Betsy Bates

PORTLAND, ORE. — A broad and diverse group of foods contains nickel, and consumption of these foods has the potential to exacerbate allergic contact dermatitis in patients, particularly those receiving more than one exposure per day, Dr. David E. Cohen said at the annual meeting of the Pacific Northwest Dermatological Society.

It's no surprise that items such as jewelry or jeans snaps might be a problem in patients with allergic contact dermatitis, since these are well-known sources of nickel that come into contact with the skin.

But edamame?

It's true. The green soybean snacks contain enough naturally occurring nickel—nearly 0.9 mg in a single serving—to have the potential of leading to systemic contact dermitis in up to 10% of nickel-sensitive patients, said Dr. Cohen, director of allergic, occupational, and contact dermatitis at New York University.

The normal daily dietary intake of nickel ranges between 0.02 mg/day and 0.48 mg/day.

The Food and Drug Administration has set 50 mcg as the tolerable upper intake level recommended in adults who are allergic to nickel.

Still, certain foods, including soybeans, cashews, lentils, figs, and raspberries, have high nickel content and could cause a patient with nickel allergy to have a flare. (See chart.)

Sometimes the allergen source in foods is even more subtle, noted Dr. Cohen, who conducted a study of three types of tomatoes to identify natural fragrances that might explain their proclivity to produce systemic contact allergy reactions in certain patients (Dermatitis 2005;16:91–100).

“I see these reactions in adult eczema patients, particularly those who are allergic to fragrance and flavor chemical on patch testing.

“These reactions can look quite banal and don't have any particular distribution to clue in the evaluating dermatologist,” Dr. Cohen said during an interview following the meeting.

Several potent constituents of the well-known allergen balsam of Peru, including cinnamic acid, were detected in various quantities in beefsteak, cherry, and plum tomatoes, he said.

In addition, the allergen coniferyl alcohol was detected in the three varieties of tomatoes.

When the source of a patient's flares is uncertain and seems to point to foods, Dr. Cohen recommends that the patient change to a diet lacking in all foods containing the suspected allergen for a period of 3 weeks.

“Then [tell them to] eat a ton of whatever they miss most,” he said.

If a flare ensues, the culprit food may be unmasked.

YENLING LIU/ELSEVIER GLOBAL MEDICAL NEWS

Soybeans, cashews, and lentils are high in nickel and could cause a patient with nickel allergy to have a flare. DR. COHEN

PORTLAND, ORE. — A broad and diverse group of foods contains nickel, and consumption of these foods has the potential to exacerbate allergic contact dermatitis in patients, particularly those receiving more than one exposure per day, Dr. David E. Cohen said at the annual meeting of the Pacific Northwest Dermatological Society.

It's no surprise that items such as jewelry or jeans snaps might be a problem in patients with allergic contact dermatitis, since these are well-known sources of nickel that come into contact with the skin.

But edamame?

It's true. The green soybean snacks contain enough naturally occurring nickel—nearly 0.9 mg in a single serving—to have the potential of leading to systemic contact dermitis in up to 10% of nickel-sensitive patients, said Dr. Cohen, director of allergic, occupational, and contact dermatitis at New York University.

The normal daily dietary intake of nickel ranges between 0.02 mg/day and 0.48 mg/day.

The Food and Drug Administration has set 50 mcg as the tolerable upper intake level recommended in adults who are allergic to nickel.

Still, certain foods, including soybeans, cashews, lentils, figs, and raspberries, have high nickel content and could cause a patient with nickel allergy to have a flare. (See chart.)

Sometimes the allergen source in foods is even more subtle, noted Dr. Cohen, who conducted a study of three types of tomatoes to identify natural fragrances that might explain their proclivity to produce systemic contact allergy reactions in certain patients (Dermatitis 2005;16:91–100).

“I see these reactions in adult eczema patients, particularly those who are allergic to fragrance and flavor chemical on patch testing.

“These reactions can look quite banal and don't have any particular distribution to clue in the evaluating dermatologist,” Dr. Cohen said during an interview following the meeting.

Several potent constituents of the well-known allergen balsam of Peru, including cinnamic acid, were detected in various quantities in beefsteak, cherry, and plum tomatoes, he said.

In addition, the allergen coniferyl alcohol was detected in the three varieties of tomatoes.

When the source of a patient's flares is uncertain and seems to point to foods, Dr. Cohen recommends that the patient change to a diet lacking in all foods containing the suspected allergen for a period of 3 weeks.

“Then [tell them to] eat a ton of whatever they miss most,” he said.

If a flare ensues, the culprit food may be unmasked.

YENLING LIU/ELSEVIER GLOBAL MEDICAL NEWS

Soybeans, cashews, and lentils are high in nickel and could cause a patient with nickel allergy to have a flare. DR. COHEN

PORTLAND, ORE. — A broad and diverse group of foods contains nickel, and consumption of these foods has the potential to exacerbate allergic contact dermatitis in patients, particularly those receiving more than one exposure per day, Dr. David E. Cohen said at the annual meeting of the Pacific Northwest Dermatological Society.

It's no surprise that items such as jewelry or jeans snaps might be a problem in patients with allergic contact dermatitis, since these are well-known sources of nickel that come into contact with the skin.

But edamame?

It's true. The green soybean snacks contain enough naturally occurring nickel—nearly 0.9 mg in a single serving—to have the potential of leading to systemic contact dermitis in up to 10% of nickel-sensitive patients, said Dr. Cohen, director of allergic, occupational, and contact dermatitis at New York University.

The normal daily dietary intake of nickel ranges between 0.02 mg/day and 0.48 mg/day.

The Food and Drug Administration has set 50 mcg as the tolerable upper intake level recommended in adults who are allergic to nickel.

Still, certain foods, including soybeans, cashews, lentils, figs, and raspberries, have high nickel content and could cause a patient with nickel allergy to have a flare. (See chart.)

Sometimes the allergen source in foods is even more subtle, noted Dr. Cohen, who conducted a study of three types of tomatoes to identify natural fragrances that might explain their proclivity to produce systemic contact allergy reactions in certain patients (Dermatitis 2005;16:91–100).

“I see these reactions in adult eczema patients, particularly those who are allergic to fragrance and flavor chemical on patch testing.

“These reactions can look quite banal and don't have any particular distribution to clue in the evaluating dermatologist,” Dr. Cohen said during an interview following the meeting.

Several potent constituents of the well-known allergen balsam of Peru, including cinnamic acid, were detected in various quantities in beefsteak, cherry, and plum tomatoes, he said.

In addition, the allergen coniferyl alcohol was detected in the three varieties of tomatoes.

When the source of a patient's flares is uncertain and seems to point to foods, Dr. Cohen recommends that the patient change to a diet lacking in all foods containing the suspected allergen for a period of 3 weeks.

“Then [tell them to] eat a ton of whatever they miss most,” he said.

If a flare ensues, the culprit food may be unmasked.

YENLING LIU/ELSEVIER GLOBAL MEDICAL NEWS

Soybeans, cashews, and lentils are high in nickel and could cause a patient with nickel allergy to have a flare. DR. COHEN

PORTLAND, ORE. — Melanoma in a pediatric patient is a lot like Sasquatch, Dr. Seth Orlow remarked at the annual meeting of the Pacific Northwest Dermatological Society.

It's a very rare thing to see, but if it's around, you surely don't want to miss it.

Drawing from case series large and small and from his own experience, Dr. Orlow painted a puzzling picture of childhood melanoma, from the hodgepodge of clinical features to highly variable survival figures.

Perhaps the only absolutely clear conclusion in the literature is that melanoma in children is exceedingly rare, even in referral centers seeing a large number of patients with suspicious lesions, said Dr. Orlow, director of pediatric and adolescent dermatology and chair of dermatology at New York University.

A SEER (Surveillance, Epidemiology, and End Results) database analysis of 140,206 cases of melanoma diagnosed between 1973 and 2001 found just 1,255 cases in patients under 20 years old; 204 of these were melanoma in situ, and just 95 occurred in children younger than 10 years of age.

The overall incidence of childhood melanoma rose 2.9% per year. In children younger than 10, the incidence rose 1.4% per year.

Younger children were less likely than older children with melanoma to be in a traditional high-risk category.

They were more likely to be nonwhite, have nodular lesions, present with head/face/neck primaries, and have metastatic disease. Many had a history of other malignancies and may have received radiation therapy and/or chemotherapy for leukemia or another cancer, Dr. Orlow said.

Other studies similarly have found few traditional risk factors, frustrating dermatologists who might hope they can simply raise the red flag for a fair-skinned child with a history of blistering sunburns.

“We feel, with some reason, we can identify adults who are at high risk. We know if you have a family history, you have many atypical nevi, you have a history of blistering sunburns, if you're red-haired and freckled, you're going to have an increased risk of melanoma” as an adult, he said.

“In prepubescent melanoma, all bets are off,” Dr. Orlow said.

Children diagnosed with melanoma represent a rainbow of skin types.

Most of them have no family history of the disease, and many have no precursor lesions.

A series from Milan's Istituto Nazionale Tumori found that 14 of 33 children under age 14 years who were diagnosed with melanoma had amelanotic lesions.

“There's no way 40% of adults' lesions would be amelanotic,” he said.

Dr. Orlow's own patients over 16 years of practicing at New York University have included a 16-year-old Jamaican girl with a primary lesion that looked like a keloid on her thigh, a 14-year-old Peruvian girl with a fingertip lesion, a 12-year-old Russian boy from Chernobyl with a lesion on the lower back, and a 12-year-old Ashkenazic girl with a small (less than 1 mm) shoulder lesion.

Another speaker at the meeting, Dr. Joseph Gruss of the University of Washington, Seattle, described a case of metastatic melanoma present at birth in an African American girl with a large scalp lesion.

The bottom line is that pediatric melanoma is a mysterious disease that calls for an open mind.

“These are not the things you're used to seeing in older children and adults. It is a very different disease,” Dr. Orlow said.

Survival of melanoma in adulthood is fairly well predicted by lesion characteristics and other factors, but the survival of childhood melanoma is neither well-characterized nor consistent from study to study.

“You'll see wildly different numbers from different centers,” he commented.

For example, among 13 cases in children under 17 years old seen at Montreal's Hopital Ste. Justine over a 22-year period, the 5-year survival was 59%.

Among 23 cases referred to Children's Hospital in Boston and reviewed by Dr. Ray Barnhill, a dermatopathologist, survival appeared linked to tumor type (Semin. Diagn. Pathol. 1998;15:189–94).

All five cases he characterized as “small cell melanoma” were fatal. There was no precursor lesion in four of the five, and two of the five were verrucous, Dr. Orlow said.

Of six cases of “adultlike melanoma,” two were fatal. Both were on the backs of older children in the series.

One of the three patients with “Spitz-like melanoma” died, but none of the nine with “atypical Spitz tumors” did. It is doubtful that the latter cases were really melanomas at all, Dr. Orlow said.

The Milan series cited a survival rate of 90% in children under age 10 years and 47% in children over 10, in a pattern that did not seem to correlate with the apparent severity of presenting features.

“It makes you wonder if all of the lesions they were calling melanoma really were melanomas,” Dr. Orlow said.

The SEER database cited survival rates of 89% and 92% in children under age 10 and aged 10–19, respectively, raising similar questions.

Indeed, a study published in 1996 highlighted the difficulty of interpreting melanoma statistics in children (Int. J. Cancer 1996;68:317–24), he said.

In this review, 42 of 60 “melanoma” lesions diagnosed in children under 16 years old in five Western European countries over a 33-year period were later reclassified as nevi.

The 5-year survival rate for the patients who had true melanoma lesions was 84%.

Case Illustrates Elusive Diagnosis

Melanoma in children is rare and often unheralded by a precursor lesion or melanocytic pigmentation, and it can elude diagnosis, Dr. Orlow said.

