Sally Koch Kubetin

SANTA MONICA, CALIF. — Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, he noted at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus. The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE. These included patients with fixed lesions with a potential for atrophy. However, data from a population-based study of inhabitants of Rochester, Minn. now show that these patients are as likely as others with CLE to progress to SLE.

The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky). hf particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249–53).

These findings “give us reason to treat these patients more aggressively than we might have done,” said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. “This is a photosensitive disease. It's photodistributed. It's photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference,” Dr. Callen noted.

First-line therapy is the antimalarial hydroxychloroquine or chloroquine. “To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus,” Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401–9). “To me, that means we need to be treating patients with antimalarials earlier than we do,” he said.

SDEF and this news organization are owned by Elsevier. Dr. Callen reported no relevant financial relationships.

Aggressive use of antimalarials, including smoking cessation, is warranted to stop progression of CLE to SLE.

Source DR. CALLEN

SANTA MONICA, CALIF. — Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, he noted at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus. The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE. These included patients with fixed lesions with a potential for atrophy. However, data from a population-based study of inhabitants of Rochester, Minn. now show that these patients are as likely as others with CLE to progress to SLE.

The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky). hf particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249–53).

These findings “give us reason to treat these patients more aggressively than we might have done,” said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. “This is a photosensitive disease. It's photodistributed. It's photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference,” Dr. Callen noted.

First-line therapy is the antimalarial hydroxychloroquine or chloroquine. “To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus,” Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401–9). “To me, that means we need to be treating patients with antimalarials earlier than we do,” he said.

SDEF and this news organization are owned by Elsevier. Dr. Callen reported no relevant financial relationships.

Aggressive use of antimalarials, including smoking cessation, is warranted to stop progression of CLE to SLE.

Source DR. CALLEN

SANTA MONICA, CALIF. — Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, he noted at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus. The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE. These included patients with fixed lesions with a potential for atrophy. However, data from a population-based study of inhabitants of Rochester, Minn. now show that these patients are as likely as others with CLE to progress to SLE.

The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky). hf particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249–53).

These findings “give us reason to treat these patients more aggressively than we might have done,” said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. “This is a photosensitive disease. It's photodistributed. It's photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference,” Dr. Callen noted.

First-line therapy is the antimalarial hydroxychloroquine or chloroquine. “To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus,” Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401–9). “To me, that means we need to be treating patients with antimalarials earlier than we do,” he said.

SDEF and this news organization are owned by Elsevier. Dr. Callen reported no relevant financial relationships.

Aggressive use of antimalarials, including smoking cessation, is warranted to stop progression of CLE to SLE.

Source DR. CALLEN

SANTA MONICA, CALIF. — Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbance, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600–10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient's fatigue, sleep, and cognition and the patient's overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3–6 and an SS score of 9 or more fell within the fibromyalgia domain; the scores correlated well with the tender point score on the ACR's 1990 classification criteria.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. “I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia, irritable bowel syndrome, and even some of our rheumatoid and lupus patients,” said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients' experience of spontaneous pain and fluctuations in pain that are unrelated to activity. In addition, the increased connectivity may have implications for cognition (Arthritis Rheum. 2010;62:2545–55).

Dr. Mease reported that he presented data from a study of 363 patients with fibromyalgia who were treated with either pregabalin alone or in combination with milnacipran at the annual meeting of the European League Against Rheumatism earlier this year. Those treated with the combination therapy (pregabalin at 150–225 mg twice daily plus 50 mg of milnacipran) for 11 weeks showed a 20-point improvement on the visual analog scale (VAS) for pain assessment. In addition, 51% considered themselves “very much improved” on the Patient Global Impression of Change (PGIC) scale.

In contrast, patients on monotherapy showed a 5-point improvement on the VAS, and 24% considered themselves very much improved on the PGIC. About one-third of the patients did not finish the trial.

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed that he has financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

SANTA MONICA, CALIF. — Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbance, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600–10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient's fatigue, sleep, and cognition and the patient's overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3–6 and an SS score of 9 or more fell within the fibromyalgia domain; the scores correlated well with the tender point score on the ACR's 1990 classification criteria.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. “I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia, irritable bowel syndrome, and even some of our rheumatoid and lupus patients,” said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients' experience of spontaneous pain and fluctuations in pain that are unrelated to activity. In addition, the increased connectivity may have implications for cognition (Arthritis Rheum. 2010;62:2545–55).

Dr. Mease reported that he presented data from a study of 363 patients with fibromyalgia who were treated with either pregabalin alone or in combination with milnacipran at the annual meeting of the European League Against Rheumatism earlier this year. Those treated with the combination therapy (pregabalin at 150–225 mg twice daily plus 50 mg of milnacipran) for 11 weeks showed a 20-point improvement on the visual analog scale (VAS) for pain assessment. In addition, 51% considered themselves “very much improved” on the Patient Global Impression of Change (PGIC) scale.

In contrast, patients on monotherapy showed a 5-point improvement on the VAS, and 24% considered themselves very much improved on the PGIC. About one-third of the patients did not finish the trial.

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed that he has financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

SANTA MONICA, CALIF. — Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbance, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600–10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient's fatigue, sleep, and cognition and the patient's overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3–6 and an SS score of 9 or more fell within the fibromyalgia domain; the scores correlated well with the tender point score on the ACR's 1990 classification criteria.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. “I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia, irritable bowel syndrome, and even some of our rheumatoid and lupus patients,” said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients' experience of spontaneous pain and fluctuations in pain that are unrelated to activity. In addition, the increased connectivity may have implications for cognition (Arthritis Rheum. 2010;62:2545–55).

Dr. Mease reported that he presented data from a study of 363 patients with fibromyalgia who were treated with either pregabalin alone or in combination with milnacipran at the annual meeting of the European League Against Rheumatism earlier this year. Those treated with the combination therapy (pregabalin at 150–225 mg twice daily plus 50 mg of milnacipran) for 11 weeks showed a 20-point improvement on the visual analog scale (VAS) for pain assessment. In addition, 51% considered themselves “very much improved” on the Patient Global Impression of Change (PGIC) scale.

In contrast, patients on monotherapy showed a 5-point improvement on the VAS, and 24% considered themselves very much improved on the PGIC. About one-third of the patients did not finish the trial.

