Sally Koch Kubetin

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.

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.

SANTA MONICA, CALIF. – Social media provide a way for physicians to engage with their patients and the community, whether the physician practices in an HMO or privately, according to Dr. Jeffrey Benabio, a dermatologist at Kaiser Permanente in San Diego.

Moreover, physicians in private practice could find social media useful in building their practices, Dr. Benabio said at the meeting, sponsored by the Skin Disease Education Foundation and the University of Louisville.

No matter what the specialty, the principles of using social media such as blogs, Facebook, Twitter, and Web sites as tools for improving patient care will apply. “Online patient communities are an ascendant means for patients to learn about their disease, and seek advice and comfort from [other] patients like them. Physicians can be part of this conversation and contribute to it. Who better to [advise] patients [on] how to live with pain, live with deformity, deal with insurance companies, than physicians?” noted Dr. Benabio in an interview.

It takes no money but lots of time to build online networks. So why bother to do it? Dr. Benabio offered several reasons.

“Patients are going online to interact with their physicians, and we are not there.

“Physicians are losing [their] status as the sole source of medical knowledge. Whereas patients always had to come to us to learn about disease and health, now they get most of their information online. Our absence online perpetuates a trend of diminishing importance of our profession. Patients are online; physicians need to be where they are, he said.

As with much in life, the secret to being effective online comes down to showing up. “A physician becomes a trusted member of the community by being present. Over time, regular blog posts, Facebook updates, and tweets allow the audience to become familiar with the physician. To know that he or she is there, is listening, is part of the community.

“Physicians should blog and have Facebook pages. They should post things that are helpful and informative for their audience. They can report news, but it must be within the law. Physicians can talk about drugs and about non-FDA–approved uses of drugs as long as they are not giving actual medical advice, and are clear about any disclosures and disclaimers,” he said.

They should Google themselves and see what they find, although they might not like it. The only content you can control is the content you create, he asserted. Google has 400 million queries daily and 75%-80% of adults have sought medical information online. The nature of information on the Internet is that it is collaborative, and physicians need to be part of that. Otherwise, the public might be offered information that is inaccurate and biased, he noted.

“It is as important to be a trusted member of the online community as it is to be a trusted member of your actual community,” Dr. Benabio said. Starting a blog and making it part of your practice's Web site will have the additional benefit of marketing the practice at the same time you are offering the public a reliable perspective on medical developments within your specialty.

Those who are interested in marketing their practices should remember that using social media is free but time consuming. But getting your name out online, making sure it is associated with reliable information, and being available as a caring, informed physician are all effective marketing strategies that are literally at your fingertips in the form of social media tools. Some say this is becoming the first choice in marketing, and that traditional marketing is dying.

Dr. Benabio warned that others will usurp physicians' role as providers of health information unless they get online to counter that trend. Certainly alternative health providers are on social media, building relationships with patients, and boosting their status among them. Just as a patient who has no access to a dermatologist will see a nurse or naturopath, patients online seek information from nonphysicians, he noted.

Physicians are on a slippery slope in this age of the Internet information highway. “This is a critical time when we are trying to demonstrate our value as practitioners,” he said. “The more comfortable people are with nonphysicians, the more difficult it will be for us to fight nonphysicians' expansion of their scope of practice.”

SDEF and this news organization are owned by Elsevier. Dr. Benabio disclosed that he is a consultant for Livestrong.com

Dr. Jeffrey Benabio encourages physicians to be active members of the online medical community by using social media.

Source Sally Koch Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. – Social media provide a way for physicians to engage with their patients and the community, whether the physician practices in an HMO or privately, according to Dr. Jeffrey Benabio, a dermatologist at Kaiser Permanente in San Diego.

Moreover, physicians in private practice could find social media useful in building their practices, Dr. Benabio said at the meeting, sponsored by the Skin Disease Education Foundation and the University of Louisville.

No matter what the specialty, the principles of using social media such as blogs, Facebook, Twitter, and Web sites as tools for improving patient care will apply. “Online patient communities are an ascendant means for patients to learn about their disease, and seek advice and comfort from [other] patients like them. Physicians can be part of this conversation and contribute to it. Who better to [advise] patients [on] how to live with pain, live with deformity, deal with insurance companies, than physicians?” noted Dr. Benabio in an interview.

It takes no money but lots of time to build online networks. So why bother to do it? Dr. Benabio offered several reasons.

“Patients are going online to interact with their physicians, and we are not there.

“Physicians are losing [their] status as the sole source of medical knowledge. Whereas patients always had to come to us to learn about disease and health, now they get most of their information online. Our absence online perpetuates a trend of diminishing importance of our profession. Patients are online; physicians need to be where they are, he said.

As with much in life, the secret to being effective online comes down to showing up. “A physician becomes a trusted member of the community by being present. Over time, regular blog posts, Facebook updates, and tweets allow the audience to become familiar with the physician. To know that he or she is there, is listening, is part of the community.

“Physicians should blog and have Facebook pages. They should post things that are helpful and informative for their audience. They can report news, but it must be within the law. Physicians can talk about drugs and about non-FDA–approved uses of drugs as long as they are not giving actual medical advice, and are clear about any disclosures and disclaimers,” he said.

They should Google themselves and see what they find, although they might not like it. The only content you can control is the content you create, he asserted. Google has 400 million queries daily and 75%-80% of adults have sought medical information online. The nature of information on the Internet is that it is collaborative, and physicians need to be part of that. Otherwise, the public might be offered information that is inaccurate and biased, he noted.

“It is as important to be a trusted member of the online community as it is to be a trusted member of your actual community,” Dr. Benabio said. Starting a blog and making it part of your practice's Web site will have the additional benefit of marketing the practice at the same time you are offering the public a reliable perspective on medical developments within your specialty.

Those who are interested in marketing their practices should remember that using social media is free but time consuming. But getting your name out online, making sure it is associated with reliable information, and being available as a caring, informed physician are all effective marketing strategies that are literally at your fingertips in the form of social media tools. Some say this is becoming the first choice in marketing, and that traditional marketing is dying.

Dr. Benabio warned that others will usurp physicians' role as providers of health information unless they get online to counter that trend. Certainly alternative health providers are on social media, building relationships with patients, and boosting their status among them. Just as a patient who has no access to a dermatologist will see a nurse or naturopath, patients online seek information from nonphysicians, he noted.

Physicians are on a slippery slope in this age of the Internet information highway. “This is a critical time when we are trying to demonstrate our value as practitioners,” he said. “The more comfortable people are with nonphysicians, the more difficult it will be for us to fight nonphysicians' expansion of their scope of practice.”

SDEF and this news organization are owned by Elsevier. Dr. Benabio disclosed that he is a consultant for Livestrong.com

Dr. Jeffrey Benabio encourages physicians to be active members of the online medical community by using social media.

Source Sally Koch Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. – Social media provide a way for physicians to engage with their patients and the community, whether the physician practices in an HMO or privately, according to Dr. Jeffrey Benabio, a dermatologist at Kaiser Permanente in San Diego.

Moreover, physicians in private practice could find social media useful in building their practices, Dr. Benabio said at the meeting, sponsored by the Skin Disease Education Foundation and the University of Louisville.

No matter what the specialty, the principles of using social media such as blogs, Facebook, Twitter, and Web sites as tools for improving patient care will apply. “Online patient communities are an ascendant means for patients to learn about their disease, and seek advice and comfort from [other] patients like them. Physicians can be part of this conversation and contribute to it. Who better to [advise] patients [on] how to live with pain, live with deformity, deal with insurance companies, than physicians?” noted Dr. Benabio in an interview.

It takes no money but lots of time to build online networks. So why bother to do it? Dr. Benabio offered several reasons.

“Patients are going online to interact with their physicians, and we are not there.

“Physicians are losing [their] status as the sole source of medical knowledge. Whereas patients always had to come to us to learn about disease and health, now they get most of their information online. Our absence online perpetuates a trend of diminishing importance of our profession. Patients are online; physicians need to be where they are, he said.

As with much in life, the secret to being effective online comes down to showing up. “A physician becomes a trusted member of the community by being present. Over time, regular blog posts, Facebook updates, and tweets allow the audience to become familiar with the physician. To know that he or she is there, is listening, is part of the community.

“Physicians should blog and have Facebook pages. They should post things that are helpful and informative for their audience. They can report news, but it must be within the law. Physicians can talk about drugs and about non-FDA–approved uses of drugs as long as they are not giving actual medical advice, and are clear about any disclosures and disclaimers,” he said.

They should Google themselves and see what they find, although they might not like it. The only content you can control is the content you create, he asserted. Google has 400 million queries daily and 75%-80% of adults have sought medical information online. The nature of information on the Internet is that it is collaborative, and physicians need to be part of that. Otherwise, the public might be offered information that is inaccurate and biased, he noted.

“It is as important to be a trusted member of the online community as it is to be a trusted member of your actual community,” Dr. Benabio said. Starting a blog and making it part of your practice's Web site will have the additional benefit of marketing the practice at the same time you are offering the public a reliable perspective on medical developments within your specialty.

Those who are interested in marketing their practices should remember that using social media is free but time consuming. But getting your name out online, making sure it is associated with reliable information, and being available as a caring, informed physician are all effective marketing strategies that are literally at your fingertips in the form of social media tools. Some say this is becoming the first choice in marketing, and that traditional marketing is dying.

Dr. Benabio warned that others will usurp physicians' role as providers of health information unless they get online to counter that trend. Certainly alternative health providers are on social media, building relationships with patients, and boosting their status among them. Just as a patient who has no access to a dermatologist will see a nurse or naturopath, patients online seek information from nonphysicians, he noted.

Physicians are on a slippery slope in this age of the Internet information highway. “This is a critical time when we are trying to demonstrate our value as practitioners,” he said. “The more comfortable people are with nonphysicians, the more difficult it will be for us to fight nonphysicians' expansion of their scope of practice.”

SDEF and this news organization are owned by Elsevier. Dr. Benabio disclosed that he is a consultant for Livestrong.com

Dr. Jeffrey Benabio encourages physicians to be active members of the online medical community by using social media.

Source Sally Koch Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. – Rheumatoid arthritis patients with a true primary failure on a first-time trial of tumor necrosis factor inhibitor therapy should change to treatment with a biologic that has a different mechanism of action. The likelihood is great that trying a second anti-TNF agent will result in just another failure and delay the initiation of effective treatment, according to Dr. Daniel E. Furst.

The key is to be sure that the failure to respond to the first anti-TNF agent is not secondary to another cause, such as too low a dose, he stressed, speaking at a meeting sponsored by Rheumatology News and Skin Disease Education Foundation.

An estimated 60%-70% of patients who begin treatment with an anti-TNF agent are still on the agent at the end of 1 year. Although some patients have to stop treatment because of problems with their insurance and other reasons, primary and secondary failure play a role, he said.

