Sally Koch Kubetin

SANTA MONICA, CALIF. — Management of pulmonary hypertension in systemic sclerosis is inching its way toward a new age of prevention.

The change is coming from the appreciation that the finding of exercise-induced pulmonary hypertension (PH) likely represents abnormal hemodynamic manifestation in patients with systemic sclerosis (SSc) who have normal resting mean pulmonary artery pressure. And that this finding may flag those patients who are most likely to benefit from early, aggressive treatment.

Currently, by the time most cases of resting PH in SSc are diagnosed, the underlying hemodynamic disease process has become irreversible. “We are able to treat it. However, we are not able to cure it,” said Dr. Rajeev Saggar. As a result, the prognosis is grim.

PH-SSc tends to have a poorer prognosis, compared with other WHO Group I diagnoses. Recently, isolated PH-SSc survival, while receiving pulmonary vasodilator therapy, was reported at 78% at 1 year and 47% at 3 years. Furthermore, survival in PH-SSc associated with interstitial lung disease is even worse, said Dr. Saggar, a pulmonologist in the lung transplant and pulmonary hypertension division of the University of California, Los Angeles.

In an investigational program at his institution, treatment is being started in patients who have exercise-induced PH.

The exercise stress regimen involves patients, with a right heart catheter in place, riding a stationary supine bicycle for 3-9 minutes.

Those with an exercise mean pulmonary artery pressure greater than or equal to 30 mm Hg and a pulmonary wedge pressure less than or equal to 18 mm Hg receive treatment with an endothelin antagonist. All of these patients have normal resting mean pulmonary artery pressures.

Recent data from a U.K. study of 42 SSc patients with exercise-induced PH showed that 8 progressed to resting PH within 2-3 years, and 4 died from complications of pulmonary vascular disease within 3 years. “By waiting to diagnose this disease until it is present in the resting state, we are losing our opportunity to treat it,” he said.

These findings support the observation that “patients with SSc should be evaluated for exercise-induced PH. It's abnormal and should be treated in the context of a clinical study,” said Dr. Saggar said at a meeting sponsored by

For now, until the concept of screening for exercise-induced PH catches on, “before you ever treat a patient with PH, you have to get a right heart catheterization. Right heart catheterization is not that invasive in the right hands. The risk of associated mortality is less than 0.05%,” he said. Prognosis can be based on the findings from this test, he added.

Not all physicians are comfortable going straight to right heart catheterization. For them, yearly echocardiography and spirometry can be used to screen for PH. Certain clinical findings in scleroderma patients can identify which patients are likely to have PH. Early screening with noninvasive studies such as an echocardiogram and pulmonary function tests may detect these patients earlier.

Typical symptoms of any patient with scleroderma who has unexplained shortness of breath should also raise the physician's concern. Likewise PH should be on the short list of the differential diagnosis in any young scleroderma patient who has syncope. “These patients tell their physicians: 'I coughed and passed out.' Or 'I stood up and passed out,'” Dr. Saggar said at the meeting.

However, once a patient develops unexplained breathlessness, it is necessary to do right heart catheterization, he said. Breathlessness in any patients with PH associated with SSc is a sign that the disease is progressing. Aggressive management is the best hope for survival in SSc patients with PH.

The available treatments for PH remain of “arguable” efficacy, especially when they are initiated late in the course of the disease, when it has become incurable, according to Dr. Saggar.

In this progressive disease, increased pulmonary pressure is only part of the pathology. The benefit of serial right heart catheterization is that it enables the physician to assess the degree of right ventricular impairment. “What you are really worried about is the right ventricle. Failure of the right heart drives death,” he said.

As long as vascular resistance continues to increase, the patient remains in jeopardy. The right ventricle begins to fail in response to the increased vascular resistance.

PH is very rare. It is estimated to occur in 2.3-10 cases per 1 million population. Patients with SSc make up about 20% of all newly diagnosed PH patients. A recent French study that screened for PH in SSc using echocardiography and right heart catheterization showed a prevalence of 7.9%. However, findings from an autopsy study show that 60% of patients with SSc have findings typical of PH.

“This disease goes undiagnosed a lot of the time,” said Dr. Saggar.

Disclosures: Dr. Saggar reported no financial relationships that are relevant to this presentation. This newspaper and Skin Disease Education Foundation are owned by Elsevier.

SANTA MONICA, CALIF. — Management of pulmonary hypertension in systemic sclerosis is inching its way toward a new age of prevention.

The change is coming from the appreciation that the finding of exercise-induced pulmonary hypertension (PH) likely represents abnormal hemodynamic manifestation in patients with systemic sclerosis (SSc) who have normal resting mean pulmonary artery pressure. And that this finding may flag those patients who are most likely to benefit from early, aggressive treatment.

Currently, by the time most cases of resting PH in SSc are diagnosed, the underlying hemodynamic disease process has become irreversible. “We are able to treat it. However, we are not able to cure it,” said Dr. Rajeev Saggar. As a result, the prognosis is grim.

PH-SSc tends to have a poorer prognosis, compared with other WHO Group I diagnoses. Recently, isolated PH-SSc survival, while receiving pulmonary vasodilator therapy, was reported at 78% at 1 year and 47% at 3 years. Furthermore, survival in PH-SSc associated with interstitial lung disease is even worse, said Dr. Saggar, a pulmonologist in the lung transplant and pulmonary hypertension division of the University of California, Los Angeles.

In an investigational program at his institution, treatment is being started in patients who have exercise-induced PH.

The exercise stress regimen involves patients, with a right heart catheter in place, riding a stationary supine bicycle for 3-9 minutes.

Those with an exercise mean pulmonary artery pressure greater than or equal to 30 mm Hg and a pulmonary wedge pressure less than or equal to 18 mm Hg receive treatment with an endothelin antagonist. All of these patients have normal resting mean pulmonary artery pressures.

Recent data from a U.K. study of 42 SSc patients with exercise-induced PH showed that 8 progressed to resting PH within 2-3 years, and 4 died from complications of pulmonary vascular disease within 3 years. “By waiting to diagnose this disease until it is present in the resting state, we are losing our opportunity to treat it,” he said.

These findings support the observation that “patients with SSc should be evaluated for exercise-induced PH. It's abnormal and should be treated in the context of a clinical study,” said Dr. Saggar said at a meeting sponsored by

For now, until the concept of screening for exercise-induced PH catches on, “before you ever treat a patient with PH, you have to get a right heart catheterization. Right heart catheterization is not that invasive in the right hands. The risk of associated mortality is less than 0.05%,” he said. Prognosis can be based on the findings from this test, he added.

Not all physicians are comfortable going straight to right heart catheterization. For them, yearly echocardiography and spirometry can be used to screen for PH. Certain clinical findings in scleroderma patients can identify which patients are likely to have PH. Early screening with noninvasive studies such as an echocardiogram and pulmonary function tests may detect these patients earlier.

Typical symptoms of any patient with scleroderma who has unexplained shortness of breath should also raise the physician's concern. Likewise PH should be on the short list of the differential diagnosis in any young scleroderma patient who has syncope. “These patients tell their physicians: 'I coughed and passed out.' Or 'I stood up and passed out,'” Dr. Saggar said at the meeting.

However, once a patient develops unexplained breathlessness, it is necessary to do right heart catheterization, he said. Breathlessness in any patients with PH associated with SSc is a sign that the disease is progressing. Aggressive management is the best hope for survival in SSc patients with PH.

The available treatments for PH remain of “arguable” efficacy, especially when they are initiated late in the course of the disease, when it has become incurable, according to Dr. Saggar.

In this progressive disease, increased pulmonary pressure is only part of the pathology. The benefit of serial right heart catheterization is that it enables the physician to assess the degree of right ventricular impairment. “What you are really worried about is the right ventricle. Failure of the right heart drives death,” he said.

As long as vascular resistance continues to increase, the patient remains in jeopardy. The right ventricle begins to fail in response to the increased vascular resistance.

PH is very rare. It is estimated to occur in 2.3-10 cases per 1 million population. Patients with SSc make up about 20% of all newly diagnosed PH patients. A recent French study that screened for PH in SSc using echocardiography and right heart catheterization showed a prevalence of 7.9%. However, findings from an autopsy study show that 60% of patients with SSc have findings typical of PH.

“This disease goes undiagnosed a lot of the time,” said Dr. Saggar.

Disclosures: Dr. Saggar reported no financial relationships that are relevant to this presentation. This newspaper and Skin Disease Education Foundation are owned by Elsevier.

SANTA MONICA, CALIF. — Management of pulmonary hypertension in systemic sclerosis is inching its way toward a new age of prevention.

The change is coming from the appreciation that the finding of exercise-induced pulmonary hypertension (PH) likely represents abnormal hemodynamic manifestation in patients with systemic sclerosis (SSc) who have normal resting mean pulmonary artery pressure. And that this finding may flag those patients who are most likely to benefit from early, aggressive treatment.

Currently, by the time most cases of resting PH in SSc are diagnosed, the underlying hemodynamic disease process has become irreversible. “We are able to treat it. However, we are not able to cure it,” said Dr. Rajeev Saggar. As a result, the prognosis is grim.

PH-SSc tends to have a poorer prognosis, compared with other WHO Group I diagnoses. Recently, isolated PH-SSc survival, while receiving pulmonary vasodilator therapy, was reported at 78% at 1 year and 47% at 3 years. Furthermore, survival in PH-SSc associated with interstitial lung disease is even worse, said Dr. Saggar, a pulmonologist in the lung transplant and pulmonary hypertension division of the University of California, Los Angeles.

In an investigational program at his institution, treatment is being started in patients who have exercise-induced PH.

The exercise stress regimen involves patients, with a right heart catheter in place, riding a stationary supine bicycle for 3-9 minutes.

Those with an exercise mean pulmonary artery pressure greater than or equal to 30 mm Hg and a pulmonary wedge pressure less than or equal to 18 mm Hg receive treatment with an endothelin antagonist. All of these patients have normal resting mean pulmonary artery pressures.

Recent data from a U.K. study of 42 SSc patients with exercise-induced PH showed that 8 progressed to resting PH within 2-3 years, and 4 died from complications of pulmonary vascular disease within 3 years. “By waiting to diagnose this disease until it is present in the resting state, we are losing our opportunity to treat it,” he said.

These findings support the observation that “patients with SSc should be evaluated for exercise-induced PH. It's abnormal and should be treated in the context of a clinical study,” said Dr. Saggar said at a meeting sponsored by

For now, until the concept of screening for exercise-induced PH catches on, “before you ever treat a patient with PH, you have to get a right heart catheterization. Right heart catheterization is not that invasive in the right hands. The risk of associated mortality is less than 0.05%,” he said. Prognosis can be based on the findings from this test, he added.