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed that he has financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

SANTA MONICA, CALIF. — Gastroenterologists seem to be taking a page from the rheumatologists' playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found the odds ratio of having both IBD and RA was 2.1–2.7, and of having IBD and ankylosing spondylitis, about 5.8–7.8 (Inflamm. Bowel Dis. 2008;14:738–43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158–63).

In the prebiologic era, the natural history of Crohn's disease also was grim. Crohn's followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244–50). “Virtually all Crohn's disease patients relapsed and most required one or more surgeries,” said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago. An estimated 10% of Crohn's patients had their colons removed surgically within 1 year of their diagnosis with IBD.

Even today, most ulcerative colitis patients are treated with steroids, and many of these patients become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255–60). There is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher (N. Engl. J. Med. 2010;362:1383–95).

SDEF and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.

SANTA MONICA, CALIF. — Gastroenterologists seem to be taking a page from the rheumatologists' playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found the odds ratio of having both IBD and RA was 2.1–2.7, and of having IBD and ankylosing spondylitis, about 5.8–7.8 (Inflamm. Bowel Dis. 2008;14:738–43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158–63).

In the prebiologic era, the natural history of Crohn's disease also was grim. Crohn's followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244–50). “Virtually all Crohn's disease patients relapsed and most required one or more surgeries,” said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago. An estimated 10% of Crohn's patients had their colons removed surgically within 1 year of their diagnosis with IBD.

Even today, most ulcerative colitis patients are treated with steroids, and many of these patients become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255–60). There is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher (N. Engl. J. Med. 2010;362:1383–95).

SDEF and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.

SANTA MONICA, CALIF. — Gastroenterologists seem to be taking a page from the rheumatologists' playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found the odds ratio of having both IBD and RA was 2.1–2.7, and of having IBD and ankylosing spondylitis, about 5.8–7.8 (Inflamm. Bowel Dis. 2008;14:738–43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158–63).

In the prebiologic era, the natural history of Crohn's disease also was grim. Crohn's followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244–50). “Virtually all Crohn's disease patients relapsed and most required one or more surgeries,” said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago. An estimated 10% of Crohn's patients had their colons removed surgically within 1 year of their diagnosis with IBD.

Even today, most ulcerative colitis patients are treated with steroids, and many of these patients become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255–60). There is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher (N. Engl. J. Med. 2010;362:1383–95).

SDEF and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.

SANTA MONICA, CALIF. — Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbances, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600-10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient's fatigue, sleep, and cognition and the patient's overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3-6 and an SS score of 9 or more fell within the fibromyalgia domain, and the scores correlated well with the tender point score on the American College of Rheumatology 1990 classification criteria.

These criteria, although already published, are considered preliminary and are being tested in clinical settings to confirm their reliability.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease. He noted that these findings confirm the observation that fibromyalgia often coexists with other chronic pain conditions.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. “I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia,” Dr. Mease said.

There have been data from clinical trials of agents targeting some of the neurobiologic pathways that are proving to be better than placebo in lessening some of the symptoms of fibromyalgia, said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients' experience of spontaneous pain and fluctuations in pain that are unrelated to activity.(Arthritis Rheum. 2010;62:2545-55).

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

Data show that 20% of patients with rheumatoid arthritis have scores indicating concomitant fibromyalgia.

Source DR. MEASE

SANTA MONICA, CALIF. — Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbances, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600-10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient's fatigue, sleep, and cognition and the patient's overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3-6 and an SS score of 9 or more fell within the fibromyalgia domain, and the scores correlated well with the tender point score on the American College of Rheumatology 1990 classification criteria.

These criteria, although already published, are considered preliminary and are being tested in clinical settings to confirm their reliability.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease. He noted that these findings confirm the observation that fibromyalgia often coexists with other chronic pain conditions.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. “I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia,” Dr. Mease said.

There have been data from clinical trials of agents targeting some of the neurobiologic pathways that are proving to be better than placebo in lessening some of the symptoms of fibromyalgia, said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients' experience of spontaneous pain and fluctuations in pain that are unrelated to activity.(Arthritis Rheum. 2010;62:2545-55).

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

Data show that 20% of patients with rheumatoid arthritis have scores indicating concomitant fibromyalgia.

Source DR. MEASE

SANTA MONICA, CALIF. — Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbances, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600-10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient's fatigue, sleep, and cognition and the patient's overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3-6 and an SS score of 9 or more fell within the fibromyalgia domain, and the scores correlated well with the tender point score on the American College of Rheumatology 1990 classification criteria.

These criteria, although already published, are considered preliminary and are being tested in clinical settings to confirm their reliability.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease. He noted that these findings confirm the observation that fibromyalgia often coexists with other chronic pain conditions.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. “I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia,” Dr. Mease said.

There have been data from clinical trials of agents targeting some of the neurobiologic pathways that are proving to be better than placebo in lessening some of the symptoms of fibromyalgia, said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients' experience of spontaneous pain and fluctuations in pain that are unrelated to activity.(Arthritis Rheum. 2010;62:2545-55).

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

Data show that 20% of patients with rheumatoid arthritis have scores indicating concomitant fibromyalgia.

Source DR. MEASE

SANTA MONICA, CALIF. — Gastroenterologists seem to be taking a page from the rheumatologists' playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at the meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis. The cartilage and bone usually are spared from destruction. Arthritis in IBD usually involves five or more joints and lasts about 3 years.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found that the prevalence of IBD was about 0.62%-0.65% and the prevalence of RA was about 0.98%–1.08% in patients aged 47-56 years old living in the Midwest or the South. The odds ratio of having both IBD and RA was 2.1-2.7, and of having IBD and ankylosing spondylitis, about 5.8-7.8 (Inflamm. Bowel Dis. 2008;14:738-43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158-63).

In the prebiologic era, the natural history of Crohn's disease also was grim. The disease followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244-50).

In the past, “virtually all Crohn's disease patients relapsed and most required one or more surgeries,” said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago (Gastroenterology 1985;88:1826-33).

An estimated 10% of Crohn's patients had their colons removed surgically within 1 year of their diagnosis with IBD. The disease tended to recur at the site of anastomosis of the previous surgery and to involve as much bowel as had been removed in the previous surgery. About half of the patients needed a second surgery.

Even today, most ulcerative colitis patients are treated with steroids, and many of these patients become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255-60).

These days, there is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher and lesions that were visible on endoscopy (N. Engl. J. Med. 2010;362:1383-95).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.