One cannot recognize a treatment failure unless one undertakes therapy with a treatment target in mind, usually remission or low disease activity levels. Treating-to-target goals have been shown to improve outcome and to lower rates of organ damage in diabetes and hypertension. Treating to target was the watchword of new treatment guidelines issued jointly earlier this year by the American College of Rheumatology and the European League Against Rheumatism. The guidelines were published jointly in the EULAR journal Annals of the Rheumatic Diseases (2010;69:1580-8) and the ACR’s Arthritis & Rheumatism (2010;62:2569-81).

Evidence that treating to target in RA is effective dates back to 1998, and this therapeutic approach has become more important in the biologics era of care. The goals of treating to target, as outlined by ACR/EULAR, are to aim for complete remission of low disease activity; to see the patient monthly for at least the first 3-6 months, depending on disease activity; to use a combination of validated response measures; to consider comorbidities; to aim for sustained remission; and to get informed consent.

So how does one tell whether a patient’s lack of response to an anti-TNF agent is a true primary failure or is secondary to something else that may be correctable, such as a longer therapeutic trial?

Findings from a secondary analysis of TEMPO (Trial of Etanercept and Methotrexate With Radiographic Patient Outcomes) data show that about half of the patients who had not responded by 12 weeks to treatment with etanercept or methotrexate, either as monotherapy or in combination, were still likely to respond by 24 weeks with either treatment (Ann. Rheum. Dis. 2008;67:1444-7).

“"If there is a hint of a response, treat beyond the usual 12 weeks,” advised Dr. Furst, who is the Carl M. Pearson Professor of Medicine at the University of California, Los Angeles.

Some patients may need a higher dose of the anti-TNF agent than they have been receiving. A retrospective chart review presented by Dr. Furst and colleagues at the 2008 annual meeting of the ACR showed that increasing the adalimumab dose from 40 mg subcutaneously every other week for 5 months to 40 mg every week for 6 months can increase the number of patients with good EULAR responses. Of 48 patients who originally had received 40 mg of adalimumab subcutaneously every other week for 5 months, 20 had good response and 28 achieved moderate or no EULAR responses. An increase in the dose to 40 mg every week for 6 months resulted in a good EULAR response in 8 of 28 nonresponders, which included 4 of 12 patients who originally had no response to the lower-dose adalimumab (Arthritis Rheum. 2008;58[suppl.]:abstract 999).

Similarly, Dr. Furst noted that one can improve treatment response to infliximab by decreasing the interval between doses. But increasing the dose and leaving the interval the same does not have the desired effect of improving treatment response. Other data from his research suggest that in the case of etanercept, increasing dose does not improve efficacy (Arthritis Rheum. 2007;56[suppl.):abstract 726).

Higher doses of anti-TNF agents are associated with higher rates of nonserious adverse events, especially with adalimumab and infliximab. Data from package inserts show that infliximab has a 5.3% rate of serious adverse events, which is higher than that seen with adalimumab (2%), etanercept (1%), golimumab (1.9%), and certolizumab (3%). Data from the French RATIO (Research Axed on Tolerance of Biotherapies) registry show that during 57,711 people-years of biologic use in 2004-2007, there were 69 cases of tuberculosis in patients who took anti-TNF agents for a variety of reasons, including RA. After adjustment for confounding risk factors, the incidence rate for TB in patients on any anti-TNF drug was shown to be 116.7 cases per 100,000 person-years of use (Arthritis Rheum. 2009;60:1884-94).

Postmarketing surveillance of anti-TNF drugs has shown hepatotoxicity to be another serious adverse event. Reports have ranged from death to the need for transplant because of cirrhosis. Most of the reports have been linked to infliximab.

The bottom line is that not only are anti-TNF agents less effective after a primary failure, but the rate of adverse events increases as well, judging from data reported at the annual meeting of the European League Against Rheumatism in 2008 by Dr. Luba Nalysnyk of United BioSource Corp. Dr. Nalysnyk and associates performed a meta-analysis of 16 articles and 15 abstracts involving 5,306 patients. In the meta-analysis, primary failure of an anti-TNF agent occurred in 48% of patients. A second anti-TNF agent did not work in 66% of those patients, and another 66% of those patients developed adverse events in response to the second agent.

Not all physicians are comfortable switching patients after one failure to a drug that works by a mechanism other than blocking TNF. But for those who are, they must decide how to choose between abatacept, rituximab, and tocilizumab, Dr. Furst said. All three agents pose the same risk of bacterial infection. Rituximab may be the drug of choice in patients with a history of lymphoma or solid tumor. The risk for infusion reaction is less with abatacept than with rituximab or tocilizumab. The data on tocilizumab look good so far. In patients with chronic or latent TB, either abatacept or rituximab may be a better choice than is tocilizumab.

SDEF and this news organization are owned by Elsevier. Dr. Furst has disclosed financial relationships with Abbott, Actelion, Amgen, Array, Biogen Idec, BMS, Celgene, Centocor, Genentech, Gilead, GSK, the National Institutes of Health, Nitec Pharma, Novartis, Roche, UCB, and Wyeth.

SANTA MONICA, CALIF. – Rheumatoid arthritis patients with a true primary failure on a first-time trial of tumor necrosis factor inhibitor therapy should change to treatment with a biologic that has a different mechanism of action. The likelihood is great that trying a second anti-TNF agent will result in just another failure and delay the initiation of effective treatment, according to Dr. Daniel E. Furst.

The key is to be sure that the failure to respond to the first anti-TNF agent is not secondary to another cause, such as too low a dose, he stressed, speaking at a meeting sponsored by Rheumatology News and Skin Disease Education Foundation.

An estimated 60%-70% of patients who begin treatment with an anti-TNF agent are still on the agent at the end of 1 year. Although some patients have to stop treatment because of problems with their insurance and other reasons, primary and secondary failure play a role, he said.

One cannot recognize a treatment failure unless one undertakes therapy with a treatment target in mind, usually remission or low disease activity levels. Treating-to-target goals have been shown to improve outcome and to lower rates of organ damage in diabetes and hypertension. Treating to target was the watchword of new treatment guidelines issued jointly earlier this year by the American College of Rheumatology and the European League Against Rheumatism. The guidelines were published jointly in the EULAR journal Annals of the Rheumatic Diseases (2010;69:1580-8) and the ACR’s Arthritis & Rheumatism (2010;62:2569-81).

Evidence that treating to target in RA is effective dates back to 1998, and this therapeutic approach has become more important in the biologics era of care. The goals of treating to target, as outlined by ACR/EULAR, are to aim for complete remission of low disease activity; to see the patient monthly for at least the first 3-6 months, depending on disease activity; to use a combination of validated response measures; to consider comorbidities; to aim for sustained remission; and to get informed consent.

So how does one tell whether a patient’s lack of response to an anti-TNF agent is a true primary failure or is secondary to something else that may be correctable, such as a longer therapeutic trial?

Findings from a secondary analysis of TEMPO (Trial of Etanercept and Methotrexate With Radiographic Patient Outcomes) data show that about half of the patients who had not responded by 12 weeks to treatment with etanercept or methotrexate, either as monotherapy or in combination, were still likely to respond by 24 weeks with either treatment (Ann. Rheum. Dis. 2008;67:1444-7).

“"If there is a hint of a response, treat beyond the usual 12 weeks,” advised Dr. Furst, who is the Carl M. Pearson Professor of Medicine at the University of California, Los Angeles.

Some patients may need a higher dose of the anti-TNF agent than they have been receiving. A retrospective chart review presented by Dr. Furst and colleagues at the 2008 annual meeting of the ACR showed that increasing the adalimumab dose from 40 mg subcutaneously every other week for 5 months to 40 mg every week for 6 months can increase the number of patients with good EULAR responses. Of 48 patients who originally had received 40 mg of adalimumab subcutaneously every other week for 5 months, 20 had good response and 28 achieved moderate or no EULAR responses. An increase in the dose to 40 mg every week for 6 months resulted in a good EULAR response in 8 of 28 nonresponders, which included 4 of 12 patients who originally had no response to the lower-dose adalimumab (Arthritis Rheum. 2008;58[suppl.]:abstract 999).

Similarly, Dr. Furst noted that one can improve treatment response to infliximab by decreasing the interval between doses. But increasing the dose and leaving the interval the same does not have the desired effect of improving treatment response. Other data from his research suggest that in the case of etanercept, increasing dose does not improve efficacy (Arthritis Rheum. 2007;56[suppl.):abstract 726).

Higher doses of anti-TNF agents are associated with higher rates of nonserious adverse events, especially with adalimumab and infliximab. Data from package inserts show that infliximab has a 5.3% rate of serious adverse events, which is higher than that seen with adalimumab (2%), etanercept (1%), golimumab (1.9%), and certolizumab (3%). Data from the French RATIO (Research Axed on Tolerance of Biotherapies) registry show that during 57,711 people-years of biologic use in 2004-2007, there were 69 cases of tuberculosis in patients who took anti-TNF agents for a variety of reasons, including RA. After adjustment for confounding risk factors, the incidence rate for TB in patients on any anti-TNF drug was shown to be 116.7 cases per 100,000 person-years of use (Arthritis Rheum. 2009;60:1884-94).

Postmarketing surveillance of anti-TNF drugs has shown hepatotoxicity to be another serious adverse event. Reports have ranged from death to the need for transplant because of cirrhosis. Most of the reports have been linked to infliximab.

The bottom line is that not only are anti-TNF agents less effective after a primary failure, but the rate of adverse events increases as well, judging from data reported at the annual meeting of the European League Against Rheumatism in 2008 by Dr. Luba Nalysnyk of United BioSource Corp. Dr. Nalysnyk and associates performed a meta-analysis of 16 articles and 15 abstracts involving 5,306 patients. In the meta-analysis, primary failure of an anti-TNF agent occurred in 48% of patients. A second anti-TNF agent did not work in 66% of those patients, and another 66% of those patients developed adverse events in response to the second agent.

Not all physicians are comfortable switching patients after one failure to a drug that works by a mechanism other than blocking TNF. But for those who are, they must decide how to choose between abatacept, rituximab, and tocilizumab, Dr. Furst said. All three agents pose the same risk of bacterial infection. Rituximab may be the drug of choice in patients with a history of lymphoma or solid tumor. The risk for infusion reaction is less with abatacept than with rituximab or tocilizumab. The data on tocilizumab look good so far. In patients with chronic or latent TB, either abatacept or rituximab may be a better choice than is tocilizumab.

SDEF and this news organization are owned by Elsevier. Dr. Furst has disclosed financial relationships with Abbott, Actelion, Amgen, Array, Biogen Idec, BMS, Celgene, Centocor, Genentech, Gilead, GSK, the National Institutes of Health, Nitec Pharma, Novartis, Roche, UCB, and Wyeth.

SANTA MONICA, CALIF. – Rheumatoid arthritis patients with a true primary failure on a first-time trial of tumor necrosis factor inhibitor therapy should change to treatment with a biologic that has a different mechanism of action. The likelihood is great that trying a second anti-TNF agent will result in just another failure and delay the initiation of effective treatment, according to Dr. Daniel E. Furst.

