M. Alexander Otto

NEWPORT BEACH, CALIF. – A history of severe cradle cap and diaper dermatitis helps to differentiate between pediatric psoriasis and atopic dermatitis, so be sure to ask, according to Dr. Alan Menter, chief of the dermatology division at the Baylor University Medical Center in Dallas.

“Both are markers for later onset of psoriasis, and are much more likely to be a marker for psoriasis than atopic eczema,” he said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

The tip to ask about cradle cap and diaper dermatitis is based largely on clinical observation, but is more useful than asking about a family history of psoriasis, because people tend to keep psoriasis to themselves, he noted; family members and even spouses might not know. “It’s a very hidden disease, so family history is of little benefit,” he said.

Recent strep infection also may provide a clue, not only for guttate psoriasis but also probably for plaque psoriasis in children, Dr. Menter said. But the sooner pediatric psoriasis is caught and controlled, the better, no matter how it is detected. Aside from the suffering it causes on its own, psoriasis in children has been linked to diabetes, hypertension, fatty liver disease, obesity, and cardiovascular problems, he noted.

The mechanism of action for these comorbidities remains under investigation. Perhaps mothers with psoriasis gain more weight during pregnancy, and their children are heavier at birth, Dr. Menter said.

Crohn’s disease is far more likely in children with psoriasis, too. Dr. Menter noted that he has had referrals where the diagnosis has been missed, even in the setting of long-standing fatigue and diarrhea. “We have to look for it [Crohn’s] in our psoriasis population,” he said.

Children with psoriasis are often teased, taunted, and bullied, sometimes as young as kindergarten age. The emotional stress, loneliness, and depression can have a major impact on school and social growth, Dr. Menter said.

“Treatment of these kids goes beyond prescribing a topical steroid; they need [both] physical and psychological support,” he emphasized. Talk to parents and teachers about how the child is doing in school and other social settings. Parents might know about grades, but not much about their child’s social interactions. To help catch problems, also “take a quality of life index on all your patients with psoriasis,” he said.

It’s important to intervene early and get children’s skin cleared quickly. “[Although] we’d love to treat [everybody] with topicals and wet compresses,” effective treatment sometimes means systemic therapy, he said.

Cyclosporine is a valid rescue option, particularly for more inflammatory disease. “Rarely, if ever, have I seen any hypertension or serum creatinine issues,” Dr. Menter said. “You just have to warn parents to be careful about gums, because you can get gingival hyperplasia, and girls don’t like the mild hypertrichosis you sometimes get around the temples and forearms,” he said.

Etanercept is another option. It not approved for pediatric psoriasis, but if you try hard enough, you can get insurance companies to cover it, Dr. Menter said. “You have to talk about quality of life and how psoriasis has impacted schooling,” among other topics, he explained.

Clinicians looking for child-oriented resources and support materials can recommend the National Psoriasis Foundation to their patients, he noted. SDEF and this news organization are owned by Frontline Medical Communications.

Dr. Menter disclosed financial relationships with Abbott, AbbVie, and numerous other companies.

aotto@frontlinemedcom.com

NEWPORT BEACH, CALIF. – A history of severe cradle cap and diaper dermatitis helps to differentiate between pediatric psoriasis and atopic dermatitis, so be sure to ask, according to Dr. Alan Menter, chief of the dermatology division at the Baylor University Medical Center in Dallas.

“Both are markers for later onset of psoriasis, and are much more likely to be a marker for psoriasis than atopic eczema,” he said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

The tip to ask about cradle cap and diaper dermatitis is based largely on clinical observation, but is more useful than asking about a family history of psoriasis, because people tend to keep psoriasis to themselves, he noted; family members and even spouses might not know. “It’s a very hidden disease, so family history is of little benefit,” he said.

Recent strep infection also may provide a clue, not only for guttate psoriasis but also probably for plaque psoriasis in children, Dr. Menter said. But the sooner pediatric psoriasis is caught and controlled, the better, no matter how it is detected. Aside from the suffering it causes on its own, psoriasis in children has been linked to diabetes, hypertension, fatty liver disease, obesity, and cardiovascular problems, he noted.

The mechanism of action for these comorbidities remains under investigation. Perhaps mothers with psoriasis gain more weight during pregnancy, and their children are heavier at birth, Dr. Menter said.

Crohn’s disease is far more likely in children with psoriasis, too. Dr. Menter noted that he has had referrals where the diagnosis has been missed, even in the setting of long-standing fatigue and diarrhea. “We have to look for it [Crohn’s] in our psoriasis population,” he said.

Children with psoriasis are often teased, taunted, and bullied, sometimes as young as kindergarten age. The emotional stress, loneliness, and depression can have a major impact on school and social growth, Dr. Menter said.

“Treatment of these kids goes beyond prescribing a topical steroid; they need [both] physical and psychological support,” he emphasized. Talk to parents and teachers about how the child is doing in school and other social settings. Parents might know about grades, but not much about their child’s social interactions. To help catch problems, also “take a quality of life index on all your patients with psoriasis,” he said.

It’s important to intervene early and get children’s skin cleared quickly. “[Although] we’d love to treat [everybody] with topicals and wet compresses,” effective treatment sometimes means systemic therapy, he said.

Cyclosporine is a valid rescue option, particularly for more inflammatory disease. “Rarely, if ever, have I seen any hypertension or serum creatinine issues,” Dr. Menter said. “You just have to warn parents to be careful about gums, because you can get gingival hyperplasia, and girls don’t like the mild hypertrichosis you sometimes get around the temples and forearms,” he said.

Etanercept is another option. It not approved for pediatric psoriasis, but if you try hard enough, you can get insurance companies to cover it, Dr. Menter said. “You have to talk about quality of life and how psoriasis has impacted schooling,” among other topics, he explained.

Clinicians looking for child-oriented resources and support materials can recommend the National Psoriasis Foundation to their patients, he noted. SDEF and this news organization are owned by Frontline Medical Communications.

Dr. Menter disclosed financial relationships with Abbott, AbbVie, and numerous other companies.

aotto@frontlinemedcom.com

NEWPORT BEACH, CALIF. – A history of severe cradle cap and diaper dermatitis helps to differentiate between pediatric psoriasis and atopic dermatitis, so be sure to ask, according to Dr. Alan Menter, chief of the dermatology division at the Baylor University Medical Center in Dallas.

“Both are markers for later onset of psoriasis, and are much more likely to be a marker for psoriasis than atopic eczema,” he said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

The tip to ask about cradle cap and diaper dermatitis is based largely on clinical observation, but is more useful than asking about a family history of psoriasis, because people tend to keep psoriasis to themselves, he noted; family members and even spouses might not know. “It’s a very hidden disease, so family history is of little benefit,” he said.

Recent strep infection also may provide a clue, not only for guttate psoriasis but also probably for plaque psoriasis in children, Dr. Menter said. But the sooner pediatric psoriasis is caught and controlled, the better, no matter how it is detected. Aside from the suffering it causes on its own, psoriasis in children has been linked to diabetes, hypertension, fatty liver disease, obesity, and cardiovascular problems, he noted.

The mechanism of action for these comorbidities remains under investigation. Perhaps mothers with psoriasis gain more weight during pregnancy, and their children are heavier at birth, Dr. Menter said.

Crohn’s disease is far more likely in children with psoriasis, too. Dr. Menter noted that he has had referrals where the diagnosis has been missed, even in the setting of long-standing fatigue and diarrhea. “We have to look for it [Crohn’s] in our psoriasis population,” he said.

Children with psoriasis are often teased, taunted, and bullied, sometimes as young as kindergarten age. The emotional stress, loneliness, and depression can have a major impact on school and social growth, Dr. Menter said.

“Treatment of these kids goes beyond prescribing a topical steroid; they need [both] physical and psychological support,” he emphasized. Talk to parents and teachers about how the child is doing in school and other social settings. Parents might know about grades, but not much about their child’s social interactions. To help catch problems, also “take a quality of life index on all your patients with psoriasis,” he said.

It’s important to intervene early and get children’s skin cleared quickly. “[Although] we’d love to treat [everybody] with topicals and wet compresses,” effective treatment sometimes means systemic therapy, he said.

Cyclosporine is a valid rescue option, particularly for more inflammatory disease. “Rarely, if ever, have I seen any hypertension or serum creatinine issues,” Dr. Menter said. “You just have to warn parents to be careful about gums, because you can get gingival hyperplasia, and girls don’t like the mild hypertrichosis you sometimes get around the temples and forearms,” he said.

Etanercept is another option. It not approved for pediatric psoriasis, but if you try hard enough, you can get insurance companies to cover it, Dr. Menter said. “You have to talk about quality of life and how psoriasis has impacted schooling,” among other topics, he explained.

Clinicians looking for child-oriented resources and support materials can recommend the National Psoriasis Foundation to their patients, he noted. SDEF and this news organization are owned by Frontline Medical Communications.

Dr. Menter disclosed financial relationships with Abbott, AbbVie, and numerous other companies.

aotto@frontlinemedcom.com

NEWPORT BEACH, CALIF.– In children with atopic dermatitis, serious superinfections are more likely to be caused by group A beta-hemolytic Streptococcus than methicillin-resistant Staphylococcus aureus, according to Dr. Victoria Barrio of the University of California, San Diego.