“The real thing you have to be on the lookout for is rapid and unexpected growth,” he emphasized.

He described the case of a boy who first presented at age 2 years with a 2-mm papule on his right ear. The lesion was treated with liquid nitrogen.

The lesion returned and measured 4 mm at age 5, 8 mm at age 6 (when it was biopsied and diagnosed as a Spitz nevus), and 10 mm at age 7, when a recurrence was excised and a second biopsy revealed “Spitz nevus with moderate atypia.”

“They were good at measuring it,” Dr. Orlow quipped.

The boy was referred to New York University at age 7. A work-up revealed cervical adenopathy, and a lymph node biopsy detected metastatic melanoma.

Although the child went into apparent remission after 9 months of biochemotherapy, a follow-up positron emission tomography scan at age 11 revealed abnormal foci in the liver, bilateral cervical triangle, and right paratracheal areas.

Despite the ominous course of this case study, Dr. Orlow recommends “restraint in biopsying” when a lesion first presents in a child.

After all, he reminded the audience, any patient destined to have 30 nevi in adulthood will be developing new, completely normal lesions at ages 8, 9, and 10.

There are lesions, like the one in this child, that should have been biopsied “much earlier,” he said. But there are many more “that show up in patients you wouldn't expect … when reasonable people couldn't have guessed it was anything like a melanoma until they took it out and discovered it was.”

An annual examination makes sense for children older than 12 years who have multiple nevi—particularly if they are atypical—and a family history of melanoma, he said.

In children under age 12, though, those factors do not seem to clearly confer elevated risk.

It all gets back to observation, so he is ever on the lookout “for peculiar lesions demonstrating unexpected growth, especially things you can't quite characterize, like a pink, eroded papule that doesn't quite look like a pyogenic granuloma,” he said.

Spotting Pediatric Melanoma

▸ Family history may be negative.

▸ Patient may be nonwhite.

▸ Child may have history of other malignancy.

▸ There is usually no precursor lesion.

▸ Amelanotic, nodular lesions are common.

▸ Rapid, unexpected growth is a red flag.

Source: Dr. Orlow

PORTLAND, ORE. — Melanoma in a pediatric patient is a lot like Sasquatch, Dr. Seth Orlow remarked at the annual meeting of the Pacific Northwest Dermatological Society.

It's a very rare thing to see, but if it's around, you surely don't want to miss it.

Drawing from case series large and small and from his own experience, Dr. Orlow painted a puzzling picture of childhood melanoma, from the hodgepodge of clinical features to highly variable survival figures.

Perhaps the only absolutely clear conclusion in the literature is that melanoma in children is exceedingly rare, even in referral centers seeing a large number of patients with suspicious lesions, said Dr. Orlow, director of pediatric and adolescent dermatology and chair of dermatology at New York University.

A SEER (Surveillance, Epidemiology, and End Results) database analysis of 140,206 cases of melanoma diagnosed between 1973 and 2001 found just 1,255 cases in patients under 20 years old; 204 of these were melanoma in situ, and just 95 occurred in children younger than 10 years of age.

The overall incidence of childhood melanoma rose 2.9% per year. In children younger than 10, the incidence rose 1.4% per year.

Younger children were less likely than older children with melanoma to be in a traditional high-risk category.

They were more likely to be nonwhite, have nodular lesions, present with head/face/neck primaries, and have metastatic disease. Many had a history of other malignancies and may have received radiation therapy and/or chemotherapy for leukemia or another cancer, Dr. Orlow said.

Other studies similarly have found few traditional risk factors, frustrating dermatologists who might hope they can simply raise the red flag for a fair-skinned child with a history of blistering sunburns.

“We feel, with some reason, we can identify adults who are at high risk. We know if you have a family history, you have many atypical nevi, you have a history of blistering sunburns, if you're red-haired and freckled, you're going to have an increased risk of melanoma” as an adult, he said.

“In prepubescent melanoma, all bets are off,” Dr. Orlow said.

Children diagnosed with melanoma represent a rainbow of skin types.

Most of them have no family history of the disease, and many have no precursor lesions.

A series from Milan's Istituto Nazionale Tumori found that 14 of 33 children under age 14 years who were diagnosed with melanoma had amelanotic lesions.

“There's no way 40% of adults' lesions would be amelanotic,” he said.

Dr. Orlow's own patients over 16 years of practicing at New York University have included a 16-year-old Jamaican girl with a primary lesion that looked like a keloid on her thigh, a 14-year-old Peruvian girl with a fingertip lesion, a 12-year-old Russian boy from Chernobyl with a lesion on the lower back, and a 12-year-old Ashkenazic girl with a small (less than 1 mm) shoulder lesion.

Another speaker at the meeting, Dr. Joseph Gruss of the University of Washington, Seattle, described a case of metastatic melanoma present at birth in an African American girl with a large scalp lesion.

The bottom line is that pediatric melanoma is a mysterious disease that calls for an open mind.

“These are not the things you're used to seeing in older children and adults. It is a very different disease,” Dr. Orlow said.

Survival of melanoma in adulthood is fairly well predicted by lesion characteristics and other factors, but the survival of childhood melanoma is neither well-characterized nor consistent from study to study.

“You'll see wildly different numbers from different centers,” he commented.

For example, among 13 cases in children under 17 years old seen at Montreal's Hopital Ste. Justine over a 22-year period, the 5-year survival was 59%.

Among 23 cases referred to Children's Hospital in Boston and reviewed by Dr. Ray Barnhill, a dermatopathologist, survival appeared linked to tumor type (Semin. Diagn. Pathol. 1998;15:189–94).

All five cases he characterized as “small cell melanoma” were fatal. There was no precursor lesion in four of the five, and two of the five were verrucous, Dr. Orlow said.

Of six cases of “adultlike melanoma,” two were fatal. Both were on the backs of older children in the series.

One of the three patients with “Spitz-like melanoma” died, but none of the nine with “atypical Spitz tumors” did. It is doubtful that the latter cases were really melanomas at all, Dr. Orlow said.

The Milan series cited a survival rate of 90% in children under age 10 years and 47% in children over 10, in a pattern that did not seem to correlate with the apparent severity of presenting features.

“It makes you wonder if all of the lesions they were calling melanoma really were melanomas,” Dr. Orlow said.

The SEER database cited survival rates of 89% and 92% in children under age 10 and aged 10–19, respectively, raising similar questions.

Indeed, a study published in 1996 highlighted the difficulty of interpreting melanoma statistics in children (Int. J. Cancer 1996;68:317–24), he said.

In this review, 42 of 60 “melanoma” lesions diagnosed in children under 16 years old in five Western European countries over a 33-year period were later reclassified as nevi.

The 5-year survival rate for the patients who had true melanoma lesions was 84%.

Case Illustrates Elusive Diagnosis

Melanoma in children is rare and often unheralded by a precursor lesion or melanocytic pigmentation, and it can elude diagnosis, Dr. Orlow said.

“The real thing you have to be on the lookout for is rapid and unexpected growth,” he emphasized.

He described the case of a boy who first presented at age 2 years with a 2-mm papule on his right ear. The lesion was treated with liquid nitrogen.

The lesion returned and measured 4 mm at age 5, 8 mm at age 6 (when it was biopsied and diagnosed as a Spitz nevus), and 10 mm at age 7, when a recurrence was excised and a second biopsy revealed “Spitz nevus with moderate atypia.”

“They were good at measuring it,” Dr. Orlow quipped.

The boy was referred to New York University at age 7. A work-up revealed cervical adenopathy, and a lymph node biopsy detected metastatic melanoma.

Although the child went into apparent remission after 9 months of biochemotherapy, a follow-up positron emission tomography scan at age 11 revealed abnormal foci in the liver, bilateral cervical triangle, and right paratracheal areas.

Despite the ominous course of this case study, Dr. Orlow recommends “restraint in biopsying” when a lesion first presents in a child.

After all, he reminded the audience, any patient destined to have 30 nevi in adulthood will be developing new, completely normal lesions at ages 8, 9, and 10.

There are lesions, like the one in this child, that should have been biopsied “much earlier,” he said. But there are many more “that show up in patients you wouldn't expect … when reasonable people couldn't have guessed it was anything like a melanoma until they took it out and discovered it was.”

An annual examination makes sense for children older than 12 years who have multiple nevi—particularly if they are atypical—and a family history of melanoma, he said.

In children under age 12, though, those factors do not seem to clearly confer elevated risk.

It all gets back to observation, so he is ever on the lookout “for peculiar lesions demonstrating unexpected growth, especially things you can't quite characterize, like a pink, eroded papule that doesn't quite look like a pyogenic granuloma,” he said.

Spotting Pediatric Melanoma

▸ Family history may be negative.

▸ Patient may be nonwhite.

▸ Child may have history of other malignancy.

▸ There is usually no precursor lesion.

▸ Amelanotic, nodular lesions are common.

▸ Rapid, unexpected growth is a red flag.

Source: Dr. Orlow

PORTLAND, ORE. — Melanoma in a pediatric patient is a lot like Sasquatch, Dr. Seth Orlow remarked at the annual meeting of the Pacific Northwest Dermatological Society.

It's a very rare thing to see, but if it's around, you surely don't want to miss it.

Drawing from case series large and small and from his own experience, Dr. Orlow painted a puzzling picture of childhood melanoma, from the hodgepodge of clinical features to highly variable survival figures.

Perhaps the only absolutely clear conclusion in the literature is that melanoma in children is exceedingly rare, even in referral centers seeing a large number of patients with suspicious lesions, said Dr. Orlow, director of pediatric and adolescent dermatology and chair of dermatology at New York University.

A SEER (Surveillance, Epidemiology, and End Results) database analysis of 140,206 cases of melanoma diagnosed between 1973 and 2001 found just 1,255 cases in patients under 20 years old; 204 of these were melanoma in situ, and just 95 occurred in children younger than 10 years of age.

The overall incidence of childhood melanoma rose 2.9% per year. In children younger than 10, the incidence rose 1.4% per year.

Younger children were less likely than older children with melanoma to be in a traditional high-risk category.

They were more likely to be nonwhite, have nodular lesions, present with head/face/neck primaries, and have metastatic disease. Many had a history of other malignancies and may have received radiation therapy and/or chemotherapy for leukemia or another cancer, Dr. Orlow said.

Other studies similarly have found few traditional risk factors, frustrating dermatologists who might hope they can simply raise the red flag for a fair-skinned child with a history of blistering sunburns.

“We feel, with some reason, we can identify adults who are at high risk. We know if you have a family history, you have many atypical nevi, you have a history of blistering sunburns, if you're red-haired and freckled, you're going to have an increased risk of melanoma” as an adult, he said.

“In prepubescent melanoma, all bets are off,” Dr. Orlow said.

Children diagnosed with melanoma represent a rainbow of skin types.

Most of them have no family history of the disease, and many have no precursor lesions.

A series from Milan's Istituto Nazionale Tumori found that 14 of 33 children under age 14 years who were diagnosed with melanoma had amelanotic lesions.

“There's no way 40% of adults' lesions would be amelanotic,” he said.

Dr. Orlow's own patients over 16 years of practicing at New York University have included a 16-year-old Jamaican girl with a primary lesion that looked like a keloid on her thigh, a 14-year-old Peruvian girl with a fingertip lesion, a 12-year-old Russian boy from Chernobyl with a lesion on the lower back, and a 12-year-old Ashkenazic girl with a small (less than 1 mm) shoulder lesion.

Another speaker at the meeting, Dr. Joseph Gruss of the University of Washington, Seattle, described a case of metastatic melanoma present at birth in an African American girl with a large scalp lesion.

The bottom line is that pediatric melanoma is a mysterious disease that calls for an open mind.

“These are not the things you're used to seeing in older children and adults. It is a very different disease,” Dr. Orlow said.