SANTA MONICA, CALIF. — Gastroenterologists seem to be taking a page from the rheumatologists' playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at the meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis. The cartilage and bone usually are spared from destruction. Arthritis in IBD usually involves five or more joints and lasts about 3 years.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found that the prevalence of IBD was about 0.62%-0.65% and the prevalence of RA was about 0.98%–1.08% in patients aged 47-56 years old living in the Midwest or the South. The odds ratio of having both IBD and RA was 2.1-2.7, and of having IBD and ankylosing spondylitis, about 5.8-7.8 (Inflamm. Bowel Dis. 2008;14:738-43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158-63).

In the prebiologic era, the natural history of Crohn's disease also was grim. The disease followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244-50).

In the past, “virtually all Crohn's disease patients relapsed and most required one or more surgeries,” said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago (Gastroenterology 1985;88:1826-33).

An estimated 10% of Crohn's patients had their colons removed surgically within 1 year of their diagnosis with IBD. The disease tended to recur at the site of anastomosis of the previous surgery and to involve as much bowel as had been removed in the previous surgery. About half of the patients needed a second surgery.

Even today, most ulcerative colitis patients are treated with steroids, and many of these patients become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255-60).

These days, there is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher and lesions that were visible on endoscopy (N. Engl. J. Med. 2010;362:1383-95).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.

SANTA MONICA, CALIF. — Gastroenterologists seem to be taking a page from the rheumatologists' playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at the meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis. The cartilage and bone usually are spared from destruction. Arthritis in IBD usually involves five or more joints and lasts about 3 years.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found that the prevalence of IBD was about 0.62%-0.65% and the prevalence of RA was about 0.98%–1.08% in patients aged 47-56 years old living in the Midwest or the South. The odds ratio of having both IBD and RA was 2.1-2.7, and of having IBD and ankylosing spondylitis, about 5.8-7.8 (Inflamm. Bowel Dis. 2008;14:738-43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158-63).

In the prebiologic era, the natural history of Crohn's disease also was grim. The disease followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244-50).

In the past, “virtually all Crohn's disease patients relapsed and most required one or more surgeries,” said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago (Gastroenterology 1985;88:1826-33).

An estimated 10% of Crohn's patients had their colons removed surgically within 1 year of their diagnosis with IBD. The disease tended to recur at the site of anastomosis of the previous surgery and to involve as much bowel as had been removed in the previous surgery. About half of the patients needed a second surgery.

Even today, most ulcerative colitis patients are treated with steroids, and many of these patients become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255-60).

These days, there is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher and lesions that were visible on endoscopy (N. Engl. J. Med. 2010;362:1383-95).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.

ATLANTA – The number of women serving as professors and division directors of rheumatology has not changed for the past 30 years, a circumstance that should prompt a policy directive from the American College of Rheumatology, according to some of its leaders.

During an annual meeting session sponsored by the Committee on Rheumatology Training and Workforce Issues and the ACR Young Investigator Subcommittee of the Research Committee, Dr. Abby Goulder Abelson noted that women accounted for 60% of graduates of rheumatology fellowships in 2009. Yet women hold just 30% of all academic appointments and comprise 15% of full professors and 7% of division heads. Those figures have been virtually unchanged for the past 30 years, according to Dr. Abelson, who chairs the committee.

Findings from a 2009 benchmarking survey by the American Association of Medical Colleges showed that women accounted for 18% of full professors, 13% of department chairs, and 12% of medical school deans.

"If [the ACR’s Research and Education Foundation (REF)] had a policy that it would not support fellowship programs that did not have more women in leadership," the problem would fix itself, said Dr. David Wofsy, past president of the ACR. "A decade ago we were tremendously short of rheumatology fellows. So REF and ACR set a goal and achieved it. ... Let’s articulate the goals and decide what practices we need to achieve these goals."

Dr. Wofsy suggested the goal should be to increase by 25% the number of women division chiefs. Dr. Wofsy is professor of medicine and microbiology/immunology and chief of rheumatology at the San Francisco VA Medical Center as well as associate dean for admissions at the University of California at San Francisco.

"We need to communicate the message that having more women in leadership in academic programs is good for training and good for society," said Dr. Christy I. Sandborg, a pediatric rheumatologist who is associate chair of the department of pediatrics at Stanford (Calif.) University.

The lack of women in academic leadership positions in rheumatology training programs is not a woman’s issue. It is a rheumatology issue and an ACR issue, said Dr. Sandborg, who cautioned against tainting any effort to promote more women with even the hint that women are in some way damaged and need help.

Data gathered in 2008 showed that 9.1% of women left their academic posts early in their careers, compared with 7.7% of men. Women cited as their reasons for leaving their observation that their gender affected their salary, their rate of promotion, and the amount of their protected time for research and teaching. As pronounced as these problems were for women in general, they were more so for minority women, said Dr. Abelson, who is interim chair of the department of rheumatologic and immunologic disease at the Cleveland Clinic.

At the same time, there is a sea change in how both men and women approach their professional lives and look for work-life integration. "This is the first time that I have attended a session on gender where 50% of the audience is male," she said.

Most rheumatology divisions around the country are actively recruiting new faculty. But to many young rheumatologists, private practice feels like the better choice. Dr. David Karp, chief of the division of rheumatology at the University of Texas Southwestern Medical Center at Dallas, acknowledged that "my young fellows feel that an academic career lacks control."

Dr. Abelson noted that young male rheumatologists want more control and a less stressful lifestyle, which is also changing academic medicine. "They start early, work through lunch, and leave early to pick up their kids from day care."

In Dr. Sandborg’s experience, young men who ask for flexible work arrangements are stigmatized because older faculty consider them to be less than serious about their careers.

Another presenter, Anne C. Talley, urged the audience: "You can’t wait for the culture to change.

"People must feel free to ask for flexible arrangements such as job sharing, even at the director level. We must push through the stigma," said Ms. Talley of Merck & Co., who spoke representing the HealthCare Businesswomen’s Association, Pittsgrove, N.J.

None of the presenters reported any financial conflicts of interest.

ATLANTA – The number of women serving as professors and division directors of rheumatology has not changed for the past 30 years, a circumstance that should prompt a policy directive from the American College of Rheumatology, according to some of its leaders.