Unless there are classic MRSA signs, “I wouldn’t start off with Bactrim [sulfamethoxazole and trimethoprim] assuming that they have MRSA; Bactrim doesn’t work for strep. You are going to be in trouble if they actually have strep,” she said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Instead, Dr. Barrio is more likely to start empirically with cephalexin (Keflex) three times daily, which also covers staph in most communities. “It’s usually well tolerated, and it does pretty well,” she said, but adding that she adjusts treatment as needed depending on culture results.

This protocol is supported in part by findings from a study by colleagues of Dr. Barrio, which showed that children with atopic dermatitis carry more S. aureus on their skin than do children without eczema, so they are less likely to be infected with community-acquired MRSA, probably because non-MRSA strains outcompete it. In the study, the MRSA the investigators found responded to clindamycin (Pediatr. Dermatol. 2011;28:6-11).

Dr. Barrio cited another study suggesting that group A strep skin infections are a more serious problem than staph is in children with eczema; the children are more likely to be febrile, have systemic involvement, and need hospitalization than those with staph superinfections (Pediatr. Dermatol. 2011;28:230-4).

“These patients are often a lot sicker. You have to be aware that strep is out there, and it can be a problem for kids with eczema,” said Dr. Barrio.

In general, for bacterial superinfections, “bleach baths are a fantastic way to try to keep kids who are always getting infected under control,” she said. It really does keep that overload of bacteria down.”

Current data support her opinion. Following a course of antibiotics, another study showed that twice-weekly baths, followed by intranasal mupirocin ointment had “significantly greater mean reductions from baseline in Eczema Area and Severity Index scores,” compared with placebo (Pediatrics 2009;123:e808-14).

For older children who don’t want to take baths, a bleach soap (CLn Bodywash) is now available, Dr. Barrio noted.

Viral eczema coxsackium skin infections, recently characterized in the literature, remain a problem for children. Presentations can vary and include widespread blisters, erosions, purpura, and petechiae around the mouth or on the arms, legs, and torso. The infection can mimic bullous impetigo, eczema herpeticum, vasculitis, and primary immunobullous disease,and it is a common cause of onychomadesis as well, Dr. Barrio noted (Pediatrics 2013;132:e149-57).

“We saw a lot of it a few years ago. I am still seeing it around. You don’t really think about it as being hand, foot, and mouth” disease, she said.

Dr. Barrio added that eczema is hard on children emotionally as well as physically. They may lose sleep, have a tough time in school, and might blame the illness on themselves, and these and other problems can lead to depression, anxiety, and a big hit to self-esteem, she said.

Clinicians at the University of Nottingham (U.K.) have created a free web resource that might help, which features stories for children. The clinicians have posted several tales, like “The Princess and the Itch,” that make eczema the villain and the child the hero, which helps to externalize the disease. The child’s name can be entered into a template to personalize the story (Pediatr. Dermatol. 2013;30:765-7). Dr. Barrio had no relevant disclosures. SDEF and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

NEWPORT BEACH, CALIF.– In children with atopic dermatitis, serious superinfections are more likely to be caused by group A beta-hemolytic Streptococcus than methicillin-resistant Staphylococcus aureus, according to Dr. Victoria Barrio of the University of California, San Diego.

Unless there are classic MRSA signs, “I wouldn’t start off with Bactrim [sulfamethoxazole and trimethoprim] assuming that they have MRSA; Bactrim doesn’t work for strep. You are going to be in trouble if they actually have strep,” she said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Instead, Dr. Barrio is more likely to start empirically with cephalexin (Keflex) three times daily, which also covers staph in most communities. “It’s usually well tolerated, and it does pretty well,” she said, but adding that she adjusts treatment as needed depending on culture results.

This protocol is supported in part by findings from a study by colleagues of Dr. Barrio, which showed that children with atopic dermatitis carry more S. aureus on their skin than do children without eczema, so they are less likely to be infected with community-acquired MRSA, probably because non-MRSA strains outcompete it. In the study, the MRSA the investigators found responded to clindamycin (Pediatr. Dermatol. 2011;28:6-11).

Dr. Barrio cited another study suggesting that group A strep skin infections are a more serious problem than staph is in children with eczema; the children are more likely to be febrile, have systemic involvement, and need hospitalization than those with staph superinfections (Pediatr. Dermatol. 2011;28:230-4).

“These patients are often a lot sicker. You have to be aware that strep is out there, and it can be a problem for kids with eczema,” said Dr. Barrio.

In general, for bacterial superinfections, “bleach baths are a fantastic way to try to keep kids who are always getting infected under control,” she said. It really does keep that overload of bacteria down.”

Current data support her opinion. Following a course of antibiotics, another study showed that twice-weekly baths, followed by intranasal mupirocin ointment had “significantly greater mean reductions from baseline in Eczema Area and Severity Index scores,” compared with placebo (Pediatrics 2009;123:e808-14).

For older children who don’t want to take baths, a bleach soap (CLn Bodywash) is now available, Dr. Barrio noted.

Viral eczema coxsackium skin infections, recently characterized in the literature, remain a problem for children. Presentations can vary and include widespread blisters, erosions, purpura, and petechiae around the mouth or on the arms, legs, and torso. The infection can mimic bullous impetigo, eczema herpeticum, vasculitis, and primary immunobullous disease,and it is a common cause of onychomadesis as well, Dr. Barrio noted (Pediatrics 2013;132:e149-57).

“We saw a lot of it a few years ago. I am still seeing it around. You don’t really think about it as being hand, foot, and mouth” disease, she said.

Dr. Barrio added that eczema is hard on children emotionally as well as physically. They may lose sleep, have a tough time in school, and might blame the illness on themselves, and these and other problems can lead to depression, anxiety, and a big hit to self-esteem, she said.

Clinicians at the University of Nottingham (U.K.) have created a free web resource that might help, which features stories for children. The clinicians have posted several tales, like “The Princess and the Itch,” that make eczema the villain and the child the hero, which helps to externalize the disease. The child’s name can be entered into a template to personalize the story (Pediatr. Dermatol. 2013;30:765-7). Dr. Barrio had no relevant disclosures. SDEF and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

NEWPORT BEACH, CALIF.– In children with atopic dermatitis, serious superinfections are more likely to be caused by group A beta-hemolytic Streptococcus than methicillin-resistant Staphylococcus aureus, according to Dr. Victoria Barrio of the University of California, San Diego.

Unless there are classic MRSA signs, “I wouldn’t start off with Bactrim [sulfamethoxazole and trimethoprim] assuming that they have MRSA; Bactrim doesn’t work for strep. You are going to be in trouble if they actually have strep,” she said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Instead, Dr. Barrio is more likely to start empirically with cephalexin (Keflex) three times daily, which also covers staph in most communities. “It’s usually well tolerated, and it does pretty well,” she said, but adding that she adjusts treatment as needed depending on culture results.

This protocol is supported in part by findings from a study by colleagues of Dr. Barrio, which showed that children with atopic dermatitis carry more S. aureus on their skin than do children without eczema, so they are less likely to be infected with community-acquired MRSA, probably because non-MRSA strains outcompete it. In the study, the MRSA the investigators found responded to clindamycin (Pediatr. Dermatol. 2011;28:6-11).

Dr. Barrio cited another study suggesting that group A strep skin infections are a more serious problem than staph is in children with eczema; the children are more likely to be febrile, have systemic involvement, and need hospitalization than those with staph superinfections (Pediatr. Dermatol. 2011;28:230-4).

“These patients are often a lot sicker. You have to be aware that strep is out there, and it can be a problem for kids with eczema,” said Dr. Barrio.

In general, for bacterial superinfections, “bleach baths are a fantastic way to try to keep kids who are always getting infected under control,” she said. It really does keep that overload of bacteria down.”

Current data support her opinion. Following a course of antibiotics, another study showed that twice-weekly baths, followed by intranasal mupirocin ointment had “significantly greater mean reductions from baseline in Eczema Area and Severity Index scores,” compared with placebo (Pediatrics 2009;123:e808-14).

For older children who don’t want to take baths, a bleach soap (CLn Bodywash) is now available, Dr. Barrio noted.

Viral eczema coxsackium skin infections, recently characterized in the literature, remain a problem for children. Presentations can vary and include widespread blisters, erosions, purpura, and petechiae around the mouth or on the arms, legs, and torso. The infection can mimic bullous impetigo, eczema herpeticum, vasculitis, and primary immunobullous disease,and it is a common cause of onychomadesis as well, Dr. Barrio noted (Pediatrics 2013;132:e149-57).

“We saw a lot of it a few years ago. I am still seeing it around. You don’t really think about it as being hand, foot, and mouth” disease, she said.

Dr. Barrio added that eczema is hard on children emotionally as well as physically. They may lose sleep, have a tough time in school, and might blame the illness on themselves, and these and other problems can lead to depression, anxiety, and a big hit to self-esteem, she said.

Clinicians at the University of Nottingham (U.K.) have created a free web resource that might help, which features stories for children. The clinicians have posted several tales, like “The Princess and the Itch,” that make eczema the villain and the child the hero, which helps to externalize the disease. The child’s name can be entered into a template to personalize the story (Pediatr. Dermatol. 2013;30:765-7). Dr. Barrio had no relevant disclosures. SDEF and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

NEWPORT BEACH, CALIF.– Desquamation is a handy way to differentiate between Staphylococcus skin infections and molluscum.