Survival of melanoma in adulthood is fairly well predicted by lesion characteristics and other factors, but the survival of childhood melanoma is neither well-characterized nor consistent from study to study.

“You'll see wildly different numbers from different centers,” he commented.

For example, among 13 cases in children under 17 years old seen at Montreal's Hopital Ste. Justine over a 22-year period, the 5-year survival was 59%.

Among 23 cases referred to Children's Hospital in Boston and reviewed by Dr. Ray Barnhill, a dermatopathologist, survival appeared linked to tumor type (Semin. Diagn. Pathol. 1998;15:189–94).

All five cases he characterized as “small cell melanoma” were fatal. There was no precursor lesion in four of the five, and two of the five were verrucous, Dr. Orlow said.

Of six cases of “adultlike melanoma,” two were fatal. Both were on the backs of older children in the series.

One of the three patients with “Spitz-like melanoma” died, but none of the nine with “atypical Spitz tumors” did. It is doubtful that the latter cases were really melanomas at all, Dr. Orlow said.

The Milan series cited a survival rate of 90% in children under age 10 years and 47% in children over 10, in a pattern that did not seem to correlate with the apparent severity of presenting features.

“It makes you wonder if all of the lesions they were calling melanoma really were melanomas,” Dr. Orlow said.

The SEER database cited survival rates of 89% and 92% in children under age 10 and aged 10–19, respectively, raising similar questions.

Indeed, a study published in 1996 highlighted the difficulty of interpreting melanoma statistics in children (Int. J. Cancer 1996;68:317–24), he said.

In this review, 42 of 60 “melanoma” lesions diagnosed in children under 16 years old in five Western European countries over a 33-year period were later reclassified as nevi.

The 5-year survival rate for the patients who had true melanoma lesions was 84%.

Case Illustrates Elusive Diagnosis

Melanoma in children is rare and often unheralded by a precursor lesion or melanocytic pigmentation, and it can elude diagnosis, Dr. Orlow said.

“The real thing you have to be on the lookout for is rapid and unexpected growth,” he emphasized.

He described the case of a boy who first presented at age 2 years with a 2-mm papule on his right ear. The lesion was treated with liquid nitrogen.

The lesion returned and measured 4 mm at age 5, 8 mm at age 6 (when it was biopsied and diagnosed as a Spitz nevus), and 10 mm at age 7, when a recurrence was excised and a second biopsy revealed “Spitz nevus with moderate atypia.”

“They were good at measuring it,” Dr. Orlow quipped.

The boy was referred to New York University at age 7. A work-up revealed cervical adenopathy, and a lymph node biopsy detected metastatic melanoma.

Although the child went into apparent remission after 9 months of biochemotherapy, a follow-up positron emission tomography scan at age 11 revealed abnormal foci in the liver, bilateral cervical triangle, and right paratracheal areas.

Despite the ominous course of this case study, Dr. Orlow recommends “restraint in biopsying” when a lesion first presents in a child.

After all, he reminded the audience, any patient destined to have 30 nevi in adulthood will be developing new, completely normal lesions at ages 8, 9, and 10.

There are lesions, like the one in this child, that should have been biopsied “much earlier,” he said. But there are many more “that show up in patients you wouldn't expect … when reasonable people couldn't have guessed it was anything like a melanoma until they took it out and discovered it was.”

An annual examination makes sense for children older than 12 years who have multiple nevi—particularly if they are atypical—and a family history of melanoma, he said.

In children under age 12, though, those factors do not seem to clearly confer elevated risk.

It all gets back to observation, so he is ever on the lookout “for peculiar lesions demonstrating unexpected growth, especially things you can't quite characterize, like a pink, eroded papule that doesn't quite look like a pyogenic granuloma,” he said.

Spotting Pediatric Melanoma

▸ Family history may be negative.

▸ Patient may be nonwhite.

▸ Child may have history of other malignancy.

▸ There is usually no precursor lesion.

▸ Amelanotic, nodular lesions are common.

▸ Rapid, unexpected growth is a red flag.

Source: Dr. Orlow

VANCOUVER, B.C. – Aggression is not a diagnosis, it's a symptom.

It may be secondary to a psychiatric diagnosis, or unrelated.

It may be a temporary response to the environment, or deeply woven into a child's personality.

Physicians need to know the whys of aggression before they can devise a plan to help, Dr. Susan Lomax said at a conference sponsored by the North Pacific Pediatric Society.

“What's driving the aggression makes a difference with the intervention,” said Dr. Lomax, an adolescent psychiatrist at British Columbia Children's Hospital and a faculty member at the University of British Columbia in Vancouver.

It may be helpful to look at aggression in the context of a child's other traits.

The Antisocial Child

You may see deliberate, proactive, or predatory aggression in an antisocial child. In this context, aggression isn't explosive, but controlled, goal-oriented, and often planned. It's rewarding to the child in some way, perhaps as a release from boredom. This type of aggression is seen when a child methodically injures animals or other children. It is the most difficult form of aggression to treat.

When contemplating a treatment plan, keep in mind that antisocial children want to know “what's in it for me?”

Therefore, concrete, reward-based therapy within a highly structured program makes sense.

One-on-one psychotherapy is rarely useful because these children “often don't have the ability to talk through problems internally,” said Dr. Lomax. Group therapy may be more helpful because these children may be sensitive to peer approval or disapproval.

Because their aggression may arise from a desire for stimulation, encourage time-consuming, prosocial activities such as organized sports, “where they can reinforce skills … and acquire skills they can feel good about.”

The Anxious Child

In sharp contrast to an antisocial child, aggression in a jittery child erupts as a fear reaction. Blowups in the morning before school represent avoidant behavior. These children may have an anxiety disorder, posttraumatic stress disorder, depression, or, rarely, psychosis. Treatment of the psychosis may reduce the high level of arousal that leads to aggressive behavior, Dr. Lomax said.

The Rigid Child

“These kids want things their way or no way,” she explained.

They may become infuriated at having to leave the computer to come to dinner.

“They think they're picked on, that there's no justice,” she said.

Rigid children “habitually misinterpret cues” from parents, teachers, and peers. As a result, they fly off the handle in anger.

Associated diagnoses may include oppositional defiant disorder, the autism spectrum, obsessive-compulsive disorder (when anger arises from interference with rituals), and nonverbal learning disabilities.

Their temperaments tend to be inflexible and stubborn.

The Impulsive Child

Frontal lobe dysfunction plays a role in the aggression of a child who becomes very angry very fast and cannot self-calm.

Beyond their inability to inhibit their impulses, “These children have a hard time planning or envisioning consequences,” said Dr. Lomax.

Possibly associated diagnoses might include ADHD, fetal alcohol syndrome, brain injury, or substance abuse.

The Dysregulated Child

Irritability, agitation, volatility, and mood instability underlie aggression in dysregulated children. Developmental or genetic issues should be explored.

For example, dysregulated aggression is common in children who experienced few nurturing, calming experiences in the first years of life.

Dysregulation may be an early sign of bipolar disorder, even if classic adult signs of euphoria and grandiosity are not present. In children, aggression and sleeplessness may alternate with depression and lethargy in a pattern of rapid cycling.

The Abused or Traumatized Child

Aggressive behaviors in such children make sense within the context of their lives, since the “fight” response to a survival threat naturally requires quick and decisive action.

“Their autonomic system is on overdrive. They become panicked if someone tries to control them,” said Dr. Lomax.

They are hypervigilant, distrustful, and show diminished cognition and a loss of impulse control when they perceive a threat.

Seemingly “minor” events may precipitate catastrophic reactions in these children, she said.

Children Whose Lives Are in Flux

It is also important to remember that aggression may be symptomatic of a situational upheaval in a child's life: a parent's divorce, for example, or a serious illness.

Consider, too, the family context in which aggression occurs.

Aggression may be a learned behavior, modeled by parents with their own history of violence and/or Axis I diagnoses.

Be forewarned: Parents may take “deep and grievous offense” at the notion that the family dynamic may be a contributor to the child's aggressive behavior. Dr. Lomax suggested a careful assessment of whether they are intellectually capable of insight and stable enough to accept suggestions about how to learn and practice anger management and training in parenting skills such as boundary and limit setting.

Sometimes, it may be necessary to go outside the immediately family for help, to grandparents or spouse equivalents, she said.

Psychoeducation, enhancing attachment, marital therapy, and parent support groups are all helpful adjuncts for parents of aggressive children.

“These families are often held hostage to their child's behavior,” Dr. Lomax said.

The treatment of a child with impulsive or affective aggression may be successful in one-on-one sessions or in group therapy. Principles include anxiety management, correction of cognitive distortions, assertiveness training, impulse control strategies, stress reduction, and, if applicable, therapy to address trauma.

In extreme cases, medications may be both necessary and helpful.

Treat any primary psychiatric disorder first, then consider risperidone in very low doses (0.5–2 mg/day), a mood stabilizer if the child is irritable and volatile, or a β-blocker in the context of hyperarousal, Dr. Lomax said.

She cautioned that antidepressants can sometimes have activating effects that exacerbate aggression in some children.

Lorazepam should be avoided for this reason in aggressive children, and children prescribed other antidepressants should be monitored very closely early in therapy for signs of akathisia, sleep problems, and “rage reactions” out of character for the child.

Questions That Should Be Asked

▸ When did the behavior start? What was the context? What is the child's age?

▸ Is the child capable of empathy and/or real regret? Does he or she laugh when confronted with the consequences of the aggressive behavior?

▸ Is the aggressive behavior situation specific?

▸ How is the child's general tolerance for frustration? (Is this a rigid child?)

▸ Has the child had a traumatic experience? Was he/she nurtured early in life?

▸ Do other children in the family have problems with aggression?

▸ How readily does the child adjust to changes in routine?

Source: Dr. Lomax

VANCOUVER, B.C. – Aggression is not a diagnosis, it's a symptom.

It may be secondary to a psychiatric diagnosis, or unrelated.

It may be a temporary response to the environment, or deeply woven into a child's personality.

Physicians need to know the whys of aggression before they can devise a plan to help, Dr. Susan Lomax said at a conference sponsored by the North Pacific Pediatric Society.

“What's driving the aggression makes a difference with the intervention,” said Dr. Lomax, an adolescent psychiatrist at British Columbia Children's Hospital and a faculty member at the University of British Columbia in Vancouver.

It may be helpful to look at aggression in the context of a child's other traits.

The Antisocial Child

You may see deliberate, proactive, or predatory aggression in an antisocial child. In this context, aggression isn't explosive, but controlled, goal-oriented, and often planned. It's rewarding to the child in some way, perhaps as a release from boredom. This type of aggression is seen when a child methodically injures animals or other children. It is the most difficult form of aggression to treat.

When contemplating a treatment plan, keep in mind that antisocial children want to know “what's in it for me?”

Therefore, concrete, reward-based therapy within a highly structured program makes sense.

One-on-one psychotherapy is rarely useful because these children “often don't have the ability to talk through problems internally,” said Dr. Lomax. Group therapy may be more helpful because these children may be sensitive to peer approval or disapproval.

Because their aggression may arise from a desire for stimulation, encourage time-consuming, prosocial activities such as organized sports, “where they can reinforce skills … and acquire skills they can feel good about.”

The Anxious Child

In sharp contrast to an antisocial child, aggression in a jittery child erupts as a fear reaction. Blowups in the morning before school represent avoidant behavior. These children may have an anxiety disorder, posttraumatic stress disorder, depression, or, rarely, psychosis. Treatment of the psychosis may reduce the high level of arousal that leads to aggressive behavior, Dr. Lomax said.

The Rigid Child

“These kids want things their way or no way,” she explained.

They may become infuriated at having to leave the computer to come to dinner.

“They think they're picked on, that there's no justice,” she said.