During an annual meeting session sponsored by the Committee on Rheumatology Training and Workforce Issues and the ACR Young Investigator Subcommittee of the Research Committee, Dr. Abby Goulder Abelson noted that women accounted for 60% of graduates of rheumatology fellowships in 2009. Yet women hold just 30% of all academic appointments and comprise 15% of full professors and 7% of division heads. Those figures have been virtually unchanged for the past 30 years, according to Dr. Abelson, who chairs the committee.

Findings from a 2009 benchmarking survey by the American Association of Medical Colleges showed that women accounted for 18% of full professors, 13% of department chairs, and 12% of medical school deans.

"If [the ACR’s Research and Education Foundation (REF)] had a policy that it would not support fellowship programs that did not have more women in leadership," the problem would fix itself, said Dr. David Wofsy, past president of the ACR. "A decade ago we were tremendously short of rheumatology fellows. So REF and ACR set a goal and achieved it. ... Let’s articulate the goals and decide what practices we need to achieve these goals."

Dr. Wofsy suggested the goal should be to increase by 25% the number of women division chiefs. Dr. Wofsy is professor of medicine and microbiology/immunology and chief of rheumatology at the San Francisco VA Medical Center as well as associate dean for admissions at the University of California at San Francisco.

"We need to communicate the message that having more women in leadership in academic programs is good for training and good for society," said Dr. Christy I. Sandborg, a pediatric rheumatologist who is associate chair of the department of pediatrics at Stanford (Calif.) University.

The lack of women in academic leadership positions in rheumatology training programs is not a woman’s issue. It is a rheumatology issue and an ACR issue, said Dr. Sandborg, who cautioned against tainting any effort to promote more women with even the hint that women are in some way damaged and need help.

Data gathered in 2008 showed that 9.1% of women left their academic posts early in their careers, compared with 7.7% of men. Women cited as their reasons for leaving their observation that their gender affected their salary, their rate of promotion, and the amount of their protected time for research and teaching. As pronounced as these problems were for women in general, they were more so for minority women, said Dr. Abelson, who is interim chair of the department of rheumatologic and immunologic disease at the Cleveland Clinic.

At the same time, there is a sea change in how both men and women approach their professional lives and look for work-life integration. "This is the first time that I have attended a session on gender where 50% of the audience is male," she said.

Most rheumatology divisions around the country are actively recruiting new faculty. But to many young rheumatologists, private practice feels like the better choice. Dr. David Karp, chief of the division of rheumatology at the University of Texas Southwestern Medical Center at Dallas, acknowledged that "my young fellows feel that an academic career lacks control."

Dr. Abelson noted that young male rheumatologists want more control and a less stressful lifestyle, which is also changing academic medicine. "They start early, work through lunch, and leave early to pick up their kids from day care."

In Dr. Sandborg’s experience, young men who ask for flexible work arrangements are stigmatized because older faculty consider them to be less than serious about their careers.

Another presenter, Anne C. Talley, urged the audience: "You can’t wait for the culture to change.

"People must feel free to ask for flexible arrangements such as job sharing, even at the director level. We must push through the stigma," said Ms. Talley of Merck & Co., who spoke representing the HealthCare Businesswomen’s Association, Pittsgrove, N.J.

None of the presenters reported any financial conflicts of interest.

ATLANTA – The number of women serving as professors and division directors of rheumatology has not changed for the past 30 years, a circumstance that should prompt a policy directive from the American College of Rheumatology, according to some of its leaders.

During an annual meeting session sponsored by the Committee on Rheumatology Training and Workforce Issues and the ACR Young Investigator Subcommittee of the Research Committee, Dr. Abby Goulder Abelson noted that women accounted for 60% of graduates of rheumatology fellowships in 2009. Yet women hold just 30% of all academic appointments and comprise 15% of full professors and 7% of division heads. Those figures have been virtually unchanged for the past 30 years, according to Dr. Abelson, who chairs the committee.

Findings from a 2009 benchmarking survey by the American Association of Medical Colleges showed that women accounted for 18% of full professors, 13% of department chairs, and 12% of medical school deans.

"If [the ACR’s Research and Education Foundation (REF)] had a policy that it would not support fellowship programs that did not have more women in leadership," the problem would fix itself, said Dr. David Wofsy, past president of the ACR. "A decade ago we were tremendously short of rheumatology fellows. So REF and ACR set a goal and achieved it. ... Let’s articulate the goals and decide what practices we need to achieve these goals."

Dr. Wofsy suggested the goal should be to increase by 25% the number of women division chiefs. Dr. Wofsy is professor of medicine and microbiology/immunology and chief of rheumatology at the San Francisco VA Medical Center as well as associate dean for admissions at the University of California at San Francisco.

"We need to communicate the message that having more women in leadership in academic programs is good for training and good for society," said Dr. Christy I. Sandborg, a pediatric rheumatologist who is associate chair of the department of pediatrics at Stanford (Calif.) University.

The lack of women in academic leadership positions in rheumatology training programs is not a woman’s issue. It is a rheumatology issue and an ACR issue, said Dr. Sandborg, who cautioned against tainting any effort to promote more women with even the hint that women are in some way damaged and need help.

Data gathered in 2008 showed that 9.1% of women left their academic posts early in their careers, compared with 7.7% of men. Women cited as their reasons for leaving their observation that their gender affected their salary, their rate of promotion, and the amount of their protected time for research and teaching. As pronounced as these problems were for women in general, they were more so for minority women, said Dr. Abelson, who is interim chair of the department of rheumatologic and immunologic disease at the Cleveland Clinic.

At the same time, there is a sea change in how both men and women approach their professional lives and look for work-life integration. "This is the first time that I have attended a session on gender where 50% of the audience is male," she said.

Most rheumatology divisions around the country are actively recruiting new faculty. But to many young rheumatologists, private practice feels like the better choice. Dr. David Karp, chief of the division of rheumatology at the University of Texas Southwestern Medical Center at Dallas, acknowledged that "my young fellows feel that an academic career lacks control."

Dr. Abelson noted that young male rheumatologists want more control and a less stressful lifestyle, which is also changing academic medicine. "They start early, work through lunch, and leave early to pick up their kids from day care."

In Dr. Sandborg’s experience, young men who ask for flexible work arrangements are stigmatized because older faculty consider them to be less than serious about their careers.

Another presenter, Anne C. Talley, urged the audience: "You can’t wait for the culture to change.