Most of the time, the presentation of molluscum “is straightforward, but it’s one of the great imitators,” according to pediatric dermatologist Dr. James Treat of the department of pediatrics at the Children’s Hospital of Philadelphia. Molluscum can present as pearly little drops, inflamed papules that look infected, or even a large cyst. Molluscum also can kick up a small patch of localized eczema that makes it easy to overlook pathognomonic signs, he said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Sometimes, patients wind up being treated for folliculitis, bug bites, and other problems they don’t have. “We see people who get multiple antibiotics. I’ve seen so many patients who have been told they have recurrent MRSA,” Dr. Treat said.

However, methicillin-resistant Staphylococcus aureus (MRSA) secretes a toxin that causes the nearby epidermis to slough off; molluscum does not. “That’s a nice little marker for a staph infection,” Dr. Treat noted. As for pruritus, “You sometimes see a child who presents with a random spot of eczema on an arm, leg, or an inguinal fold that they’ve never had before. Look for molluscum in the center of it. When in doubt, culture,” he said.

Lesions often become inflamed, which makes parents worry about infection, but “the reality is that molluscum is almost never infected. If you take a little blade or needle and pop into it, you are not going to get pus out,” Dr. Treat said.

Instead, inflammation is a sign that the body is attacking the virus, which “is a really good thing.” The phenomenon was recently dubbed the beginning-of-the-end (BOTE) sign. If kids come in with inflamed molluscum, it’s time to “talk parents off the ledge. The body has already done your job for you.” Dr. Treat said.

If the body hasn’t yet done it’s job, the goal of treatment is to irritate the lesion to draw the immune system’s attention to it.

Scraping is the most reliable one-time treatment, but the blood and pain are too much for small children. Salicylic acid and topical imiquimod do the job the first time around in about half of kids, and cantharidin in about a third, Dr. Treat said (Pediatr. Dermatol. 2006;23:574-9).

Freezing and comedone extraction work, too, but they hurt, so are best used in older, “highly motivated” children. Don’t overdo freezing either; it might cause pigment changes, said Dr. Treat.

Also, “it’s reasonable to treat those itchy, red patches” with a low-potency topical steroid “because that’s what’s making the kid uncomfortable,” he said.

Doing nothing is reasonable, too, because molluscum is self-limiting, but it’s wise to tell parents it can take as long as 2 or more years for the condition to burn itself out.

Whether or not observation is the treatment of choice, parents need to know that molluscum can spread through bathing with siblings, and via wet washcloths, bathing suits, towels, and pool toys. Wrestling, assisting other children in gymnastics, and other skin-on-skin activities can spread molluscum, too.

Parents also need to know that molluscum on the face can present as unilateral conjunctivitis. “A random red eye should be evaluated. This is where I might use oral cimetidine. It’s totally off label and has limited data, but it’s also over the counter and reasonable to try,” Dr. Treat said.

Dr. Treat has no relevant disclosures. SDEF and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

NEWPORT BEACH, CALIF.– Desquamation is a handy way to differentiate between Staphylococcus skin infections and molluscum.

Most of the time, the presentation of molluscum “is straightforward, but it’s one of the great imitators,” according to pediatric dermatologist Dr. James Treat of the department of pediatrics at the Children’s Hospital of Philadelphia. Molluscum can present as pearly little drops, inflamed papules that look infected, or even a large cyst. Molluscum also can kick up a small patch of localized eczema that makes it easy to overlook pathognomonic signs, he said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Sometimes, patients wind up being treated for folliculitis, bug bites, and other problems they don’t have. “We see people who get multiple antibiotics. I’ve seen so many patients who have been told they have recurrent MRSA,” Dr. Treat said.

However, methicillin-resistant Staphylococcus aureus (MRSA) secretes a toxin that causes the nearby epidermis to slough off; molluscum does not. “That’s a nice little marker for a staph infection,” Dr. Treat noted. As for pruritus, “You sometimes see a child who presents with a random spot of eczema on an arm, leg, or an inguinal fold that they’ve never had before. Look for molluscum in the center of it. When in doubt, culture,” he said.

Lesions often become inflamed, which makes parents worry about infection, but “the reality is that molluscum is almost never infected. If you take a little blade or needle and pop into it, you are not going to get pus out,” Dr. Treat said.

Instead, inflammation is a sign that the body is attacking the virus, which “is a really good thing.” The phenomenon was recently dubbed the beginning-of-the-end (BOTE) sign. If kids come in with inflamed molluscum, it’s time to “talk parents off the ledge. The body has already done your job for you.” Dr. Treat said.

If the body hasn’t yet done it’s job, the goal of treatment is to irritate the lesion to draw the immune system’s attention to it.

Scraping is the most reliable one-time treatment, but the blood and pain are too much for small children. Salicylic acid and topical imiquimod do the job the first time around in about half of kids, and cantharidin in about a third, Dr. Treat said (Pediatr. Dermatol. 2006;23:574-9).

Freezing and comedone extraction work, too, but they hurt, so are best used in older, “highly motivated” children. Don’t overdo freezing either; it might cause pigment changes, said Dr. Treat.

Also, “it’s reasonable to treat those itchy, red patches” with a low-potency topical steroid “because that’s what’s making the kid uncomfortable,” he said.

Doing nothing is reasonable, too, because molluscum is self-limiting, but it’s wise to tell parents it can take as long as 2 or more years for the condition to burn itself out.

Whether or not observation is the treatment of choice, parents need to know that molluscum can spread through bathing with siblings, and via wet washcloths, bathing suits, towels, and pool toys. Wrestling, assisting other children in gymnastics, and other skin-on-skin activities can spread molluscum, too.

Parents also need to know that molluscum on the face can present as unilateral conjunctivitis. “A random red eye should be evaluated. This is where I might use oral cimetidine. It’s totally off label and has limited data, but it’s also over the counter and reasonable to try,” Dr. Treat said.

Dr. Treat has no relevant disclosures. SDEF and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

NEWPORT BEACH, CALIF.– Desquamation is a handy way to differentiate between Staphylococcus skin infections and molluscum.

Most of the time, the presentation of molluscum “is straightforward, but it’s one of the great imitators,” according to pediatric dermatologist Dr. James Treat of the department of pediatrics at the Children’s Hospital of Philadelphia. Molluscum can present as pearly little drops, inflamed papules that look infected, or even a large cyst. Molluscum also can kick up a small patch of localized eczema that makes it easy to overlook pathognomonic signs, he said at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Sometimes, patients wind up being treated for folliculitis, bug bites, and other problems they don’t have. “We see people who get multiple antibiotics. I’ve seen so many patients who have been told they have recurrent MRSA,” Dr. Treat said.

However, methicillin-resistant Staphylococcus aureus (MRSA) secretes a toxin that causes the nearby epidermis to slough off; molluscum does not. “That’s a nice little marker for a staph infection,” Dr. Treat noted. As for pruritus, “You sometimes see a child who presents with a random spot of eczema on an arm, leg, or an inguinal fold that they’ve never had before. Look for molluscum in the center of it. When in doubt, culture,” he said.

Lesions often become inflamed, which makes parents worry about infection, but “the reality is that molluscum is almost never infected. If you take a little blade or needle and pop into it, you are not going to get pus out,” Dr. Treat said.

Instead, inflammation is a sign that the body is attacking the virus, which “is a really good thing.” The phenomenon was recently dubbed the beginning-of-the-end (BOTE) sign. If kids come in with inflamed molluscum, it’s time to “talk parents off the ledge. The body has already done your job for you.” Dr. Treat said.

If the body hasn’t yet done it’s job, the goal of treatment is to irritate the lesion to draw the immune system’s attention to it.

Scraping is the most reliable one-time treatment, but the blood and pain are too much for small children. Salicylic acid and topical imiquimod do the job the first time around in about half of kids, and cantharidin in about a third, Dr. Treat said (Pediatr. Dermatol. 2006;23:574-9).

Freezing and comedone extraction work, too, but they hurt, so are best used in older, “highly motivated” children. Don’t overdo freezing either; it might cause pigment changes, said Dr. Treat.

Also, “it’s reasonable to treat those itchy, red patches” with a low-potency topical steroid “because that’s what’s making the kid uncomfortable,” he said.

Doing nothing is reasonable, too, because molluscum is self-limiting, but it’s wise to tell parents it can take as long as 2 or more years for the condition to burn itself out.

Whether or not observation is the treatment of choice, parents need to know that molluscum can spread through bathing with siblings, and via wet washcloths, bathing suits, towels, and pool toys. Wrestling, assisting other children in gymnastics, and other skin-on-skin activities can spread molluscum, too.

Parents also need to know that molluscum on the face can present as unilateral conjunctivitis. “A random red eye should be evaluated. This is where I might use oral cimetidine. It’s totally off label and has limited data, but it’s also over the counter and reasonable to try,” Dr. Treat said.

Dr. Treat has no relevant disclosures. SDEF and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

The Food and Drug Administration on Oct. 15 approved two new oral medications for idiopathic pulmonary fibrosis, Boehringer Ingelheim’s nintedanib (Ofev) and Roche’s pirfenidone (Esbriet).

The drugs significantly slowed the decline of forced vital capacity (FVC), compared with placebo, in phase III testing. They did not significantly reduce mortality. The FDA granted both agents fast track, priority review, orphan product, and breakthrough designations. Both were also approved ahead of schedule, according to the agency. Each of the drugs should be available for patients within the next 2 weeks, according to their manufacturers.

For pirfenidone, already on the market in Europe and Canada, Roche said it plans “a comprehensive patient support program designed to help with access, financial support, and ongoing education.”