Rigid children “habitually misinterpret cues” from parents, teachers, and peers. As a result, they fly off the handle in anger.

Associated diagnoses may include oppositional defiant disorder, the autism spectrum, obsessive-compulsive disorder (when anger arises from interference with rituals), and nonverbal learning disabilities.

Their temperaments tend to be inflexible and stubborn.

The Impulsive Child

Frontal lobe dysfunction plays a role in the aggression of a child who becomes very angry very fast and cannot self-calm.

Beyond their inability to inhibit their impulses, “These children have a hard time planning or envisioning consequences,” said Dr. Lomax.

Possibly associated diagnoses might include ADHD, fetal alcohol syndrome, brain injury, or substance abuse.

The Dysregulated Child

Irritability, agitation, volatility, and mood instability underlie aggression in dysregulated children. Developmental or genetic issues should be explored.

For example, dysregulated aggression is common in children who experienced few nurturing, calming experiences in the first years of life.

Dysregulation may be an early sign of bipolar disorder, even if classic adult signs of euphoria and grandiosity are not present. In children, aggression and sleeplessness may alternate with depression and lethargy in a pattern of rapid cycling.

The Abused or Traumatized Child

Aggressive behaviors in such children make sense within the context of their lives, since the “fight” response to a survival threat naturally requires quick and decisive action.

“Their autonomic system is on overdrive. They become panicked if someone tries to control them,” said Dr. Lomax.

They are hypervigilant, distrustful, and show diminished cognition and a loss of impulse control when they perceive a threat.

Seemingly “minor” events may precipitate catastrophic reactions in these children, she said.

Children Whose Lives Are in Flux

It is also important to remember that aggression may be symptomatic of a situational upheaval in a child's life: a parent's divorce, for example, or a serious illness.

Consider, too, the family context in which aggression occurs.

Aggression may be a learned behavior, modeled by parents with their own history of violence and/or Axis I diagnoses.

Be forewarned: Parents may take “deep and grievous offense” at the notion that the family dynamic may be a contributor to the child's aggressive behavior. Dr. Lomax suggested a careful assessment of whether they are intellectually capable of insight and stable enough to accept suggestions about how to learn and practice anger management and training in parenting skills such as boundary and limit setting.

Sometimes, it may be necessary to go outside the immediately family for help, to grandparents or spouse equivalents, she said.

Psychoeducation, enhancing attachment, marital therapy, and parent support groups are all helpful adjuncts for parents of aggressive children.

“These families are often held hostage to their child's behavior,” Dr. Lomax said.

The treatment of a child with impulsive or affective aggression may be successful in one-on-one sessions or in group therapy. Principles include anxiety management, correction of cognitive distortions, assertiveness training, impulse control strategies, stress reduction, and, if applicable, therapy to address trauma.

In extreme cases, medications may be both necessary and helpful.

Treat any primary psychiatric disorder first, then consider risperidone in very low doses (0.5–2 mg/day), a mood stabilizer if the child is irritable and volatile, or a β-blocker in the context of hyperarousal, Dr. Lomax said.

She cautioned that antidepressants can sometimes have activating effects that exacerbate aggression in some children.

Lorazepam should be avoided for this reason in aggressive children, and children prescribed other antidepressants should be monitored very closely early in therapy for signs of akathisia, sleep problems, and “rage reactions” out of character for the child.

Questions That Should Be Asked

▸ When did the behavior start? What was the context? What is the child's age?

▸ Is the child capable of empathy and/or real regret? Does he or she laugh when confronted with the consequences of the aggressive behavior?

▸ Is the aggressive behavior situation specific?

▸ How is the child's general tolerance for frustration? (Is this a rigid child?)

▸ Has the child had a traumatic experience? Was he/she nurtured early in life?

▸ Do other children in the family have problems with aggression?

▸ How readily does the child adjust to changes in routine?

Source: Dr. Lomax

VANCOUVER, B.C. – Aggression is not a diagnosis, it's a symptom.

It may be secondary to a psychiatric diagnosis, or unrelated.

It may be a temporary response to the environment, or deeply woven into a child's personality.

Physicians need to know the whys of aggression before they can devise a plan to help, Dr. Susan Lomax said at a conference sponsored by the North Pacific Pediatric Society.

“What's driving the aggression makes a difference with the intervention,” said Dr. Lomax, an adolescent psychiatrist at British Columbia Children's Hospital and a faculty member at the University of British Columbia in Vancouver.

It may be helpful to look at aggression in the context of a child's other traits.

The Antisocial Child

You may see deliberate, proactive, or predatory aggression in an antisocial child. In this context, aggression isn't explosive, but controlled, goal-oriented, and often planned. It's rewarding to the child in some way, perhaps as a release from boredom. This type of aggression is seen when a child methodically injures animals or other children. It is the most difficult form of aggression to treat.

When contemplating a treatment plan, keep in mind that antisocial children want to know “what's in it for me?”

Therefore, concrete, reward-based therapy within a highly structured program makes sense.

One-on-one psychotherapy is rarely useful because these children “often don't have the ability to talk through problems internally,” said Dr. Lomax. Group therapy may be more helpful because these children may be sensitive to peer approval or disapproval.

Because their aggression may arise from a desire for stimulation, encourage time-consuming, prosocial activities such as organized sports, “where they can reinforce skills … and acquire skills they can feel good about.”

The Anxious Child

In sharp contrast to an antisocial child, aggression in a jittery child erupts as a fear reaction. Blowups in the morning before school represent avoidant behavior. These children may have an anxiety disorder, posttraumatic stress disorder, depression, or, rarely, psychosis. Treatment of the psychosis may reduce the high level of arousal that leads to aggressive behavior, Dr. Lomax said.

The Rigid Child

“These kids want things their way or no way,” she explained.

They may become infuriated at having to leave the computer to come to dinner.

“They think they're picked on, that there's no justice,” she said.

Rigid children “habitually misinterpret cues” from parents, teachers, and peers. As a result, they fly off the handle in anger.

Associated diagnoses may include oppositional defiant disorder, the autism spectrum, obsessive-compulsive disorder (when anger arises from interference with rituals), and nonverbal learning disabilities.

Their temperaments tend to be inflexible and stubborn.

The Impulsive Child

Frontal lobe dysfunction plays a role in the aggression of a child who becomes very angry very fast and cannot self-calm.

Beyond their inability to inhibit their impulses, “These children have a hard time planning or envisioning consequences,” said Dr. Lomax.

Possibly associated diagnoses might include ADHD, fetal alcohol syndrome, brain injury, or substance abuse.

The Dysregulated Child

Irritability, agitation, volatility, and mood instability underlie aggression in dysregulated children. Developmental or genetic issues should be explored.

For example, dysregulated aggression is common in children who experienced few nurturing, calming experiences in the first years of life.

Dysregulation may be an early sign of bipolar disorder, even if classic adult signs of euphoria and grandiosity are not present. In children, aggression and sleeplessness may alternate with depression and lethargy in a pattern of rapid cycling.

The Abused or Traumatized Child

Aggressive behaviors in such children make sense within the context of their lives, since the “fight” response to a survival threat naturally requires quick and decisive action.

“Their autonomic system is on overdrive. They become panicked if someone tries to control them,” said Dr. Lomax.

They are hypervigilant, distrustful, and show diminished cognition and a loss of impulse control when they perceive a threat.

Seemingly “minor” events may precipitate catastrophic reactions in these children, she said.

Children Whose Lives Are in Flux

It is also important to remember that aggression may be symptomatic of a situational upheaval in a child's life: a parent's divorce, for example, or a serious illness.

Consider, too, the family context in which aggression occurs.

Aggression may be a learned behavior, modeled by parents with their own history of violence and/or Axis I diagnoses.

Be forewarned: Parents may take “deep and grievous offense” at the notion that the family dynamic may be a contributor to the child's aggressive behavior. Dr. Lomax suggested a careful assessment of whether they are intellectually capable of insight and stable enough to accept suggestions about how to learn and practice anger management and training in parenting skills such as boundary and limit setting.

Sometimes, it may be necessary to go outside the immediately family for help, to grandparents or spouse equivalents, she said.

Psychoeducation, enhancing attachment, marital therapy, and parent support groups are all helpful adjuncts for parents of aggressive children.

“These families are often held hostage to their child's behavior,” Dr. Lomax said.

The treatment of a child with impulsive or affective aggression may be successful in one-on-one sessions or in group therapy. Principles include anxiety management, correction of cognitive distortions, assertiveness training, impulse control strategies, stress reduction, and, if applicable, therapy to address trauma.

In extreme cases, medications may be both necessary and helpful.

Treat any primary psychiatric disorder first, then consider risperidone in very low doses (0.5–2 mg/day), a mood stabilizer if the child is irritable and volatile, or a β-blocker in the context of hyperarousal, Dr. Lomax said.

She cautioned that antidepressants can sometimes have activating effects that exacerbate aggression in some children.

Lorazepam should be avoided for this reason in aggressive children, and children prescribed other antidepressants should be monitored very closely early in therapy for signs of akathisia, sleep problems, and “rage reactions” out of character for the child.

Questions That Should Be Asked

▸ When did the behavior start? What was the context? What is the child's age?

▸ Is the child capable of empathy and/or real regret? Does he or she laugh when confronted with the consequences of the aggressive behavior?

▸ Is the aggressive behavior situation specific?

▸ How is the child's general tolerance for frustration? (Is this a rigid child?)

▸ Has the child had a traumatic experience? Was he/she nurtured early in life?

▸ Do other children in the family have problems with aggression?

▸ How readily does the child adjust to changes in routine?

Source: Dr. Lomax

LOS ANGELES– Acute confusional migraines in children and adolescents are most common in young boys and are often associated with head trauma, Dr. A. David Rothner reported at the annual scientific meeting of the American Headache Society.

A review of 90 cases–22 from the Cleveland Clinic and 68 from a literature review–portrayed clear patterns of symptoms that may appear alarming to pediatricians and emergency department physicians. Confusion lasted from 10 minutes to 2 days, with the majority of patients remaining confused for 4 hours or less, but 25 (28%) were confused for 5 to 8 hours.

Not all children described headache, but some were so confused they were unable to communicate information about their symptoms. All were disoriented, 72 had amnesia, 63 had speech impairment, 49 had agitation, 49 had emesis, 36 had visual disturbances, and 33 had somnolence.

Notably, 74 children had a family history of migraine, and 52 had a personal history of migraine.

Acute confusional migraines were recurrent in more than a third of patients.

Boys aged 5–12 years, followed by boys aged 13–17 years, were most often affected. Proximal head trauma, often very mild, was present in more than a third of cases.

“When we're talking about confusion, for the most part we're not talking about a little bit of confusion,” said Dr. Rothner, a pediatric neurologist and director of the Pediatric/Adolescent Headache Clinic at the Cleveland Clinic.

As an example, he described the case of a 14-year-old girl who experienced an aura followed by a bifrontal headache and a 5-hour period of progressive disorientation, confusion, incontinence, bizarre behavior, and extreme combativeness that included kicking, screaming, scratching, and attempting to bite medical personnel. She was unresponsive to benzodiazepines. Once the confusion passed, the patient had no recollection of these events.

Her parents recalled two previous episodes that were less severe and involved nausea and vomiting. “There seems to be something special about this group of patients that predisposes them to recurrent attacks of a very, very unusual phenomenon,” Dr. Rothner noted.

Toxicology screens in 76 patients were all negative, as were examinations of cerebrospinal fluid in 29. Computed tomography or MRI in 63 patients was normal in 57 and showed unrelated abnormalities in 6. Electroencephalograms were performed in 55 patients and were abnormal in 44, with the majority showing unilateral or bilateral slowing.

“The differential diagnosis can be the most difficult and problematic issue,” Dr. Rothner explained. “If there is any doubt regarding the condition, transportation to an emergency room or trauma center is wise.”