"People must feel free to ask for flexible arrangements such as job sharing, even at the director level. We must push through the stigma," said Ms. Talley of Merck & Co., who spoke representing the HealthCare Businesswomen’s Association, Pittsgrove, N.J.

None of the presenters reported any financial conflicts of interest.

SANTA MONICA, Calif. – Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their clinical response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, Dr. Callen noted at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus (CLE). The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE (SLE). These included patients with fixed lesions with a potential for atrophy. However, data now show that these patients are as likely as others with CLE to progress to SLE.

The data come from a population-based study of inhabitants of Rochester, Minn. The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky).

Of particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249-53).

These findings "give us reason to treat these patients more aggressively than we might have done," said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. "This is a photosensitive disease. It’s photodistributed. It’s photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference," Dr. Callen noted.

Some patients also respond to topical corticosteroids, selected according to the lesion and the site that are being treated. Topical calcineurin inhibitors have been used off label.

But first-line therapy is the antimalarial hydroxychloroquine or chloroquine. "To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus," Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401-9). "To me, that means we need to be treating patients with antimalarials earlier than we do," he said.

If those therapies do not work, "we may combine hydroxychloroquine or chloroquine with quinacrine, but we do not combine hydroxychloroquine and chloroquine. I am a little bit fearful of exacerbating potential ocular toxicity."

Or one can use a second-line therapy that ranges from immunosuppressive therapy to thalidomide.

"We ask first if the patients are taking drugs that may exacerbate the disease, especially in the setting of subacute cutaneous LE. And stop those drugs if at all possible. Is the patient smoking? Try to get them to stop," he said.

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Callen reported that he does not have any relevant financial relationships with any commercial interests.

Jeffrey Callen

SANTA MONICA, Calif. – Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their clinical response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, Dr. Callen noted at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus (CLE). The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE (SLE). These included patients with fixed lesions with a potential for atrophy. However, data now show that these patients are as likely as others with CLE to progress to SLE.

The data come from a population-based study of inhabitants of Rochester, Minn. The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky).

Of particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249-53).

These findings "give us reason to treat these patients more aggressively than we might have done," said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. "This is a photosensitive disease. It’s photodistributed. It’s photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference," Dr. Callen noted.

Some patients also respond to topical corticosteroids, selected according to the lesion and the site that are being treated. Topical calcineurin inhibitors have been used off label.

But first-line therapy is the antimalarial hydroxychloroquine or chloroquine. "To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus," Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401-9). "To me, that means we need to be treating patients with antimalarials earlier than we do," he said.

If those therapies do not work, "we may combine hydroxychloroquine or chloroquine with quinacrine, but we do not combine hydroxychloroquine and chloroquine. I am a little bit fearful of exacerbating potential ocular toxicity."

Or one can use a second-line therapy that ranges from immunosuppressive therapy to thalidomide.

"We ask first if the patients are taking drugs that may exacerbate the disease, especially in the setting of subacute cutaneous LE. And stop those drugs if at all possible. Is the patient smoking? Try to get them to stop," he said.

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Callen reported that he does not have any relevant financial relationships with any commercial interests.

Jeffrey Callen

SANTA MONICA, Calif. – Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their clinical response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, Dr. Callen noted at the meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus (CLE). The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE (SLE). These included patients with fixed lesions with a potential for atrophy. However, data now show that these patients are as likely as others with CLE to progress to SLE.

The data come from a population-based study of inhabitants of Rochester, Minn. The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky).

Of particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249-53).

These findings "give us reason to treat these patients more aggressively than we might have done," said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. "This is a photosensitive disease. It’s photodistributed. It’s photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference," Dr. Callen noted.

Some patients also respond to topical corticosteroids, selected according to the lesion and the site that are being treated. Topical calcineurin inhibitors have been used off label.

But first-line therapy is the antimalarial hydroxychloroquine or chloroquine. "To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus," Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401-9). "To me, that means we need to be treating patients with antimalarials earlier than we do," he said.

If those therapies do not work, "we may combine hydroxychloroquine or chloroquine with quinacrine, but we do not combine hydroxychloroquine and chloroquine. I am a little bit fearful of exacerbating potential ocular toxicity."

Or one can use a second-line therapy that ranges from immunosuppressive therapy to thalidomide.

"We ask first if the patients are taking drugs that may exacerbate the disease, especially in the setting of subacute cutaneous LE. And stop those drugs if at all possible. Is the patient smoking? Try to get them to stop," he said.

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Callen reported that he does not have any relevant financial relationships with any commercial interests.

Jeffrey Callen

SANTA MONICA, Calif. – Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their clinical response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, Dr. Callen noted at a rheumatology seminar sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Photo Credit: (c) PhotoDisc

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus (CLE). The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE (SLE). These included patients with fixed lesions with a potential for atrophy. However, data now show that these patients are as likely as others with CLE to progress to SLE.

The data come from a population-based study of inhabitants of Rochester, Minn. The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky).

Of particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249-53).

These findings "give us reason to treat these patients more aggressively than we might have done," said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. "This is a photosensitive disease. It’s photodistributed. It’s photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference," Dr. Callen noted.

Some patients also respond to topical corticosteroids, selected according to the lesion and the site that are being treated. Topical calcineurin inhibitors have been used off label.

But first-line therapy is the antimalarial hydroxychloroquine or chloroquine. "To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus," Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401-9). "To me, that means we need to be treating patients with antimalarials earlier than we do," he said.

If those therapies do not work, "we may combine hydroxychloroquine or chloroquine with quinacrine, but we do not combine hydroxychloroquine and chloroquine. I am a little bit fearful of exacerbating potential ocular toxicity."

Or one can use a second-line therapy that ranges from immunosuppressive therapy to thalidomide.

"We ask first if the patients are taking drugs that may exacerbate the disease, especially in the setting of subacute cutaneous LE. And stop those drugs if at all possible. Is the patient smoking? Try to get them to stop," he said.

SDEF and this news organization are owned by Elsevier. Dr. Callen reported that he does not have any relevant financial relationships with any commercial interests.

SANTA MONICA, Calif. – Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their clinical response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, Dr. Callen noted at a rheumatology seminar sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Photo Credit: (c) PhotoDisc

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus (CLE). The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE (SLE). These included patients with fixed lesions with a potential for atrophy. However, data now show that these patients are as likely as others with CLE to progress to SLE.

The data come from a population-based study of inhabitants of Rochester, Minn. The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky).

Of particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249-53).