For nintedanib, Boehringer Ingelheim plans “a comprehensive patient support program that will provide a broad range of financial and nursing support services,” called “Open Doors.” In testing, the most frequent serious adverse reactions with nintedanib, versus placebo, were bronchitis (1.2% versus 0.8%) and myocardial infarction (1.5% versus 0.4%). Pneumonia (0.7% versus 0.6%), lung cancer (0.3% versus 0%), and MI (0.3% versus 0.2%) were the most common fatal adverse events.

The most common side effects of nintedanib were diarrhea, nausea, abdominal pain, vomiting, liver enzyme elevation, decreased appetite, headache, weight loss, and high blood pressure. Nintedanib is not recommended for patients who have moderate to severe liver problems or are pregnancy class D. Women of childbearing potential should use contraception for at least 3 months after stopping the drug, according to the FDA.

For pirfenidone, the most serious adverse events versus placebo were liver enzyme elevations (3.7% versus 0.8%), sensitivity to light or rash (9.0% versus 1.0%), and gastrointestinal side effects that caused 2.2 % of patients to discontinue treatment compared with 1.0% of those who received placebo.

The most common side effects of pirfenidone were nausea, rash, abdominal pain, upper respiratory tract infection, diarrhea, fatigue, headache, dyspepsia, dizziness, vomiting, loss of appetite, gastroesophageal reflux, sinusitis, insomnia, decreased weight, and arthralgia.

The FDA warned about use of pirfenidone in patients with severe liver problems or end-stage kidney disease, or in those who require dialysis. Patients taking pirfenidone also must monitor and guard against sun exposure.

Clinical trials of pirfenidone included 1,247 idiopathic pulmonary fibrosis patients. In one with 555 patients, 17% of pirfenidone patients had an FVC decline of at least 10% after a year, compared with 32% who received placebo, Roche said.

Trials of nintedanib included 1,231 patients. One with 513 showed a relative reduction in annual FVC decline of 52% (–115 versus –240 mL for placebo) at 1 year, Boehringer Ingelheim noted.

aotto@frontlinemedcom.com

The Food and Drug Administration on Oct. 15 approved two new oral medications for idiopathic pulmonary fibrosis, Boehringer Ingelheim’s nintedanib (Ofev) and Roche’s pirfenidone (Esbriet).

The drugs significantly slowed the decline of forced vital capacity (FVC), compared with placebo, in phase III testing. They did not significantly reduce mortality. The FDA granted both agents fast track, priority review, orphan product, and breakthrough designations. Both were also approved ahead of schedule, according to the agency. Each of the drugs should be available for patients within the next 2 weeks, according to their manufacturers.

For pirfenidone, already on the market in Europe and Canada, Roche said it plans “a comprehensive patient support program designed to help with access, financial support, and ongoing education.”

For nintedanib, Boehringer Ingelheim plans “a comprehensive patient support program that will provide a broad range of financial and nursing support services,” called “Open Doors.” In testing, the most frequent serious adverse reactions with nintedanib, versus placebo, were bronchitis (1.2% versus 0.8%) and myocardial infarction (1.5% versus 0.4%). Pneumonia (0.7% versus 0.6%), lung cancer (0.3% versus 0%), and MI (0.3% versus 0.2%) were the most common fatal adverse events.

The most common side effects of nintedanib were diarrhea, nausea, abdominal pain, vomiting, liver enzyme elevation, decreased appetite, headache, weight loss, and high blood pressure. Nintedanib is not recommended for patients who have moderate to severe liver problems or are pregnancy class D. Women of childbearing potential should use contraception for at least 3 months after stopping the drug, according to the FDA.

For pirfenidone, the most serious adverse events versus placebo were liver enzyme elevations (3.7% versus 0.8%), sensitivity to light or rash (9.0% versus 1.0%), and gastrointestinal side effects that caused 2.2 % of patients to discontinue treatment compared with 1.0% of those who received placebo.

The most common side effects of pirfenidone were nausea, rash, abdominal pain, upper respiratory tract infection, diarrhea, fatigue, headache, dyspepsia, dizziness, vomiting, loss of appetite, gastroesophageal reflux, sinusitis, insomnia, decreased weight, and arthralgia.

The FDA warned about use of pirfenidone in patients with severe liver problems or end-stage kidney disease, or in those who require dialysis. Patients taking pirfenidone also must monitor and guard against sun exposure.

Clinical trials of pirfenidone included 1,247 idiopathic pulmonary fibrosis patients. In one with 555 patients, 17% of pirfenidone patients had an FVC decline of at least 10% after a year, compared with 32% who received placebo, Roche said.

Trials of nintedanib included 1,231 patients. One with 513 showed a relative reduction in annual FVC decline of 52% (–115 versus –240 mL for placebo) at 1 year, Boehringer Ingelheim noted.

aotto@frontlinemedcom.com

The Food and Drug Administration on Oct. 15 approved two new oral medications for idiopathic pulmonary fibrosis, Boehringer Ingelheim’s nintedanib (Ofev) and Roche’s pirfenidone (Esbriet).

The drugs significantly slowed the decline of forced vital capacity (FVC), compared with placebo, in phase III testing. They did not significantly reduce mortality. The FDA granted both agents fast track, priority review, orphan product, and breakthrough designations. Both were also approved ahead of schedule, according to the agency. Each of the drugs should be available for patients within the next 2 weeks, according to their manufacturers.

For pirfenidone, already on the market in Europe and Canada, Roche said it plans “a comprehensive patient support program designed to help with access, financial support, and ongoing education.”

For nintedanib, Boehringer Ingelheim plans “a comprehensive patient support program that will provide a broad range of financial and nursing support services,” called “Open Doors.” In testing, the most frequent serious adverse reactions with nintedanib, versus placebo, were bronchitis (1.2% versus 0.8%) and myocardial infarction (1.5% versus 0.4%). Pneumonia (0.7% versus 0.6%), lung cancer (0.3% versus 0%), and MI (0.3% versus 0.2%) were the most common fatal adverse events.

The most common side effects of nintedanib were diarrhea, nausea, abdominal pain, vomiting, liver enzyme elevation, decreased appetite, headache, weight loss, and high blood pressure. Nintedanib is not recommended for patients who have moderate to severe liver problems or are pregnancy class D. Women of childbearing potential should use contraception for at least 3 months after stopping the drug, according to the FDA.

For pirfenidone, the most serious adverse events versus placebo were liver enzyme elevations (3.7% versus 0.8%), sensitivity to light or rash (9.0% versus 1.0%), and gastrointestinal side effects that caused 2.2 % of patients to discontinue treatment compared with 1.0% of those who received placebo.

The most common side effects of pirfenidone were nausea, rash, abdominal pain, upper respiratory tract infection, diarrhea, fatigue, headache, dyspepsia, dizziness, vomiting, loss of appetite, gastroesophageal reflux, sinusitis, insomnia, decreased weight, and arthralgia.

The FDA warned about use of pirfenidone in patients with severe liver problems or end-stage kidney disease, or in those who require dialysis. Patients taking pirfenidone also must monitor and guard against sun exposure.

Clinical trials of pirfenidone included 1,247 idiopathic pulmonary fibrosis patients. In one with 555 patients, 17% of pirfenidone patients had an FVC decline of at least 10% after a year, compared with 32% who received placebo, Roche said.

Trials of nintedanib included 1,231 patients. One with 513 showed a relative reduction in annual FVC decline of 52% (–115 versus –240 mL for placebo) at 1 year, Boehringer Ingelheim noted.

aotto@frontlinemedcom.com

The risk of cataracts more than doubles if patients with systemic lupus erythematosus have been on 10 mg/day of prednisone, or its equivalent, for 3 or more years, according to a retrospective review of 2,109 patients at Johns Hopkins University in Baltimore.

After the researchers controlled for age, sex, and other potential confounders, they found that the risk triples when patients have been on that dose for 10 or more years (relative risk, 3.1; 95% confidence interval, 1.6-5.7; P = .0005). The doubling of risk was found in those who had been on 10 mg/day, or its equivalent, for 3-10 years (RR, 2.3; 95% CI, 1.3-4.3; P = .0065). Shorter courses did not increase the risk of cataracts (Rheumatol. Int. 2014 Sept. 26 [doi:10.1007/s00296-014-3129-5]).

It’s not news that long-term prednisone causes cataracts, but the findings give an idea of how long it takes – and how much drug is needed – for problems to emerge. Overall, in patients with systemic lupus erythematosus (SLE), “the cumulative prednisone dose was the most important risk factor for cataract[s],” concluded Dr. Khaled Alderaan, a postdoctoral fellow in rheumatology at Johns Hopkins University, and his team. Also, the risk of cataracts doubled if patients had a mean systolic blood pressure above 140 mm Hg over a median of 4.1 years of follow-up (RR, 2.2; 95% CI, 1.4-3.3; P = .0006 ), and the risk increased 30% for every 2-point increase in disease activity, as measured on the SELENA–SLEDAI (Systemic Lupus Erythematosus Disease Activity Index, as modified for the Safety of Estrogens in Lupus Erythematosus National Assessment) (RR, 1.3; 95% CI, 1.1-1.5; P = .0005).

“These results provide further incentive for controlling blood pressure and disease activity in SLE,” the authors concluded.

The patients, all members of the Hopkins Lupus Cohort, were seen quarterly by their rheumatologists and examined every half year by their ophthalmologists. About half were under 40 years old when they enrolled, and the rest were under 60 years old. Most of the patients (93%) were women, and most were either white (54%) or black (39%). They had no cataract history when they joined the cohort.