Not all physicians are comfortable going straight to right heart catheterization. For them, yearly echocardiography and spirometry can be used to screen for PH. Certain clinical findings in scleroderma patients can identify which patients are likely to have PH. Early screening with noninvasive studies such as an echocardiogram and pulmonary function tests may detect these patients earlier.

Typical symptoms of any patient with scleroderma who has unexplained shortness of breath should also raise the physician's concern. Likewise PH should be on the short list of the differential diagnosis in any young scleroderma patient who has syncope. “These patients tell their physicians: 'I coughed and passed out.' Or 'I stood up and passed out,'” Dr. Saggar said at the meeting.

However, once a patient develops unexplained breathlessness, it is necessary to do right heart catheterization, he said. Breathlessness in any patients with PH associated with SSc is a sign that the disease is progressing. Aggressive management is the best hope for survival in SSc patients with PH.

The available treatments for PH remain of “arguable” efficacy, especially when they are initiated late in the course of the disease, when it has become incurable, according to Dr. Saggar.

In this progressive disease, increased pulmonary pressure is only part of the pathology. The benefit of serial right heart catheterization is that it enables the physician to assess the degree of right ventricular impairment. “What you are really worried about is the right ventricle. Failure of the right heart drives death,” he said.

As long as vascular resistance continues to increase, the patient remains in jeopardy. The right ventricle begins to fail in response to the increased vascular resistance.

PH is very rare. It is estimated to occur in 2.3-10 cases per 1 million population. Patients with SSc make up about 20% of all newly diagnosed PH patients. A recent French study that screened for PH in SSc using echocardiography and right heart catheterization showed a prevalence of 7.9%. However, findings from an autopsy study show that 60% of patients with SSc have findings typical of PH.

“This disease goes undiagnosed a lot of the time,” said Dr. Saggar.

Disclosures: Dr. Saggar reported no financial relationships that are relevant to this presentation. This newspaper and Skin Disease Education Foundation are owned by Elsevier.

SANTA MONICA, CALIF. — Recommendations that you adjust your default coding for an office visit upward and appeal all denied insurance claims were among numerous tips on how to increase income that were offered by Dr. Joseph S. Eastern at a meeting sponsored by

With the demise of consultation codes on Jan. 1, 2010, many rheumatologists are concerned about balancing their budgets. When assessing their bottom line, physicians tend to put undue emphasis on reducing their practice overhead. However, it is unlikely that overhead is the problem.

Most practices have cut overhead to the bone, said Dr. Eastern, a dermatologist in Belleville, N.J. Cutting overhead too much, by reducing the number of office staff and/or hiring unskilled workers, will lessen practice efficiency and—in the end—reduce revenue.

“Your ability to decrease costs is limited, while your ability to increase revenue is unlimited. Putting it another way: Would you rather keep 60% of $800,000 or 40% of $2 million?” challenged Dr. Eastern, who also is on the faculty of Seton Hall University, South Orange, N.J.

So rather than asking how to decrease overhead, the better question is how to increase revenue. The first step is to renegotiate your contracts with your third-party payers every year. This is not a time to be shy. Third-party payers are not going to call to announce they've been underpaying you. When Dr. Eastern asked the attendees to raise their hands if they renegotiated their contracts yearly, few hands went up.

“Every year, we send a letter to the lowest payer that says: 'We'll keep you if you pay us the going rate rather than what you are paying us now.' They may not give you what you ask for, but they'll give you more if you make a good case for the increase.”

Most physicians tend to under-code because of their fear of being audited. But they do more than they are coding for. By changing their default office visit code from level 2 to level 3, physicians can increase their income by about $100,000 a year. “That's pure profit,” said Dr. Eastern, who said his observation is based on a study he did of N.J. physicians.

“If you are doing level 3 worth of work, you should code for it. You are entitled to it. According to the CPR code book, a level 3 exam involves an established patient with either one worsening problem or one new problem or two or more chronic or inactive problems, plus documentation of a pertinent review of systems, which in rheumatology comes down to asking 'How are your joints? Are you having problems with any of your joints?' Then a 99213 code is justified. The key word is documentation,” he said.

Appeal all denied claims, he advised. The code examiner often knows nothing about medicine and has just a few months experience in the job. Data on dermatologists show that they file 30 million Medicare claims yearly. An estimated 6%, or almost 2 million claims, are denied. Of those, fewer than 5% are appealed, “which is just inexcusable,” Dr. Eastern said. The data on dermatologists show the chance that the appeal will increase payment is 50%. “What else are you doing that has a 50% return?” Dr. Eastern challenged.

People in other lines of business are amazed that physicians let patients walk out without paying. Instead, he said, take an imprint of each patient's credit card. Then, when the insurance payment comes in, charge the balance on the credit card. “We have decreased our accounts receivable by 50% just by having people do this.

“Patients sign an authorization that we can charge the unpaid balance to their card. Our office manager calls the patient if the charge is greater than $50. We keep the credit card number in the patient's chart, with all the other confidential information,” Dr. Eastern said.

Disclosures: Dr. Eastern reported that he has no financial disclosures to make. SDEF and

Rather than letting people walk out of your office without paying, take an imprint of their credit card.

Source DR. EASTERN

SANTA MONICA, CALIF. — Recommendations that you adjust your default coding for an office visit upward and appeal all denied insurance claims were among numerous tips on how to increase income that were offered by Dr. Joseph S. Eastern at a meeting sponsored by

With the demise of consultation codes on Jan. 1, 2010, many rheumatologists are concerned about balancing their budgets. When assessing their bottom line, physicians tend to put undue emphasis on reducing their practice overhead. However, it is unlikely that overhead is the problem.

Most practices have cut overhead to the bone, said Dr. Eastern, a dermatologist in Belleville, N.J. Cutting overhead too much, by reducing the number of office staff and/or hiring unskilled workers, will lessen practice efficiency and—in the end—reduce revenue.

“Your ability to decrease costs is limited, while your ability to increase revenue is unlimited. Putting it another way: Would you rather keep 60% of $800,000 or 40% of $2 million?” challenged Dr. Eastern, who also is on the faculty of Seton Hall University, South Orange, N.J.

So rather than asking how to decrease overhead, the better question is how to increase revenue. The first step is to renegotiate your contracts with your third-party payers every year. This is not a time to be shy. Third-party payers are not going to call to announce they've been underpaying you. When Dr. Eastern asked the attendees to raise their hands if they renegotiated their contracts yearly, few hands went up.

“Every year, we send a letter to the lowest payer that says: 'We'll keep you if you pay us the going rate rather than what you are paying us now.' They may not give you what you ask for, but they'll give you more if you make a good case for the increase.”

Most physicians tend to under-code because of their fear of being audited. But they do more than they are coding for. By changing their default office visit code from level 2 to level 3, physicians can increase their income by about $100,000 a year. “That's pure profit,” said Dr. Eastern, who said his observation is based on a study he did of N.J. physicians.

“If you are doing level 3 worth of work, you should code for it. You are entitled to it. According to the CPR code book, a level 3 exam involves an established patient with either one worsening problem or one new problem or two or more chronic or inactive problems, plus documentation of a pertinent review of systems, which in rheumatology comes down to asking 'How are your joints? Are you having problems with any of your joints?' Then a 99213 code is justified. The key word is documentation,” he said.

Appeal all denied claims, he advised. The code examiner often knows nothing about medicine and has just a few months experience in the job. Data on dermatologists show that they file 30 million Medicare claims yearly. An estimated 6%, or almost 2 million claims, are denied. Of those, fewer than 5% are appealed, “which is just inexcusable,” Dr. Eastern said. The data on dermatologists show the chance that the appeal will increase payment is 50%. “What else are you doing that has a 50% return?” Dr. Eastern challenged.

People in other lines of business are amazed that physicians let patients walk out without paying. Instead, he said, take an imprint of each patient's credit card. Then, when the insurance payment comes in, charge the balance on the credit card. “We have decreased our accounts receivable by 50% just by having people do this.

“Patients sign an authorization that we can charge the unpaid balance to their card. Our office manager calls the patient if the charge is greater than $50. We keep the credit card number in the patient's chart, with all the other confidential information,” Dr. Eastern said.

Disclosures: Dr. Eastern reported that he has no financial disclosures to make. SDEF and

Rather than letting people walk out of your office without paying, take an imprint of their credit card.

Source DR. EASTERN

SANTA MONICA, CALIF. — Recommendations that you adjust your default coding for an office visit upward and appeal all denied insurance claims were among numerous tips on how to increase income that were offered by Dr. Joseph S. Eastern at a meeting sponsored by

With the demise of consultation codes on Jan. 1, 2010, many rheumatologists are concerned about balancing their budgets. When assessing their bottom line, physicians tend to put undue emphasis on reducing their practice overhead. However, it is unlikely that overhead is the problem.

Most practices have cut overhead to the bone, said Dr. Eastern, a dermatologist in Belleville, N.J. Cutting overhead too much, by reducing the number of office staff and/or hiring unskilled workers, will lessen practice efficiency and—in the end—reduce revenue.

“Your ability to decrease costs is limited, while your ability to increase revenue is unlimited. Putting it another way: Would you rather keep 60% of $800,000 or 40% of $2 million?” challenged Dr. Eastern, who also is on the faculty of Seton Hall University, South Orange, N.J.

So rather than asking how to decrease overhead, the better question is how to increase revenue. The first step is to renegotiate your contracts with your third-party payers every year. This is not a time to be shy. Third-party payers are not going to call to announce they've been underpaying you. When Dr. Eastern asked the attendees to raise their hands if they renegotiated their contracts yearly, few hands went up.

“Every year, we send a letter to the lowest payer that says: 'We'll keep you if you pay us the going rate rather than what you are paying us now.' They may not give you what you ask for, but they'll give you more if you make a good case for the increase.”

Most physicians tend to under-code because of their fear of being audited. But they do more than they are coding for. By changing their default office visit code from level 2 to level 3, physicians can increase their income by about $100,000 a year. “That's pure profit,” said Dr. Eastern, who said his observation is based on a study he did of N.J. physicians.

“If you are doing level 3 worth of work, you should code for it. You are entitled to it. According to the CPR code book, a level 3 exam involves an established patient with either one worsening problem or one new problem or two or more chronic or inactive problems, plus documentation of a pertinent review of systems, which in rheumatology comes down to asking 'How are your joints? Are you having problems with any of your joints?' Then a 99213 code is justified. The key word is documentation,” he said.

Appeal all denied claims, he advised. The code examiner often knows nothing about medicine and has just a few months experience in the job. Data on dermatologists show that they file 30 million Medicare claims yearly. An estimated 6%, or almost 2 million claims, are denied. Of those, fewer than 5% are appealed, “which is just inexcusable,” Dr. Eastern said. The data on dermatologists show the chance that the appeal will increase payment is 50%. “What else are you doing that has a 50% return?” Dr. Eastern challenged.