In the short term, “Care must be taken to make sure that one does not overlook a more ominous problem, like an epidural or subdural hematoma,” he said in an interview following the meeting.

A careful description of the injury may be helpful in ruling out concussion. “Concussion often but not always involves a bigger hit and often but not always, immediate loss of consciousness,” he said.

In these cases, mild trauma often occurred quite some time before the development of migraine-like symptoms, and then confusion. Visual disturbances were much more prevalent in patients with acute confusional migraine than in children with typical migraines.

Until the etiology is known, he cautioned against sedating patients, although he acknowledged that the agitation and confusion can be difficult to manage. Dr. Rothner also hesitates to prescribe triptans in the presence of a neurologic deficit.

Providing pain relief and antiemetics are key in the acute setting, and patients and families should be counseled about the high rate of recurrence of acute confusional migraine.

LOS ANGELES– Acute confusional migraines in children and adolescents are most common in young boys and are often associated with head trauma, Dr. A. David Rothner reported at the annual scientific meeting of the American Headache Society.

A review of 90 cases–22 from the Cleveland Clinic and 68 from a literature review–portrayed clear patterns of symptoms that may appear alarming to pediatricians and emergency department physicians. Confusion lasted from 10 minutes to 2 days, with the majority of patients remaining confused for 4 hours or less, but 25 (28%) were confused for 5 to 8 hours.

Not all children described headache, but some were so confused they were unable to communicate information about their symptoms. All were disoriented, 72 had amnesia, 63 had speech impairment, 49 had agitation, 49 had emesis, 36 had visual disturbances, and 33 had somnolence.

Notably, 74 children had a family history of migraine, and 52 had a personal history of migraine.

Acute confusional migraines were recurrent in more than a third of patients.

Boys aged 5–12 years, followed by boys aged 13–17 years, were most often affected. Proximal head trauma, often very mild, was present in more than a third of cases.

“When we're talking about confusion, for the most part we're not talking about a little bit of confusion,” said Dr. Rothner, a pediatric neurologist and director of the Pediatric/Adolescent Headache Clinic at the Cleveland Clinic.

As an example, he described the case of a 14-year-old girl who experienced an aura followed by a bifrontal headache and a 5-hour period of progressive disorientation, confusion, incontinence, bizarre behavior, and extreme combativeness that included kicking, screaming, scratching, and attempting to bite medical personnel. She was unresponsive to benzodiazepines. Once the confusion passed, the patient had no recollection of these events.

Her parents recalled two previous episodes that were less severe and involved nausea and vomiting. “There seems to be something special about this group of patients that predisposes them to recurrent attacks of a very, very unusual phenomenon,” Dr. Rothner noted.

Toxicology screens in 76 patients were all negative, as were examinations of cerebrospinal fluid in 29. Computed tomography or MRI in 63 patients was normal in 57 and showed unrelated abnormalities in 6. Electroencephalograms were performed in 55 patients and were abnormal in 44, with the majority showing unilateral or bilateral slowing.

“The differential diagnosis can be the most difficult and problematic issue,” Dr. Rothner explained. “If there is any doubt regarding the condition, transportation to an emergency room or trauma center is wise.”

In the short term, “Care must be taken to make sure that one does not overlook a more ominous problem, like an epidural or subdural hematoma,” he said in an interview following the meeting.

A careful description of the injury may be helpful in ruling out concussion. “Concussion often but not always involves a bigger hit and often but not always, immediate loss of consciousness,” he said.

In these cases, mild trauma often occurred quite some time before the development of migraine-like symptoms, and then confusion. Visual disturbances were much more prevalent in patients with acute confusional migraine than in children with typical migraines.

Until the etiology is known, he cautioned against sedating patients, although he acknowledged that the agitation and confusion can be difficult to manage. Dr. Rothner also hesitates to prescribe triptans in the presence of a neurologic deficit.

Providing pain relief and antiemetics are key in the acute setting, and patients and families should be counseled about the high rate of recurrence of acute confusional migraine.

LOS ANGELES– Acute confusional migraines in children and adolescents are most common in young boys and are often associated with head trauma, Dr. A. David Rothner reported at the annual scientific meeting of the American Headache Society.

A review of 90 cases–22 from the Cleveland Clinic and 68 from a literature review–portrayed clear patterns of symptoms that may appear alarming to pediatricians and emergency department physicians. Confusion lasted from 10 minutes to 2 days, with the majority of patients remaining confused for 4 hours or less, but 25 (28%) were confused for 5 to 8 hours.

Not all children described headache, but some were so confused they were unable to communicate information about their symptoms. All were disoriented, 72 had amnesia, 63 had speech impairment, 49 had agitation, 49 had emesis, 36 had visual disturbances, and 33 had somnolence.

Notably, 74 children had a family history of migraine, and 52 had a personal history of migraine.

Acute confusional migraines were recurrent in more than a third of patients.

Boys aged 5–12 years, followed by boys aged 13–17 years, were most often affected. Proximal head trauma, often very mild, was present in more than a third of cases.

“When we're talking about confusion, for the most part we're not talking about a little bit of confusion,” said Dr. Rothner, a pediatric neurologist and director of the Pediatric/Adolescent Headache Clinic at the Cleveland Clinic.

As an example, he described the case of a 14-year-old girl who experienced an aura followed by a bifrontal headache and a 5-hour period of progressive disorientation, confusion, incontinence, bizarre behavior, and extreme combativeness that included kicking, screaming, scratching, and attempting to bite medical personnel. She was unresponsive to benzodiazepines. Once the confusion passed, the patient had no recollection of these events.

Her parents recalled two previous episodes that were less severe and involved nausea and vomiting. “There seems to be something special about this group of patients that predisposes them to recurrent attacks of a very, very unusual phenomenon,” Dr. Rothner noted.

Toxicology screens in 76 patients were all negative, as were examinations of cerebrospinal fluid in 29. Computed tomography or MRI in 63 patients was normal in 57 and showed unrelated abnormalities in 6. Electroencephalograms were performed in 55 patients and were abnormal in 44, with the majority showing unilateral or bilateral slowing.

“The differential diagnosis can be the most difficult and problematic issue,” Dr. Rothner explained. “If there is any doubt regarding the condition, transportation to an emergency room or trauma center is wise.”

In the short term, “Care must be taken to make sure that one does not overlook a more ominous problem, like an epidural or subdural hematoma,” he said in an interview following the meeting.

A careful description of the injury may be helpful in ruling out concussion. “Concussion often but not always involves a bigger hit and often but not always, immediate loss of consciousness,” he said.

In these cases, mild trauma often occurred quite some time before the development of migraine-like symptoms, and then confusion. Visual disturbances were much more prevalent in patients with acute confusional migraine than in children with typical migraines.

Until the etiology is known, he cautioned against sedating patients, although he acknowledged that the agitation and confusion can be difficult to manage. Dr. Rothner also hesitates to prescribe triptans in the presence of a neurologic deficit.

Providing pain relief and antiemetics are key in the acute setting, and patients and families should be counseled about the high rate of recurrence of acute confusional migraine.

LOS ANGELES — Migraine headaches were twice as likely during the menstrual cycle, and menstrual migraines lasted longer, were somewhat more painful, and proved significantly more resistant to treatment than migraines suffered during other times of the month, according to a study released at the annual meeting of the American Headache Society.

Dr. Brenda F. Pinkerman of the James A. Haley Veterans' Hospital in Tampa, Fla., reported a sharp spike in migraines on day 1 of the menstrual cycle in a prospective study of 107 women with a history of menstrual-related migraine.

The women were subjects in a larger study cosponsored by Ohio University in Athens and the National Institutes of Health. To be eligible, patients had to have a history of disabling migraines 3–20 days a month. Those enrolled in the menstrual migraine portion of the study had a mean age of 35 and suffered from migraines a mean 9 days per month.

The odds ratio of a migraine was 1.91—almost a doubling of risk—in a 4-day window beginning 2 days prior to and ending 2 days after day 1 of the menstrual cycle, compared with any other time of the month.

Perimenstrual migraines were significantly different from those occurring at other times of the month in a few ways, including the following:

▸ Duration: 23 hours, compared with 16 hours.

▸ Disability: occurs in conjunction with 86% of menstrual headaches vs. 76% of other headaches.

▸ Doses of triptans: two vs. 1.6; and rescue medications: 2.3 vs. 1.7.

▸ Pain-free response to medication at 2 hours: 7% vs. 13%.

▸ Recurrence after 4 pain-free hours: 36%, compared with 20%.

Other poster presentations at the meeting detailed the efficacy of rizatriptan administered early in the course of menstrual migraines and the safety and tolerability of frovatriptan taken prophylactically each month in women with regular menstrual cycles.

The TAME (Treat a Migraine Early) trials randomized 94 patients to take a single 10-mg dose of rizatriptan or placebo within 1 hour of the onset of any migraine occurring during the 2 days before to 3 days following day 1 of their menstrual cycles.

Freedom from pain at 2 hours was reported by 40 of 63 subjects (63.5%) taking rizatriptan, compared with 9 of 31 (29%) assigned to placebo, a highly significant difference. Nausea was significantly less common in subjects taking rizatriptan, although photophobia and phonophobia responses did not reach significance in the Merck-sponsored, multicenter study presented by Dr. Vincent Martin of the University of Cincinnati.

A final poster featured results from a yearlong, open-label extension study of frovatriptan used to prevent migraines in 308 patients with regular menstrual cycles and a history of menstrual migraine. Women were instructed to take two 5-mg doses of frovatriptan 2 days before the expected onset of menstruation, followed by 2.5 mg of frovatriptan twice daily for the next 5 days.

Dizziness, the most common side effect, occurred in about 7% of patients. The drug was well tolerated, with just 25 patients discontinuing long-term treatment for reasons other than migraine, reported Dr. Anne MacGregor of the City of London Migraine Clinic.

Perimenstrual migraines occurred in 44% of women taking prophylactic frovatriptan for a year—on par with the 41% who experienced perimenstrual migraines during a 3-month randomized, double-blind, placebo-controlled trial of 433 patients. In that pivotal study, 67% patients assigned to placebo experienced migraines.

The consistency of incidence data in the two trials suggests “durability of effect with continued use,” Dr. MacGregor and associates noted in their poster's conclusion. “In addition, there was no evidence of rebound migraine.”

The study was sponsored by Endo Pharmaceuticals of Chadds Ford, Pa., manufacturer of frovatriptan.

LOS ANGELES — Migraine headaches were twice as likely during the menstrual cycle, and menstrual migraines lasted longer, were somewhat more painful, and proved significantly more resistant to treatment than migraines suffered during other times of the month, according to a study released at the annual meeting of the American Headache Society.

Dr. Brenda F. Pinkerman of the James A. Haley Veterans' Hospital in Tampa, Fla., reported a sharp spike in migraines on day 1 of the menstrual cycle in a prospective study of 107 women with a history of menstrual-related migraine.

The women were subjects in a larger study cosponsored by Ohio University in Athens and the National Institutes of Health. To be eligible, patients had to have a history of disabling migraines 3–20 days a month. Those enrolled in the menstrual migraine portion of the study had a mean age of 35 and suffered from migraines a mean 9 days per month.

The odds ratio of a migraine was 1.91—almost a doubling of risk—in a 4-day window beginning 2 days prior to and ending 2 days after day 1 of the menstrual cycle, compared with any other time of the month.

Perimenstrual migraines were significantly different from those occurring at other times of the month in a few ways, including the following:

▸ Duration: 23 hours, compared with 16 hours.

▸ Disability: occurs in conjunction with 86% of menstrual headaches vs. 76% of other headaches.

▸ Doses of triptans: two vs. 1.6; and rescue medications: 2.3 vs. 1.7.

▸ Pain-free response to medication at 2 hours: 7% vs. 13%.