Cataracts were not associated with lupus duration, diabetes, smoking, high cholesterol, renal involvement, immunological profile, and medication history other than prednisone. Diabetes, smoking, and high cholesterol are all known to increase the risk of cataracts in the general population.

During a total of 11,887 persons-years, the cohort had a cataract incidence of 13.2/1,000 persons-years.

“High disease activity would be an indication for higher corticosteroid doses. However, in our multivariate analysis, the association of disease activity with cataract persisted after we controlled for corticosteroid doses. Another potential explanation of the association between disease activity and cataract is an immunological impact of SLE on ocular cytokines and growth factors. Imbalance between these cytokines can facilitate the formation of cataract, as proposed in the general population,” the investigators noted.

“In the general population, the relationship between hypertension and cataract has been inconsistent. Moreover, the pathophysiological mechanism of hypertension-induced cataract remains uncertain. Some have debated the potential association may be affected by confounding factors such as diabetes or smoking. In our study, the association persisted after controlling for all other confounding factors,” they wrote.

Men in the study had a 20 % lower risk of cataracts than did women. “Although this finding was not statistically significant, it is consistent with general population studies.” The reasons for the sex differences are unknown, the researchers wrote.

The work was funded by the National Institutes of Health. The investigators have no competing financial interests.

aotto@frontlinemedcom.com

The risk of cataracts more than doubles if patients with systemic lupus erythematosus have been on 10 mg/day of prednisone, or its equivalent, for 3 or more years, according to a retrospective review of 2,109 patients at Johns Hopkins University in Baltimore.

After the researchers controlled for age, sex, and other potential confounders, they found that the risk triples when patients have been on that dose for 10 or more years (relative risk, 3.1; 95% confidence interval, 1.6-5.7; P = .0005). The doubling of risk was found in those who had been on 10 mg/day, or its equivalent, for 3-10 years (RR, 2.3; 95% CI, 1.3-4.3; P = .0065). Shorter courses did not increase the risk of cataracts (Rheumatol. Int. 2014 Sept. 26 [doi:10.1007/s00296-014-3129-5]).

It’s not news that long-term prednisone causes cataracts, but the findings give an idea of how long it takes – and how much drug is needed – for problems to emerge. Overall, in patients with systemic lupus erythematosus (SLE), “the cumulative prednisone dose was the most important risk factor for cataract[s],” concluded Dr. Khaled Alderaan, a postdoctoral fellow in rheumatology at Johns Hopkins University, and his team. Also, the risk of cataracts doubled if patients had a mean systolic blood pressure above 140 mm Hg over a median of 4.1 years of follow-up (RR, 2.2; 95% CI, 1.4-3.3; P = .0006 ), and the risk increased 30% for every 2-point increase in disease activity, as measured on the SELENA–SLEDAI (Systemic Lupus Erythematosus Disease Activity Index, as modified for the Safety of Estrogens in Lupus Erythematosus National Assessment) (RR, 1.3; 95% CI, 1.1-1.5; P = .0005).

“These results provide further incentive for controlling blood pressure and disease activity in SLE,” the authors concluded.

The patients, all members of the Hopkins Lupus Cohort, were seen quarterly by their rheumatologists and examined every half year by their ophthalmologists. About half were under 40 years old when they enrolled, and the rest were under 60 years old. Most of the patients (93%) were women, and most were either white (54%) or black (39%). They had no cataract history when they joined the cohort.

Cataracts were not associated with lupus duration, diabetes, smoking, high cholesterol, renal involvement, immunological profile, and medication history other than prednisone. Diabetes, smoking, and high cholesterol are all known to increase the risk of cataracts in the general population.

During a total of 11,887 persons-years, the cohort had a cataract incidence of 13.2/1,000 persons-years.

“High disease activity would be an indication for higher corticosteroid doses. However, in our multivariate analysis, the association of disease activity with cataract persisted after we controlled for corticosteroid doses. Another potential explanation of the association between disease activity and cataract is an immunological impact of SLE on ocular cytokines and growth factors. Imbalance between these cytokines can facilitate the formation of cataract, as proposed in the general population,” the investigators noted.

“In the general population, the relationship between hypertension and cataract has been inconsistent. Moreover, the pathophysiological mechanism of hypertension-induced cataract remains uncertain. Some have debated the potential association may be affected by confounding factors such as diabetes or smoking. In our study, the association persisted after controlling for all other confounding factors,” they wrote.

Men in the study had a 20 % lower risk of cataracts than did women. “Although this finding was not statistically significant, it is consistent with general population studies.” The reasons for the sex differences are unknown, the researchers wrote.

The work was funded by the National Institutes of Health. The investigators have no competing financial interests.

aotto@frontlinemedcom.com

The risk of cataracts more than doubles if patients with systemic lupus erythematosus have been on 10 mg/day of prednisone, or its equivalent, for 3 or more years, according to a retrospective review of 2,109 patients at Johns Hopkins University in Baltimore.

After the researchers controlled for age, sex, and other potential confounders, they found that the risk triples when patients have been on that dose for 10 or more years (relative risk, 3.1; 95% confidence interval, 1.6-5.7; P = .0005). The doubling of risk was found in those who had been on 10 mg/day, or its equivalent, for 3-10 years (RR, 2.3; 95% CI, 1.3-4.3; P = .0065). Shorter courses did not increase the risk of cataracts (Rheumatol. Int. 2014 Sept. 26 [doi:10.1007/s00296-014-3129-5]).

It’s not news that long-term prednisone causes cataracts, but the findings give an idea of how long it takes – and how much drug is needed – for problems to emerge. Overall, in patients with systemic lupus erythematosus (SLE), “the cumulative prednisone dose was the most important risk factor for cataract[s],” concluded Dr. Khaled Alderaan, a postdoctoral fellow in rheumatology at Johns Hopkins University, and his team. Also, the risk of cataracts doubled if patients had a mean systolic blood pressure above 140 mm Hg over a median of 4.1 years of follow-up (RR, 2.2; 95% CI, 1.4-3.3; P = .0006 ), and the risk increased 30% for every 2-point increase in disease activity, as measured on the SELENA–SLEDAI (Systemic Lupus Erythematosus Disease Activity Index, as modified for the Safety of Estrogens in Lupus Erythematosus National Assessment) (RR, 1.3; 95% CI, 1.1-1.5; P = .0005).

“These results provide further incentive for controlling blood pressure and disease activity in SLE,” the authors concluded.

The patients, all members of the Hopkins Lupus Cohort, were seen quarterly by their rheumatologists and examined every half year by their ophthalmologists. About half were under 40 years old when they enrolled, and the rest were under 60 years old. Most of the patients (93%) were women, and most were either white (54%) or black (39%). They had no cataract history when they joined the cohort.

Cataracts were not associated with lupus duration, diabetes, smoking, high cholesterol, renal involvement, immunological profile, and medication history other than prednisone. Diabetes, smoking, and high cholesterol are all known to increase the risk of cataracts in the general population.

During a total of 11,887 persons-years, the cohort had a cataract incidence of 13.2/1,000 persons-years.

“High disease activity would be an indication for higher corticosteroid doses. However, in our multivariate analysis, the association of disease activity with cataract persisted after we controlled for corticosteroid doses. Another potential explanation of the association between disease activity and cataract is an immunological impact of SLE on ocular cytokines and growth factors. Imbalance between these cytokines can facilitate the formation of cataract, as proposed in the general population,” the investigators noted.

“In the general population, the relationship between hypertension and cataract has been inconsistent. Moreover, the pathophysiological mechanism of hypertension-induced cataract remains uncertain. Some have debated the potential association may be affected by confounding factors such as diabetes or smoking. In our study, the association persisted after controlling for all other confounding factors,” they wrote.

Men in the study had a 20 % lower risk of cataracts than did women. “Although this finding was not statistically significant, it is consistent with general population studies.” The reasons for the sex differences are unknown, the researchers wrote.

The work was funded by the National Institutes of Health. The investigators have no competing financial interests.

aotto@frontlinemedcom.com

Fatal heroin overdoses doubled in the United States from 2010 to 2012, according to a report published online Oct. 2 in the Morbidity and Mortality Weekly Report.

In a representative sample of 28 states, heroin deaths climbed from 1,779 to 3,635, a rate increase from 1.0 to 2.1 per 100,000 population. Meanwhile, deaths from prescription opioids fell from 10,427 to 9,869, a decrease from 6.0 to 5.6 per 100,000 population (MMWR 2014;63:849-54).

In Northeastern states, fatal heroin overdoses increased 211.2%. Southern states had an increase of 180.9%, Midwestern states an increase of 62.1%, and Western states an increase of 90.7%, based on state health department data.

The report did not give numbers for individual states, only regions, but it did note that Kentucky reported a 279% increase in heroin deaths from 2010 to 2012, and Ohio had an increase of approximately 300% from 2007 to 2012.

The investigators found no statistically significant relationship between the increase in heroin deaths and the decrease in prescription opioid fatalities. However, they noted that about 75% of heroin users report using prescription opioids first, then switching to heroin, a cheaper, more readily available alternative that gives a more potent high.

Others have reported that young adults are sometimes unaware that prescription pain pills are opioids and that their abuse can slip into heroin use. Particularly hard hit communities have reduced opioid fatalities by getting that message out through education campaigns, and also by distributing intranasal naloxone kits to the people most likely to need them: first responders, family members, and opioid abusers who might need to rescue a friend (See, for example, BMJ 2013;346:f174.).