People in other lines of business are amazed that physicians let patients walk out without paying. Instead, he said, take an imprint of each patient's credit card. Then, when the insurance payment comes in, charge the balance on the credit card. “We have decreased our accounts receivable by 50% just by having people do this.

“Patients sign an authorization that we can charge the unpaid balance to their card. Our office manager calls the patient if the charge is greater than $50. We keep the credit card number in the patient's chart, with all the other confidential information,” Dr. Eastern said.

Disclosures: Dr. Eastern reported that he has no financial disclosures to make. SDEF and

Rather than letting people walk out of your office without paying, take an imprint of their credit card.

Source DR. EASTERN

SANTA MONICA, CALIF. — There is only one cause of joint inflammation in childhood that the child will typically outgrow: true oligoarthritis. Even though the inflammation will eventually pass, affected children still need treatment to prevent limb-length discrepancy or blindness resulting from uveitis, according to Dr. Thomas J.A. Lehman.

Because of the shortage of pediatric rheumatologists, adult rheumatologists often end up treating children with new-onset joint symptoms, he noted at the meeting sponsored by

Without genetic markers, it is difficult to separate all the types of arthritis—which are not limited to just the eight subtypes listed in the official diagnostic criteria—that occur in children. “There may be anywhere from 30 to 50 subtypes” of arthritis in children. This matters, because they will not all respond to the same treatment or have the same disease course, said Dr. Lehman, chief of the division of pediatric rheumatology at the Hospital for Special Surgery in New York.

Oligoarthritis is not a systemic disease, which makes it harder to diagnose early. The onset of joint swelling and pain should be limited to four or fewer large joints during the first 6 months, and most often only a single joint is affected. Because the stiffness and pain are worse upon awakening and tend to ease as the day progresses, parents often let it continue awhile and often cannot pinpoint when the symptoms started. Also, onset usually occurs at age 1–5 years (and typical oligoarthritis never begins after age 9 years), which means that the children are too young to describe their symptoms. A limp in the morning and a swollen knee may be the only sign that something is wrong; sometimes a visiting grandmother notices what the parents have overlooked.

Laboratory findings—or lack thereof—can help confirm the diagnosis. Because this is not a systemic disease, the hemoglobin level is never less than 11.0 g/dL and the erythrocyte sedimentation rate is never greater than 40 mm/h, according to Dr. Lehman. There is never fever, rash, or elevated white blood cell count. Oligoarthritis affects more girls than boys. The children are often positive for antinuclear antibodies and often have eye disease, usually uveitis.

It is important to make the diagnosis of true oligoarthritis as early as possible, according to Dr. Lehman. Too many children are allowed to continue limping without a diagnosis because some criteria require joint pain for at least 6 weeks, and others say 3 months. That doesn't mean children can't be treated before a definitive diagnosis of oligoarthritis is made, he said. Continued pain produces muscle loss and joint damage. In addition, it hinders a child's emotional development when they can's keep up with their friends and participate in normal activities.

Many children with true oligoarthritis will respond to NSAIDs, but physicians should use all the medication necessary to control the disease, he noted. Corticosteroid injections may be helpful if there is a single “stubborn” joint.

This arthritis never involves the fingers or hips and never more than four joints. “True oligoarthritis affects only the knees,” said Dr. Lehman, who stressed that these diagnostic criteria are his own and are not accepted by any accrediting body.

Children who present after age 9 years or who have involvement of four or fewer joints that expand to more than four joints do not have true oligoarthritis. Theirs is likely to be a debilitating arthritis, and they will not outgrow it, he stressed.

Disclosures: Dr. Lehman has financial relationships with Celgene Corp., BioMarin Pharmaceutical Inc., Genentech Inc., Bristol-Myers Squibb Co., Abbott Laboratories, Wyeth (now owned by Pfizer Inc.), and Amgen Inc. SDEF and

To see an interview with Dr. Lehman, please go to www.youtube.com/rheumatologynews

SANTA MONICA, CALIF. — There is only one cause of joint inflammation in childhood that the child will typically outgrow: true oligoarthritis. Even though the inflammation will eventually pass, affected children still need treatment to prevent limb-length discrepancy or blindness resulting from uveitis, according to Dr. Thomas J.A. Lehman.

Because of the shortage of pediatric rheumatologists, adult rheumatologists often end up treating children with new-onset joint symptoms, he noted at the meeting sponsored by

Without genetic markers, it is difficult to separate all the types of arthritis—which are not limited to just the eight subtypes listed in the official diagnostic criteria—that occur in children. “There may be anywhere from 30 to 50 subtypes” of arthritis in children. This matters, because they will not all respond to the same treatment or have the same disease course, said Dr. Lehman, chief of the division of pediatric rheumatology at the Hospital for Special Surgery in New York.

Oligoarthritis is not a systemic disease, which makes it harder to diagnose early. The onset of joint swelling and pain should be limited to four or fewer large joints during the first 6 months, and most often only a single joint is affected. Because the stiffness and pain are worse upon awakening and tend to ease as the day progresses, parents often let it continue awhile and often cannot pinpoint when the symptoms started. Also, onset usually occurs at age 1–5 years (and typical oligoarthritis never begins after age 9 years), which means that the children are too young to describe their symptoms. A limp in the morning and a swollen knee may be the only sign that something is wrong; sometimes a visiting grandmother notices what the parents have overlooked.

Laboratory findings—or lack thereof—can help confirm the diagnosis. Because this is not a systemic disease, the hemoglobin level is never less than 11.0 g/dL and the erythrocyte sedimentation rate is never greater than 40 mm/h, according to Dr. Lehman. There is never fever, rash, or elevated white blood cell count. Oligoarthritis affects more girls than boys. The children are often positive for antinuclear antibodies and often have eye disease, usually uveitis.

It is important to make the diagnosis of true oligoarthritis as early as possible, according to Dr. Lehman. Too many children are allowed to continue limping without a diagnosis because some criteria require joint pain for at least 6 weeks, and others say 3 months. That doesn't mean children can't be treated before a definitive diagnosis of oligoarthritis is made, he said. Continued pain produces muscle loss and joint damage. In addition, it hinders a child's emotional development when they can's keep up with their friends and participate in normal activities.

Many children with true oligoarthritis will respond to NSAIDs, but physicians should use all the medication necessary to control the disease, he noted. Corticosteroid injections may be helpful if there is a single “stubborn” joint.

This arthritis never involves the fingers or hips and never more than four joints. “True oligoarthritis affects only the knees,” said Dr. Lehman, who stressed that these diagnostic criteria are his own and are not accepted by any accrediting body.

Children who present after age 9 years or who have involvement of four or fewer joints that expand to more than four joints do not have true oligoarthritis. Theirs is likely to be a debilitating arthritis, and they will not outgrow it, he stressed.

Disclosures: Dr. Lehman has financial relationships with Celgene Corp., BioMarin Pharmaceutical Inc., Genentech Inc., Bristol-Myers Squibb Co., Abbott Laboratories, Wyeth (now owned by Pfizer Inc.), and Amgen Inc. SDEF and

To see an interview with Dr. Lehman, please go to www.youtube.com/rheumatologynews

SANTA MONICA, CALIF. — There is only one cause of joint inflammation in childhood that the child will typically outgrow: true oligoarthritis. Even though the inflammation will eventually pass, affected children still need treatment to prevent limb-length discrepancy or blindness resulting from uveitis, according to Dr. Thomas J.A. Lehman.

Because of the shortage of pediatric rheumatologists, adult rheumatologists often end up treating children with new-onset joint symptoms, he noted at the meeting sponsored by

Without genetic markers, it is difficult to separate all the types of arthritis—which are not limited to just the eight subtypes listed in the official diagnostic criteria—that occur in children. “There may be anywhere from 30 to 50 subtypes” of arthritis in children. This matters, because they will not all respond to the same treatment or have the same disease course, said Dr. Lehman, chief of the division of pediatric rheumatology at the Hospital for Special Surgery in New York.

Oligoarthritis is not a systemic disease, which makes it harder to diagnose early. The onset of joint swelling and pain should be limited to four or fewer large joints during the first 6 months, and most often only a single joint is affected. Because the stiffness and pain are worse upon awakening and tend to ease as the day progresses, parents often let it continue awhile and often cannot pinpoint when the symptoms started. Also, onset usually occurs at age 1–5 years (and typical oligoarthritis never begins after age 9 years), which means that the children are too young to describe their symptoms. A limp in the morning and a swollen knee may be the only sign that something is wrong; sometimes a visiting grandmother notices what the parents have overlooked.

Laboratory findings—or lack thereof—can help confirm the diagnosis. Because this is not a systemic disease, the hemoglobin level is never less than 11.0 g/dL and the erythrocyte sedimentation rate is never greater than 40 mm/h, according to Dr. Lehman. There is never fever, rash, or elevated white blood cell count. Oligoarthritis affects more girls than boys. The children are often positive for antinuclear antibodies and often have eye disease, usually uveitis.

It is important to make the diagnosis of true oligoarthritis as early as possible, according to Dr. Lehman. Too many children are allowed to continue limping without a diagnosis because some criteria require joint pain for at least 6 weeks, and others say 3 months. That doesn't mean children can't be treated before a definitive diagnosis of oligoarthritis is made, he said. Continued pain produces muscle loss and joint damage. In addition, it hinders a child's emotional development when they can's keep up with their friends and participate in normal activities.

Many children with true oligoarthritis will respond to NSAIDs, but physicians should use all the medication necessary to control the disease, he noted. Corticosteroid injections may be helpful if there is a single “stubborn” joint.

This arthritis never involves the fingers or hips and never more than four joints. “True oligoarthritis affects only the knees,” said Dr. Lehman, who stressed that these diagnostic criteria are his own and are not accepted by any accrediting body.

Children who present after age 9 years or who have involvement of four or fewer joints that expand to more than four joints do not have true oligoarthritis. Theirs is likely to be a debilitating arthritis, and they will not outgrow it, he stressed.

Disclosures: Dr. Lehman has financial relationships with Celgene Corp., BioMarin Pharmaceutical Inc., Genentech Inc., Bristol-Myers Squibb Co., Abbott Laboratories, Wyeth (now owned by Pfizer Inc.), and Amgen Inc. SDEF and

To see an interview with Dr. Lehman, please go to www.youtube.com/rheumatologynews

SANTA MONICA, CALIF. — How to treat a patient with concurrent inflammatory bowel disease and rheumatic disease depends on which condition is “hot” and which is quiescent.