▸ Recurrence after 4 pain-free hours: 36%, compared with 20%.

Other poster presentations at the meeting detailed the efficacy of rizatriptan administered early in the course of menstrual migraines and the safety and tolerability of frovatriptan taken prophylactically each month in women with regular menstrual cycles.

The TAME (Treat a Migraine Early) trials randomized 94 patients to take a single 10-mg dose of rizatriptan or placebo within 1 hour of the onset of any migraine occurring during the 2 days before to 3 days following day 1 of their menstrual cycles.

Freedom from pain at 2 hours was reported by 40 of 63 subjects (63.5%) taking rizatriptan, compared with 9 of 31 (29%) assigned to placebo, a highly significant difference. Nausea was significantly less common in subjects taking rizatriptan, although photophobia and phonophobia responses did not reach significance in the Merck-sponsored, multicenter study presented by Dr. Vincent Martin of the University of Cincinnati.

A final poster featured results from a yearlong, open-label extension study of frovatriptan used to prevent migraines in 308 patients with regular menstrual cycles and a history of menstrual migraine. Women were instructed to take two 5-mg doses of frovatriptan 2 days before the expected onset of menstruation, followed by 2.5 mg of frovatriptan twice daily for the next 5 days.

Dizziness, the most common side effect, occurred in about 7% of patients. The drug was well tolerated, with just 25 patients discontinuing long-term treatment for reasons other than migraine, reported Dr. Anne MacGregor of the City of London Migraine Clinic.

Perimenstrual migraines occurred in 44% of women taking prophylactic frovatriptan for a year—on par with the 41% who experienced perimenstrual migraines during a 3-month randomized, double-blind, placebo-controlled trial of 433 patients. In that pivotal study, 67% patients assigned to placebo experienced migraines.

The consistency of incidence data in the two trials suggests “durability of effect with continued use,” Dr. MacGregor and associates noted in their poster's conclusion. “In addition, there was no evidence of rebound migraine.”

The study was sponsored by Endo Pharmaceuticals of Chadds Ford, Pa., manufacturer of frovatriptan.

LOS ANGELES — Migraine headaches were twice as likely during the menstrual cycle, and menstrual migraines lasted longer, were somewhat more painful, and proved significantly more resistant to treatment than migraines suffered during other times of the month, according to a study released at the annual meeting of the American Headache Society.

Dr. Brenda F. Pinkerman of the James A. Haley Veterans' Hospital in Tampa, Fla., reported a sharp spike in migraines on day 1 of the menstrual cycle in a prospective study of 107 women with a history of menstrual-related migraine.

The women were subjects in a larger study cosponsored by Ohio University in Athens and the National Institutes of Health. To be eligible, patients had to have a history of disabling migraines 3–20 days a month. Those enrolled in the menstrual migraine portion of the study had a mean age of 35 and suffered from migraines a mean 9 days per month.

The odds ratio of a migraine was 1.91—almost a doubling of risk—in a 4-day window beginning 2 days prior to and ending 2 days after day 1 of the menstrual cycle, compared with any other time of the month.

Perimenstrual migraines were significantly different from those occurring at other times of the month in a few ways, including the following:

▸ Duration: 23 hours, compared with 16 hours.

▸ Disability: occurs in conjunction with 86% of menstrual headaches vs. 76% of other headaches.

▸ Doses of triptans: two vs. 1.6; and rescue medications: 2.3 vs. 1.7.

▸ Pain-free response to medication at 2 hours: 7% vs. 13%.

▸ Recurrence after 4 pain-free hours: 36%, compared with 20%.

Other poster presentations at the meeting detailed the efficacy of rizatriptan administered early in the course of menstrual migraines and the safety and tolerability of frovatriptan taken prophylactically each month in women with regular menstrual cycles.

The TAME (Treat a Migraine Early) trials randomized 94 patients to take a single 10-mg dose of rizatriptan or placebo within 1 hour of the onset of any migraine occurring during the 2 days before to 3 days following day 1 of their menstrual cycles.

Freedom from pain at 2 hours was reported by 40 of 63 subjects (63.5%) taking rizatriptan, compared with 9 of 31 (29%) assigned to placebo, a highly significant difference. Nausea was significantly less common in subjects taking rizatriptan, although photophobia and phonophobia responses did not reach significance in the Merck-sponsored, multicenter study presented by Dr. Vincent Martin of the University of Cincinnati.

A final poster featured results from a yearlong, open-label extension study of frovatriptan used to prevent migraines in 308 patients with regular menstrual cycles and a history of menstrual migraine. Women were instructed to take two 5-mg doses of frovatriptan 2 days before the expected onset of menstruation, followed by 2.5 mg of frovatriptan twice daily for the next 5 days.

Dizziness, the most common side effect, occurred in about 7% of patients. The drug was well tolerated, with just 25 patients discontinuing long-term treatment for reasons other than migraine, reported Dr. Anne MacGregor of the City of London Migraine Clinic.

Perimenstrual migraines occurred in 44% of women taking prophylactic frovatriptan for a year—on par with the 41% who experienced perimenstrual migraines during a 3-month randomized, double-blind, placebo-controlled trial of 433 patients. In that pivotal study, 67% patients assigned to placebo experienced migraines.

The consistency of incidence data in the two trials suggests “durability of effect with continued use,” Dr. MacGregor and associates noted in their poster's conclusion. “In addition, there was no evidence of rebound migraine.”

The study was sponsored by Endo Pharmaceuticals of Chadds Ford, Pa., manufacturer of frovatriptan.

SAN FRANCISCO — Pigmented lesions revealed few clues as to their true histologic identities in a 5-year retrospective study, Dr. Roland M. Strauss said in a poster presentation at the annual meeting of the American Academy of Dermatology.

Of 434 excised lesions, nearly half proved to be benign melanocytic nevi, but more than 100 were invasive melanomas or displayed severely dysplastic features or in situ melanoma.

Telling the difference proved difficult, even for specialists at a pigmented lesion clinic at Leeds (England) General Infirmary. The best predictors of melanoma in the study were older patient age, larger lesion diameter, blue or blue-gray lesion hue, and male sex, said Dr. Strauss of the infirmary.

Only advanced age was predictive of severe histologic dysplasia or in situ melanoma vs. nevi with mild to moderate atypia, he said in his poster presentation.

“Our results confirm the difficulty experienced by dermatologists in distinguishing atypical nevi with mild to moderate histologic atypia from those with severe histologic dysplasia or melanoma in situ,” Dr. Strauss wrote. “In order not to miss any lesions with severe dysplasia/melanoma in situ, the excision of a number of benign lesions with only mild to moderate dysplastic features will therefore have to be accepted,” he suggested.

SAN FRANCISCO — Pigmented lesions revealed few clues as to their true histologic identities in a 5-year retrospective study, Dr. Roland M. Strauss said in a poster presentation at the annual meeting of the American Academy of Dermatology.

Of 434 excised lesions, nearly half proved to be benign melanocytic nevi, but more than 100 were invasive melanomas or displayed severely dysplastic features or in situ melanoma.

Telling the difference proved difficult, even for specialists at a pigmented lesion clinic at Leeds (England) General Infirmary. The best predictors of melanoma in the study were older patient age, larger lesion diameter, blue or blue-gray lesion hue, and male sex, said Dr. Strauss of the infirmary.

Only advanced age was predictive of severe histologic dysplasia or in situ melanoma vs. nevi with mild to moderate atypia, he said in his poster presentation.

“Our results confirm the difficulty experienced by dermatologists in distinguishing atypical nevi with mild to moderate histologic atypia from those with severe histologic dysplasia or melanoma in situ,” Dr. Strauss wrote. “In order not to miss any lesions with severe dysplasia/melanoma in situ, the excision of a number of benign lesions with only mild to moderate dysplastic features will therefore have to be accepted,” he suggested.

SAN FRANCISCO — Pigmented lesions revealed few clues as to their true histologic identities in a 5-year retrospective study, Dr. Roland M. Strauss said in a poster presentation at the annual meeting of the American Academy of Dermatology.

Of 434 excised lesions, nearly half proved to be benign melanocytic nevi, but more than 100 were invasive melanomas or displayed severely dysplastic features or in situ melanoma.

Telling the difference proved difficult, even for specialists at a pigmented lesion clinic at Leeds (England) General Infirmary. The best predictors of melanoma in the study were older patient age, larger lesion diameter, blue or blue-gray lesion hue, and male sex, said Dr. Strauss of the infirmary.

Only advanced age was predictive of severe histologic dysplasia or in situ melanoma vs. nevi with mild to moderate atypia, he said in his poster presentation.

“Our results confirm the difficulty experienced by dermatologists in distinguishing atypical nevi with mild to moderate histologic atypia from those with severe histologic dysplasia or melanoma in situ,” Dr. Strauss wrote. “In order not to miss any lesions with severe dysplasia/melanoma in situ, the excision of a number of benign lesions with only mild to moderate dysplastic features will therefore have to be accepted,” he suggested.

PORTLAND, ORE. — A broad and diverse group of foods contains nickel, and consumption of these foods has the potential to exacerbate allergic contact dermatitis, particularly in patients receiving more than one exposure per day, Dr. David E. Cohen said at the annual meeting of the Pacific Northwest Dermatological Society.

It's no surprise that items such as jewelry or jeans snaps might be a problem in patients with allergic contact dermatitis, since these are well-known sources of nickel that come into contact with the skin.

But edamame? It's true. The green soybean snacks contain enough naturally occurring nickel—nearly 0.9 mg per serving—to have the potential of leading to systemic contact dermitis in up to 10% of nickel-sensitive patients, said Dr. Cohen, director of allergic, occupational, and contact dermatitis at New York University.

The normal dietary intake of nickel ranges from 0.02 mg to 0.48 mg/day, and the Food and Drug Administration has set 50 mcg as the tolerable upper intake level recommended in nickel allergic adults. Still, certain foods, including soybeans, cashews, lentils, figs, and raspberries, have high nickel content and could cause a flare in allergic patients. (See chart.)

Sometimes the allergen source in foods is even more subtle, noted Dr. Cohen, who conducted a study of three types of tomatoes to identify natural fragrances that might explain their proclivity to produce systemic contact allergy reactions in certain patients (Dermatitis 2005;16:91–100).

Several potent constituents of the well-known allergen balsam of Peru, including cinnamic acid, and coniferyl alcohol were detected in various quantities in beefsteak, cherry, and plum tomatoes, he said.

“These reactions can look quite banal and don't have any particular distribution to clue in the evaluating [physician],” Dr. Cohen said during an interview following the meeting.

When the cause of the flares is uncertain and seems to point to foods, Dr. Cohen recommends eliminating all foods containing the suspected allergen for 3 weeks. “Then [tell them to] eat a ton of whatever they miss most,” he said. If a flare ensues, the culprit food may be unmasked.

YENLING LIU, DESIGNER/ELSEVIER GLOBAL MEDICAL NEWS

'These reactions can look quite banal and don't have any particular distribution to clue in the evaluating [physician].' DR. COHEN

PORTLAND, ORE. — A broad and diverse group of foods contains nickel, and consumption of these foods has the potential to exacerbate allergic contact dermatitis, particularly in patients receiving more than one exposure per day, Dr. David E. Cohen said at the annual meeting of the Pacific Northwest Dermatological Society.

It's no surprise that items such as jewelry or jeans snaps might be a problem in patients with allergic contact dermatitis, since these are well-known sources of nickel that come into contact with the skin.

But edamame? It's true. The green soybean snacks contain enough naturally occurring nickel—nearly 0.9 mg per serving—to have the potential of leading to systemic contact dermitis in up to 10% of nickel-sensitive patients, said Dr. Cohen, director of allergic, occupational, and contact dermatitis at New York University.