“State policies that increase access to naloxone, a drug that can reverse potentially fatal respiratory depression in persons who have overdosed from either OPRs [opioid pain relievers] or heroin, or policies that reduce or eliminate penalties when someone reports an overdose, are potentially useful strategies” to counter the problem, said the investigators, led by Rose A. Rudd, a statistician at the Centers for Disease Control and Prevention.

Also, “efforts to prevent expansion of the number of OPR users who might use heroin when it is available should continue [including] screening for substance abuse, urine testing for drug use, and referral to substance abuse treatment. The use of prescription drug monitoring programs can address inappropriate opioid prescribing and further prevent OPR abuse,” they said.

In 2012, 25- to 34-year-olds had the highest heroin fatality rate; OPR fatalities were highest in those aged 45-54 years. Non-Hispanic whites had the highest rates for both. Men were four times more likely than women to die from a heroin overdose, but only slightly more likely to die from prescription pain pills.

“Heroin overdose death rates increased significantly for both sexes, all age groups, all census regions, and all racial/ethnic groups other than American Indians/Alaska Natives,” the investigators noted.

Meanwhile, from 2010 to 2012 pain pill overdoses declined significantly in men, people under 45 years old, those who live in the South, and non-Hispanic whites. They increased in people aged 55-64 years.

The MMWR is published by the Centers for Disease Control and Prevention.

aotto@frontlinemedcom.com

Fatal heroin overdoses doubled in the United States from 2010 to 2012, according to a report published online Oct. 2 in the Morbidity and Mortality Weekly Report.

In a representative sample of 28 states, heroin deaths climbed from 1,779 to 3,635, a rate increase from 1.0 to 2.1 per 100,000 population. Meanwhile, deaths from prescription opioids fell from 10,427 to 9,869, a decrease from 6.0 to 5.6 per 100,000 population (MMWR 2014;63:849-54).

In Northeastern states, fatal heroin overdoses increased 211.2%. Southern states had an increase of 180.9%, Midwestern states an increase of 62.1%, and Western states an increase of 90.7%, based on state health department data.

The report did not give numbers for individual states, only regions, but it did note that Kentucky reported a 279% increase in heroin deaths from 2010 to 2012, and Ohio had an increase of approximately 300% from 2007 to 2012.

The investigators found no statistically significant relationship between the increase in heroin deaths and the decrease in prescription opioid fatalities. However, they noted that about 75% of heroin users report using prescription opioids first, then switching to heroin, a cheaper, more readily available alternative that gives a more potent high.

Others have reported that young adults are sometimes unaware that prescription pain pills are opioids and that their abuse can slip into heroin use. Particularly hard hit communities have reduced opioid fatalities by getting that message out through education campaigns, and also by distributing intranasal naloxone kits to the people most likely to need them: first responders, family members, and opioid abusers who might need to rescue a friend (See, for example, BMJ 2013;346:f174.).

“State policies that increase access to naloxone, a drug that can reverse potentially fatal respiratory depression in persons who have overdosed from either OPRs [opioid pain relievers] or heroin, or policies that reduce or eliminate penalties when someone reports an overdose, are potentially useful strategies” to counter the problem, said the investigators, led by Rose A. Rudd, a statistician at the Centers for Disease Control and Prevention.

Also, “efforts to prevent expansion of the number of OPR users who might use heroin when it is available should continue [including] screening for substance abuse, urine testing for drug use, and referral to substance abuse treatment. The use of prescription drug monitoring programs can address inappropriate opioid prescribing and further prevent OPR abuse,” they said.

In 2012, 25- to 34-year-olds had the highest heroin fatality rate; OPR fatalities were highest in those aged 45-54 years. Non-Hispanic whites had the highest rates for both. Men were four times more likely than women to die from a heroin overdose, but only slightly more likely to die from prescription pain pills.

“Heroin overdose death rates increased significantly for both sexes, all age groups, all census regions, and all racial/ethnic groups other than American Indians/Alaska Natives,” the investigators noted.

Meanwhile, from 2010 to 2012 pain pill overdoses declined significantly in men, people under 45 years old, those who live in the South, and non-Hispanic whites. They increased in people aged 55-64 years.

The MMWR is published by the Centers for Disease Control and Prevention.

aotto@frontlinemedcom.com

Fatal heroin overdoses doubled in the United States from 2010 to 2012, according to a report published online Oct. 2 in the Morbidity and Mortality Weekly Report.

In a representative sample of 28 states, heroin deaths climbed from 1,779 to 3,635, a rate increase from 1.0 to 2.1 per 100,000 population. Meanwhile, deaths from prescription opioids fell from 10,427 to 9,869, a decrease from 6.0 to 5.6 per 100,000 population (MMWR 2014;63:849-54).

In Northeastern states, fatal heroin overdoses increased 211.2%. Southern states had an increase of 180.9%, Midwestern states an increase of 62.1%, and Western states an increase of 90.7%, based on state health department data.

The report did not give numbers for individual states, only regions, but it did note that Kentucky reported a 279% increase in heroin deaths from 2010 to 2012, and Ohio had an increase of approximately 300% from 2007 to 2012.

The investigators found no statistically significant relationship between the increase in heroin deaths and the decrease in prescription opioid fatalities. However, they noted that about 75% of heroin users report using prescription opioids first, then switching to heroin, a cheaper, more readily available alternative that gives a more potent high.

Others have reported that young adults are sometimes unaware that prescription pain pills are opioids and that their abuse can slip into heroin use. Particularly hard hit communities have reduced opioid fatalities by getting that message out through education campaigns, and also by distributing intranasal naloxone kits to the people most likely to need them: first responders, family members, and opioid abusers who might need to rescue a friend (See, for example, BMJ 2013;346:f174.).

“State policies that increase access to naloxone, a drug that can reverse potentially fatal respiratory depression in persons who have overdosed from either OPRs [opioid pain relievers] or heroin, or policies that reduce or eliminate penalties when someone reports an overdose, are potentially useful strategies” to counter the problem, said the investigators, led by Rose A. Rudd, a statistician at the Centers for Disease Control and Prevention.

Also, “efforts to prevent expansion of the number of OPR users who might use heroin when it is available should continue [including] screening for substance abuse, urine testing for drug use, and referral to substance abuse treatment. The use of prescription drug monitoring programs can address inappropriate opioid prescribing and further prevent OPR abuse,” they said.

In 2012, 25- to 34-year-olds had the highest heroin fatality rate; OPR fatalities were highest in those aged 45-54 years. Non-Hispanic whites had the highest rates for both. Men were four times more likely than women to die from a heroin overdose, but only slightly more likely to die from prescription pain pills.

“Heroin overdose death rates increased significantly for both sexes, all age groups, all census regions, and all racial/ethnic groups other than American Indians/Alaska Natives,” the investigators noted.

Meanwhile, from 2010 to 2012 pain pill overdoses declined significantly in men, people under 45 years old, those who live in the South, and non-Hispanic whites. They increased in people aged 55-64 years.

The MMWR is published by the Centers for Disease Control and Prevention.

aotto@frontlinemedcom.com

LAS VEGAS – When methotrexate doesn’t work in rheumatoid arthritis and patients are still suffering after their first tumor necrosis factor inhibitor, it’s worthwhile to try a second TNF inhibitor, according to Dr. Daniel Furst, the Carl M Pearson Professor in Rheumatology at University of California, Los Angeles.

Even just side effects from the first TNF inhibitor indicate that the second one might work, he said at the conference held by Global Academy for Medical Education.

Dr. Furst also explains in the video how to safely use steroids in RA patients, and when to move them to non–TNF inhibitor biologics.

Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

LAS VEGAS – When methotrexate doesn’t work in rheumatoid arthritis and patients are still suffering after their first tumor necrosis factor inhibitor, it’s worthwhile to try a second TNF inhibitor, according to Dr. Daniel Furst, the Carl M Pearson Professor in Rheumatology at University of California, Los Angeles.

Even just side effects from the first TNF inhibitor indicate that the second one might work, he said at the conference held by Global Academy for Medical Education.

Dr. Furst also explains in the video how to safely use steroids in RA patients, and when to move them to non–TNF inhibitor biologics.

Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

LAS VEGAS – When methotrexate doesn’t work in rheumatoid arthritis and patients are still suffering after their first tumor necrosis factor inhibitor, it’s worthwhile to try a second TNF inhibitor, according to Dr. Daniel Furst, the Carl M Pearson Professor in Rheumatology at University of California, Los Angeles.

Even just side effects from the first TNF inhibitor indicate that the second one might work, he said at the conference held by Global Academy for Medical Education.

Dr. Furst also explains in the video how to safely use steroids in RA patients, and when to move them to non–TNF inhibitor biologics.

Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

LAS VEGAS– With the help of newer equipment, ophthalmologists are catching hydroxychloroquine-associated retina changes earlier than ever before, but it’s not clear if early changes signal trouble and a need to discontinue the drug, a linchpin of lupus therapy, according to Dr. Susan Manzi.

Hydroxychloroquine (Plaquenil) causes eye damage in an estimated 1% of users after about 5-7 years of use. Bilateral “bull’s-eye” retinal pigment-change lesions are the traditional telltale signs; by the time they appear, patients already have some permanent vision loss.