The key is to be sure that the failure to respond to the first anti-TNF agent is not secondary to another cause, such as too low a dose, he stressed, speaking at a meeting sponsored by Rheumatology News and Skin Disease Education Foundation.

An estimated 60%-70% of patients who begin treatment with an anti-TNF agent are still on the agent at the end of 1 year. Although some patients have to stop treatment because of problems with their insurance and other reasons, primary and secondary failure play a role, he said.

One cannot recognize a treatment failure unless one undertakes therapy with a treatment target in mind, usually remission or low disease activity levels. Treating-to-target goals have been shown to improve outcome and to lower rates of organ damage in diabetes and hypertension. Treating to target was the watchword of new treatment guidelines issued jointly earlier this year by the American College of Rheumatology and the European League Against Rheumatism. The guidelines were published jointly in the EULAR journal Annals of the Rheumatic Diseases (2010;69:1580-8) and the ACR’s Arthritis & Rheumatism (2010;62:2569-81).

Evidence that treating to target in RA is effective dates back to 1998, and this therapeutic approach has become more important in the biologics era of care. The goals of treating to target, as outlined by ACR/EULAR, are to aim for complete remission of low disease activity; to see the patient monthly for at least the first 3-6 months, depending on disease activity; to use a combination of validated response measures; to consider comorbidities; to aim for sustained remission; and to get informed consent.

So how does one tell whether a patient’s lack of response to an anti-TNF agent is a true primary failure or is secondary to something else that may be correctable, such as a longer therapeutic trial?

Findings from a secondary analysis of TEMPO (Trial of Etanercept and Methotrexate With Radiographic Patient Outcomes) data show that about half of the patients who had not responded by 12 weeks to treatment with etanercept or methotrexate, either as monotherapy or in combination, were still likely to respond by 24 weeks with either treatment (Ann. Rheum. Dis. 2008;67:1444-7).

“"If there is a hint of a response, treat beyond the usual 12 weeks,” advised Dr. Furst, who is the Carl M. Pearson Professor of Medicine at the University of California, Los Angeles.

Some patients may need a higher dose of the anti-TNF agent than they have been receiving. A retrospective chart review presented by Dr. Furst and colleagues at the 2008 annual meeting of the ACR showed that increasing the adalimumab dose from 40 mg subcutaneously every other week for 5 months to 40 mg every week for 6 months can increase the number of patients with good EULAR responses. Of 48 patients who originally had received 40 mg of adalimumab subcutaneously every other week for 5 months, 20 had good response and 28 achieved moderate or no EULAR responses. An increase in the dose to 40 mg every week for 6 months resulted in a good EULAR response in 8 of 28 nonresponders, which included 4 of 12 patients who originally had no response to the lower-dose adalimumab (Arthritis Rheum. 2008;58[suppl.]:abstract 999).

Similarly, Dr. Furst noted that one can improve treatment response to infliximab by decreasing the interval between doses. But increasing the dose and leaving the interval the same does not have the desired effect of improving treatment response. Other data from his research suggest that in the case of etanercept, increasing dose does not improve efficacy (Arthritis Rheum. 2007;56[suppl.):abstract 726).

Higher doses of anti-TNF agents are associated with higher rates of nonserious adverse events, especially with adalimumab and infliximab. Data from package inserts show that infliximab has a 5.3% rate of serious adverse events, which is higher than that seen with adalimumab (2%), etanercept (1%), golimumab (1.9%), and certolizumab (3%). Data from the French RATIO (Research Axed on Tolerance of Biotherapies) registry show that during 57,711 people-years of biologic use in 2004-2007, there were 69 cases of tuberculosis in patients who took anti-TNF agents for a variety of reasons, including RA. After adjustment for confounding risk factors, the incidence rate for TB in patients on any anti-TNF drug was shown to be 116.7 cases per 100,000 person-years of use (Arthritis Rheum. 2009;60:1884-94).

Postmarketing surveillance of anti-TNF drugs has shown hepatotoxicity to be another serious adverse event. Reports have ranged from death to the need for transplant because of cirrhosis. Most of the reports have been linked to infliximab.

The bottom line is that not only are anti-TNF agents less effective after a primary failure, but the rate of adverse events increases as well, judging from data reported at the annual meeting of the European League Against Rheumatism in 2008 by Dr. Luba Nalysnyk of United BioSource Corp. Dr. Nalysnyk and associates performed a meta-analysis of 16 articles and 15 abstracts involving 5,306 patients. In the meta-analysis, primary failure of an anti-TNF agent occurred in 48% of patients. A second anti-TNF agent did not work in 66% of those patients, and another 66% of those patients developed adverse events in response to the second agent.

Not all physicians are comfortable switching patients after one failure to a drug that works by a mechanism other than blocking TNF. But for those who are, they must decide how to choose between abatacept, rituximab, and tocilizumab, Dr. Furst said. All three agents pose the same risk of bacterial infection. Rituximab may be the drug of choice in patients with a history of lymphoma or solid tumor. The risk for infusion reaction is less with abatacept than with rituximab or tocilizumab. The data on tocilizumab look good so far. In patients with chronic or latent TB, either abatacept or rituximab may be a better choice than is tocilizumab.

SDEF and this news organization are owned by Elsevier. Dr. Furst has disclosed financial relationships with Abbott, Actelion, Amgen, Array, Biogen Idec, BMS, Celgene, Centocor, Genentech, Gilead, GSK, the National Institutes of Health, Nitec Pharma, Novartis, Roche, UCB, and Wyeth.

SANTA MONICA, CALIF. – Advances in biomarker research and imaging may eventually make earlier diagnosis of osteoarthritis a reality. Unfortunately, such technologies remain prohibitively expensive for routine use.

And there's another problem: nothing to offer patients by way of an effective early therapy for knee OA.

"Clearly, the benefit of early diagnosis is in the setting of an effective treatment that could prevent progression to more severe changes," Dr. Amanda E. Nelson noted. "So at the present time, when such treatments are not available, the benefit of early diagnosis is really to identify individuals at an early stage when an investigational therapy might be of use, and such individuals can be enrolled in clinical trials.

"In the absence of specific disease-modifying treatments, the extra expense of an MRI for diagnosis is not warranted in daily practice at this time," advised Dr. Nelson of the division of rheumatology, allergy, and immunology at the University of North Carolina at Chapel Hill.

"The ideal therapy for knee OA is to be able to tailor therapy to an individual and their specific set of risk factors," Dr. Nelson said, noting that in such an ideal world, there would not be one OA treatment that was applied to everyone.

What has stymied the development of effective drugs for altering the course of knee OA?

The progress is slow for a few reasons, according to Dr. Nelson. Among them are lack of sensitive, cost-effective early diagnostics to best identify candidates for treatment, medicine's as-yet poor understanding of the causes of progression in OA, and its inability to identify which patients will progress to knee OA. This disease has a very long natural history: An injury in one's 20s may not lead to OA until after age 40 years. These things make trials difficult to conduct and to fund.

So for now, physicians who manage patients with knee OA are left with some poor choices.

Current treatment is directed toward late-stage disease, and by and large these therapies focus on easing pain, not on modifying the course of the disease, Dr. Nelson said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Corticosteroids have no effect on function, but do relieve pain for 1-3 weeks. Administration of intra-articular hyaluronans eases pain and preserves or improves function for 5-13 weeks, judging from findings of a systematic review (Cochrane Database Syst. Rev. 2006 [doi:10.1002/14651858.CD005328.pub2]).

On the investigational front, at least one phase III trial of the cyclooxygenase/lipoxygenase (COX/LOX) agent licofelone has been completed.

This investigational agent is an anti-inflammatory agent without the adverse effects of COX inhibition. Specifically, licofelone blocks synthesis of leukotriene, which contributes to inflammation and vasoconstriction. Metabolites of leukotriene synthesis cause gastrointestinal damage.

Findings from a trial of 355 patients with knee OA showed that licofelone given in a 200-mg dose twice daily preserved the volume of knee cartilage as well as did naproxen given in a 500-mg dose twice daily, with less GI toxicity. Cartilage volume was assessed using MRI (Ann. Rheum. Dis. 2009;68:938-47).

Another category of symptomatic treatment that has gone through a phase III trial is COX-inhibiting nitric oxide donators (CINODs). These compounds are created by fusing an existing NSAID to nitric oxide. These agents have anti-inflammatory properties similar to those of NSAIDs, but – unlike NSAIDs – CINODS protect the gastric mucosa and acts as both a vasodilator and an inhibitor of platelet aggregation, thereby preventing vascular damage (J. Pharm. Pharm. Sci. 2008;11:81s-110s).

Findings from research using intra-articular injection of the cytokine inhibitor IL-1Ra in humans has been disappointing. The drug did not ease pain at 12 weeks but did provide more short-term pain relief. The role of this agent may prove to be in the prevention of posttraumatic OA if it is given soon enough after injury.

Pain management is one of the major challenges in OA clinical care. "The pain management choices we have are often minimally or not effective and carry with them significant side effects. There are no great answers and a large need for better options," she said.

Some investigators were keeping a close eye on trials of tanezumab, a monoclonal antibody against nerve growth factor that showed early efficacy in OA pain. Although Pfizer Inc. has halted the trials because of increased progression and higher numbers of joint replacement, it is unclear whether that was related to the drug or to increased activity by the study subjects who experienced pain relief.

The SDEF and this news organization are owned by Elsevier. Dr. Nelson reported that her funding sources include a National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases loan repayment grant and an American College of Rheumatology Research and Education Foundation Clinical Investigator Fellowship Award. She reported having no other disclosures to make.

SANTA MONICA, CALIF. – Advances in biomarker research and imaging may eventually make earlier diagnosis of osteoarthritis a reality. Unfortunately, such technologies remain prohibitively expensive for routine use.

And there's another problem: nothing to offer patients by way of an effective early therapy for knee OA.

"Clearly, the benefit of early diagnosis is in the setting of an effective treatment that could prevent progression to more severe changes," Dr. Amanda E. Nelson noted. "So at the present time, when such treatments are not available, the benefit of early diagnosis is really to identify individuals at an early stage when an investigational therapy might be of use, and such individuals can be enrolled in clinical trials.

"In the absence of specific disease-modifying treatments, the extra expense of an MRI for diagnosis is not warranted in daily practice at this time," advised Dr. Nelson of the division of rheumatology, allergy, and immunology at the University of North Carolina at Chapel Hill.

"The ideal therapy for knee OA is to be able to tailor therapy to an individual and their specific set of risk factors," Dr. Nelson said, noting that in such an ideal world, there would not be one OA treatment that was applied to everyone.

What has stymied the development of effective drugs for altering the course of knee OA?