Using standard anti-inflammatory agents to treat the rheumatic disease is problematic because it may exacerbate the IBD. Conventional NSAIDs are associated with reversible colitis and ulceration in patients without IBD, and NSAID enteropathy—often subclinical—is present in up to 60% of patients who take these agents, according to Dr. Bennett E. Roth, director of the digestive disease center and chief of clinical gastroenterology at the University of California, Los Angeles.

Data do support the use of available cyclooxygenase-2 (COX-2) inhibitors in patients with both active IBD and active joint disease, Dr. Roth said at a meeting sponsored by

Why some patients develop both IBD and arthritis is not fully understood, Dr. Roth noted. Possible explanations include the potential relocation of the immune reaction from the intestine to the joints and the activation of immune cells in the gut.

IBD arthropathy can take two forms: spondyloarthropathy (SpA) and peripheral arthropathy. Each has its own course and relationship to IBD, Dr. Roth said.

The degree of SpA activity in IBD patients is independent of the IBD activity. Among patients with both conditions, 20%–25% have sacroiliitis on x-ray; 50% of cases of sacroiliitis in IBD are asymptomatic. Ankylosing spondylitis (AS)—be it HLA-B27 negative or positive—has a prevalence of 3%–10% in this population, according to Dr. Roth.

Young patients who present with axial arthropathy may be candidates for a gastrointestinal evaluation, said Dr. Roth, who is also director of the center for esophageal disorders at UCLA.

The treatment regimen for AS includes physiotherapy, 5-amino-salicylic acid (5-ASA) or immunomodulatory therapy with agents such as 6-mercaptopurine or azathioprine (6MP/AZA), or methotrexate. Fallback treatments are short courses of steroids. If these are insufficient, biologic anti-TNF antibodies may be effective.

One large study showed that infliximab was efficacious in 61% of a group of IBD patients with peripheral arthritis (Am. J. Gastroenterol. 2002;97:2688–90). Infliximab has been shown to be effective in 53% of patients with AS, regardless of the presence of concurrent IBD (Lancet 2002;359:1187–93). Findings from randomized controlled trials of patients who had both AS and IBD and were treated with infliximab show a significant drop in BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) scores but not CDAI (Crohn's Disease Activity Index) scores (Ann. Rheum. Dis. 2004;63:1664–9).

Peripheral arthropathy is divided into types 1 and 2 for classification purposes. Type 1 peripheral arthropathy can involve the large joints, specifically ankles, knees, hips, elbows, and shoulders, in a pauciarticular pattern.

When it comes to the treatment of type 1, Dr. Roth said that as the IBD goes, “so goes the arthritis.” In other words, because the joint inflammation corresponds to the activity of the disease in the gut, there is likely to be a concomitant joint response once the bowel disease is placed into remission. Standard approaches to treating the IBD are employed, including anti-inflammatory agents such as 5-ASA and steroids with the additional use of immunosuppressants 6MP/AZA, or anti-TNF agents as needed.

Type 2 peripheral arthropathy involves the small joints of the hands, is persistent and polyarticular, and follows a course that is independent of the IBD course. Treatment consists of physical therapy, simple analgesics, short courses of steroids with progression to immunosuppressive agents, and/or biologics.

Dr. Roth reported that he has no financial disclosures that are relevant to the topic of his presentation. Skin Disease Education Foundation and this news organization are owned by Elsevier.

SANTA MONICA, CALIF. — How to treat a patient with concurrent inflammatory bowel disease and rheumatic disease depends on which condition is “hot” and which is quiescent.

Using standard anti-inflammatory agents to treat the rheumatic disease is problematic because it may exacerbate the IBD. Conventional NSAIDs are associated with reversible colitis and ulceration in patients without IBD, and NSAID enteropathy—often subclinical—is present in up to 60% of patients who take these agents, according to Dr. Bennett E. Roth, director of the digestive disease center and chief of clinical gastroenterology at the University of California, Los Angeles.

Data do support the use of available cyclooxygenase-2 (COX-2) inhibitors in patients with both active IBD and active joint disease, Dr. Roth said at a meeting sponsored by

Why some patients develop both IBD and arthritis is not fully understood, Dr. Roth noted. Possible explanations include the potential relocation of the immune reaction from the intestine to the joints and the activation of immune cells in the gut.

IBD arthropathy can take two forms: spondyloarthropathy (SpA) and peripheral arthropathy. Each has its own course and relationship to IBD, Dr. Roth said.

The degree of SpA activity in IBD patients is independent of the IBD activity. Among patients with both conditions, 20%–25% have sacroiliitis on x-ray; 50% of cases of sacroiliitis in IBD are asymptomatic. Ankylosing spondylitis (AS)—be it HLA-B27 negative or positive—has a prevalence of 3%–10% in this population, according to Dr. Roth.

Young patients who present with axial arthropathy may be candidates for a gastrointestinal evaluation, said Dr. Roth, who is also director of the center for esophageal disorders at UCLA.

The treatment regimen for AS includes physiotherapy, 5-amino-salicylic acid (5-ASA) or immunomodulatory therapy with agents such as 6-mercaptopurine or azathioprine (6MP/AZA), or methotrexate. Fallback treatments are short courses of steroids. If these are insufficient, biologic anti-TNF antibodies may be effective.

One large study showed that infliximab was efficacious in 61% of a group of IBD patients with peripheral arthritis (Am. J. Gastroenterol. 2002;97:2688–90). Infliximab has been shown to be effective in 53% of patients with AS, regardless of the presence of concurrent IBD (Lancet 2002;359:1187–93). Findings from randomized controlled trials of patients who had both AS and IBD and were treated with infliximab show a significant drop in BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) scores but not CDAI (Crohn's Disease Activity Index) scores (Ann. Rheum. Dis. 2004;63:1664–9).

Peripheral arthropathy is divided into types 1 and 2 for classification purposes. Type 1 peripheral arthropathy can involve the large joints, specifically ankles, knees, hips, elbows, and shoulders, in a pauciarticular pattern.

When it comes to the treatment of type 1, Dr. Roth said that as the IBD goes, “so goes the arthritis.” In other words, because the joint inflammation corresponds to the activity of the disease in the gut, there is likely to be a concomitant joint response once the bowel disease is placed into remission. Standard approaches to treating the IBD are employed, including anti-inflammatory agents such as 5-ASA and steroids with the additional use of immunosuppressants 6MP/AZA, or anti-TNF agents as needed.

Type 2 peripheral arthropathy involves the small joints of the hands, is persistent and polyarticular, and follows a course that is independent of the IBD course. Treatment consists of physical therapy, simple analgesics, short courses of steroids with progression to immunosuppressive agents, and/or biologics.

Dr. Roth reported that he has no financial disclosures that are relevant to the topic of his presentation. Skin Disease Education Foundation and this news organization are owned by Elsevier.

SANTA MONICA, CALIF. — How to treat a patient with concurrent inflammatory bowel disease and rheumatic disease depends on which condition is “hot” and which is quiescent.

Using standard anti-inflammatory agents to treat the rheumatic disease is problematic because it may exacerbate the IBD. Conventional NSAIDs are associated with reversible colitis and ulceration in patients without IBD, and NSAID enteropathy—often subclinical—is present in up to 60% of patients who take these agents, according to Dr. Bennett E. Roth, director of the digestive disease center and chief of clinical gastroenterology at the University of California, Los Angeles.

Data do support the use of available cyclooxygenase-2 (COX-2) inhibitors in patients with both active IBD and active joint disease, Dr. Roth said at a meeting sponsored by

Why some patients develop both IBD and arthritis is not fully understood, Dr. Roth noted. Possible explanations include the potential relocation of the immune reaction from the intestine to the joints and the activation of immune cells in the gut.

IBD arthropathy can take two forms: spondyloarthropathy (SpA) and peripheral arthropathy. Each has its own course and relationship to IBD, Dr. Roth said.

The degree of SpA activity in IBD patients is independent of the IBD activity. Among patients with both conditions, 20%–25% have sacroiliitis on x-ray; 50% of cases of sacroiliitis in IBD are asymptomatic. Ankylosing spondylitis (AS)—be it HLA-B27 negative or positive—has a prevalence of 3%–10% in this population, according to Dr. Roth.

Young patients who present with axial arthropathy may be candidates for a gastrointestinal evaluation, said Dr. Roth, who is also director of the center for esophageal disorders at UCLA.

The treatment regimen for AS includes physiotherapy, 5-amino-salicylic acid (5-ASA) or immunomodulatory therapy with agents such as 6-mercaptopurine or azathioprine (6MP/AZA), or methotrexate. Fallback treatments are short courses of steroids. If these are insufficient, biologic anti-TNF antibodies may be effective.

One large study showed that infliximab was efficacious in 61% of a group of IBD patients with peripheral arthritis (Am. J. Gastroenterol. 2002;97:2688–90). Infliximab has been shown to be effective in 53% of patients with AS, regardless of the presence of concurrent IBD (Lancet 2002;359:1187–93). Findings from randomized controlled trials of patients who had both AS and IBD and were treated with infliximab show a significant drop in BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) scores but not CDAI (Crohn's Disease Activity Index) scores (Ann. Rheum. Dis. 2004;63:1664–9).

Peripheral arthropathy is divided into types 1 and 2 for classification purposes. Type 1 peripheral arthropathy can involve the large joints, specifically ankles, knees, hips, elbows, and shoulders, in a pauciarticular pattern.

When it comes to the treatment of type 1, Dr. Roth said that as the IBD goes, “so goes the arthritis.” In other words, because the joint inflammation corresponds to the activity of the disease in the gut, there is likely to be a concomitant joint response once the bowel disease is placed into remission. Standard approaches to treating the IBD are employed, including anti-inflammatory agents such as 5-ASA and steroids with the additional use of immunosuppressants 6MP/AZA, or anti-TNF agents as needed.

Type 2 peripheral arthropathy involves the small joints of the hands, is persistent and polyarticular, and follows a course that is independent of the IBD course. Treatment consists of physical therapy, simple analgesics, short courses of steroids with progression to immunosuppressive agents, and/or biologics.

Dr. Roth reported that he has no financial disclosures that are relevant to the topic of his presentation. Skin Disease Education Foundation and this news organization are owned by Elsevier.

SANTA MONICA, CALIF. — Progression of early rheumatoid arthritis is likely in any woman who smokes, has active disease at the time of presentation, and is positive for both rheumatoid factor and anti–cyclic citrullinated peptide antibodies.

Sex and clinical disease activity are the most frequent risk factors for progression of rheumatoid arthritis (RA), and rheumatoid factor and anti–cyclic citrullinated peptide (anti-CCP) antibodies are the most frequent tests that physicians use to assess the likelihood of such progression. Other genetic tests that offer information about progression risk, such as that for HLA-DRB1, are not widely used. And yet other tests for genetic determinants of treatment response and the likelihood of developing adverse events in response to treatment are encouraging, but remain largely in the realm of research, according to Dr. Daniel E. Furst, who is the Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles.

