved. Photos courtesy Dr. Bernard Noel

FLORENCE, ITALY — An alternative to the classic, 150-year-old surgical technique for repairing ingrown toenails may be associated with fewer recurrences and a much-improved aesthetic result, two dermatologists reported at the 13th Congress of the European Academy of Dermatology and Venereology.

Bernard Noel, M.D., and his coauthor Renatto G. Panizzon, M.D., maintain that their technique is superior to Emmert plasty, a procedure that consists of a rather superficial wedge excision of granulation tissue, as well as the adjacent nail bed and the corresponding matrix.

To refine Emmert plasty, however, they first had to scrutinize its steps to understand why it has a recurrence rate as high as 10%–30%.

Dr. Noel and Dr. Panizzon, professor of dermatology at the University of Lausanne (Switzerland), theorized that recurrences may be related to the surgical target of Emmert plasty: the nail, which is narrowed by the radical surgery and sometimes left in a dystrophic state that may be vulnerable to the same pressure that led to the ingrown nail initially.

Moreover, when a significant portion of the nail bed is sacrificed and the nail width is permanently reduced, aesthetic results are often “unsatisfactory,” according to Dr. Noel, chief of dermatologic surgery and the wound healing clinic at Centre Hospitalier Universitaire Vaudois of the University of Lausanne.

By contrast, their approach preserves the nail apparatus while deeply targeting the granulation tissue and reducing the size of the toe itself. “The breadth of the toe extremity is clearly reduced in a way that radically reduces the lateral pressure exerted by the shoes,” Dr. Noel said.

“The great toe looks thinner, with a nail plate covering almost completely the distal phalange, reducing, therefore, the risk of recurrence,” he noted.

The procedure is performed using a digital block and tourniquet at the toe base. Large, deep excisions remove granulation tissue before the wounds are closed in standard fashion. Among 10 patients followed for a year or more, there has been a 100% success rate and no incidence of recurrence, Dr. Noel and Dr. Panizzon reported in their detailed poster presentation.

The authors believe their findings bode well for patients who are prone to develop ingrown toenails, which are the most common of all toenail disorders, believed to account for as many as 20% of foot-related physician visits.

Excessive pressure on the lateral toenail due to body weight, ill-fitting shoes, or improperly cut toenails all have been cited as contributors to the inflammation and the formation of granulation tissue that causes nails, usually of the great toe, to become ingrown.

When patient education and conservative therapy fail, repeated recurrences can lead to infections and extreme discomfort.

Granulation tissue is removed by using large and deep excisions.

The breadth of the toe is clearly reduced but the nail apparatus is preserved. Photos courtesy Dr. Bernard Noel

FLORENCE, ITALY — An alternative to the classic, 150-year-old surgical technique for repairing ingrown toenails may be associated with fewer recurrences and a much-improved aesthetic result, two dermatologists reported at the 13th Congress of the European Academy of Dermatology and Venereology.

Bernard Noel, M.D., and his coauthor Renatto G. Panizzon, M.D., maintain that their technique is superior to Emmert plasty, a procedure that consists of a rather superficial wedge excision of granulation tissue, as well as the adjacent nail bed and the corresponding matrix.

To refine Emmert plasty, however, they first had to scrutinize its steps to understand why it has a recurrence rate as high as 10%–30%.

Dr. Noel and Dr. Panizzon, professor of dermatology at the University of Lausanne (Switzerland), theorized that recurrences may be related to the surgical target of Emmert plasty: the nail, which is narrowed by the radical surgery and sometimes left in a dystrophic state that may be vulnerable to the same pressure that led to the ingrown nail initially.

Moreover, when a significant portion of the nail bed is sacrificed and the nail width is permanently reduced, aesthetic results are often “unsatisfactory,” according to Dr. Noel, chief of dermatologic surgery and the wound healing clinic at Centre Hospitalier Universitaire Vaudois of the University of Lausanne.

By contrast, their approach preserves the nail apparatus while deeply targeting the granulation tissue and reducing the size of the toe itself. “The breadth of the toe extremity is clearly reduced in a way that radically reduces the lateral pressure exerted by the shoes,” Dr. Noel said.

“The great toe looks thinner, with a nail plate covering almost completely the distal phalange, reducing, therefore, the risk of recurrence,” he noted.

The procedure is performed using a digital block and tourniquet at the toe base. Large, deep excisions remove granulation tissue before the wounds are closed in standard fashion. Among 10 patients followed for a year or more, there has been a 100% success rate and no incidence of recurrence, Dr. Noel and Dr. Panizzon reported in their detailed poster presentation.

The authors believe their findings bode well for patients who are prone to develop ingrown toenails, which are the most common of all toenail disorders, believed to account for as many as 20% of foot-related physician visits.

Excessive pressure on the lateral toenail due to body weight, ill-fitting shoes, or improperly cut toenails all have been cited as contributors to the inflammation and the formation of granulation tissue that causes nails, usually of the great toe, to become ingrown.