The hope is to catch problems earlier. Newer ophthalmologic techniques – optical coherence tomography, fundus autofluorescence screening, and others – detect far more subtle retina changes earlier in the course of treatment, but the importance of those early changes is not clear. This uncertainty makes it hard for patients and rheumatologists to know what to do when they hear about such findings, especially when hydroxychloroquine is working, Dr. Manzi said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“Before, they used to look in the eye for pigment changes. Now, [we are] getting calls from ophthalmologists with concerns about” retinal edema and other less obvious problems, which are sometimes described as “early maculopathy, so we have to stop the drug” even if there are no vision problems. “We really don’t know what to make of it when [maybe] there’s just a little edema. It reminds me of the era when we started doing MRIs. We weren’t sure if all the things we found were relevant; I think we are going to be hearing more from ophthalmologists about some of these changes” and how much to worry about them, said Dr. Manzi, chair of the Allegheny Health Network department of medicine and director of the Lupus Center of Excellence, both in Pittsburgh.

In the meantime, “I can count the times I’ve stopped” hydroxychloroquine for eye issues, “and mostly it was because of [concomitant] macular degeneration or diabetic retinopathy,” not hydroxychloroquine-induced damage, she said.

In 2011, the American Academy of Ophthalmology recommended baseline screening with the newer technologies, and follow-up screening after 5 years. When “possible” toxicity is found, the group recommends screening every 3-6 months.

“There is no firm definition of ‘early’ toxicity, so that subtle changes (especially if parafoveal) – in visual field sensitivity, macular pigmentation, or any of the objective screening tests … should be taken seriously. If such changes occur, the tests should be repeated for verification or verified with other procedures. However, mild and nonspecific changes can appear in all tests for reasons other than toxicity (including cataract, early macular degeneration, and testing variation of the visual field …), and a relationship to [hydroxychloroquine] is difficult to confirm without evidence of paracentral functional or structural loss,” the group said (Ophthalmology 2011;118:415-22).

Dr. Manzi follows this screening advice. She also requests repeat testing if ophthalmologists find a problem on somewhat subjective measures, such as peripheral vision. Repeat testing sometimes alleviates worries.

Her practice also mirrors the academy’s dosing guidelines, which aim to minimize eye and other toxicities. For most lupus patients, that means 200 mg twice a day, or 400 mg once daily. “Most people do fine with that,” although 200 mg a day is a better call in small women and adolescents, she said.

Dr. Manzi is an adviser or consultant for Genentech, Eli Lilly, Bristol-Myers Squibb, GlaxoSmithKline, and other companies. Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

LAS VEGAS– With the help of newer equipment, ophthalmologists are catching hydroxychloroquine-associated retina changes earlier than ever before, but it’s not clear if early changes signal trouble and a need to discontinue the drug, a linchpin of lupus therapy, according to Dr. Susan Manzi.

Hydroxychloroquine (Plaquenil) causes eye damage in an estimated 1% of users after about 5-7 years of use. Bilateral “bull’s-eye” retinal pigment-change lesions are the traditional telltale signs; by the time they appear, patients already have some permanent vision loss.

The hope is to catch problems earlier. Newer ophthalmologic techniques – optical coherence tomography, fundus autofluorescence screening, and others – detect far more subtle retina changes earlier in the course of treatment, but the importance of those early changes is not clear. This uncertainty makes it hard for patients and rheumatologists to know what to do when they hear about such findings, especially when hydroxychloroquine is working, Dr. Manzi said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“Before, they used to look in the eye for pigment changes. Now, [we are] getting calls from ophthalmologists with concerns about” retinal edema and other less obvious problems, which are sometimes described as “early maculopathy, so we have to stop the drug” even if there are no vision problems. “We really don’t know what to make of it when [maybe] there’s just a little edema. It reminds me of the era when we started doing MRIs. We weren’t sure if all the things we found were relevant; I think we are going to be hearing more from ophthalmologists about some of these changes” and how much to worry about them, said Dr. Manzi, chair of the Allegheny Health Network department of medicine and director of the Lupus Center of Excellence, both in Pittsburgh.

In the meantime, “I can count the times I’ve stopped” hydroxychloroquine for eye issues, “and mostly it was because of [concomitant] macular degeneration or diabetic retinopathy,” not hydroxychloroquine-induced damage, she said.

In 2011, the American Academy of Ophthalmology recommended baseline screening with the newer technologies, and follow-up screening after 5 years. When “possible” toxicity is found, the group recommends screening every 3-6 months.

“There is no firm definition of ‘early’ toxicity, so that subtle changes (especially if parafoveal) – in visual field sensitivity, macular pigmentation, or any of the objective screening tests … should be taken seriously. If such changes occur, the tests should be repeated for verification or verified with other procedures. However, mild and nonspecific changes can appear in all tests for reasons other than toxicity (including cataract, early macular degeneration, and testing variation of the visual field …), and a relationship to [hydroxychloroquine] is difficult to confirm without evidence of paracentral functional or structural loss,” the group said (Ophthalmology 2011;118:415-22).

Dr. Manzi follows this screening advice. She also requests repeat testing if ophthalmologists find a problem on somewhat subjective measures, such as peripheral vision. Repeat testing sometimes alleviates worries.

Her practice also mirrors the academy’s dosing guidelines, which aim to minimize eye and other toxicities. For most lupus patients, that means 200 mg twice a day, or 400 mg once daily. “Most people do fine with that,” although 200 mg a day is a better call in small women and adolescents, she said.

Dr. Manzi is an adviser or consultant for Genentech, Eli Lilly, Bristol-Myers Squibb, GlaxoSmithKline, and other companies. Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

LAS VEGAS– With the help of newer equipment, ophthalmologists are catching hydroxychloroquine-associated retina changes earlier than ever before, but it’s not clear if early changes signal trouble and a need to discontinue the drug, a linchpin of lupus therapy, according to Dr. Susan Manzi.

Hydroxychloroquine (Plaquenil) causes eye damage in an estimated 1% of users after about 5-7 years of use. Bilateral “bull’s-eye” retinal pigment-change lesions are the traditional telltale signs; by the time they appear, patients already have some permanent vision loss.

The hope is to catch problems earlier. Newer ophthalmologic techniques – optical coherence tomography, fundus autofluorescence screening, and others – detect far more subtle retina changes earlier in the course of treatment, but the importance of those early changes is not clear. This uncertainty makes it hard for patients and rheumatologists to know what to do when they hear about such findings, especially when hydroxychloroquine is working, Dr. Manzi said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“Before, they used to look in the eye for pigment changes. Now, [we are] getting calls from ophthalmologists with concerns about” retinal edema and other less obvious problems, which are sometimes described as “early maculopathy, so we have to stop the drug” even if there are no vision problems. “We really don’t know what to make of it when [maybe] there’s just a little edema. It reminds me of the era when we started doing MRIs. We weren’t sure if all the things we found were relevant; I think we are going to be hearing more from ophthalmologists about some of these changes” and how much to worry about them, said Dr. Manzi, chair of the Allegheny Health Network department of medicine and director of the Lupus Center of Excellence, both in Pittsburgh.

In the meantime, “I can count the times I’ve stopped” hydroxychloroquine for eye issues, “and mostly it was because of [concomitant] macular degeneration or diabetic retinopathy,” not hydroxychloroquine-induced damage, she said.

In 2011, the American Academy of Ophthalmology recommended baseline screening with the newer technologies, and follow-up screening after 5 years. When “possible” toxicity is found, the group recommends screening every 3-6 months.

“There is no firm definition of ‘early’ toxicity, so that subtle changes (especially if parafoveal) – in visual field sensitivity, macular pigmentation, or any of the objective screening tests … should be taken seriously. If such changes occur, the tests should be repeated for verification or verified with other procedures. However, mild and nonspecific changes can appear in all tests for reasons other than toxicity (including cataract, early macular degeneration, and testing variation of the visual field …), and a relationship to [hydroxychloroquine] is difficult to confirm without evidence of paracentral functional or structural loss,” the group said (Ophthalmology 2011;118:415-22).

Dr. Manzi follows this screening advice. She also requests repeat testing if ophthalmologists find a problem on somewhat subjective measures, such as peripheral vision. Repeat testing sometimes alleviates worries.

Her practice also mirrors the academy’s dosing guidelines, which aim to minimize eye and other toxicities. For most lupus patients, that means 200 mg twice a day, or 400 mg once daily. “Most people do fine with that,” although 200 mg a day is a better call in small women and adolescents, she said.

Dr. Manzi is an adviser or consultant for Genentech, Eli Lilly, Bristol-Myers Squibb, GlaxoSmithKline, and other companies. Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

LAS VEGAS – If patients don’t respond to an antidepressant within 2 weeks, it’s probably time to switch them to another antidepressant or think about add-on therapy. If symptoms have gotten worse, however, it’s time to stop the antidepressant altogether, according to Dr. Charles Raison, professor of psychiatry at the University of Arizona in Tucson.

It doesn’t take 6-8 weeks for antidepressants to work; that commonly held notion is “100% wrong,” he said.

Imaging studies show brain activity changes within 2 hours of a single dose, and in trials where antidepressants separate from placebo, they do so in a week or 2 (Arch. Gen. Psychiatry 2006;63:1217-23). “Most of the action is early on,” Dr. Raison said at the annual Perspectives in Rheumatic Diseases conference held by the Global Academy for Medical Education.