No single marker can absolutely predict disease progression, at least in part because RA is probably more than one disease, dependent on the presence or absence of anti-CCP antibodies. Anti-CCP antibodies are the result of a genetic predisposition and a systemic stress, such as smoking. However, Dr. Furst pointed out that even among all anti-CCP antibody–positive people, the course of RA may vary because of the effects of environmental stimuli, immune events, and interventions (Annu. Rev. Immunol. 2008;26:651-75).

Citrullination is present in a wide range of inflammatory tissues, suggesting that this process is a nonspecific response to inflammation, rather than a disease-specific response, Dr. Furst noted at a meeting sponsored by

Subset analyses of data from the PROMPT (Probable Rheumatoid Arthritis: Methotrexate vs. Placebo Treatment) study, presented by Dr. Henrike Van Dongen of Leiden (the Netherlands) University Medical Center at the 2006 congress of the European League Against Rheumatism (EULAR), demonstrated that the presence of anti-CCP determined response to methotrexate. Responses at 15 months after diagnosis in a group of 27 anti-CCP antibody–positive patients were below 10% in those on placebo, but were close to 50% in those on methotrexate. There was no treatment effect in a group of 83 anti-CCP–negative patients (Arthritis Rheum. 2007; 56:1424).

The HLA-DRB1 gene is associated with extra-articular manifestations of RA and the development of Felty's syndrome. That syndrome occurs in fewer than 1% of RA patients and is considered to be a complication of long-standing disease. It involves a triad of conditions: RA, splenomegaly, and an abnormally low white blood count. Findings from an unpublished study show that Felty's syndrome was associated with HLA-DRB1.0401.

Other extra-articular manifestations of RA (such as pericarditis, vasculitis, interstitial lung disease, and neurologic involvement) were seen not with individual alleles, but with DRB1.04SE double-dose genotypes.

Findings from numerous other studies show that multiple single nucleotide polymorphisms (SNPs) of the PTPN22 gene have a significant association with RA, as does TRAF1-C5 (on chromosome 9).

Smoking and anti-CCP antibody status seem to be associated in RA, but PTPN22 is an independent risk factor for developing RA, according to Dr. Furst. Although not yet directly applicable to clinical care, attempts are being made to predict response to RA medications using genetic signatures or gene SNPs.

For now, other factors are more practical predictors of good response.

SDEF and this news organization are owned by Elsevier.

For a video interview with Dr. Furst, go to www.youtube.com/rheumatologynews

Disclosures: Dr. Furst reported financial relationships with numerous pharmaceutical companies and the National Institutes of Health.

Dr. Daniel E. Furst noted that anti-CCP antibodies are the result of a genetic predisposition and a systemic stress.

Source Sally Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. — Progression of early rheumatoid arthritis is likely in any woman who smokes, has active disease at the time of presentation, and is positive for both rheumatoid factor and anti–cyclic citrullinated peptide antibodies.

Sex and clinical disease activity are the most frequent risk factors for progression of rheumatoid arthritis (RA), and rheumatoid factor and anti–cyclic citrullinated peptide (anti-CCP) antibodies are the most frequent tests that physicians use to assess the likelihood of such progression. Other genetic tests that offer information about progression risk, such as that for HLA-DRB1, are not widely used. And yet other tests for genetic determinants of treatment response and the likelihood of developing adverse events in response to treatment are encouraging, but remain largely in the realm of research, according to Dr. Daniel E. Furst, who is the Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles.

No single marker can absolutely predict disease progression, at least in part because RA is probably more than one disease, dependent on the presence or absence of anti-CCP antibodies. Anti-CCP antibodies are the result of a genetic predisposition and a systemic stress, such as smoking. However, Dr. Furst pointed out that even among all anti-CCP antibody–positive people, the course of RA may vary because of the effects of environmental stimuli, immune events, and interventions (Annu. Rev. Immunol. 2008;26:651-75).

Citrullination is present in a wide range of inflammatory tissues, suggesting that this process is a nonspecific response to inflammation, rather than a disease-specific response, Dr. Furst noted at a meeting sponsored by

Subset analyses of data from the PROMPT (Probable Rheumatoid Arthritis: Methotrexate vs. Placebo Treatment) study, presented by Dr. Henrike Van Dongen of Leiden (the Netherlands) University Medical Center at the 2006 congress of the European League Against Rheumatism (EULAR), demonstrated that the presence of anti-CCP determined response to methotrexate. Responses at 15 months after diagnosis in a group of 27 anti-CCP antibody–positive patients were below 10% in those on placebo, but were close to 50% in those on methotrexate. There was no treatment effect in a group of 83 anti-CCP–negative patients (Arthritis Rheum. 2007; 56:1424).

The HLA-DRB1 gene is associated with extra-articular manifestations of RA and the development of Felty's syndrome. That syndrome occurs in fewer than 1% of RA patients and is considered to be a complication of long-standing disease. It involves a triad of conditions: RA, splenomegaly, and an abnormally low white blood count. Findings from an unpublished study show that Felty's syndrome was associated with HLA-DRB1.0401.

Other extra-articular manifestations of RA (such as pericarditis, vasculitis, interstitial lung disease, and neurologic involvement) were seen not with individual alleles, but with DRB1.04SE double-dose genotypes.

Findings from numerous other studies show that multiple single nucleotide polymorphisms (SNPs) of the PTPN22 gene have a significant association with RA, as does TRAF1-C5 (on chromosome 9).

Smoking and anti-CCP antibody status seem to be associated in RA, but PTPN22 is an independent risk factor for developing RA, according to Dr. Furst. Although not yet directly applicable to clinical care, attempts are being made to predict response to RA medications using genetic signatures or gene SNPs.

For now, other factors are more practical predictors of good response.

SDEF and this news organization are owned by Elsevier.

For a video interview with Dr. Furst, go to www.youtube.com/rheumatologynews

Disclosures: Dr. Furst reported financial relationships with numerous pharmaceutical companies and the National Institutes of Health.

Dr. Daniel E. Furst noted that anti-CCP antibodies are the result of a genetic predisposition and a systemic stress.

Source Sally Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. — Progression of early rheumatoid arthritis is likely in any woman who smokes, has active disease at the time of presentation, and is positive for both rheumatoid factor and anti–cyclic citrullinated peptide antibodies.

Sex and clinical disease activity are the most frequent risk factors for progression of rheumatoid arthritis (RA), and rheumatoid factor and anti–cyclic citrullinated peptide (anti-CCP) antibodies are the most frequent tests that physicians use to assess the likelihood of such progression. Other genetic tests that offer information about progression risk, such as that for HLA-DRB1, are not widely used. And yet other tests for genetic determinants of treatment response and the likelihood of developing adverse events in response to treatment are encouraging, but remain largely in the realm of research, according to Dr. Daniel E. Furst, who is the Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles.

No single marker can absolutely predict disease progression, at least in part because RA is probably more than one disease, dependent on the presence or absence of anti-CCP antibodies. Anti-CCP antibodies are the result of a genetic predisposition and a systemic stress, such as smoking. However, Dr. Furst pointed out that even among all anti-CCP antibody–positive people, the course of RA may vary because of the effects of environmental stimuli, immune events, and interventions (Annu. Rev. Immunol. 2008;26:651-75).

Citrullination is present in a wide range of inflammatory tissues, suggesting that this process is a nonspecific response to inflammation, rather than a disease-specific response, Dr. Furst noted at a meeting sponsored by

Subset analyses of data from the PROMPT (Probable Rheumatoid Arthritis: Methotrexate vs. Placebo Treatment) study, presented by Dr. Henrike Van Dongen of Leiden (the Netherlands) University Medical Center at the 2006 congress of the European League Against Rheumatism (EULAR), demonstrated that the presence of anti-CCP determined response to methotrexate. Responses at 15 months after diagnosis in a group of 27 anti-CCP antibody–positive patients were below 10% in those on placebo, but were close to 50% in those on methotrexate. There was no treatment effect in a group of 83 anti-CCP–negative patients (Arthritis Rheum. 2007; 56:1424).

The HLA-DRB1 gene is associated with extra-articular manifestations of RA and the development of Felty's syndrome. That syndrome occurs in fewer than 1% of RA patients and is considered to be a complication of long-standing disease. It involves a triad of conditions: RA, splenomegaly, and an abnormally low white blood count. Findings from an unpublished study show that Felty's syndrome was associated with HLA-DRB1.0401.

Other extra-articular manifestations of RA (such as pericarditis, vasculitis, interstitial lung disease, and neurologic involvement) were seen not with individual alleles, but with DRB1.04SE double-dose genotypes.

Findings from numerous other studies show that multiple single nucleotide polymorphisms (SNPs) of the PTPN22 gene have a significant association with RA, as does TRAF1-C5 (on chromosome 9).

Smoking and anti-CCP antibody status seem to be associated in RA, but PTPN22 is an independent risk factor for developing RA, according to Dr. Furst. Although not yet directly applicable to clinical care, attempts are being made to predict response to RA medications using genetic signatures or gene SNPs.

For now, other factors are more practical predictors of good response.

SDEF and this news organization are owned by Elsevier.

For a video interview with Dr. Furst, go to www.youtube.com/rheumatologynews

Disclosures: Dr. Furst reported financial relationships with numerous pharmaceutical companies and the National Institutes of Health.

Dr. Daniel E. Furst noted that anti-CCP antibodies are the result of a genetic predisposition and a systemic stress.

Source Sally Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. — Although good drugs are available, it takes more than medications to manage fibromyalgia, according to Dr. Chad S. Boomershine.

“I recommend that fibromyalgia patients perform stretches every morning and, on alternating days, engage in aerobic and resistance exercise a total of 6 days per week,” counseled Dr. Boomershine, a rheumatologist at Vanderbilt University, Nashville, Tenn., where he specializes in treating fibromyalgia in collaboration with the Vanderbilt Center for Integrative Health and the Vanderbilt Dayani Center.

“The combination of aerobic and resistance exercise is particularly effective in improving symptoms. Since many patients don't live near an exercise facility, I provide patients with instructional handouts and [professional elastic resistance bands] for resistance exercise on their initial visit so they can exercise at home,” Dr. Boomershine said at a meeting sponsored by

Dr. Boomershine said he refers his patients to the exercise guide on the National Institute on Aging Web site (www.nia.nih.gov/HealthInformation/Publications/ExerciseGuide

He also recommends the National Center on Physical Activity and Disability Web site's exercise fact sheet (www.ncpad.org/exercise/fact_sheet.php?sheet=259

Additionally, he recommends that patients learn more about fibromyalgia and find support groups in their area. “Due to the severity of their symptoms, patients are often afraid they have a terminal illness,” he noted. “Understanding that fibromyalgia is not progressive and realizing they can manage their symptoms by learning self-help techniques is empowering and necessary if patients are to have lasting symptom improvement.”