The progress is slow for a few reasons, according to Dr. Nelson. Among them are lack of sensitive, cost-effective early diagnostics to best identify candidates for treatment, medicine's as-yet poor understanding of the causes of progression in OA, and its inability to identify which patients will progress to knee OA. This disease has a very long natural history: An injury in one's 20s may not lead to OA until after age 40 years. These things make trials difficult to conduct and to fund.

So for now, physicians who manage patients with knee OA are left with some poor choices.

Current treatment is directed toward late-stage disease, and by and large these therapies focus on easing pain, not on modifying the course of the disease, Dr. Nelson said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Corticosteroids have no effect on function, but do relieve pain for 1-3 weeks. Administration of intra-articular hyaluronans eases pain and preserves or improves function for 5-13 weeks, judging from findings of a systematic review (Cochrane Database Syst. Rev. 2006 [doi:10.1002/14651858.CD005328.pub2]).

On the investigational front, at least one phase III trial of the cyclooxygenase/lipoxygenase (COX/LOX) agent licofelone has been completed.

This investigational agent is an anti-inflammatory agent without the adverse effects of COX inhibition. Specifically, licofelone blocks synthesis of leukotriene, which contributes to inflammation and vasoconstriction. Metabolites of leukotriene synthesis cause gastrointestinal damage.

Findings from a trial of 355 patients with knee OA showed that licofelone given in a 200-mg dose twice daily preserved the volume of knee cartilage as well as did naproxen given in a 500-mg dose twice daily, with less GI toxicity. Cartilage volume was assessed using MRI (Ann. Rheum. Dis. 2009;68:938-47).

Another category of symptomatic treatment that has gone through a phase III trial is COX-inhibiting nitric oxide donators (CINODs). These compounds are created by fusing an existing NSAID to nitric oxide. These agents have anti-inflammatory properties similar to those of NSAIDs, but – unlike NSAIDs – CINODS protect the gastric mucosa and acts as both a vasodilator and an inhibitor of platelet aggregation, thereby preventing vascular damage (J. Pharm. Pharm. Sci. 2008;11:81s-110s).

Findings from research using intra-articular injection of the cytokine inhibitor IL-1Ra in humans has been disappointing. The drug did not ease pain at 12 weeks but did provide more short-term pain relief. The role of this agent may prove to be in the prevention of posttraumatic OA if it is given soon enough after injury.

Pain management is one of the major challenges in OA clinical care. "The pain management choices we have are often minimally or not effective and carry with them significant side effects. There are no great answers and a large need for better options," she said.

Some investigators were keeping a close eye on trials of tanezumab, a monoclonal antibody against nerve growth factor that showed early efficacy in OA pain. Although Pfizer Inc. has halted the trials because of increased progression and higher numbers of joint replacement, it is unclear whether that was related to the drug or to increased activity by the study subjects who experienced pain relief.

The SDEF and this news organization are owned by Elsevier. Dr. Nelson reported that her funding sources include a National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases loan repayment grant and an American College of Rheumatology Research and Education Foundation Clinical Investigator Fellowship Award. She reported having no other disclosures to make.

SANTA MONICA, CALIF. – Advances in biomarker research and imaging may eventually make earlier diagnosis of osteoarthritis a reality. Unfortunately, such technologies remain prohibitively expensive for routine use.

And there's another problem: nothing to offer patients by way of an effective early therapy for knee OA.

"Clearly, the benefit of early diagnosis is in the setting of an effective treatment that could prevent progression to more severe changes," Dr. Amanda E. Nelson noted. "So at the present time, when such treatments are not available, the benefit of early diagnosis is really to identify individuals at an early stage when an investigational therapy might be of use, and such individuals can be enrolled in clinical trials.

"In the absence of specific disease-modifying treatments, the extra expense of an MRI for diagnosis is not warranted in daily practice at this time," advised Dr. Nelson of the division of rheumatology, allergy, and immunology at the University of North Carolina at Chapel Hill.

"The ideal therapy for knee OA is to be able to tailor therapy to an individual and their specific set of risk factors," Dr. Nelson said, noting that in such an ideal world, there would not be one OA treatment that was applied to everyone.

What has stymied the development of effective drugs for altering the course of knee OA?

The progress is slow for a few reasons, according to Dr. Nelson. Among them are lack of sensitive, cost-effective early diagnostics to best identify candidates for treatment, medicine's as-yet poor understanding of the causes of progression in OA, and its inability to identify which patients will progress to knee OA. This disease has a very long natural history: An injury in one's 20s may not lead to OA until after age 40 years. These things make trials difficult to conduct and to fund.

So for now, physicians who manage patients with knee OA are left with some poor choices.

Current treatment is directed toward late-stage disease, and by and large these therapies focus on easing pain, not on modifying the course of the disease, Dr. Nelson said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Corticosteroids have no effect on function, but do relieve pain for 1-3 weeks. Administration of intra-articular hyaluronans eases pain and preserves or improves function for 5-13 weeks, judging from findings of a systematic review (Cochrane Database Syst. Rev. 2006 [doi:10.1002/14651858.CD005328.pub2]).

On the investigational front, at least one phase III trial of the cyclooxygenase/lipoxygenase (COX/LOX) agent licofelone has been completed.

This investigational agent is an anti-inflammatory agent without the adverse effects of COX inhibition. Specifically, licofelone blocks synthesis of leukotriene, which contributes to inflammation and vasoconstriction. Metabolites of leukotriene synthesis cause gastrointestinal damage.

Findings from a trial of 355 patients with knee OA showed that licofelone given in a 200-mg dose twice daily preserved the volume of knee cartilage as well as did naproxen given in a 500-mg dose twice daily, with less GI toxicity. Cartilage volume was assessed using MRI (Ann. Rheum. Dis. 2009;68:938-47).

Another category of symptomatic treatment that has gone through a phase III trial is COX-inhibiting nitric oxide donators (CINODs). These compounds are created by fusing an existing NSAID to nitric oxide. These agents have anti-inflammatory properties similar to those of NSAIDs, but – unlike NSAIDs – CINODS protect the gastric mucosa and acts as both a vasodilator and an inhibitor of platelet aggregation, thereby preventing vascular damage (J. Pharm. Pharm. Sci. 2008;11:81s-110s).

Findings from research using intra-articular injection of the cytokine inhibitor IL-1Ra in humans has been disappointing. The drug did not ease pain at 12 weeks but did provide more short-term pain relief. The role of this agent may prove to be in the prevention of posttraumatic OA if it is given soon enough after injury.

Pain management is one of the major challenges in OA clinical care. "The pain management choices we have are often minimally or not effective and carry with them significant side effects. There are no great answers and a large need for better options," she said.

Some investigators were keeping a close eye on trials of tanezumab, a monoclonal antibody against nerve growth factor that showed early efficacy in OA pain. Although Pfizer Inc. has halted the trials because of increased progression and higher numbers of joint replacement, it is unclear whether that was related to the drug or to increased activity by the study subjects who experienced pain relief.

The SDEF and this news organization are owned by Elsevier. Dr. Nelson reported that her funding sources include a National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases loan repayment grant and an American College of Rheumatology Research and Education Foundation Clinical Investigator Fellowship Award. She reported having no other disclosures to make.

SANTA MONICA, CALIF. — Rheumatoid arthritis patients with a true primary failure on a first-time trial of tumor necrosis factor inhibitor therapy should change to treatment with a biologic that has a different mechanism of action. The likelihood is great that trying a second anti-TNF agent will result in just another failure and delay the initiation of effective treatment, according to Dr. Daniel E. Furst.

The key is to be sure that failure to respond to the first anti-TNF agent is not secondary to another cause, such as too low a dose, he said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

An estimated 60%–70% of patients who begin treatment with an anti-TNF agent are still on the agent at the end of 1 year. Although some patients have to stop treatment because of problems with their insurance and other reasons, primary and secondary failure play a role, he said.

One cannot recognize a treatment failure unless one undertakes therapy with a treatment target in mind, usually remission or low disease activity levels. Treating-to-target goals have been shown to improve outcome and to lower rates of organ damage in diabetes and hypertension. Treating to target was the watchword of new treatment guidelines issued jointly earlier this year by the American College of Rheumatology and the European League Against Rheumatism (

Evidence that treating to target in RA is effective dates back to 1998, and this therapeutic approach has become more important in the biologics era of care. The goals of treating to target, as outlined by ACR/EULAR, are to aim for complete remission of low disease activity; to see the patient monthly for at least the first 3–6 months, depending on disease activity; to use a combination of validated response measures; to consider comorbidities; to aim for sustained remission; and to get informed consent.

So how does one tell whether a patient's lack of response to an anti-TNF agent is a true primary failure or is secondary to something else that may be correctable, such as a longer therapeutic trial?

Findings from a secondary analysis of TEMPO (Trial of Etanercept and Methotrexate With Radiographic Patient Outcomes) data show that about half of the patients who had not responded by 12 weeks to treatment with etanercept or methotrexate, either as monotherapy or in combination, were still likely to respond by 24 weeks with either treatment (Ann. Rheum. Dis. 2008;67:1444–7).

“If there is a hint of a response, treat beyond the usual 12 weeks,” advised Dr. Furst, who is the Carl M. Pearson Professor of Medicine at the University of California, Los Angeles.

Some patients may need a higher dose of the anti-TNF agent than they have been receiving. A chart review presented by Dr. Furst and colleagues at the 2008 annual meeting of the ACR showed that increasing the adalimumab dose from 40 mg subcutaneously every other week for 5 months to 40 mg every week for 6 months can increase the number of patients with good EULAR responses. Of 48 patients who originally had received 40 mg of adalimumab subcutaneously every other week for 5 months, 20 had good response and 28 achieved moderate or no EULAR responses. An increase in the dose to 40 mg every week for 6 months resulted in a good EULAR response in 8 of 28 nonresponders, which included 4 of 12 patients who originally had no response to the lower-dose adalimumab (Arthritis Rheum. 2008;58[suppl.]:abstract 999).

One can improve treatment response to infliximab by decreasing the interval between doses. But increasing the dose and leaving the interval the same does not have the desired effect. Other data from Dr. Furst's research suggest that in the case of etanercept, increasing dose does not improve efficacy (Arthritis Rheum. 2007;56[suppl.]:abstract 726).

Higher doses of anti-TNF agents are associated with higher rates of nonserious adverse events, especially with adalimumab and infliximab. Data from package inserts show that infliximab has a 5.3% rate of serious adverse events, which is higher than that seen with adalimumab (2%), etanercept (1%), golimumab (1.9%), and certolizumab (3%). Data from the French RATIO registry show that, during 57,711 people-years of biologic use in 2004–2007, there were 69 cases of tuberculosis in patients who took anti-TNF agents for a variety of reasons, including RA. After adjustment for confounding risk factors, the incidence rate for TB in patients on any anti-TNF drug was shown to be 116.7 cases per 100,000 person-years of use (Arthritis Rheum. 2009;60:1884–94).