When patient education and conservative therapy fail, repeated recurrences can lead to infections and extreme discomfort.

Granulation tissue is removed by using large and deep excisions.

The breadth of the toe is clearly reduced but the nail apparatus is preserved. Photos courtesy Dr. Bernard Noel

PARIS — At least one abnormal biologic liver parameter was found in 20 of 22 patients with generalized pustular psoriasis, highlighting a previously underestimated connection between liver involvement and the disease, French researchers reported at the European Congress on Psoriasis 2004.

Extracutaneous manifestations, such as arthritis and mucosal involvement, of pustular psoriasis are well recognized.

Although liver abnormalities have been noted in isolated cases, the full extent of liver involvement has not been fully explored, noted Manuelle A. Viguier, M.D., of the department of dermatology at Saint-Louis Hospital in Paris.

Liver tests were performed on 22 consecutive patients admitted to the hospital for a flare of their generalized pustular psoriasis; tests were done at the time of the flare and several weeks later.

Patients with abnormal biologic tests (bilirubin, γ-glutamyl transferase, alkaline phosphatase, aspartate aminotransferase, or alanine aminotransferase serum counts) underwent a more extensive liver work-up, which included a drug intake analysis, serologic detection of hepatitis B virus and hepatitis C virus infections, abdominal ultrasound examination, liver histology, and endoscopic retrograde cholangiopancreatography or magnetic resonance cholangiopancreatography.

Abnormal biologic liver tests were a very common finding at the time of a psoriasis flare, occurring in nearly all patients.

Half of the 22 patients studied had pronounced abnormalities: jaundice in 4, γ-glutamyl transferase higher than four times the normal value in 10, alkaline phosphatase higher than twice the normal value in 7, and transaminases higher than three times the normal value in 7.

“These abnormalities returned to [the] normal range at the time of remission of pustular psoriasis and relapsed when new cutaneous attacks occurred,” the researchers noted in their poster.

Liver biopsies revealed neutrophilic cholangitis. Magnetic resonance studies showed features characteristic of sclerosing cholangitis in three of four patients who underwent such examinations.

“Biliary involvement related to neutrophilic cholangitis should be added to the spectrum of extracutaneous manifestations of this disease, and physicians should be aware of such complications in order to avoid both invasive liver investigations [that aren't useful] and withdrawal of drugs with potentially deleterious consequences on the course of the disease,” Dr. Viguier said.

PARIS — At least one abnormal biologic liver parameter was found in 20 of 22 patients with generalized pustular psoriasis, highlighting a previously underestimated connection between liver involvement and the disease, French researchers reported at the European Congress on Psoriasis 2004.

Extracutaneous manifestations, such as arthritis and mucosal involvement, of pustular psoriasis are well recognized.

Although liver abnormalities have been noted in isolated cases, the full extent of liver involvement has not been fully explored, noted Manuelle A. Viguier, M.D., of the department of dermatology at Saint-Louis Hospital in Paris.

Liver tests were performed on 22 consecutive patients admitted to the hospital for a flare of their generalized pustular psoriasis; tests were done at the time of the flare and several weeks later.

Patients with abnormal biologic tests (bilirubin, γ-glutamyl transferase, alkaline phosphatase, aspartate aminotransferase, or alanine aminotransferase serum counts) underwent a more extensive liver work-up, which included a drug intake analysis, serologic detection of hepatitis B virus and hepatitis C virus infections, abdominal ultrasound examination, liver histology, and endoscopic retrograde cholangiopancreatography or magnetic resonance cholangiopancreatography.

Abnormal biologic liver tests were a very common finding at the time of a psoriasis flare, occurring in nearly all patients.

Half of the 22 patients studied had pronounced abnormalities: jaundice in 4, γ-glutamyl transferase higher than four times the normal value in 10, alkaline phosphatase higher than twice the normal value in 7, and transaminases higher than three times the normal value in 7.

“These abnormalities returned to [the] normal range at the time of remission of pustular psoriasis and relapsed when new cutaneous attacks occurred,” the researchers noted in their poster.

Liver biopsies revealed neutrophilic cholangitis. Magnetic resonance studies showed features characteristic of sclerosing cholangitis in three of four patients who underwent such examinations.

“Biliary involvement related to neutrophilic cholangitis should be added to the spectrum of extracutaneous manifestations of this disease, and physicians should be aware of such complications in order to avoid both invasive liver investigations [that aren't useful] and withdrawal of drugs with potentially deleterious consequences on the course of the disease,” Dr. Viguier said.

PARIS — At least one abnormal biologic liver parameter was found in 20 of 22 patients with generalized pustular psoriasis, highlighting a previously underestimated connection between liver involvement and the disease, French researchers reported at the European Congress on Psoriasis 2004.

Extracutaneous manifestations, such as arthritis and mucosal involvement, of pustular psoriasis are well recognized.

Although liver abnormalities have been noted in isolated cases, the full extent of liver involvement has not been fully explored, noted Manuelle A. Viguier, M.D., of the department of dermatology at Saint-Louis Hospital in Paris.