The Web sites www.knowfibro.comwww.fmaware.org

Between 2% and 4% of the U.S. population meet the fibromyalgia classification criteria issued in 1990 by the American College of Rheumatology. However, the true prevalence is estimated to be about twice as high, and—as prevalence increases with age—fibromyalgia is expected to become increasingly common with the aging of the population, he said.

Of those who have the condition, the reported 9:1 ratio of women to men is incorrect, as women have more tender points and men are more likely to self-medicate rather than to seek medical care.

There are no official figures on how many people are unable to work due to fibromyalgia because the Social Security Adminustration does not recognize it as a cause of disability.

SDEF and this news organization are owned by Elsevier.

SANTA MONICA, CALIF. — Although good drugs are available, it takes more than medications to manage fibromyalgia, according to Dr. Chad S. Boomershine.

“I recommend that fibromyalgia patients perform stretches every morning and, on alternating days, engage in aerobic and resistance exercise a total of 6 days per week,” counseled Dr. Boomershine, a rheumatologist at Vanderbilt University, Nashville, Tenn., where he specializes in treating fibromyalgia in collaboration with the Vanderbilt Center for Integrative Health and the Vanderbilt Dayani Center.

“The combination of aerobic and resistance exercise is particularly effective in improving symptoms. Since many patients don't live near an exercise facility, I provide patients with instructional handouts and [professional elastic resistance bands] for resistance exercise on their initial visit so they can exercise at home,” Dr. Boomershine said at a meeting sponsored by

Dr. Boomershine said he refers his patients to the exercise guide on the National Institute on Aging Web site (www.nia.nih.gov/HealthInformation/Publications/ExerciseGuide

He also recommends the National Center on Physical Activity and Disability Web site's exercise fact sheet (www.ncpad.org/exercise/fact_sheet.php?sheet=259

Additionally, he recommends that patients learn more about fibromyalgia and find support groups in their area. “Due to the severity of their symptoms, patients are often afraid they have a terminal illness,” he noted. “Understanding that fibromyalgia is not progressive and realizing they can manage their symptoms by learning self-help techniques is empowering and necessary if patients are to have lasting symptom improvement.”

The Web sites www.knowfibro.comwww.fmaware.org

Between 2% and 4% of the U.S. population meet the fibromyalgia classification criteria issued in 1990 by the American College of Rheumatology. However, the true prevalence is estimated to be about twice as high, and—as prevalence increases with age—fibromyalgia is expected to become increasingly common with the aging of the population, he said.

Of those who have the condition, the reported 9:1 ratio of women to men is incorrect, as women have more tender points and men are more likely to self-medicate rather than to seek medical care.

There are no official figures on how many people are unable to work due to fibromyalgia because the Social Security Adminustration does not recognize it as a cause of disability.

SDEF and this news organization are owned by Elsevier.

SANTA MONICA, CALIF. — Although good drugs are available, it takes more than medications to manage fibromyalgia, according to Dr. Chad S. Boomershine.

“I recommend that fibromyalgia patients perform stretches every morning and, on alternating days, engage in aerobic and resistance exercise a total of 6 days per week,” counseled Dr. Boomershine, a rheumatologist at Vanderbilt University, Nashville, Tenn., where he specializes in treating fibromyalgia in collaboration with the Vanderbilt Center for Integrative Health and the Vanderbilt Dayani Center.

“The combination of aerobic and resistance exercise is particularly effective in improving symptoms. Since many patients don't live near an exercise facility, I provide patients with instructional handouts and [professional elastic resistance bands] for resistance exercise on their initial visit so they can exercise at home,” Dr. Boomershine said at a meeting sponsored by

Dr. Boomershine said he refers his patients to the exercise guide on the National Institute on Aging Web site (www.nia.nih.gov/HealthInformation/Publications/ExerciseGuide

He also recommends the National Center on Physical Activity and Disability Web site's exercise fact sheet (www.ncpad.org/exercise/fact_sheet.php?sheet=259

Additionally, he recommends that patients learn more about fibromyalgia and find support groups in their area. “Due to the severity of their symptoms, patients are often afraid they have a terminal illness,” he noted. “Understanding that fibromyalgia is not progressive and realizing they can manage their symptoms by learning self-help techniques is empowering and necessary if patients are to have lasting symptom improvement.”

The Web sites www.knowfibro.comwww.fmaware.org

Between 2% and 4% of the U.S. population meet the fibromyalgia classification criteria issued in 1990 by the American College of Rheumatology. However, the true prevalence is estimated to be about twice as high, and—as prevalence increases with age—fibromyalgia is expected to become increasingly common with the aging of the population, he said.

Of those who have the condition, the reported 9:1 ratio of women to men is incorrect, as women have more tender points and men are more likely to self-medicate rather than to seek medical care.

There are no official figures on how many people are unable to work due to fibromyalgia because the Social Security Adminustration does not recognize it as a cause of disability.

SDEF and this news organization are owned by Elsevier.

Major Finding: Fibromyalgia therapies need to be used in combination, and sometimes at doses other than those recommended by the manufacturer, depending upon the overarching symptom of the individual patient.

Source of Data: Expert opinion.

Disclosures: Dr. Boomershine reported that he is an investigator for Pfizer Inc. and the National Institutes of Health, and is a consultant for Pfizer, Eli Lilly & Co., Forest Pharmaceuticals Inc., and Takeda Pharmaceutical Co.

SANTA MONICA, CALIF. — Effective treatments exist for fibromyalgia syndrome, but many physicians still do a poor job of treating affected patients, Dr. Chad S. Boomershine said at a meeting sponsored by

Could it be that these physicians don't consider fibromyalgia to be a “real” disease, that they perceive affected patients as being too time consuming and unlikely to get better? asked Dr. Boomershine, a rheumatologist at Vanderbilt University in Nashville, Tenn., where he specializes in treating fibromyalgia in collaboration with the Vanderbilt Center for Integrative Health and the Vanderbilt Dayani Center.

About 2%-4% of the U.S. population meets the fibromyalgia classification criteria issued in 1990 by the ACR. The true prevalence is estimated to be about twice as high, and—as prevalence increases with age—fibromyalgia is expected to become more common with the aging of the population.

The ACR classification criteria for fibromyalgia include widespread pain for at least 3 months' duration, and pain at a minimum of 11 of 18 specified tender points when enough pressure to just blanch the examiner's thumbnail is applied. The reported 9:1 ratio of women to men with the condition is incorrect, he said, as women have more tender points and men are more likely to self-medicate rather than to seek medical care.

Fibromyalgia typically involves symptoms other than pain, which Dr. Boomershine teaches using the FIBRO mnemonic (F for fatigue and 'fibrofog' [cognitive dysfunction], I for insomnia [nonrestorative sleep], B for blues [depression and anxiety], R for rigidity [muscle and joint stiffness], and O for Ow! [pain and work disability]). Nevertheless, pharmacologic management should start by treating pain because it is the one symptom common to all fibromyalgia patients, he said.

When choosing among the three indicated medications, a physician should individualize therapy based on the associated symptom that is most disabling for the patient, he recommended.

Pain associated with insomnia is best treated with pregabalin (Lyrica), he said. The label states that pregabalin should be given in two divided doses daily beginning with a total of 150 mg/day and increasing to as much as 450 mg/day if needed. In an effort to avoid the typical side effects of dizziness, somnolence, fatigue, and cognitive dysfunction, however, Dr. Boomershine recommends beginning with 25-75 mg once daily at bedtime and titrating up to 150-225 mg at night before adding a morning dose.

Pain with depression and/or anxiety is best managed with duloxetine (Cymbalta) every morning, he said. The label states that the recommended dosage for fibromyalgia is 60 mg/day, but Dr. Boomershine recommends starting with 20-30 mg and increasing to 60 mg only if necessary. Trial data indicate that many patients do well on lower doses, he noted, and higher doses are associated with increased risk for side effects, including nausea, headache, and insomnia.

For pain associated with fatigue or fibrofog, the treatment of choice is milnacipran (Savella), he said. The label for this agent recommends starting at a dose of 12.5 mg once daily and gradually working up to 50 mg twice daily after 1 week and a maximum dosage of 100 mg twice daily if needed. Dr. Boomershine said he recommends a more gradual up-titration and noted that the dose should be increased only if needed because of the patient's symptoms. Milnacipran is available in 12.5-, 25-, 50- and 100-mg tablets, allowing for dosing flexibility.

Physicians with years of experience in successfully managing fibromyalgia are accustomed to using other drugs that lack Food and Drug Administration approval specifically for use in fibromyalgia.

Amitriptyline given as a 25-mg dose at bedtime in combination with fluoxetine (20 mg) in the morning is a “particularly good combination,” said Dr. Boomershine. He noted that the combination has shown good efficacy and likely provides balanced norepinephrine and serotonin reuptake inhibition similar to that provided by duloxetine and milnacipran, but at a much lower cost.

Dr. Boomershine recommends avoiding the use of narcotics, benzodiazepines, or steroids in treating fibromyalgia symptoms.

SDEF and this news organization are owned by Elsevier.

For a video interview with Dr. Boomershine, go to www.youtube.com/rheumatologynews

Treatment needs to address the fact that pain is only one symptom of fibromyalgia, Dr. Chad S. Boomershine said.

Source Sally Kubetin/Elsevier Global Medical News

Major Finding: Fibromyalgia therapies need to be used in combination, and sometimes at doses other than those recommended by the manufacturer, depending upon the overarching symptom of the individual patient.

Source of Data: Expert opinion.

Disclosures: Dr. Boomershine reported that he is an investigator for Pfizer Inc. and the National Institutes of Health, and is a consultant for Pfizer, Eli Lilly & Co., Forest Pharmaceuticals Inc., and Takeda Pharmaceutical Co.

SANTA MONICA, CALIF. — Effective treatments exist for fibromyalgia syndrome, but many physicians still do a poor job of treating affected patients, Dr. Chad S. Boomershine said at a meeting sponsored by

Could it be that these physicians don't consider fibromyalgia to be a “real” disease, that they perceive affected patients as being too time consuming and unlikely to get better? asked Dr. Boomershine, a rheumatologist at Vanderbilt University in Nashville, Tenn., where he specializes in treating fibromyalgia in collaboration with the Vanderbilt Center for Integrative Health and the Vanderbilt Dayani Center.

About 2%-4% of the U.S. population meets the fibromyalgia classification criteria issued in 1990 by the ACR. The true prevalence is estimated to be about twice as high, and—as prevalence increases with age—fibromyalgia is expected to become more common with the aging of the population.