The bottom line is that not only are anti-TNF agents less effective after a primary failure, but the rate of adverse events increases as well, judging from data reported at the annual meeting of the European League Against Rheumatism in 2008 by Dr. Luba Nalysnyk of United BioSource Corp. Dr. Nalysnyk and associates performed a meta-analysis of 16 articles and 15 abstracts involving 5,306 patients. In the meta-analysis, primary failure of an anti-TNF agent occurred in 48% of patients. A second anti-TNF agent did not work in 66% of those patients, and another 66% of those patients developed adverse events in response to the second agent.

SDEF and

A video interview with Dr. Daniel E. Furst is available at

Source Sally Kubetin/ELsevier Global Medical Newswww.rheumatologynews.com/

SANTA MONICA, CALIF. — Rheumatoid arthritis patients with a true primary failure on a first-time trial of tumor necrosis factor inhibitor therapy should change to treatment with a biologic that has a different mechanism of action. The likelihood is great that trying a second anti-TNF agent will result in just another failure and delay the initiation of effective treatment, according to Dr. Daniel E. Furst.

The key is to be sure that failure to respond to the first anti-TNF agent is not secondary to another cause, such as too low a dose, he said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

An estimated 60%–70% of patients who begin treatment with an anti-TNF agent are still on the agent at the end of 1 year. Although some patients have to stop treatment because of problems with their insurance and other reasons, primary and secondary failure play a role, he said.

One cannot recognize a treatment failure unless one undertakes therapy with a treatment target in mind, usually remission or low disease activity levels. Treating-to-target goals have been shown to improve outcome and to lower rates of organ damage in diabetes and hypertension. Treating to target was the watchword of new treatment guidelines issued jointly earlier this year by the American College of Rheumatology and the European League Against Rheumatism (

Evidence that treating to target in RA is effective dates back to 1998, and this therapeutic approach has become more important in the biologics era of care. The goals of treating to target, as outlined by ACR/EULAR, are to aim for complete remission of low disease activity; to see the patient monthly for at least the first 3–6 months, depending on disease activity; to use a combination of validated response measures; to consider comorbidities; to aim for sustained remission; and to get informed consent.

So how does one tell whether a patient's lack of response to an anti-TNF agent is a true primary failure or is secondary to something else that may be correctable, such as a longer therapeutic trial?

Findings from a secondary analysis of TEMPO (Trial of Etanercept and Methotrexate With Radiographic Patient Outcomes) data show that about half of the patients who had not responded by 12 weeks to treatment with etanercept or methotrexate, either as monotherapy or in combination, were still likely to respond by 24 weeks with either treatment (Ann. Rheum. Dis. 2008;67:1444–7).

“If there is a hint of a response, treat beyond the usual 12 weeks,” advised Dr. Furst, who is the Carl M. Pearson Professor of Medicine at the University of California, Los Angeles.

Some patients may need a higher dose of the anti-TNF agent than they have been receiving. A chart review presented by Dr. Furst and colleagues at the 2008 annual meeting of the ACR showed that increasing the adalimumab dose from 40 mg subcutaneously every other week for 5 months to 40 mg every week for 6 months can increase the number of patients with good EULAR responses. Of 48 patients who originally had received 40 mg of adalimumab subcutaneously every other week for 5 months, 20 had good response and 28 achieved moderate or no EULAR responses. An increase in the dose to 40 mg every week for 6 months resulted in a good EULAR response in 8 of 28 nonresponders, which included 4 of 12 patients who originally had no response to the lower-dose adalimumab (Arthritis Rheum. 2008;58[suppl.]:abstract 999).

One can improve treatment response to infliximab by decreasing the interval between doses. But increasing the dose and leaving the interval the same does not have the desired effect. Other data from Dr. Furst's research suggest that in the case of etanercept, increasing dose does not improve efficacy (Arthritis Rheum. 2007;56[suppl.]:abstract 726).

Higher doses of anti-TNF agents are associated with higher rates of nonserious adverse events, especially with adalimumab and infliximab. Data from package inserts show that infliximab has a 5.3% rate of serious adverse events, which is higher than that seen with adalimumab (2%), etanercept (1%), golimumab (1.9%), and certolizumab (3%). Data from the French RATIO registry show that, during 57,711 people-years of biologic use in 2004–2007, there were 69 cases of tuberculosis in patients who took anti-TNF agents for a variety of reasons, including RA. After adjustment for confounding risk factors, the incidence rate for TB in patients on any anti-TNF drug was shown to be 116.7 cases per 100,000 person-years of use (Arthritis Rheum. 2009;60:1884–94).

The bottom line is that not only are anti-TNF agents less effective after a primary failure, but the rate of adverse events increases as well, judging from data reported at the annual meeting of the European League Against Rheumatism in 2008 by Dr. Luba Nalysnyk of United BioSource Corp. Dr. Nalysnyk and associates performed a meta-analysis of 16 articles and 15 abstracts involving 5,306 patients. In the meta-analysis, primary failure of an anti-TNF agent occurred in 48% of patients. A second anti-TNF agent did not work in 66% of those patients, and another 66% of those patients developed adverse events in response to the second agent.

SDEF and

A video interview with Dr. Daniel E. Furst is available at

Source Sally Kubetin/ELsevier Global Medical Newswww.rheumatologynews.com/

SANTA MONICA, CALIF. — Rheumatoid arthritis patients with a true primary failure on a first-time trial of tumor necrosis factor inhibitor therapy should change to treatment with a biologic that has a different mechanism of action. The likelihood is great that trying a second anti-TNF agent will result in just another failure and delay the initiation of effective treatment, according to Dr. Daniel E. Furst.

The key is to be sure that failure to respond to the first anti-TNF agent is not secondary to another cause, such as too low a dose, he said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

An estimated 60%–70% of patients who begin treatment with an anti-TNF agent are still on the agent at the end of 1 year. Although some patients have to stop treatment because of problems with their insurance and other reasons, primary and secondary failure play a role, he said.

One cannot recognize a treatment failure unless one undertakes therapy with a treatment target in mind, usually remission or low disease activity levels. Treating-to-target goals have been shown to improve outcome and to lower rates of organ damage in diabetes and hypertension. Treating to target was the watchword of new treatment guidelines issued jointly earlier this year by the American College of Rheumatology and the European League Against Rheumatism (

Evidence that treating to target in RA is effective dates back to 1998, and this therapeutic approach has become more important in the biologics era of care. The goals of treating to target, as outlined by ACR/EULAR, are to aim for complete remission of low disease activity; to see the patient monthly for at least the first 3–6 months, depending on disease activity; to use a combination of validated response measures; to consider comorbidities; to aim for sustained remission; and to get informed consent.

So how does one tell whether a patient's lack of response to an anti-TNF agent is a true primary failure or is secondary to something else that may be correctable, such as a longer therapeutic trial?

Findings from a secondary analysis of TEMPO (Trial of Etanercept and Methotrexate With Radiographic Patient Outcomes) data show that about half of the patients who had not responded by 12 weeks to treatment with etanercept or methotrexate, either as monotherapy or in combination, were still likely to respond by 24 weeks with either treatment (Ann. Rheum. Dis. 2008;67:1444–7).

“If there is a hint of a response, treat beyond the usual 12 weeks,” advised Dr. Furst, who is the Carl M. Pearson Professor of Medicine at the University of California, Los Angeles.

Some patients may need a higher dose of the anti-TNF agent than they have been receiving. A chart review presented by Dr. Furst and colleagues at the 2008 annual meeting of the ACR showed that increasing the adalimumab dose from 40 mg subcutaneously every other week for 5 months to 40 mg every week for 6 months can increase the number of patients with good EULAR responses. Of 48 patients who originally had received 40 mg of adalimumab subcutaneously every other week for 5 months, 20 had good response and 28 achieved moderate or no EULAR responses. An increase in the dose to 40 mg every week for 6 months resulted in a good EULAR response in 8 of 28 nonresponders, which included 4 of 12 patients who originally had no response to the lower-dose adalimumab (Arthritis Rheum. 2008;58[suppl.]:abstract 999).

One can improve treatment response to infliximab by decreasing the interval between doses. But increasing the dose and leaving the interval the same does not have the desired effect. Other data from Dr. Furst's research suggest that in the case of etanercept, increasing dose does not improve efficacy (Arthritis Rheum. 2007;56[suppl.]:abstract 726).

Higher doses of anti-TNF agents are associated with higher rates of nonserious adverse events, especially with adalimumab and infliximab. Data from package inserts show that infliximab has a 5.3% rate of serious adverse events, which is higher than that seen with adalimumab (2%), etanercept (1%), golimumab (1.9%), and certolizumab (3%). Data from the French RATIO registry show that, during 57,711 people-years of biologic use in 2004–2007, there were 69 cases of tuberculosis in patients who took anti-TNF agents for a variety of reasons, including RA. After adjustment for confounding risk factors, the incidence rate for TB in patients on any anti-TNF drug was shown to be 116.7 cases per 100,000 person-years of use (Arthritis Rheum. 2009;60:1884–94).

The bottom line is that not only are anti-TNF agents less effective after a primary failure, but the rate of adverse events increases as well, judging from data reported at the annual meeting of the European League Against Rheumatism in 2008 by Dr. Luba Nalysnyk of United BioSource Corp. Dr. Nalysnyk and associates performed a meta-analysis of 16 articles and 15 abstracts involving 5,306 patients. In the meta-analysis, primary failure of an anti-TNF agent occurred in 48% of patients. A second anti-TNF agent did not work in 66% of those patients, and another 66% of those patients developed adverse events in response to the second agent.

SDEF and

A video interview with Dr. Daniel E. Furst is available at

Source Sally Kubetin/ELsevier Global Medical Newswww.rheumatologynews.com/

SANTA MONICA, CALIF. — The fact that many patients with rheumatoid arthritis are not smokers, have normal lipid levels, are not overweight, and do not have a family history of heart disease belies their elevated risk for cardiovascular disease.

Rheumatoid arthritis (RA) is an inflammatory disease, and physicians need to screen patients with RA more closely for cardiovascular disease (CVD) risks. Unfortunately, practitioners currently lack a screening tool since the Framingham Heart Study risk score falls woefully short of accurately predicting CVD risk in patients with RA, Dr. Sherine E. Gabriel said at a meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

With colleagues at the Mayo Clinic, Dr. Gabriel is developing just such a tool for screening RA patients. In an interview, Dr. Gabriel didn't divulge details of the tool, because it is still being tested. She advised physicians, for now, to screen their RA patients for CVD risks using standard laboratory tests and to intervene earlier than in other populations.

Severe, intractable RA often goes hand-in-hand with elevated risk for CVD. The patient who is positive for rheumatoid factor and always has an elevated level of C-reactive protein and a high erythrocyte sedimentation rate needs early intervention. Some physicians may want to consider using echocardiogram to screen for early signs of heart failure while it may be still treatable, said Dr. Gabriel, professor of medicine and epidemiology at the Mayo Clinic, Rochester, Minn.