The normal dietary intake of nickel ranges from 0.02 mg to 0.48 mg/day, and the Food and Drug Administration has set 50 mcg as the tolerable upper intake level recommended in nickel allergic adults. Still, certain foods, including soybeans, cashews, lentils, figs, and raspberries, have high nickel content and could cause a flare in allergic patients. (See chart.)

Sometimes the allergen source in foods is even more subtle, noted Dr. Cohen, who conducted a study of three types of tomatoes to identify natural fragrances that might explain their proclivity to produce systemic contact allergy reactions in certain patients (Dermatitis 2005;16:91–100).

Several potent constituents of the well-known allergen balsam of Peru, including cinnamic acid, and coniferyl alcohol were detected in various quantities in beefsteak, cherry, and plum tomatoes, he said.

“These reactions can look quite banal and don't have any particular distribution to clue in the evaluating [physician],” Dr. Cohen said during an interview following the meeting.

When the cause of the flares is uncertain and seems to point to foods, Dr. Cohen recommends eliminating all foods containing the suspected allergen for 3 weeks. “Then [tell them to] eat a ton of whatever they miss most,” he said. If a flare ensues, the culprit food may be unmasked.

YENLING LIU, DESIGNER/ELSEVIER GLOBAL MEDICAL NEWS

'These reactions can look quite banal and don't have any particular distribution to clue in the evaluating [physician].' DR. COHEN

PORTLAND, ORE. — A broad and diverse group of foods contains nickel, and consumption of these foods has the potential to exacerbate allergic contact dermatitis, particularly in patients receiving more than one exposure per day, Dr. David E. Cohen said at the annual meeting of the Pacific Northwest Dermatological Society.

It's no surprise that items such as jewelry or jeans snaps might be a problem in patients with allergic contact dermatitis, since these are well-known sources of nickel that come into contact with the skin.

But edamame? It's true. The green soybean snacks contain enough naturally occurring nickel—nearly 0.9 mg per serving—to have the potential of leading to systemic contact dermitis in up to 10% of nickel-sensitive patients, said Dr. Cohen, director of allergic, occupational, and contact dermatitis at New York University.

The normal dietary intake of nickel ranges from 0.02 mg to 0.48 mg/day, and the Food and Drug Administration has set 50 mcg as the tolerable upper intake level recommended in nickel allergic adults. Still, certain foods, including soybeans, cashews, lentils, figs, and raspberries, have high nickel content and could cause a flare in allergic patients. (See chart.)

Sometimes the allergen source in foods is even more subtle, noted Dr. Cohen, who conducted a study of three types of tomatoes to identify natural fragrances that might explain their proclivity to produce systemic contact allergy reactions in certain patients (Dermatitis 2005;16:91–100).

Several potent constituents of the well-known allergen balsam of Peru, including cinnamic acid, and coniferyl alcohol were detected in various quantities in beefsteak, cherry, and plum tomatoes, he said.

“These reactions can look quite banal and don't have any particular distribution to clue in the evaluating [physician],” Dr. Cohen said during an interview following the meeting.

When the cause of the flares is uncertain and seems to point to foods, Dr. Cohen recommends eliminating all foods containing the suspected allergen for 3 weeks. “Then [tell them to] eat a ton of whatever they miss most,” he said. If a flare ensues, the culprit food may be unmasked.

YENLING LIU, DESIGNER/ELSEVIER GLOBAL MEDICAL NEWS

'These reactions can look quite banal and don't have any particular distribution to clue in the evaluating [physician].' DR. COHEN

TUCSON, ARIZ. — A randomized crossover trial suggests that symptom relief and satisfaction can be obtained with either of two commonly used pessary types, but that patient selection and patience are both key to success.

The multicenter study enrolled 134 women ages 30–89 (mean age 61) with symptomatic pelvic organ prolapse. They were randomized to be fitted with one of two types of pessary and to wear it, if possible, for 3 months before being switched to the other pessary design for 3 months. Subjects could discontinue using either pessary at any time.

Only 62 of 134 subjects stayed in the study long enough to complete satisfaction scores on both types of pessaries and of those, just 22 were highly satisfied with both. “Some could not be fitted. Some did not like pessaries. Some had had enough of pessaries after one trial,” said Dr. Geoffrey W. Cundiff, professor of obstetrics and gynecology at Johns Hopkins School of Medicine in Baltimore.

Surprisingly, younger women were far less likely to complete the trial comparing a ring pessary with support and a gellhorn pessary, reported Dr. Cundiff at the annual meeting of the Society of Gynecologic Surgeons.

Satisfaction rates were similar for the two pessary types, but there was a clear difference in the types of patients who preferred each design. The 36 women who reported high satisfaction with the ring pessary were older and had weaker pelvic floor muscles. They were more likely to be nonwhite and to be more parous than those who preferred the gellhorn pessary.

Meanwhile, the 39 women who strongly preferred the gellhorn pessary were more likely to have anterior wall prolapse and less likely to have had a hysterectomy or prior prolapse surgery.

Refusal to wear a pessary for 3 months was significantly more common among younger women (mean age 57, compared with 66) and nonwhite women. The nine subjects who wore the pessaries but were dissatisfied with both were more likely to be white, have a history of prior prolapse surgery, and have stage II prolapse.

A subanalysis of the data showed that patients who wore either pessary for 3 months experienced a significant reduction in lower urinary tract symptoms, particularly obstructive symptoms.

Among 97 patients who completed the Pelvic Floor Distress Inventory, no differences were seen in symptomatic relief offered by the ring or gellhorn pessaries, reported Dr. Joseph I. Schaffer, chief of gynecology at the University of Texas Southwestern Medical Center in Dallas.

Scores on the Obstructive/Discomfort subscale declined from a mean 20.32 at baseline to 8.61. Irritative subscale scores declined from a baseline mean of 15.85 to 10, and Stress subscale scores declined from 15.55 at baseline to 12.24.

On another measure, the Urinary Distress Inventory, scores improved from a baseline mean of 51.31 to 31.45.

“This study challenges common beliefs about pessaries,” said Dr. Cundiff, and audience members agreed. One attendee, Dr. Marc Toglia of Philadelphia, admitted the results “challenge my belief system.”

Both physicians acknowledged their surprise that so many women would find the gellhorn pessary preferable to a ring pessary.

A formal discussant on the study, Dr. Deborah Myers of Brown University School of Medicine in Providence, R.I., noted that a third of the patients required refitting of a pessary. “This is important information for patients and physicians,” she said. “Don't give up on the first try.”

The 39 women who strongly preferred the gellhorn pessary were more likely to have anterior wall prolapse. DR. CUNDIFF

TUCSON, ARIZ. — A randomized crossover trial suggests that symptom relief and satisfaction can be obtained with either of two commonly used pessary types, but that patient selection and patience are both key to success.

The multicenter study enrolled 134 women ages 30–89 (mean age 61) with symptomatic pelvic organ prolapse. They were randomized to be fitted with one of two types of pessary and to wear it, if possible, for 3 months before being switched to the other pessary design for 3 months. Subjects could discontinue using either pessary at any time.

Only 62 of 134 subjects stayed in the study long enough to complete satisfaction scores on both types of pessaries and of those, just 22 were highly satisfied with both. “Some could not be fitted. Some did not like pessaries. Some had had enough of pessaries after one trial,” said Dr. Geoffrey W. Cundiff, professor of obstetrics and gynecology at Johns Hopkins School of Medicine in Baltimore.

Surprisingly, younger women were far less likely to complete the trial comparing a ring pessary with support and a gellhorn pessary, reported Dr. Cundiff at the annual meeting of the Society of Gynecologic Surgeons.

Satisfaction rates were similar for the two pessary types, but there was a clear difference in the types of patients who preferred each design. The 36 women who reported high satisfaction with the ring pessary were older and had weaker pelvic floor muscles. They were more likely to be nonwhite and to be more parous than those who preferred the gellhorn pessary.

Meanwhile, the 39 women who strongly preferred the gellhorn pessary were more likely to have anterior wall prolapse and less likely to have had a hysterectomy or prior prolapse surgery.

Refusal to wear a pessary for 3 months was significantly more common among younger women (mean age 57, compared with 66) and nonwhite women. The nine subjects who wore the pessaries but were dissatisfied with both were more likely to be white, have a history of prior prolapse surgery, and have stage II prolapse.

A subanalysis of the data showed that patients who wore either pessary for 3 months experienced a significant reduction in lower urinary tract symptoms, particularly obstructive symptoms.

Among 97 patients who completed the Pelvic Floor Distress Inventory, no differences were seen in symptomatic relief offered by the ring or gellhorn pessaries, reported Dr. Joseph I. Schaffer, chief of gynecology at the University of Texas Southwestern Medical Center in Dallas.

Scores on the Obstructive/Discomfort subscale declined from a mean 20.32 at baseline to 8.61. Irritative subscale scores declined from a baseline mean of 15.85 to 10, and Stress subscale scores declined from 15.55 at baseline to 12.24.

On another measure, the Urinary Distress Inventory, scores improved from a baseline mean of 51.31 to 31.45.

“This study challenges common beliefs about pessaries,” said Dr. Cundiff, and audience members agreed. One attendee, Dr. Marc Toglia of Philadelphia, admitted the results “challenge my belief system.”

Both physicians acknowledged their surprise that so many women would find the gellhorn pessary preferable to a ring pessary.

A formal discussant on the study, Dr. Deborah Myers of Brown University School of Medicine in Providence, R.I., noted that a third of the patients required refitting of a pessary. “This is important information for patients and physicians,” she said. “Don't give up on the first try.”

The 39 women who strongly preferred the gellhorn pessary were more likely to have anterior wall prolapse. DR. CUNDIFF

TUCSON, ARIZ. — A randomized crossover trial suggests that symptom relief and satisfaction can be obtained with either of two commonly used pessary types, but that patient selection and patience are both key to success.

The multicenter study enrolled 134 women ages 30–89 (mean age 61) with symptomatic pelvic organ prolapse. They were randomized to be fitted with one of two types of pessary and to wear it, if possible, for 3 months before being switched to the other pessary design for 3 months. Subjects could discontinue using either pessary at any time.

Only 62 of 134 subjects stayed in the study long enough to complete satisfaction scores on both types of pessaries and of those, just 22 were highly satisfied with both. “Some could not be fitted. Some did not like pessaries. Some had had enough of pessaries after one trial,” said Dr. Geoffrey W. Cundiff, professor of obstetrics and gynecology at Johns Hopkins School of Medicine in Baltimore.

Surprisingly, younger women were far less likely to complete the trial comparing a ring pessary with support and a gellhorn pessary, reported Dr. Cundiff at the annual meeting of the Society of Gynecologic Surgeons.

Satisfaction rates were similar for the two pessary types, but there was a clear difference in the types of patients who preferred each design. The 36 women who reported high satisfaction with the ring pessary were older and had weaker pelvic floor muscles. They were more likely to be nonwhite and to be more parous than those who preferred the gellhorn pessary.

Meanwhile, the 39 women who strongly preferred the gellhorn pessary were more likely to have anterior wall prolapse and less likely to have had a hysterectomy or prior prolapse surgery.

Refusal to wear a pessary for 3 months was significantly more common among younger women (mean age 57, compared with 66) and nonwhite women. The nine subjects who wore the pessaries but were dissatisfied with both were more likely to be white, have a history of prior prolapse surgery, and have stage II prolapse.

A subanalysis of the data showed that patients who wore either pessary for 3 months experienced a significant reduction in lower urinary tract symptoms, particularly obstructive symptoms.

Among 97 patients who completed the Pelvic Floor Distress Inventory, no differences were seen in symptomatic relief offered by the ring or gellhorn pessaries, reported Dr. Joseph I. Schaffer, chief of gynecology at the University of Texas Southwestern Medical Center in Dallas.