Liver tests were performed on 22 consecutive patients admitted to the hospital for a flare of their generalized pustular psoriasis; tests were done at the time of the flare and several weeks later.

Patients with abnormal biologic tests (bilirubin, γ-glutamyl transferase, alkaline phosphatase, aspartate aminotransferase, or alanine aminotransferase serum counts) underwent a more extensive liver work-up, which included a drug intake analysis, serologic detection of hepatitis B virus and hepatitis C virus infections, abdominal ultrasound examination, liver histology, and endoscopic retrograde cholangiopancreatography or magnetic resonance cholangiopancreatography.

Abnormal biologic liver tests were a very common finding at the time of a psoriasis flare, occurring in nearly all patients.

Half of the 22 patients studied had pronounced abnormalities: jaundice in 4, γ-glutamyl transferase higher than four times the normal value in 10, alkaline phosphatase higher than twice the normal value in 7, and transaminases higher than three times the normal value in 7.

“These abnormalities returned to [the] normal range at the time of remission of pustular psoriasis and relapsed when new cutaneous attacks occurred,” the researchers noted in their poster.

Liver biopsies revealed neutrophilic cholangitis. Magnetic resonance studies showed features characteristic of sclerosing cholangitis in three of four patients who underwent such examinations.

“Biliary involvement related to neutrophilic cholangitis should be added to the spectrum of extracutaneous manifestations of this disease, and physicians should be aware of such complications in order to avoid both invasive liver investigations [that aren't useful] and withdrawal of drugs with potentially deleterious consequences on the course of the disease,” Dr. Viguier said.

PARIS — Patients colonized with certain enterotoxic strains of Staphylococcus aureus had significantly worse Psoriasis Area and Severity Index scores than did patients not colonized with these bacterial strains, raising the possibility that antibiotics might have an adjunctive role in treatment, Austrian dermatologists reported at the European Congress on Psoriasis 2004.

Nordwig S. Tomi, M.D., and Elisabeth Aberer, M.D., of Karl Franzens University in Graz, Austria, took sample swabs from the lesional skin and nares of 25 patients with psoriasis for evidence of S. aureus colonization and identification of enterotoxins A, B, C, or D.

Samples from 15 of 25 patients grew positive cultures; these samples were from the nares alone in 1 patient, skin only in 4 patients, and skin and nares in 10. Sixty percent of the strains produced S. aureus enterotoxins.

Four patients had enterotoxin B, two had enterotoxin C, one had D, and combinations of A plus D and B plus C were found in one patient each. The Psoriasis Area and Severity Index score was significantly higher (P = .001) in patients with enterotoxin-producing staphylococcal strains, the investigators reported in a poster presentation at the meeting.

PARIS — Patients colonized with certain enterotoxic strains of Staphylococcus aureus had significantly worse Psoriasis Area and Severity Index scores than did patients not colonized with these bacterial strains, raising the possibility that antibiotics might have an adjunctive role in treatment, Austrian dermatologists reported at the European Congress on Psoriasis 2004.

Nordwig S. Tomi, M.D., and Elisabeth Aberer, M.D., of Karl Franzens University in Graz, Austria, took sample swabs from the lesional skin and nares of 25 patients with psoriasis for evidence of S. aureus colonization and identification of enterotoxins A, B, C, or D.

Samples from 15 of 25 patients grew positive cultures; these samples were from the nares alone in 1 patient, skin only in 4 patients, and skin and nares in 10. Sixty percent of the strains produced S. aureus enterotoxins.

Four patients had enterotoxin B, two had enterotoxin C, one had D, and combinations of A plus D and B plus C were found in one patient each. The Psoriasis Area and Severity Index score was significantly higher (P = .001) in patients with enterotoxin-producing staphylococcal strains, the investigators reported in a poster presentation at the meeting.

PARIS — Patients colonized with certain enterotoxic strains of Staphylococcus aureus had significantly worse Psoriasis Area and Severity Index scores than did patients not colonized with these bacterial strains, raising the possibility that antibiotics might have an adjunctive role in treatment, Austrian dermatologists reported at the European Congress on Psoriasis 2004.

Nordwig S. Tomi, M.D., and Elisabeth Aberer, M.D., of Karl Franzens University in Graz, Austria, took sample swabs from the lesional skin and nares of 25 patients with psoriasis for evidence of S. aureus colonization and identification of enterotoxins A, B, C, or D.

Samples from 15 of 25 patients grew positive cultures; these samples were from the nares alone in 1 patient, skin only in 4 patients, and skin and nares in 10. Sixty percent of the strains produced S. aureus enterotoxins.

Four patients had enterotoxin B, two had enterotoxin C, one had D, and combinations of A plus D and B plus C were found in one patient each. The Psoriasis Area and Severity Index score was significantly higher (P = .001) in patients with enterotoxin-producing staphylococcal strains, the investigators reported in a poster presentation at the meeting.