These findings "give us reason to treat these patients more aggressively than we might have done," said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. "This is a photosensitive disease. It’s photodistributed. It’s photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference," Dr. Callen noted.

Some patients also respond to topical corticosteroids, selected according to the lesion and the site that are being treated. Topical calcineurin inhibitors have been used off label.

But first-line therapy is the antimalarial hydroxychloroquine or chloroquine. "To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus," Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401-9). "To me, that means we need to be treating patients with antimalarials earlier than we do," he said.

If those therapies do not work, "we may combine hydroxychloroquine or chloroquine with quinacrine, but we do not combine hydroxychloroquine and chloroquine. I am a little bit fearful of exacerbating potential ocular toxicity."

Or one can use a second-line therapy that ranges from immunosuppressive therapy to thalidomide.

"We ask first if the patients are taking drugs that may exacerbate the disease, especially in the setting of subacute cutaneous LE. And stop those drugs if at all possible. Is the patient smoking? Try to get them to stop," he said.

SDEF and this news organization are owned by Elsevier. Dr. Callen reported that he does not have any relevant financial relationships with any commercial interests.

SANTA MONICA, Calif. – Quitting smoking is the most important thing patients with cutaneous lupus erythematosus can do to increase their clinical response to antimalarials, according to Dr. Jeffrey P. Callen.

Smokers are already at risk of having more severe disease than their nonsmoking CLE counterparts, Dr. Callen noted at a rheumatology seminar sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Photo Credit: (c) PhotoDisc

Antimalarial drugs are the basis of therapy for cutaneous lupus erythematosus (CLE). The need for maximizing treatment response has recently become clearer. In the past, certain patients with CLE were considered to be at low risk for progression to systemic LE (SLE). These included patients with fixed lesions with a potential for atrophy. However, data now show that these patients are as likely as others with CLE to progress to SLE.

The data come from a population-based study of inhabitants of Rochester, Minn. The researchers found that the incidence of CLE and SLE were equal. But of the 156 patients with CLE, 12% (19 patients) progressed to SLE within a mean of 8.2 years from the time of their CLE diagnosis, said Dr. Callen, professor of medicine (dermatology) and chief of the division of dermatology at the University of Louisville (Ky).

Of particular interest was the subtype of SLE that the researchers found in the 19 patients who progressed to SLE – there were 9 cases of the localized discoid subtype of CLE, 4 cases of the generalized discoid CLE subtype, 2 with the panniculitis CLE subtype, and 4 with the psoriasiform subtype of CLE (Arch. Dermatol. 2009;145:249-53).

These findings "give us reason to treat these patients more aggressively than we might have done," said Dr. Callen, and part of that more aggressive treatment is to get patients who smoke to stop.

Another tool is to get patients to use sunblock. "This is a photosensitive disease. It’s photodistributed. It’s photoexacerbated. We can reproduce it with phototesting. So sunscreens are important, but even more so is photoprotection. Patients need to change their behavior and wear photoprotective clothing. Whenever we do that, patients are going to have vitamin D deficiency. Data have come out recently that lupus patients in general have vitamin D deficiency. So we need to address that and [ensure that they] get adequate vitamin D. No one has done a study to see if [supplementation with vitamin D] makes a difference," Dr. Callen noted.

Some patients also respond to topical corticosteroids, selected according to the lesion and the site that are being treated. Topical calcineurin inhibitors have been used off label.

But first-line therapy is the antimalarial hydroxychloroquine or chloroquine. "To me, systemic corticosteroid therapy is not a therapy for cutaneous lupus," Dr. Callen said.

Data from one study suggest that giving patients hydroxychloroquine delays the time from onset of CLE to progression to SLE (Lupus 2007;16:401-9). "To me, that means we need to be treating patients with antimalarials earlier than we do," he said.

If those therapies do not work, "we may combine hydroxychloroquine or chloroquine with quinacrine, but we do not combine hydroxychloroquine and chloroquine. I am a little bit fearful of exacerbating potential ocular toxicity."

Or one can use a second-line therapy that ranges from immunosuppressive therapy to thalidomide.

"We ask first if the patients are taking drugs that may exacerbate the disease, especially in the setting of subacute cutaneous LE. And stop those drugs if at all possible. Is the patient smoking? Try to get them to stop," he said.

SDEF and this news organization are owned by Elsevier. Dr. Callen reported that he does not have any relevant financial relationships with any commercial interests.

SANTA MONICA, CALIF. – Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbance, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600-10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient’s fatigue, sleep, and cognition and the patient’s overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3-6 and an SS score of 9 or more fell within the fibromyalgia domain, and the scores correlated well with the tender point score on the American College of Rheumatology 1990 classification criteria.

These criteria, although already published, are considered preliminary and are being tested in clinical settings to confirm their reliability.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease. He noted that these findings confirm the observation that fibromyalgia often coexists with other chronic pain conditions.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. "I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia, irritable bowel syndrome, and even some of our rheumatoid and lupus patients," Dr. Mease said.

In parallel with the increased appreciation for the role of neurobiology in the pathogenesis of fibromyalgia, there have been data from clinical trials of agents targeting some of the neurobiologic pathways that are proving to be better than placebo in lessening some of the symptoms of fibromyalgia, said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Many rheumatologists might roll their eyes when the discussion turns to fibromyalgia, but recent findings are confirming quantitatively that these patients feel pain with unusual intensity. Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients’ experience of spontaneous pain and fluctuations in pain that are unrelated to activity. In addition, the increased connectivity may have implications for cognition (Arthritis Rheum. 2010;62:2545-55).

Dr. Mease reported that?he presented data from a study of 363 patients with fibromyalgia who were treated with either pregabalin alone or in combination with milnacipran at the annual meeting of the European League Against Rheumatism earlier this year. Those treated with the combination therapy (pregabalin at 150-225 mg twice daily plus 50 mg of milnacipran) for 11 weeks showed a 20-point improvement on the visual analog scale (VAS) for pain assessment. In addition, 51% considered themselves "very much improved" on the Patient Global Impression of Change (PGIC) scale.

In contrast, patients on monotherapy showed a 5-point improvement on the VAS, and 24% considered themselves very much improved on the PGIC. About one-third of the patients did not finish the trial.

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed that he has financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

SANTA MONICA, CALIF. – Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbance, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600-10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient’s fatigue, sleep, and cognition and the patient’s overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3-6 and an SS score of 9 or more fell within the fibromyalgia domain, and the scores correlated well with the tender point score on the American College of Rheumatology 1990 classification criteria.