The ACR classification criteria for fibromyalgia include widespread pain for at least 3 months' duration, and pain at a minimum of 11 of 18 specified tender points when enough pressure to just blanch the examiner's thumbnail is applied. The reported 9:1 ratio of women to men with the condition is incorrect, he said, as women have more tender points and men are more likely to self-medicate rather than to seek medical care.

Fibromyalgia typically involves symptoms other than pain, which Dr. Boomershine teaches using the FIBRO mnemonic (F for fatigue and 'fibrofog' [cognitive dysfunction], I for insomnia [nonrestorative sleep], B for blues [depression and anxiety], R for rigidity [muscle and joint stiffness], and O for Ow! [pain and work disability]). Nevertheless, pharmacologic management should start by treating pain because it is the one symptom common to all fibromyalgia patients, he said.

When choosing among the three indicated medications, a physician should individualize therapy based on the associated symptom that is most disabling for the patient, he recommended.

Pain associated with insomnia is best treated with pregabalin (Lyrica), he said. The label states that pregabalin should be given in two divided doses daily beginning with a total of 150 mg/day and increasing to as much as 450 mg/day if needed. In an effort to avoid the typical side effects of dizziness, somnolence, fatigue, and cognitive dysfunction, however, Dr. Boomershine recommends beginning with 25-75 mg once daily at bedtime and titrating up to 150-225 mg at night before adding a morning dose.

Pain with depression and/or anxiety is best managed with duloxetine (Cymbalta) every morning, he said. The label states that the recommended dosage for fibromyalgia is 60 mg/day, but Dr. Boomershine recommends starting with 20-30 mg and increasing to 60 mg only if necessary. Trial data indicate that many patients do well on lower doses, he noted, and higher doses are associated with increased risk for side effects, including nausea, headache, and insomnia.

For pain associated with fatigue or fibrofog, the treatment of choice is milnacipran (Savella), he said. The label for this agent recommends starting at a dose of 12.5 mg once daily and gradually working up to 50 mg twice daily after 1 week and a maximum dosage of 100 mg twice daily if needed. Dr. Boomershine said he recommends a more gradual up-titration and noted that the dose should be increased only if needed because of the patient's symptoms. Milnacipran is available in 12.5-, 25-, 50- and 100-mg tablets, allowing for dosing flexibility.

Physicians with years of experience in successfully managing fibromyalgia are accustomed to using other drugs that lack Food and Drug Administration approval specifically for use in fibromyalgia.

Amitriptyline given as a 25-mg dose at bedtime in combination with fluoxetine (20 mg) in the morning is a “particularly good combination,” said Dr. Boomershine. He noted that the combination has shown good efficacy and likely provides balanced norepinephrine and serotonin reuptake inhibition similar to that provided by duloxetine and milnacipran, but at a much lower cost.

Dr. Boomershine recommends avoiding the use of narcotics, benzodiazepines, or steroids in treating fibromyalgia symptoms.

SDEF and this news organization are owned by Elsevier.

For a video interview with Dr. Boomershine, go to www.youtube.com/rheumatologynews

Treatment needs to address the fact that pain is only one symptom of fibromyalgia, Dr. Chad S. Boomershine said.

Source Sally Kubetin/Elsevier Global Medical News

Major Finding: Fibromyalgia therapies need to be used in combination, and sometimes at doses other than those recommended by the manufacturer, depending upon the overarching symptom of the individual patient.

Source of Data: Expert opinion.

Disclosures: Dr. Boomershine reported that he is an investigator for Pfizer Inc. and the National Institutes of Health, and is a consultant for Pfizer, Eli Lilly & Co., Forest Pharmaceuticals Inc., and Takeda Pharmaceutical Co.

SANTA MONICA, CALIF. — Effective treatments exist for fibromyalgia syndrome, but many physicians still do a poor job of treating affected patients, Dr. Chad S. Boomershine said at a meeting sponsored by

Could it be that these physicians don't consider fibromyalgia to be a “real” disease, that they perceive affected patients as being too time consuming and unlikely to get better? asked Dr. Boomershine, a rheumatologist at Vanderbilt University in Nashville, Tenn., where he specializes in treating fibromyalgia in collaboration with the Vanderbilt Center for Integrative Health and the Vanderbilt Dayani Center.

About 2%-4% of the U.S. population meets the fibromyalgia classification criteria issued in 1990 by the ACR. The true prevalence is estimated to be about twice as high, and—as prevalence increases with age—fibromyalgia is expected to become more common with the aging of the population.

The ACR classification criteria for fibromyalgia include widespread pain for at least 3 months' duration, and pain at a minimum of 11 of 18 specified tender points when enough pressure to just blanch the examiner's thumbnail is applied. The reported 9:1 ratio of women to men with the condition is incorrect, he said, as women have more tender points and men are more likely to self-medicate rather than to seek medical care.

Fibromyalgia typically involves symptoms other than pain, which Dr. Boomershine teaches using the FIBRO mnemonic (F for fatigue and 'fibrofog' [cognitive dysfunction], I for insomnia [nonrestorative sleep], B for blues [depression and anxiety], R for rigidity [muscle and joint stiffness], and O for Ow! [pain and work disability]). Nevertheless, pharmacologic management should start by treating pain because it is the one symptom common to all fibromyalgia patients, he said.

When choosing among the three indicated medications, a physician should individualize therapy based on the associated symptom that is most disabling for the patient, he recommended.

Pain associated with insomnia is best treated with pregabalin (Lyrica), he said. The label states that pregabalin should be given in two divided doses daily beginning with a total of 150 mg/day and increasing to as much as 450 mg/day if needed. In an effort to avoid the typical side effects of dizziness, somnolence, fatigue, and cognitive dysfunction, however, Dr. Boomershine recommends beginning with 25-75 mg once daily at bedtime and titrating up to 150-225 mg at night before adding a morning dose.

Pain with depression and/or anxiety is best managed with duloxetine (Cymbalta) every morning, he said. The label states that the recommended dosage for fibromyalgia is 60 mg/day, but Dr. Boomershine recommends starting with 20-30 mg and increasing to 60 mg only if necessary. Trial data indicate that many patients do well on lower doses, he noted, and higher doses are associated with increased risk for side effects, including nausea, headache, and insomnia.

For pain associated with fatigue or fibrofog, the treatment of choice is milnacipran (Savella), he said. The label for this agent recommends starting at a dose of 12.5 mg once daily and gradually working up to 50 mg twice daily after 1 week and a maximum dosage of 100 mg twice daily if needed. Dr. Boomershine said he recommends a more gradual up-titration and noted that the dose should be increased only if needed because of the patient's symptoms. Milnacipran is available in 12.5-, 25-, 50- and 100-mg tablets, allowing for dosing flexibility.

Physicians with years of experience in successfully managing fibromyalgia are accustomed to using other drugs that lack Food and Drug Administration approval specifically for use in fibromyalgia.

Amitriptyline given as a 25-mg dose at bedtime in combination with fluoxetine (20 mg) in the morning is a “particularly good combination,” said Dr. Boomershine. He noted that the combination has shown good efficacy and likely provides balanced norepinephrine and serotonin reuptake inhibition similar to that provided by duloxetine and milnacipran, but at a much lower cost.

Dr. Boomershine recommends avoiding the use of narcotics, benzodiazepines, or steroids in treating fibromyalgia symptoms.

SDEF and this news organization are owned by Elsevier.

For a video interview with Dr. Boomershine, go to www.youtube.com/rheumatologynews

Treatment needs to address the fact that pain is only one symptom of fibromyalgia, Dr. Chad S. Boomershine said.

Source Sally Kubetin/Elsevier Global Medical News

SANTA MONICA, CALIF. — Progression of early rheumatoid arthritis is likely in any woman who smokes, has active disease at the time of presentation, and is positive for both rheumatoid factor and anti–cyclic citrullinated peptide antibodies.

Gender and clinical disease activity are the most common risk factors for progression of rheumatoid arthritis (RA), and rheumatoid factor and anti–cyclic citrullinated peptide (anti-CCP) antibodies are the tests used most frequently to assess the likelihood of such progression. Other genetic tests that offer information about progression risk, such as that for HLA-DRB1, are not widely used. And yet other tests for genetic determinants of treatment response and the likelihood of treatment-related adverse events show promise but remain largely in the realm of research, said Dr. Daniel E. Furst, who is the Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles.

No single marker can absolutely predict disease progression, at least in part because RA is probably more than one disease, dependent on the presence or absence of anti-CCP antibodies. Anti-CCP antibodies are the result of a genetic predisposition and a systemic stress, such as smoking. However, Dr. Furst pointed out that even among all anti-CCP antibody–positive people, the course of RA may vary because of the effects of environmental stimuli, immune events, and interventions (Annu. Rev. Immunol. 2008;26:651–75).

Citrullination is present in a wide range of inflammatory tissues, suggesting that this process is a nonspecific response to inflammation, rather than a disease-specific response, Dr. Furst noted at a meeting sponsored by

Subset analyses of data from the PROMPT (Probable Rheumatoid Arthritis: Methotrexate vs. Placebo Treatment) study, presented by Dr. Henrike Van Dongen of Leiden (the Netherlands) University Medical Center at the 2006 congress of the European League Against Rheumatism (EULAR), demonstrated that the presence of anti-CCP determined response to methotrexate. Responses at 15 months after diagnosis in a group of 27 anti-CCP antibody–positive patients were below 10% in those on placebo, but were close to 50% in those on methotrexate. There was no treatment effect in a group of 83 anti-CCP–negative patients (Arthritis Rheum. 2007;56:1424).

The HLA-DRB1 gene is associated with extra-articular manifestations of RA and the development of Felty's syndrome. That syndrome occurs in fewer than 1% of RA patients and is considered to be a complication of long-standing disease. It involves a triad of conditions: RA, splenomegaly, and an abnormally low white blood count. Findings from an unpublished study show that Felty's syndrome was associated with HLA-DRB1.0401. Other extra-articular manifestations of RA (such as pericarditis, vasculitis, interstitial lung disease, and neurologic involvement) were seen not with individual alleles, but with DRB1.04SE double-dose genotypes.

Findings from many other studies show that multiple single nucleotide polymorphisms (SNPs) of the PTPN22 gene have a significant association with RA, as does TRAF1-C5 (on chromosome 9).

Smoking and anti-CCP antibody status seem to be associated in RA, but PTPN22 is an independent risk factor for developing RA, according to Dr. Furst. Although not yet directly applicable to clinical care, attempts are being made to predict response to RA medications using genetic signatures or gene SNPs.