Scores on the Obstructive/Discomfort subscale declined from a mean 20.32 at baseline to 8.61. Irritative subscale scores declined from a baseline mean of 15.85 to 10, and Stress subscale scores declined from 15.55 at baseline to 12.24.

On another measure, the Urinary Distress Inventory, scores improved from a baseline mean of 51.31 to 31.45.

“This study challenges common beliefs about pessaries,” said Dr. Cundiff, and audience members agreed. One attendee, Dr. Marc Toglia of Philadelphia, admitted the results “challenge my belief system.”

Both physicians acknowledged their surprise that so many women would find the gellhorn pessary preferable to a ring pessary.

A formal discussant on the study, Dr. Deborah Myers of Brown University School of Medicine in Providence, R.I., noted that a third of the patients required refitting of a pessary. “This is important information for patients and physicians,” she said. “Don't give up on the first try.”

The 39 women who strongly preferred the gellhorn pessary were more likely to have anterior wall prolapse. DR. CUNDIFF

TUCSON, ARIZ. — A homemade stool-bulking agent was just as effective as commercial psyllium in relieving symptoms of constipation in a randomized trial conducted by researchers at the University of Texas Southwestern Medical Center in Dallas.

The recipe containing applesauce, unprocessed wheat bran, and prune juice cost about half as much as a commercial psyllium product, Konsyl, reported Dr. Peter Drewes and his associates from the medical center in a poster presented at the annual meeting of the Society of Gynecologic Surgeons.

Constipation is a problem for 4.5 million Americans, particularly older women, the authors noted. It is the primary reason for 2.5 million physician visits and drives the sale of $800 million in over-the-counter products each year.

Participants for the trial were drawn from patients presenting to the university's urogynecology clinic who met Rome II criteria for constipation (at least 12 weeks in the prior 12 months of at least two symptoms, including fewer than three defecations/week, straining, hard stools, and incomplete evacuation).

A total of 82 patients were randomized and 53 completed the 6-week study, including 30 randomized to take 1 teaspoon of psyllium in 8 ounces of liquid daily for 6 weeks or 4 tablespoons a day of the bowel recipe.

All of the participants received educational information on how dietary choices and fluids can influence constipation. They all kept bowel diaries.

Results were calculated using pre- and posttrial scores on a 30-point constipation scoring system, with a higher score indicating more severe constipation.

Constipation was relieved in both groups, with scores declining from 13.9 to 9.0 for the psyllium users and 13.6 to 8.5 for the recipe users during the 6-week trial.

The cost of 6 weeks' worth of the bowel recipe was $8.65, compared with $16.72 for the commercial psyllium product.

The authors of the poster concluded that the homemade recipe was “an effective and economical stool bulking agent for the treatment of constipation.”

ELSEVIER GLOBAL MEDICAL NEWS

The Pantry Solution

1 cup applesauce

1 cup coarse, unprocessed wheat bran

1/4 cup prune juice

Source: Dr. Drewes

TUCSON, ARIZ. — A homemade stool-bulking agent was just as effective as commercial psyllium in relieving symptoms of constipation in a randomized trial conducted by researchers at the University of Texas Southwestern Medical Center in Dallas.

The recipe containing applesauce, unprocessed wheat bran, and prune juice cost about half as much as a commercial psyllium product, Konsyl, reported Dr. Peter Drewes and his associates from the medical center in a poster presented at the annual meeting of the Society of Gynecologic Surgeons.

Constipation is a problem for 4.5 million Americans, particularly older women, the authors noted. It is the primary reason for 2.5 million physician visits and drives the sale of $800 million in over-the-counter products each year.

Participants for the trial were drawn from patients presenting to the university's urogynecology clinic who met Rome II criteria for constipation (at least 12 weeks in the prior 12 months of at least two symptoms, including fewer than three defecations/week, straining, hard stools, and incomplete evacuation).

A total of 82 patients were randomized and 53 completed the 6-week study, including 30 randomized to take 1 teaspoon of psyllium in 8 ounces of liquid daily for 6 weeks or 4 tablespoons a day of the bowel recipe.

All of the participants received educational information on how dietary choices and fluids can influence constipation. They all kept bowel diaries.

Results were calculated using pre- and posttrial scores on a 30-point constipation scoring system, with a higher score indicating more severe constipation.

Constipation was relieved in both groups, with scores declining from 13.9 to 9.0 for the psyllium users and 13.6 to 8.5 for the recipe users during the 6-week trial.

The cost of 6 weeks' worth of the bowel recipe was $8.65, compared with $16.72 for the commercial psyllium product.

The authors of the poster concluded that the homemade recipe was “an effective and economical stool bulking agent for the treatment of constipation.”

ELSEVIER GLOBAL MEDICAL NEWS

The Pantry Solution

1 cup applesauce

1 cup coarse, unprocessed wheat bran

1/4 cup prune juice

Source: Dr. Drewes

TUCSON, ARIZ. — A homemade stool-bulking agent was just as effective as commercial psyllium in relieving symptoms of constipation in a randomized trial conducted by researchers at the University of Texas Southwestern Medical Center in Dallas.

The recipe containing applesauce, unprocessed wheat bran, and prune juice cost about half as much as a commercial psyllium product, Konsyl, reported Dr. Peter Drewes and his associates from the medical center in a poster presented at the annual meeting of the Society of Gynecologic Surgeons.

Constipation is a problem for 4.5 million Americans, particularly older women, the authors noted. It is the primary reason for 2.5 million physician visits and drives the sale of $800 million in over-the-counter products each year.

Participants for the trial were drawn from patients presenting to the university's urogynecology clinic who met Rome II criteria for constipation (at least 12 weeks in the prior 12 months of at least two symptoms, including fewer than three defecations/week, straining, hard stools, and incomplete evacuation).

A total of 82 patients were randomized and 53 completed the 6-week study, including 30 randomized to take 1 teaspoon of psyllium in 8 ounces of liquid daily for 6 weeks or 4 tablespoons a day of the bowel recipe.

All of the participants received educational information on how dietary choices and fluids can influence constipation. They all kept bowel diaries.

Results were calculated using pre- and posttrial scores on a 30-point constipation scoring system, with a higher score indicating more severe constipation.

Constipation was relieved in both groups, with scores declining from 13.9 to 9.0 for the psyllium users and 13.6 to 8.5 for the recipe users during the 6-week trial.

The cost of 6 weeks' worth of the bowel recipe was $8.65, compared with $16.72 for the commercial psyllium product.

The authors of the poster concluded that the homemade recipe was “an effective and economical stool bulking agent for the treatment of constipation.”

ELSEVIER GLOBAL MEDICAL NEWS

The Pantry Solution

1 cup applesauce

1 cup coarse, unprocessed wheat bran

1/4 cup prune juice

Source: Dr. Drewes

LOS ANGELES — Patients with irritable bowel syndrome are eight times more likely than are other patients to develop ischemic colitis, according to a database study presented in poster form at the annual Digestive Disease Week.

Constipation was another notable risk factor, conferring a 2.6-fold increased risk of the potentially life-threatening condition, reported Mark Cziraky, Pharm.D., vice president of HealthCore Inc., a Wilmington, Del.-based research firm.

The study was funded and conducted on behalf of Novartis Pharmaceuticals Corp., manufacturer of several drugs for irritable bowel syndrome (IBS) and constipation.

Dr. Cziraky and his associates identified 100,143 patients with newly diagnosed IBS in the HealthCore Managed Care Database, which contains medical records for 12 million people. They matched these patients by age and gender to 100,143 controls who saw a physician for a reason other than irritable bowel syndrome during the study period from January 2000 to February 2005.

The same database was used to identify 81,399 patients with newly diagnosed constipation and age- and gender-matched controls.

During a median follow-up time of about 18 months, there were 167 cases of ischemic colitis among the IBS patients, compared with 77 cases among the matched controls (90.37 cases per 100,000 patient-years, compared with 41.47 cases per 100,000 patient-years). In a multivariate model, the relative risk of ischemic colitis was 8.16 for the IBS patients, compared with the controls.

Among the constipation patients, there were 199 cases of ischemic colitis, compared with 64 cases in matched controls (80.44 cases per 100,000 patient-years, compared with 43.03 cases per 100,000 patient-years).

In the multivariate model, the relative risk of ischemic colitis was 2.6 for the constipation patients, compared with the control patients.

When the researchers examined 1-year follow-up data, the data supported “an even stronger relationship” between IBS or constipation and ischemic colitis, they reported in the poster presentation.

LOS ANGELES — Patients with irritable bowel syndrome are eight times more likely than are other patients to develop ischemic colitis, according to a database study presented in poster form at the annual Digestive Disease Week.

Constipation was another notable risk factor, conferring a 2.6-fold increased risk of the potentially life-threatening condition, reported Mark Cziraky, Pharm.D., vice president of HealthCore Inc., a Wilmington, Del.-based research firm.

The study was funded and conducted on behalf of Novartis Pharmaceuticals Corp., manufacturer of several drugs for irritable bowel syndrome (IBS) and constipation.

Dr. Cziraky and his associates identified 100,143 patients with newly diagnosed IBS in the HealthCore Managed Care Database, which contains medical records for 12 million people. They matched these patients by age and gender to 100,143 controls who saw a physician for a reason other than irritable bowel syndrome during the study period from January 2000 to February 2005.

The same database was used to identify 81,399 patients with newly diagnosed constipation and age- and gender-matched controls.

During a median follow-up time of about 18 months, there were 167 cases of ischemic colitis among the IBS patients, compared with 77 cases among the matched controls (90.37 cases per 100,000 patient-years, compared with 41.47 cases per 100,000 patient-years). In a multivariate model, the relative risk of ischemic colitis was 8.16 for the IBS patients, compared with the controls.

Among the constipation patients, there were 199 cases of ischemic colitis, compared with 64 cases in matched controls (80.44 cases per 100,000 patient-years, compared with 43.03 cases per 100,000 patient-years).

In the multivariate model, the relative risk of ischemic colitis was 2.6 for the constipation patients, compared with the control patients.

When the researchers examined 1-year follow-up data, the data supported “an even stronger relationship” between IBS or constipation and ischemic colitis, they reported in the poster presentation.

LOS ANGELES — Patients with irritable bowel syndrome are eight times more likely than are other patients to develop ischemic colitis, according to a database study presented in poster form at the annual Digestive Disease Week.

Constipation was another notable risk factor, conferring a 2.6-fold increased risk of the potentially life-threatening condition, reported Mark Cziraky, Pharm.D., vice president of HealthCore Inc., a Wilmington, Del.-based research firm.

The study was funded and conducted on behalf of Novartis Pharmaceuticals Corp., manufacturer of several drugs for irritable bowel syndrome (IBS) and constipation.

Dr. Cziraky and his associates identified 100,143 patients with newly diagnosed IBS in the HealthCore Managed Care Database, which contains medical records for 12 million people. They matched these patients by age and gender to 100,143 controls who saw a physician for a reason other than irritable bowel syndrome during the study period from January 2000 to February 2005.

The same database was used to identify 81,399 patients with newly diagnosed constipation and age- and gender-matched controls.

During a median follow-up time of about 18 months, there were 167 cases of ischemic colitis among the IBS patients, compared with 77 cases among the matched controls (90.37 cases per 100,000 patient-years, compared with 41.47 cases per 100,000 patient-years). In a multivariate model, the relative risk of ischemic colitis was 8.16 for the IBS patients, compared with the controls.

Among the constipation patients, there were 199 cases of ischemic colitis, compared with 64 cases in matched controls (80.44 cases per 100,000 patient-years, compared with 43.03 cases per 100,000 patient-years).

In the multivariate model, the relative risk of ischemic colitis was 2.6 for the constipation patients, compared with the control patients.

When the researchers examined 1-year follow-up data, the data supported “an even stronger relationship” between IBS or constipation and ischemic colitis, they reported in the poster presentation.