Many of the insights into CVD risk in RA come from studies that Dr. Gabriel and other Mayo Clinic investigators have conducted over several years. The Mayo Clinic has followed a cohort of 1,179 residents of Olmsted County, Minn., who were diagnosed with RA between 1955 and 2007. The researchers compared the patients' rates of heart disease and survival with those of three other cohorts: 1,179 people without RA, 852 people with congestive heart failure, and 3,256 people with acute myocardial infarctions. Overall, survival among the RA patients was significantly shorter than would have been expected, particularly in women (Arthritis Rheum. 2003;48:54–8).

A second longitudinal study of residents of the city of Rochester, Minn., which is in Olmsted County, followed 603 patients with RA beginning when they were an average of 58 years old. During a mean follow-up of 15 years, 354 patients died, and CVD was the primary cause of death in 176 patients. The increased risk for CVD was associated with three markers of systemic inflammation: erythrocyte sedimentation rate above 60 mm/hour on three consecutive measurements, the presence of RA vasculitis, and the presence of RA lung disease (Arthritis Rheum. 2005;52:722–32).

In another study, 603 residents who were diagnosed with RA were significantly more likely to have been hospitalized for acute MI or to have experienced unrecognized MIs in the 2 years before diagnosis than were controls during a corresponding 2-year period. After diagnosis, RA patients were twice as likely to experience unrecognized MIs and sudden deaths and less likely to undergo coronary artery bypass grafting compared with non-RA subjects (Arthritis Rheum. 2005;52:402–11).

SDEF and

A new score is needed to predict CVD risk in RA, said Dr. Sherine E. Gabriel.

Source Sally Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. — The fact that many patients with rheumatoid arthritis are not smokers, have normal lipid levels, are not overweight, and do not have a family history of heart disease belies their elevated risk for cardiovascular disease.

Rheumatoid arthritis (RA) is an inflammatory disease, and physicians need to screen patients with RA more closely for cardiovascular disease (CVD) risks. Unfortunately, practitioners currently lack a screening tool since the Framingham Heart Study risk score falls woefully short of accurately predicting CVD risk in patients with RA, Dr. Sherine E. Gabriel said at a meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

With colleagues at the Mayo Clinic, Dr. Gabriel is developing just such a tool for screening RA patients. In an interview, Dr. Gabriel didn't divulge details of the tool, because it is still being tested. She advised physicians, for now, to screen their RA patients for CVD risks using standard laboratory tests and to intervene earlier than in other populations.

Severe, intractable RA often goes hand-in-hand with elevated risk for CVD. The patient who is positive for rheumatoid factor and always has an elevated level of C-reactive protein and a high erythrocyte sedimentation rate needs early intervention. Some physicians may want to consider using echocardiogram to screen for early signs of heart failure while it may be still treatable, said Dr. Gabriel, professor of medicine and epidemiology at the Mayo Clinic, Rochester, Minn.

Many of the insights into CVD risk in RA come from studies that Dr. Gabriel and other Mayo Clinic investigators have conducted over several years. The Mayo Clinic has followed a cohort of 1,179 residents of Olmsted County, Minn., who were diagnosed with RA between 1955 and 2007. The researchers compared the patients' rates of heart disease and survival with those of three other cohorts: 1,179 people without RA, 852 people with congestive heart failure, and 3,256 people with acute myocardial infarctions. Overall, survival among the RA patients was significantly shorter than would have been expected, particularly in women (Arthritis Rheum. 2003;48:54–8).

A second longitudinal study of residents of the city of Rochester, Minn., which is in Olmsted County, followed 603 patients with RA beginning when they were an average of 58 years old. During a mean follow-up of 15 years, 354 patients died, and CVD was the primary cause of death in 176 patients. The increased risk for CVD was associated with three markers of systemic inflammation: erythrocyte sedimentation rate above 60 mm/hour on three consecutive measurements, the presence of RA vasculitis, and the presence of RA lung disease (Arthritis Rheum. 2005;52:722–32).

In another study, 603 residents who were diagnosed with RA were significantly more likely to have been hospitalized for acute MI or to have experienced unrecognized MIs in the 2 years before diagnosis than were controls during a corresponding 2-year period. After diagnosis, RA patients were twice as likely to experience unrecognized MIs and sudden deaths and less likely to undergo coronary artery bypass grafting compared with non-RA subjects (Arthritis Rheum. 2005;52:402–11).

SDEF and

A new score is needed to predict CVD risk in RA, said Dr. Sherine E. Gabriel.

Source Sally Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. — The fact that many patients with rheumatoid arthritis are not smokers, have normal lipid levels, are not overweight, and do not have a family history of heart disease belies their elevated risk for cardiovascular disease.

Rheumatoid arthritis (RA) is an inflammatory disease, and physicians need to screen patients with RA more closely for cardiovascular disease (CVD) risks. Unfortunately, practitioners currently lack a screening tool since the Framingham Heart Study risk score falls woefully short of accurately predicting CVD risk in patients with RA, Dr. Sherine E. Gabriel said at a meeting sponsored by Skin Disease Education Foundation (SDEF) and the University of Louisville.

With colleagues at the Mayo Clinic, Dr. Gabriel is developing just such a tool for screening RA patients. In an interview, Dr. Gabriel didn't divulge details of the tool, because it is still being tested. She advised physicians, for now, to screen their RA patients for CVD risks using standard laboratory tests and to intervene earlier than in other populations.

Severe, intractable RA often goes hand-in-hand with elevated risk for CVD. The patient who is positive for rheumatoid factor and always has an elevated level of C-reactive protein and a high erythrocyte sedimentation rate needs early intervention. Some physicians may want to consider using echocardiogram to screen for early signs of heart failure while it may be still treatable, said Dr. Gabriel, professor of medicine and epidemiology at the Mayo Clinic, Rochester, Minn.

Many of the insights into CVD risk in RA come from studies that Dr. Gabriel and other Mayo Clinic investigators have conducted over several years. The Mayo Clinic has followed a cohort of 1,179 residents of Olmsted County, Minn., who were diagnosed with RA between 1955 and 2007. The researchers compared the patients' rates of heart disease and survival with those of three other cohorts: 1,179 people without RA, 852 people with congestive heart failure, and 3,256 people with acute myocardial infarctions. Overall, survival among the RA patients was significantly shorter than would have been expected, particularly in women (Arthritis Rheum. 2003;48:54–8).

A second longitudinal study of residents of the city of Rochester, Minn., which is in Olmsted County, followed 603 patients with RA beginning when they were an average of 58 years old. During a mean follow-up of 15 years, 354 patients died, and CVD was the primary cause of death in 176 patients. The increased risk for CVD was associated with three markers of systemic inflammation: erythrocyte sedimentation rate above 60 mm/hour on three consecutive measurements, the presence of RA vasculitis, and the presence of RA lung disease (Arthritis Rheum. 2005;52:722–32).

In another study, 603 residents who were diagnosed with RA were significantly more likely to have been hospitalized for acute MI or to have experienced unrecognized MIs in the 2 years before diagnosis than were controls during a corresponding 2-year period. After diagnosis, RA patients were twice as likely to experience unrecognized MIs and sudden deaths and less likely to undergo coronary artery bypass grafting compared with non-RA subjects (Arthritis Rheum. 2005;52:402–11).

SDEF and

A new score is needed to predict CVD risk in RA, said Dr. Sherine E. Gabriel.

Source Sally Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. — Advances in biomarker research and imaging may eventually make earlier diagnosis of osteoarthritis a reality. Unfortunately, such technologies remain prohibitively expensive for routine use.

And there's another problem: nothing to offer patients by way of an effective early therapy for knee OA.

“So at the present time, when such treatments are not available, the benefit of early diagnosis is really to identify individuals at an early stage when an investigational therapy might be of use, and such individuals can be enrolled in clinical trials,” Dr. Amanda E. Nelson noted.

“In the absence of specific disease-modifying treatments, the extra expense of an MRI for diagnosis is not warranted in daily practice at this time,” advised Dr. Nelson of the University of North Carolina at Chapel Hill.

What has stymied the development of effective drugs for altering the course of knee OA?

The progress is slow for a few reasons, according to Dr. Nelson. Among them are lack of sensitive, cost-effective early diagnostics to best identify candidates for treatment, medicine's as-yet poor understanding of the causes of progression in OA, and its inability to identify which patients will progress to knee OA. This disease has a very long natural history: An injury in one's 20s may not lead to OA until after age 40 years. These things make trials difficult to conduct and to fund.

Current treatment is directed toward late-stage disease, and by and large these therapies focus on easing pain, not on modifying the course of the disease, Dr. Nelson said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Corticosteroids have no effect on function, but they do relieve pain for 1–3 weeks. The administration of intra-articular hyaluronans eases pain and preserves or improves function for 5–13 weeks, judging from a systematic review (Cochrane Database Syst. Rev. 2006 [doi:10.1002/14651858.CD005328.pub2]).

On the investigational front, at least one phase III trial of the cyclooxygenase/lipoxygenase (COX/LOX) agent licofelone has been completed.

This investigational agent is an anti-inflammatory agent without the adverse effects of COX inhibition. Findings from a trial of 355 patients with knee OA showed that licofelone given in a 200-mg dose twice daily preserved the volume of knee cartilage as well as did naproxen given in a 500-mg dose twice daily, with less GI toxicity (Ann. Rheum. Dis. 2009;68:938–47).

Another category of symptomatic treatment that has gone through a phase III trial is COX-inhibiting nitric oxide donators (CINODs). These agents have anti-inflammatory properties similar to those of NSAIDs, but – unlike NSAIDs – CINODS protect the gastric mucosa and act as both a vasodilator and an inhibitor of platelet aggregation, thereby preventing vascular damage (J. Pharm. Pharm. Sci. 2008; Sep 20;11:81s-110s).

Findings from research using intra-articular injection of the cytokine inhibitor IL-1Ra in humans has been disappointing. The drug did not ease pain at 12 weeks but did provide more short-term pain relief.

Some investigators were keeping a close eye on trials of tanezumab, a monoclonal antibody against nerve growth factor that showed early efficacy in OA pain.

Although Pfizer Inc. has halted the trials because of increased progression and higher numbers of joint replacement, it is unclear whether that was related to the drug or to increased activity by the study subjects who experienced pain relief.

SDEF and

A video interview with Dr. Amanda E. Nelson is available at

Source Sally Kubetin/Elsevier Global Medical Newshttp://www.rheumatologynews.com/

SANTA MONICA, CALIF. — Advances in biomarker research and imaging may eventually make earlier diagnosis of osteoarthritis a reality. Unfortunately, such technologies remain prohibitively expensive for routine use.

And there's another problem: nothing to offer patients by way of an effective early therapy for knee OA.

“So at the present time, when such treatments are not available, the benefit of early diagnosis is really to identify individuals at an early stage when an investigational therapy might be of use, and such individuals can be enrolled in clinical trials,” Dr. Amanda E. Nelson noted.