These criteria, although already published, are considered preliminary and are being tested in clinical settings to confirm their reliability.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease. He noted that these findings confirm the observation that fibromyalgia often coexists with other chronic pain conditions.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. "I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia, irritable bowel syndrome, and even some of our rheumatoid and lupus patients," Dr. Mease said.

In parallel with the increased appreciation for the role of neurobiology in the pathogenesis of fibromyalgia, there have been data from clinical trials of agents targeting some of the neurobiologic pathways that are proving to be better than placebo in lessening some of the symptoms of fibromyalgia, said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Many rheumatologists might roll their eyes when the discussion turns to fibromyalgia, but recent findings are confirming quantitatively that these patients feel pain with unusual intensity. Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients’ experience of spontaneous pain and fluctuations in pain that are unrelated to activity. In addition, the increased connectivity may have implications for cognition (Arthritis Rheum. 2010;62:2545-55).

Dr. Mease reported that?he presented data from a study of 363 patients with fibromyalgia who were treated with either pregabalin alone or in combination with milnacipran at the annual meeting of the European League Against Rheumatism earlier this year. Those treated with the combination therapy (pregabalin at 150-225 mg twice daily plus 50 mg of milnacipran) for 11 weeks showed a 20-point improvement on the visual analog scale (VAS) for pain assessment. In addition, 51% considered themselves "very much improved" on the Patient Global Impression of Change (PGIC) scale.

In contrast, patients on monotherapy showed a 5-point improvement on the VAS, and 24% considered themselves very much improved on the PGIC. About one-third of the patients did not finish the trial.

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed that he has financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

SANTA MONICA, CALIF. – Exercise and cognitive-behavioral therapy complement rather than replace pharmacology in the management of fibromyalgia, according to Dr. Philip J. Mease.

Findings from several studies have shown that such nonpharmacologic treatments may lessen the primary symptoms of fibromyalgia while helping to correct some maladaptive behaviors, mood disturbance, and deconditioning.

Not all nonpharmacologic therapies are equally effective. The literature suggests that aerobic exercise, cognitive-behavioral therapy, and patient education all lessen pain and improve function. The same benefits are not reported with strength training, acupuncture, biofeedback, balneotherapy, and hypnotherapy, Dr. Mease said at the meeting, sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

This year the American College of Rheumatology published diagnostic criteria for fibromyalgia that shifted the emphasis from tender point examination and focused instead on the other symptoms that cause misery in these patients, such as sleep disturbance and fatigue (Arthritis Care Res. 2010;62:600-10).

Specifically, the diagnostic criteria are composed of two parts: a widespread pain index (WPI) that establishes the absence or presence of pain in up to 19 body areas but does not require the physician to press on those areas, and the symptom severity (SS) scale, that grades the patient’s fatigue, sleep, and cognition and the patient’s overall symptom burden.

Patients who have an overall symptom burden of 7 or more on the WPI and an SS score of 5 or more or a WPI score of 3-6 and an SS score of 9 or more fell within the fibromyalgia domain, and the scores correlated well with the tender point score on the American College of Rheumatology 1990 classification criteria.

These criteria, although already published, are considered preliminary and are being tested in clinical settings to confirm their reliability.

Data from recent, unpublished research out of the National Data Bank of Rheumatic Diseases show that 20% of patients with rheumatoid arthritis have scores that indicate concomitant fibromyalgia and 10% of patients with osteoarthritis have scores consistent with fibromyalgia, according to Dr. Mease. He noted that these findings confirm the observation that fibromyalgia often coexists with other chronic pain conditions.

In addition to the recognized role for nonpharmacologic therapies, there has been a sea change in pharmacologic management of fibromyalgia. "I am intrigued by the emergence of a better understanding of the neurobiologic basis of central pain, central fatigue, and central dyscognition as they relate to fibromyalgia, irritable bowel syndrome, and even some of our rheumatoid and lupus patients," Dr. Mease said.

In parallel with the increased appreciation for the role of neurobiology in the pathogenesis of fibromyalgia, there have been data from clinical trials of agents targeting some of the neurobiologic pathways that are proving to be better than placebo in lessening some of the symptoms of fibromyalgia, said Dr. Mease, a rheumatologist at the University of Washington, Seattle, as well as director of the division of rheumatology research at the Swedish Medical Center there.

Many rheumatologists might roll their eyes when the discussion turns to fibromyalgia, but recent findings are confirming quantitatively that these patients feel pain with unusual intensity. Findings from functional MRI studies have shown that, even at rest, the brain of patients with fibromyalgia has increased connectivity within multiple brain networks that may explain both the patients’ experience of spontaneous pain and fluctuations in pain that are unrelated to activity. In addition, the increased connectivity may have implications for cognition (Arthritis Rheum. 2010;62:2545-55).

Dr. Mease reported that?he presented data from a study of 363 patients with fibromyalgia who were treated with either pregabalin alone or in combination with milnacipran at the annual meeting of the European League Against Rheumatism earlier this year. Those treated with the combination therapy (pregabalin at 150-225 mg twice daily plus 50 mg of milnacipran) for 11 weeks showed a 20-point improvement on the visual analog scale (VAS) for pain assessment. In addition, 51% considered themselves "very much improved" on the Patient Global Impression of Change (PGIC) scale.

In contrast, patients on monotherapy showed a 5-point improvement on the VAS, and 24% considered themselves very much improved on the PGIC. About one-third of the patients did not finish the trial.

SDEF and this news organization are owned by Elsevier. Dr. Mease disclosed that he has financial relationships with Cypress Bioscience, Forest, Lilly, Pfizer, and UCB.

SANTA MONICA, Calif. – Gastroenterologists seem to be taking a page from the rheumatologists’ playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at a rheumatology seminar sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis. The cartilage and bone usually are spared from destruction. Arthritis in IBD usually involves five or more joints and lasts about 3 years.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found that the prevalence of IBD was about 0.62%-0.65% and the prevalence of RA was about 0.98%-1.08% in patients aged 47-56 years old living in the Midwest or the South. The odds ratio of having both IBD and RA was 2.1-2.7, and of having IBD and ankylosing spondylitis, about 5.8-7.8 (Inflamm. Bowel Dis. 2008;14:738-43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158-63).