“Monitoring response in the first 2 weeks is essential, because it’s going to tell you whether you’ve got the right” treatment. With any given antidepressant, about 75% of patients will respond, but about 25% will get “much, much worse. If a patient gets worse, stop. You should take that extremely seriously,” he said (Arch. Gen. Psychiatry 2011;68:1227-37).

In general, anxious people and suicidal people don’t do as well on antidepressants. Also, people with a history of childhood neglect, abuse, or trauma respond better to psychotherapy, so it’s worth asking about such issues. It’s also worth asking patients what they want to do, be it pharmaceuticals, psychotherapy, or both. Success is more likely if patients get what they want, Dr. Raison said.

“Pain is a powerful predictor of not doing well,” especially with SSRIs, so “unfortunately, [rheumatologists] deal with populations that are less likely to have a robust response.” Even so, “if you can help people with their pain, you’ll probably help” relieve their depression and help their antidepressant work, he said.

When patients don’t respond after a few weeks, “the first thing most of us do is increase the dose; for SSRIs, the data” indicate it doesn’t work. In one study, for instance, people did just as well on a lower dose as on a higher one, he said (Br. J. Psychiatry 2006;189:309-16).

Up to a quarter of patients, however, will do better if switched to another antidepressant. Some studies suggest staying in the same class of drugs; others suggest trying a different class. For now, which one to pick “depends [mostly] on side effects. There isn’t a best antidepressant; the best one is the one that works in any given patient,” Dr. Raison said (Eur. Neuropsychopharmacol. 2012;22:453-68).

Augmentation is another option, with atypical antipsychotics currently the most popular choice. There’s convincing evidence that they help, but they also have well-known and serious side effects, including extrapyramidal syndromes, metabolic derangements, and weight gain.

There’s also strong evidence for psychotherapy as an adjunct, and good data for lithium and a range of other agents. Whole-body hyperthermia is emerging as a possible depression treatment, as well.

Dr. Raison recommended actively treating nausea, jitteriness, diarrhea, and other short-term SSRI side effects; it makes it more likely that patients will stay on their treatment. Also, anxious patients and those with somatic complaints are more likely to tolerate antidepressants if they are started on subtherapeutic doses, then are titrated slowly up to a recommended dose.

Of all the SSRIs, paroxetine (Paxil) “is the one I most highly recommend you do not use. There’s no evidence it’s better than any of the others,” and it’s the one most likely to cause weight gain, sexual dysfunction, and cardiac issues, he said.

“We don’t know how long you should treat” with antidepressants; “probably at least 6-9 months,” he noted.

Dr. Raison is a consultant for Pamlab, Lilly, and Lundbeck. He is on the speakers bureaus of Pamlab and Sunovion.

LAS VEGAS – If patients don’t respond to an antidepressant within 2 weeks, it’s probably time to switch them to another antidepressant or think about add-on therapy. If symptoms have gotten worse, however, it’s time to stop the antidepressant altogether, according to Dr. Charles Raison, professor of psychiatry at the University of Arizona in Tucson.

It doesn’t take 6-8 weeks for antidepressants to work; that commonly held notion is “100% wrong,” he said.

Imaging studies show brain activity changes within 2 hours of a single dose, and in trials where antidepressants separate from placebo, they do so in a week or 2 (Arch. Gen. Psychiatry 2006;63:1217-23). “Most of the action is early on,” Dr. Raison said at the annual Perspectives in Rheumatic Diseases conference held by the Global Academy for Medical Education.

“Monitoring response in the first 2 weeks is essential, because it’s going to tell you whether you’ve got the right” treatment. With any given antidepressant, about 75% of patients will respond, but about 25% will get “much, much worse. If a patient gets worse, stop. You should take that extremely seriously,” he said (Arch. Gen. Psychiatry 2011;68:1227-37).

In general, anxious people and suicidal people don’t do as well on antidepressants. Also, people with a history of childhood neglect, abuse, or trauma respond better to psychotherapy, so it’s worth asking about such issues. It’s also worth asking patients what they want to do, be it pharmaceuticals, psychotherapy, or both. Success is more likely if patients get what they want, Dr. Raison said.

“Pain is a powerful predictor of not doing well,” especially with SSRIs, so “unfortunately, [rheumatologists] deal with populations that are less likely to have a robust response.” Even so, “if you can help people with their pain, you’ll probably help” relieve their depression and help their antidepressant work, he said.

When patients don’t respond after a few weeks, “the first thing most of us do is increase the dose; for SSRIs, the data” indicate it doesn’t work. In one study, for instance, people did just as well on a lower dose as on a higher one, he said (Br. J. Psychiatry 2006;189:309-16).

Up to a quarter of patients, however, will do better if switched to another antidepressant. Some studies suggest staying in the same class of drugs; others suggest trying a different class. For now, which one to pick “depends [mostly] on side effects. There isn’t a best antidepressant; the best one is the one that works in any given patient,” Dr. Raison said (Eur. Neuropsychopharmacol. 2012;22:453-68).

Augmentation is another option, with atypical antipsychotics currently the most popular choice. There’s convincing evidence that they help, but they also have well-known and serious side effects, including extrapyramidal syndromes, metabolic derangements, and weight gain.

There’s also strong evidence for psychotherapy as an adjunct, and good data for lithium and a range of other agents. Whole-body hyperthermia is emerging as a possible depression treatment, as well.

Dr. Raison recommended actively treating nausea, jitteriness, diarrhea, and other short-term SSRI side effects; it makes it more likely that patients will stay on their treatment. Also, anxious patients and those with somatic complaints are more likely to tolerate antidepressants if they are started on subtherapeutic doses, then are titrated slowly up to a recommended dose.

Of all the SSRIs, paroxetine (Paxil) “is the one I most highly recommend you do not use. There’s no evidence it’s better than any of the others,” and it’s the one most likely to cause weight gain, sexual dysfunction, and cardiac issues, he said.

“We don’t know how long you should treat” with antidepressants; “probably at least 6-9 months,” he noted.

Dr. Raison is a consultant for Pamlab, Lilly, and Lundbeck. He is on the speakers bureaus of Pamlab and Sunovion.

LAS VEGAS – If patients don’t respond to an antidepressant within 2 weeks, it’s probably time to switch them to another antidepressant or think about add-on therapy. If symptoms have gotten worse, however, it’s time to stop the antidepressant altogether, according to Dr. Charles Raison, professor of psychiatry at the University of Arizona in Tucson.

It doesn’t take 6-8 weeks for antidepressants to work; that commonly held notion is “100% wrong,” he said.

Imaging studies show brain activity changes within 2 hours of a single dose, and in trials where antidepressants separate from placebo, they do so in a week or 2 (Arch. Gen. Psychiatry 2006;63:1217-23). “Most of the action is early on,” Dr. Raison said at the annual Perspectives in Rheumatic Diseases conference held by the Global Academy for Medical Education.

“Monitoring response in the first 2 weeks is essential, because it’s going to tell you whether you’ve got the right” treatment. With any given antidepressant, about 75% of patients will respond, but about 25% will get “much, much worse. If a patient gets worse, stop. You should take that extremely seriously,” he said (Arch. Gen. Psychiatry 2011;68:1227-37).

In general, anxious people and suicidal people don’t do as well on antidepressants. Also, people with a history of childhood neglect, abuse, or trauma respond better to psychotherapy, so it’s worth asking about such issues. It’s also worth asking patients what they want to do, be it pharmaceuticals, psychotherapy, or both. Success is more likely if patients get what they want, Dr. Raison said.

“Pain is a powerful predictor of not doing well,” especially with SSRIs, so “unfortunately, [rheumatologists] deal with populations that are less likely to have a robust response.” Even so, “if you can help people with their pain, you’ll probably help” relieve their depression and help their antidepressant work, he said.

When patients don’t respond after a few weeks, “the first thing most of us do is increase the dose; for SSRIs, the data” indicate it doesn’t work. In one study, for instance, people did just as well on a lower dose as on a higher one, he said (Br. J. Psychiatry 2006;189:309-16).

Up to a quarter of patients, however, will do better if switched to another antidepressant. Some studies suggest staying in the same class of drugs; others suggest trying a different class. For now, which one to pick “depends [mostly] on side effects. There isn’t a best antidepressant; the best one is the one that works in any given patient,” Dr. Raison said (Eur. Neuropsychopharmacol. 2012;22:453-68).

Augmentation is another option, with atypical antipsychotics currently the most popular choice. There’s convincing evidence that they help, but they also have well-known and serious side effects, including extrapyramidal syndromes, metabolic derangements, and weight gain.

There’s also strong evidence for psychotherapy as an adjunct, and good data for lithium and a range of other agents. Whole-body hyperthermia is emerging as a possible depression treatment, as well.

Dr. Raison recommended actively treating nausea, jitteriness, diarrhea, and other short-term SSRI side effects; it makes it more likely that patients will stay on their treatment. Also, anxious patients and those with somatic complaints are more likely to tolerate antidepressants if they are started on subtherapeutic doses, then are titrated slowly up to a recommended dose.

Of all the SSRIs, paroxetine (Paxil) “is the one I most highly recommend you do not use. There’s no evidence it’s better than any of the others,” and it’s the one most likely to cause weight gain, sexual dysfunction, and cardiac issues, he said.

“We don’t know how long you should treat” with antidepressants; “probably at least 6-9 months,” he noted.

Dr. Raison is a consultant for Pamlab, Lilly, and Lundbeck. He is on the speakers bureaus of Pamlab and Sunovion.