“In the absence of specific disease-modifying treatments, the extra expense of an MRI for diagnosis is not warranted in daily practice at this time,” advised Dr. Nelson of the University of North Carolina at Chapel Hill.

What has stymied the development of effective drugs for altering the course of knee OA?

The progress is slow for a few reasons, according to Dr. Nelson. Among them are lack of sensitive, cost-effective early diagnostics to best identify candidates for treatment, medicine's as-yet poor understanding of the causes of progression in OA, and its inability to identify which patients will progress to knee OA. This disease has a very long natural history: An injury in one's 20s may not lead to OA until after age 40 years. These things make trials difficult to conduct and to fund.

Current treatment is directed toward late-stage disease, and by and large these therapies focus on easing pain, not on modifying the course of the disease, Dr. Nelson said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Corticosteroids have no effect on function, but they do relieve pain for 1–3 weeks. The administration of intra-articular hyaluronans eases pain and preserves or improves function for 5–13 weeks, judging from a systematic review (Cochrane Database Syst. Rev. 2006 [doi:10.1002/14651858.CD005328.pub2]).

On the investigational front, at least one phase III trial of the cyclooxygenase/lipoxygenase (COX/LOX) agent licofelone has been completed.

This investigational agent is an anti-inflammatory agent without the adverse effects of COX inhibition. Findings from a trial of 355 patients with knee OA showed that licofelone given in a 200-mg dose twice daily preserved the volume of knee cartilage as well as did naproxen given in a 500-mg dose twice daily, with less GI toxicity (Ann. Rheum. Dis. 2009;68:938–47).

Another category of symptomatic treatment that has gone through a phase III trial is COX-inhibiting nitric oxide donators (CINODs). These agents have anti-inflammatory properties similar to those of NSAIDs, but – unlike NSAIDs – CINODS protect the gastric mucosa and act as both a vasodilator and an inhibitor of platelet aggregation, thereby preventing vascular damage (J. Pharm. Pharm. Sci. 2008; Sep 20;11:81s-110s).

Findings from research using intra-articular injection of the cytokine inhibitor IL-1Ra in humans has been disappointing. The drug did not ease pain at 12 weeks but did provide more short-term pain relief.

Some investigators were keeping a close eye on trials of tanezumab, a monoclonal antibody against nerve growth factor that showed early efficacy in OA pain.

Although Pfizer Inc. has halted the trials because of increased progression and higher numbers of joint replacement, it is unclear whether that was related to the drug or to increased activity by the study subjects who experienced pain relief.

SDEF and

A video interview with Dr. Amanda E. Nelson is available at

Source Sally Kubetin/Elsevier Global Medical Newshttp://www.rheumatologynews.com/

SANTA MONICA, CALIF. — Advances in biomarker research and imaging may eventually make earlier diagnosis of osteoarthritis a reality. Unfortunately, such technologies remain prohibitively expensive for routine use.

And there's another problem: nothing to offer patients by way of an effective early therapy for knee OA.

“So at the present time, when such treatments are not available, the benefit of early diagnosis is really to identify individuals at an early stage when an investigational therapy might be of use, and such individuals can be enrolled in clinical trials,” Dr. Amanda E. Nelson noted.

“In the absence of specific disease-modifying treatments, the extra expense of an MRI for diagnosis is not warranted in daily practice at this time,” advised Dr. Nelson of the University of North Carolina at Chapel Hill.

What has stymied the development of effective drugs for altering the course of knee OA?

The progress is slow for a few reasons, according to Dr. Nelson. Among them are lack of sensitive, cost-effective early diagnostics to best identify candidates for treatment, medicine's as-yet poor understanding of the causes of progression in OA, and its inability to identify which patients will progress to knee OA. This disease has a very long natural history: An injury in one's 20s may not lead to OA until after age 40 years. These things make trials difficult to conduct and to fund.

Current treatment is directed toward late-stage disease, and by and large these therapies focus on easing pain, not on modifying the course of the disease, Dr. Nelson said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Corticosteroids have no effect on function, but they do relieve pain for 1–3 weeks. The administration of intra-articular hyaluronans eases pain and preserves or improves function for 5–13 weeks, judging from a systematic review (Cochrane Database Syst. Rev. 2006 [doi:10.1002/14651858.CD005328.pub2]).

On the investigational front, at least one phase III trial of the cyclooxygenase/lipoxygenase (COX/LOX) agent licofelone has been completed.

This investigational agent is an anti-inflammatory agent without the adverse effects of COX inhibition. Findings from a trial of 355 patients with knee OA showed that licofelone given in a 200-mg dose twice daily preserved the volume of knee cartilage as well as did naproxen given in a 500-mg dose twice daily, with less GI toxicity (Ann. Rheum. Dis. 2009;68:938–47).

Another category of symptomatic treatment that has gone through a phase III trial is COX-inhibiting nitric oxide donators (CINODs). These agents have anti-inflammatory properties similar to those of NSAIDs, but – unlike NSAIDs – CINODS protect the gastric mucosa and act as both a vasodilator and an inhibitor of platelet aggregation, thereby preventing vascular damage (J. Pharm. Pharm. Sci. 2008; Sep 20;11:81s-110s).

Findings from research using intra-articular injection of the cytokine inhibitor IL-1Ra in humans has been disappointing. The drug did not ease pain at 12 weeks but did provide more short-term pain relief.

Some investigators were keeping a close eye on trials of tanezumab, a monoclonal antibody against nerve growth factor that showed early efficacy in OA pain.

Although Pfizer Inc. has halted the trials because of increased progression and higher numbers of joint replacement, it is unclear whether that was related to the drug or to increased activity by the study subjects who experienced pain relief.

SDEF and

A video interview with Dr. Amanda E. Nelson is available at

Source Sally Kubetin/Elsevier Global Medical Newshttp://www.rheumatologynews.com/

SANTA MONICA, CALIF. – Social media provides a way for you to engage with your patients and the community, whether you practice in an HMO or privately, according to Dr. Jeffrey Benabio, a dermatologist at Kaiser Permanente in San Diego.

No matter what your specialty, the principles of using social media such as blogs, Facebook, and Twitter as tools for improving patient care will apply. “Online patient communities are an ascendant means for patients to learn about their disease, and seek advice and comfort from [other] patients like them,” Dr. Benabio said in an interview. “Physicians can be part of this conversation and contribute to it. Who better to [advise] patients [on] how to live with pain, live with deformity, deal with insurance companies, than physicians?”

It takes no money but lots of time to build online networks. So why bother? “Patients are going online to interact with their physicians, and we are not there. Whereas patients always had to come to us to learn about disease and health, now they get most of their information online. Our absence online perpetuates a trend of diminishing importance of our profession,” he said.

As with much in life, the secret to being effective online comes down to showing up. “A physician becomes a trusted member of the community by being present. Over time, regular blog posts, Facebook updates, and Tweets allow the audience to become familiar with you.

If you decide to post, focus on information that is helpful and informative to your audience. You can discuss medications and non–Food and Drug Administration uses of medications – as long as you do not give actual medical advice, and are clear about any disclosures and disclaimers, Dr. Benabio said.

Google yourself and see what you find.“It is as important to be a trusted member of the online community as it is to be a trusted member of your actual community,” Dr. Benabio said.

Despite the opportunities offered by establishing an online presence, keep in mind that you are on a slippery slope, he said. “This is a critical time when we are trying to demonstrate our value as practitioners. The more comfortable people are with nonphysicians, the more difficult it will be for us to fight nonphysicians' expansion of their scope of practice.”

The seminar was sponsored by

SDEF and this news organization are owned by Elsevier. Dr. Benabio disclosed that he is a consultant for Livestrong.com

SANTA MONICA, CALIF. – Social media provides a way for you to engage with your patients and the community, whether you practice in an HMO or privately, according to Dr. Jeffrey Benabio, a dermatologist at Kaiser Permanente in San Diego.

No matter what your specialty, the principles of using social media such as blogs, Facebook, and Twitter as tools for improving patient care will apply. “Online patient communities are an ascendant means for patients to learn about their disease, and seek advice and comfort from [other] patients like them,” Dr. Benabio said in an interview. “Physicians can be part of this conversation and contribute to it. Who better to [advise] patients [on] how to live with pain, live with deformity, deal with insurance companies, than physicians?”

It takes no money but lots of time to build online networks. So why bother? “Patients are going online to interact with their physicians, and we are not there. Whereas patients always had to come to us to learn about disease and health, now they get most of their information online. Our absence online perpetuates a trend of diminishing importance of our profession,” he said.

As with much in life, the secret to being effective online comes down to showing up. “A physician becomes a trusted member of the community by being present. Over time, regular blog posts, Facebook updates, and Tweets allow the audience to become familiar with you.

If you decide to post, focus on information that is helpful and informative to your audience. You can discuss medications and non–Food and Drug Administration uses of medications – as long as you do not give actual medical advice, and are clear about any disclosures and disclaimers, Dr. Benabio said.

Google yourself and see what you find.“It is as important to be a trusted member of the online community as it is to be a trusted member of your actual community,” Dr. Benabio said.

Despite the opportunities offered by establishing an online presence, keep in mind that you are on a slippery slope, he said. “This is a critical time when we are trying to demonstrate our value as practitioners. The more comfortable people are with nonphysicians, the more difficult it will be for us to fight nonphysicians' expansion of their scope of practice.”

The seminar was sponsored by

SDEF and this news organization are owned by Elsevier. Dr. Benabio disclosed that he is a consultant for Livestrong.com

SANTA MONICA, CALIF. – Social media provides a way for you to engage with your patients and the community, whether you practice in an HMO or privately, according to Dr. Jeffrey Benabio, a dermatologist at Kaiser Permanente in San Diego.

No matter what your specialty, the principles of using social media such as blogs, Facebook, and Twitter as tools for improving patient care will apply. “Online patient communities are an ascendant means for patients to learn about their disease, and seek advice and comfort from [other] patients like them,” Dr. Benabio said in an interview. “Physicians can be part of this conversation and contribute to it. Who better to [advise] patients [on] how to live with pain, live with deformity, deal with insurance companies, than physicians?”

It takes no money but lots of time to build online networks. So why bother? “Patients are going online to interact with their physicians, and we are not there. Whereas patients always had to come to us to learn about disease and health, now they get most of their information online. Our absence online perpetuates a trend of diminishing importance of our profession,” he said.

As with much in life, the secret to being effective online comes down to showing up. “A physician becomes a trusted member of the community by being present. Over time, regular blog posts, Facebook updates, and Tweets allow the audience to become familiar with you.

If you decide to post, focus on information that is helpful and informative to your audience. You can discuss medications and non–Food and Drug Administration uses of medications – as long as you do not give actual medical advice, and are clear about any disclosures and disclaimers, Dr. Benabio said.

Google yourself and see what you find.“It is as important to be a trusted member of the online community as it is to be a trusted member of your actual community,” Dr. Benabio said.