In the prebiologic era, the natural history of Crohn’s disease also was grim. The disease followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244-50).

In the past, "virtually all Crohn’s disease patients relapsed and most required one or more surgeries," said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago. He noted that there was a 70% probability that Crohn’s would recur over a 10-year period (Gastroenterology 1985;88:1826-33).

An estimated 10% of Crohn’s patients had their colons removed surgically within 1 year of their diagnosis with IBD, and an estimated 70% of patients who had one surgery for Crohn’s would require another. The disease tended to recur at the site of anastomosis of the previous surgery and to involve as much bowel as had been removed in the previous surgery. About half of the patients needed a second surgery.

Even today, most ulcerative colitis patients are treated with steroids and many of them become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255-60).

These days, there is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher and lesions that were visible on endoscopy (N. Engl. J. Med. 2010;362:1383-95).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.

SANTA MONICA, Calif. – Gastroenterologists seem to be taking a page from the rheumatologists’ playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at a rheumatology seminar sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis. The cartilage and bone usually are spared from destruction. Arthritis in IBD usually involves five or more joints and lasts about 3 years.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found that the prevalence of IBD was about 0.62%-0.65% and the prevalence of RA was about 0.98%-1.08% in patients aged 47-56 years old living in the Midwest or the South. The odds ratio of having both IBD and RA was 2.1-2.7, and of having IBD and ankylosing spondylitis, about 5.8-7.8 (Inflamm. Bowel Dis. 2008;14:738-43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158-63).

In the prebiologic era, the natural history of Crohn’s disease also was grim. The disease followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244-50).

In the past, "virtually all Crohn’s disease patients relapsed and most required one or more surgeries," said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago. He noted that there was a 70% probability that Crohn’s would recur over a 10-year period (Gastroenterology 1985;88:1826-33).

An estimated 10% of Crohn’s patients had their colons removed surgically within 1 year of their diagnosis with IBD, and an estimated 70% of patients who had one surgery for Crohn’s would require another. The disease tended to recur at the site of anastomosis of the previous surgery and to involve as much bowel as had been removed in the previous surgery. About half of the patients needed a second surgery.

Even today, most ulcerative colitis patients are treated with steroids and many of them become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255-60).

These days, there is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher and lesions that were visible on endoscopy (N. Engl. J. Med. 2010;362:1383-95).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.

SANTA MONICA, Calif. – Gastroenterologists seem to be taking a page from the rheumatologists’ playbook and are starting patients with inflammatory bowel disease on a biologic agent much sooner after diagnosis than has been standard practice.

By doing so, they hope to improve the natural history of the disease, just as rheumatologists have done in rheumatoid arthritis patients, according to Dr. Russell D. Cohen, who spoke at a rheumatology seminar sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

Arthritis and inflammatory bowel disease (IBD) have more in common than the drugs used to treat them. Arthritis is the most common extraintestinal manifestation of IBD. Onset of joint symptoms may precede the onset of IBD, develop in parallel to it, or be unrelated, he said.

Arthritis is most likely to occur in IBD patients who have other extraintestinal manifestations such as dermatologic, ocular, or renal symptoms. The most commonly involved central joints are in the spine, where the arthritis takes the form of ankylosing spondylitis or sacroiliitis. Peripheral joints can develop arthropathies in IBD as well. About 5%-20% of IBD patients get arthritis. The cartilage and bone usually are spared from destruction. Arthritis in IBD usually involves five or more joints and lasts about 3 years.

The incidence of IBD in rheumatoid arthritis is not well defined. One of the few studies to address this question involved a review of the data sets from two large insurance companies involving 17 million people. The researchers found that the prevalence of IBD was about 0.62%-0.65% and the prevalence of RA was about 0.98%-1.08% in patients aged 47-56 years old living in the Midwest or the South. The odds ratio of having both IBD and RA was 2.1-2.7, and of having IBD and ankylosing spondylitis, about 5.8-7.8 (Inflamm. Bowel Dis. 2008;14:738-43).

The advent of biologics has changed the natural history of ulcerative colitis (UC). But before these agents became available, data from a Danish study showed that during the first year after diagnosis, 10% of UC patients lost their colon, about 23% had lost their colon after 10 years, and 31% had lost their colon 18 years out (Gut 1985;26:158-63).

In the prebiologic era, the natural history of Crohn’s disease also was grim. The disease followed an inflammatory path for the first 5 years, then became penetrating with fistula formation between years 5 and 10 in a subset of patients; stricturing could develop after year 10 (Inflamm. Bowel Dis. 2002;8:244-50).

In the past, "virtually all Crohn’s disease patients relapsed and most required one or more surgeries," said Dr. Cohen, who is codirector of the inflammatory bowel disease center at the University of Chicago. He noted that there was a 70% probability that Crohn’s would recur over a 10-year period (Gastroenterology 1985;88:1826-33).

An estimated 10% of Crohn’s patients had their colons removed surgically within 1 year of their diagnosis with IBD, and an estimated 70% of patients who had one surgery for Crohn’s would require another. The disease tended to recur at the site of anastomosis of the previous surgery and to involve as much bowel as had been removed in the previous surgery. About half of the patients needed a second surgery.

Even today, most ulcerative colitis patients are treated with steroids and many of them become steroid dependent. Findings from a study of 63 UC patients placed on steroids showed that at the end of 1 month, 34 achieved complete remission, 19 had a partial remission, and 10 had no response. Follow-up data at 1 year showed that 31 had a prolonged response, 14 were steroid dependent, and 18 needed surgery (Gastroenterology 2001;121:255-60).

These days, there is a move away from making steroids the first drug in the treatment regimen and instead starting with a biologic and adding a steroid only if necessary.

There is some overlap between the biologics used to treat rheumatologic diseases and those used to treat IBD. Recent data show that infliximab in combination with azathioprine induced a steroid-free clinical remission in 44 of 64 patients. In the same study, infliximab plus placebo induced remission in 37 of 65 patients, and azathioprine plus placebo induced remission in 21 of 75 patients. All of the patients had active IBD with a C-reactive protein level of 0.8 mg/dL or higher and lesions that were visible on endoscopy (N. Engl. J. Med. 2010;362:1383-95).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Cohen disclosed financial relationships with Abbott Labs, Axcan Pharma, Elan, Centocor, Procter & Gamble, Prometheus Laboratories, Salix, Shire, UCB, and Warner Chilcott.