Despite the opportunities offered by establishing an online presence, keep in mind that you are on a slippery slope, he said. “This is a critical time when we are trying to demonstrate our value as practitioners. The more comfortable people are with nonphysicians, the more difficult it will be for us to fight nonphysicians' expansion of their scope of practice.”

The seminar was sponsored by

SDEF and this news organization are owned by Elsevier. Dr. Benabio disclosed that he is a consultant for Livestrong.com

SANTA MONICA, CALIF. – The fact that many patients with rheumatoid arthritis are not smokers, have normal lipid levels, are not overweight, and do not have a family history of heart disease belies their elevated risk for cardiovascular disease

Rheumatoid arthritis (RA) as an inflammatory disease conveys an elevated risk for cardiovascular disease (CVD), Dr. Sherine E. Gabriel said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Physicians need to screen patients with RA more closely for CVD risks than they have been. Unfortunately, practitioners currently lack a screening tool that is finely tuned to the risk factors for this population. The Framingham Heart Study risk score is a widely used screening tool, but it falls woefully short of accurately predicting the CVD risk in patients with RA, said Dr. Gabriel, who is professor of medicine and epidemiology at the Mayo Clinic, Rochester, Minn.

With colleagues at the Mayo Clinic, Dr. Gabriel is developing a tool for screening RA patients. In an interview, Dr. Gabriel didn't divulge details of the tool, because it is still being tested. She advised physicians, for now, to screen their RA patients for CVD risks using standard laboratory tests and to intervene earlier than in other populations. Doctors should prescribe statins to people with even modestly elevated serum lipid levels, for instance.

Severe, intractable RA often goes hand-in-hand with elevated risk for CVD. The patient who is positive for rheumatoid factor and always has an elevated level of C-reactive protein and a high erythrocyte sedimentation rate needs early intervention. Some physicians may want to consider using echocardiogram to screen for early signs of heart failure while it may be still treatable.

Many of the insights into CVD risk in RA come from studies that Dr. Gabriel and other Mayo Clinic investigators have conducted over several years.

The Mayo Clinic has followed a cohort of 1,179 residents of Olmsted County, Minn., who were diagnosed with RA between 1955 and 2007. The researchers compared the patients' rates of heart disease and survival with those of three other cohorts: 1,179 people without RA, 852 people with congestive heart failure, and 3,256 people with acute myocardial infarctions. Overall, survival among the RA patients was significantly shorter than would have been expected, with excess mortality being particularly pronounced in women (Arthritis Rheum. 2003;48:54-8).

A second longitudinal study of residents of the city of Rochester, Minn., which is in Olmsted County, followed 603 patients with RA beginning when they were an average of 58 years old. During a mean follow-up of 15 years, 354 patients died, and CVD was the primary cause of death in 176 patients. The increased risk for CVD was associated with three markers of systemic inflammation: erythrocyte sedimentation rate above 60 mm/hour on three consecutive measurements, the presence of RA vasculitis, and the presence of RA lung disease (Arthritis Rheum. 2005;52:722-32).

Another longitudinal population-based study conducted in Rochester County, Minn., by Dr. Gabriel and her associates examined CVD risk in 603 residents who were diagnosed with RA between 1955 and 1995 and an equal number of matched controls. A review of medical records revealed that within 2 years before diagnosis, the patients with RA were significantly more likely to have been hospitalized for acute MI or to have experienced unrecognized MIs than were controls during a corresponding 2-year period. However, they were less likely to have a history of angina pectoris than were controls. After diagnosis, RA patients were twice as likely to experience unrecognized MIs and sudden deaths and less likely to undergo coronary artery bypass grafting compared with non-RA subjects. Adjustment for the CVD risk factors did not substantially change the risk estimates (Arthritis Rheum. 2005;52:402-11).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Gabriel disclosed the following financial relationships: She is on the Actemra pharmacoepidemiology board and the Hoffmann-LaRoche CV Outcomes Trial Steering Committee, and she has received grant support from Roche Laboratories.

SANTA MONICA, CALIF. – The fact that many patients with rheumatoid arthritis are not smokers, have normal lipid levels, are not overweight, and do not have a family history of heart disease belies their elevated risk for cardiovascular disease

Rheumatoid arthritis (RA) as an inflammatory disease conveys an elevated risk for cardiovascular disease (CVD), Dr. Sherine E. Gabriel said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Physicians need to screen patients with RA more closely for CVD risks than they have been. Unfortunately, practitioners currently lack a screening tool that is finely tuned to the risk factors for this population. The Framingham Heart Study risk score is a widely used screening tool, but it falls woefully short of accurately predicting the CVD risk in patients with RA, said Dr. Gabriel, who is professor of medicine and epidemiology at the Mayo Clinic, Rochester, Minn.

With colleagues at the Mayo Clinic, Dr. Gabriel is developing a tool for screening RA patients. In an interview, Dr. Gabriel didn't divulge details of the tool, because it is still being tested. She advised physicians, for now, to screen their RA patients for CVD risks using standard laboratory tests and to intervene earlier than in other populations. Doctors should prescribe statins to people with even modestly elevated serum lipid levels, for instance.

Severe, intractable RA often goes hand-in-hand with elevated risk for CVD. The patient who is positive for rheumatoid factor and always has an elevated level of C-reactive protein and a high erythrocyte sedimentation rate needs early intervention. Some physicians may want to consider using echocardiogram to screen for early signs of heart failure while it may be still treatable.

Many of the insights into CVD risk in RA come from studies that Dr. Gabriel and other Mayo Clinic investigators have conducted over several years.

The Mayo Clinic has followed a cohort of 1,179 residents of Olmsted County, Minn., who were diagnosed with RA between 1955 and 2007. The researchers compared the patients' rates of heart disease and survival with those of three other cohorts: 1,179 people without RA, 852 people with congestive heart failure, and 3,256 people with acute myocardial infarctions. Overall, survival among the RA patients was significantly shorter than would have been expected, with excess mortality being particularly pronounced in women (Arthritis Rheum. 2003;48:54-8).

A second longitudinal study of residents of the city of Rochester, Minn., which is in Olmsted County, followed 603 patients with RA beginning when they were an average of 58 years old. During a mean follow-up of 15 years, 354 patients died, and CVD was the primary cause of death in 176 patients. The increased risk for CVD was associated with three markers of systemic inflammation: erythrocyte sedimentation rate above 60 mm/hour on three consecutive measurements, the presence of RA vasculitis, and the presence of RA lung disease (Arthritis Rheum. 2005;52:722-32).

Another longitudinal population-based study conducted in Rochester County, Minn., by Dr. Gabriel and her associates examined CVD risk in 603 residents who were diagnosed with RA between 1955 and 1995 and an equal number of matched controls. A review of medical records revealed that within 2 years before diagnosis, the patients with RA were significantly more likely to have been hospitalized for acute MI or to have experienced unrecognized MIs than were controls during a corresponding 2-year period. However, they were less likely to have a history of angina pectoris than were controls. After diagnosis, RA patients were twice as likely to experience unrecognized MIs and sudden deaths and less likely to undergo coronary artery bypass grafting compared with non-RA subjects. Adjustment for the CVD risk factors did not substantially change the risk estimates (Arthritis Rheum. 2005;52:402-11).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Gabriel disclosed the following financial relationships: She is on the Actemra pharmacoepidemiology board and the Hoffmann-LaRoche CV Outcomes Trial Steering Committee, and she has received grant support from Roche Laboratories.

SANTA MONICA, CALIF. – The fact that many patients with rheumatoid arthritis are not smokers, have normal lipid levels, are not overweight, and do not have a family history of heart disease belies their elevated risk for cardiovascular disease

Rheumatoid arthritis (RA) as an inflammatory disease conveys an elevated risk for cardiovascular disease (CVD), Dr. Sherine E. Gabriel said at a meeting sponsored by Skin Disease Education Foundation and the University of Louisville.

Physicians need to screen patients with RA more closely for CVD risks than they have been. Unfortunately, practitioners currently lack a screening tool that is finely tuned to the risk factors for this population. The Framingham Heart Study risk score is a widely used screening tool, but it falls woefully short of accurately predicting the CVD risk in patients with RA, said Dr. Gabriel, who is professor of medicine and epidemiology at the Mayo Clinic, Rochester, Minn.

With colleagues at the Mayo Clinic, Dr. Gabriel is developing a tool for screening RA patients. In an interview, Dr. Gabriel didn't divulge details of the tool, because it is still being tested. She advised physicians, for now, to screen their RA patients for CVD risks using standard laboratory tests and to intervene earlier than in other populations. Doctors should prescribe statins to people with even modestly elevated serum lipid levels, for instance.

Severe, intractable RA often goes hand-in-hand with elevated risk for CVD. The patient who is positive for rheumatoid factor and always has an elevated level of C-reactive protein and a high erythrocyte sedimentation rate needs early intervention. Some physicians may want to consider using echocardiogram to screen for early signs of heart failure while it may be still treatable.

Many of the insights into CVD risk in RA come from studies that Dr. Gabriel and other Mayo Clinic investigators have conducted over several years.

The Mayo Clinic has followed a cohort of 1,179 residents of Olmsted County, Minn., who were diagnosed with RA between 1955 and 2007. The researchers compared the patients' rates of heart disease and survival with those of three other cohorts: 1,179 people without RA, 852 people with congestive heart failure, and 3,256 people with acute myocardial infarctions. Overall, survival among the RA patients was significantly shorter than would have been expected, with excess mortality being particularly pronounced in women (Arthritis Rheum. 2003;48:54-8).

A second longitudinal study of residents of the city of Rochester, Minn., which is in Olmsted County, followed 603 patients with RA beginning when they were an average of 58 years old. During a mean follow-up of 15 years, 354 patients died, and CVD was the primary cause of death in 176 patients. The increased risk for CVD was associated with three markers of systemic inflammation: erythrocyte sedimentation rate above 60 mm/hour on three consecutive measurements, the presence of RA vasculitis, and the presence of RA lung disease (Arthritis Rheum. 2005;52:722-32).

Another longitudinal population-based study conducted in Rochester County, Minn., by Dr. Gabriel and her associates examined CVD risk in 603 residents who were diagnosed with RA between 1955 and 1995 and an equal number of matched controls. A review of medical records revealed that within 2 years before diagnosis, the patients with RA were significantly more likely to have been hospitalized for acute MI or to have experienced unrecognized MIs than were controls during a corresponding 2-year period. However, they were less likely to have a history of angina pectoris than were controls. After diagnosis, RA patients were twice as likely to experience unrecognized MIs and sudden deaths and less likely to undergo coronary artery bypass grafting compared with non-RA subjects. Adjustment for the CVD risk factors did not substantially change the risk estimates (Arthritis Rheum. 2005;52:402-11).

Skin Disease Education Foundation and this news organization are owned by Elsevier. Dr. Gabriel disclosed the following financial relationships: She is on the Actemra pharmacoepidemiology board and the Hoffmann-LaRoche CV Outcomes Trial Steering Committee, and she has received grant support from Roche Laboratories.