For example, 37 RA patients with the G/G polymorphism of the TNF promoter gene has been shown to have good response as measured by changes in DAS-28 to TNF antagonists. The same response was not seen in 3 RA patients with the A/A polymorphism or 14 RA patients with the A/G polymorphism. The same benefit of the G/A polymorphism on treatment response has been shown in patients with ankylosing spondylitis and psoriatic arthritis, according to Dr. Furst (Rheumatology 2007;46:93–96).

“We can't send off to [a commercial testing laboratory] to do this test at the moment. But I believe it is coming down the pike,” he noted.

For now, other factors are more practical predictors of good response. For example, low disease activity and few bony erosions at the beginning of TNF inhibitor therapy imply that early TNF use may be appropriate. When to change TNF inhibitors and whether to try another TNF blocker are practical questions that have been tested. It appears that if a patient has no response to two TNF blockers, a third TNF blocker is unlikely to be helpful and it is time to try a drug with a different mechanism of action.

Dr. Furst reported financial relationships with numerous pharmaceutical companies and the National Institutes of Health.

SDEF and this news organization are owned by Elsevier.

A related video is at www.youtube.com/InternalMedicineNews

SANTA MONICA, CALIF. — Progression of early rheumatoid arthritis is likely in any woman who smokes, has active disease at the time of presentation, and is positive for both rheumatoid factor and anti–cyclic citrullinated peptide antibodies.

Gender and clinical disease activity are the most common risk factors for progression of rheumatoid arthritis (RA), and rheumatoid factor and anti–cyclic citrullinated peptide (anti-CCP) antibodies are the tests used most frequently to assess the likelihood of such progression. Other genetic tests that offer information about progression risk, such as that for HLA-DRB1, are not widely used. And yet other tests for genetic determinants of treatment response and the likelihood of treatment-related adverse events show promise but remain largely in the realm of research, said Dr. Daniel E. Furst, who is the Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles.

No single marker can absolutely predict disease progression, at least in part because RA is probably more than one disease, dependent on the presence or absence of anti-CCP antibodies. Anti-CCP antibodies are the result of a genetic predisposition and a systemic stress, such as smoking. However, Dr. Furst pointed out that even among all anti-CCP antibody–positive people, the course of RA may vary because of the effects of environmental stimuli, immune events, and interventions (Annu. Rev. Immunol. 2008;26:651–75).

Citrullination is present in a wide range of inflammatory tissues, suggesting that this process is a nonspecific response to inflammation, rather than a disease-specific response, Dr. Furst noted at a meeting sponsored by

Subset analyses of data from the PROMPT (Probable Rheumatoid Arthritis: Methotrexate vs. Placebo Treatment) study, presented by Dr. Henrike Van Dongen of Leiden (the Netherlands) University Medical Center at the 2006 congress of the European League Against Rheumatism (EULAR), demonstrated that the presence of anti-CCP determined response to methotrexate. Responses at 15 months after diagnosis in a group of 27 anti-CCP antibody–positive patients were below 10% in those on placebo, but were close to 50% in those on methotrexate. There was no treatment effect in a group of 83 anti-CCP–negative patients (Arthritis Rheum. 2007;56:1424).

The HLA-DRB1 gene is associated with extra-articular manifestations of RA and the development of Felty's syndrome. That syndrome occurs in fewer than 1% of RA patients and is considered to be a complication of long-standing disease. It involves a triad of conditions: RA, splenomegaly, and an abnormally low white blood count. Findings from an unpublished study show that Felty's syndrome was associated with HLA-DRB1.0401. Other extra-articular manifestations of RA (such as pericarditis, vasculitis, interstitial lung disease, and neurologic involvement) were seen not with individual alleles, but with DRB1.04SE double-dose genotypes.

Findings from many other studies show that multiple single nucleotide polymorphisms (SNPs) of the PTPN22 gene have a significant association with RA, as does TRAF1-C5 (on chromosome 9).

Smoking and anti-CCP antibody status seem to be associated in RA, but PTPN22 is an independent risk factor for developing RA, according to Dr. Furst. Although not yet directly applicable to clinical care, attempts are being made to predict response to RA medications using genetic signatures or gene SNPs.

For example, 37 RA patients with the G/G polymorphism of the TNF promoter gene has been shown to have good response as measured by changes in DAS-28 to TNF antagonists. The same response was not seen in 3 RA patients with the A/A polymorphism or 14 RA patients with the A/G polymorphism. The same benefit of the G/A polymorphism on treatment response has been shown in patients with ankylosing spondylitis and psoriatic arthritis, according to Dr. Furst (Rheumatology 2007;46:93–96).

“We can't send off to [a commercial testing laboratory] to do this test at the moment. But I believe it is coming down the pike,” he noted.

For now, other factors are more practical predictors of good response. For example, low disease activity and few bony erosions at the beginning of TNF inhibitor therapy imply that early TNF use may be appropriate. When to change TNF inhibitors and whether to try another TNF blocker are practical questions that have been tested. It appears that if a patient has no response to two TNF blockers, a third TNF blocker is unlikely to be helpful and it is time to try a drug with a different mechanism of action.

Dr. Furst reported financial relationships with numerous pharmaceutical companies and the National Institutes of Health.

SDEF and this news organization are owned by Elsevier.

A related video is at www.youtube.com/InternalMedicineNews

SANTA MONICA, CALIF. — Progression of early rheumatoid arthritis is likely in any woman who smokes, has active disease at the time of presentation, and is positive for both rheumatoid factor and anti–cyclic citrullinated peptide antibodies.

Gender and clinical disease activity are the most common risk factors for progression of rheumatoid arthritis (RA), and rheumatoid factor and anti–cyclic citrullinated peptide (anti-CCP) antibodies are the tests used most frequently to assess the likelihood of such progression. Other genetic tests that offer information about progression risk, such as that for HLA-DRB1, are not widely used. And yet other tests for genetic determinants of treatment response and the likelihood of treatment-related adverse events show promise but remain largely in the realm of research, said Dr. Daniel E. Furst, who is the Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles.

No single marker can absolutely predict disease progression, at least in part because RA is probably more than one disease, dependent on the presence or absence of anti-CCP antibodies. Anti-CCP antibodies are the result of a genetic predisposition and a systemic stress, such as smoking. However, Dr. Furst pointed out that even among all anti-CCP antibody–positive people, the course of RA may vary because of the effects of environmental stimuli, immune events, and interventions (Annu. Rev. Immunol. 2008;26:651–75).

Citrullination is present in a wide range of inflammatory tissues, suggesting that this process is a nonspecific response to inflammation, rather than a disease-specific response, Dr. Furst noted at a meeting sponsored by

Subset analyses of data from the PROMPT (Probable Rheumatoid Arthritis: Methotrexate vs. Placebo Treatment) study, presented by Dr. Henrike Van Dongen of Leiden (the Netherlands) University Medical Center at the 2006 congress of the European League Against Rheumatism (EULAR), demonstrated that the presence of anti-CCP determined response to methotrexate. Responses at 15 months after diagnosis in a group of 27 anti-CCP antibody–positive patients were below 10% in those on placebo, but were close to 50% in those on methotrexate. There was no treatment effect in a group of 83 anti-CCP–negative patients (Arthritis Rheum. 2007;56:1424).

The HLA-DRB1 gene is associated with extra-articular manifestations of RA and the development of Felty's syndrome. That syndrome occurs in fewer than 1% of RA patients and is considered to be a complication of long-standing disease. It involves a triad of conditions: RA, splenomegaly, and an abnormally low white blood count. Findings from an unpublished study show that Felty's syndrome was associated with HLA-DRB1.0401. Other extra-articular manifestations of RA (such as pericarditis, vasculitis, interstitial lung disease, and neurologic involvement) were seen not with individual alleles, but with DRB1.04SE double-dose genotypes.

Findings from many other studies show that multiple single nucleotide polymorphisms (SNPs) of the PTPN22 gene have a significant association with RA, as does TRAF1-C5 (on chromosome 9).

Smoking and anti-CCP antibody status seem to be associated in RA, but PTPN22 is an independent risk factor for developing RA, according to Dr. Furst. Although not yet directly applicable to clinical care, attempts are being made to predict response to RA medications using genetic signatures or gene SNPs.

For example, 37 RA patients with the G/G polymorphism of the TNF promoter gene has been shown to have good response as measured by changes in DAS-28 to TNF antagonists. The same response was not seen in 3 RA patients with the A/A polymorphism or 14 RA patients with the A/G polymorphism. The same benefit of the G/A polymorphism on treatment response has been shown in patients with ankylosing spondylitis and psoriatic arthritis, according to Dr. Furst (Rheumatology 2007;46:93–96).

“We can't send off to [a commercial testing laboratory] to do this test at the moment. But I believe it is coming down the pike,” he noted.

For now, other factors are more practical predictors of good response. For example, low disease activity and few bony erosions at the beginning of TNF inhibitor therapy imply that early TNF use may be appropriate. When to change TNF inhibitors and whether to try another TNF blocker are practical questions that have been tested. It appears that if a patient has no response to two TNF blockers, a third TNF blocker is unlikely to be helpful and it is time to try a drug with a different mechanism of action.

Dr. Furst reported financial relationships with numerous pharmaceutical companies and the National Institutes of Health.

SDEF and this news organization are owned by Elsevier.

A related video is at www.youtube.com/InternalMedicineNews

SANTA MONICA, CALIF. — The treatment of rheumatoid arthritis has undergone a sea change, word of which has not reached beyond rheumatology in many cases.

Primary among the new rules of RA care is the admonition to use the best drug first and that “overtreatment” is good. Physicians should move more quickly to using combinations of agents, because the “data show we undertreat,” said Dr. John J. Cush, director of clinical rheumatology for the Baylor Research Institute and professor of medicine and rheumatology at Baylor University Medical Center at Dallas.

In addition to the aggressive use of disease-modifying antirheumatic drugs (DMARDs), optimal treatment of RA requires that physicians seize the opportunity to diagnose and manage cases of early disease. Many measures can be adopted to help achieve this goal, but Dr. Cush advocates the “promotion of practice policies to facilitate referral and [ensure] that every patient seeking an appointment for joint pain should be seen within 2 weeks or sooner.”

The integration of disease activity metrics can enhance outcomes by guiding treatment changes to achieve a specific goal. “Use of metrics yields a fourfold increase in remission rates,” Dr. Cush said at a meeting sponsored by

Word of the negative impact of comorbidities in RA has not spread far beyond rheumatology to primary care specialties. Given the cardiovascular disease (CVD) risks alone, physicians need to treat comorbidities in this population, he said.

RA patients develop CVD 10 years earlier than their unaffected peers, they have twice the malignancy rate of the general population, their rate of serious infection is six to nine times that of the general population, and their risk for both pulmonary disease and gastrointestinal bleeding is elevated. As a result, the life expectancy of RA patients is shorter than that of their age-matched peers (10 years shorter for women and 4 years shorter for men).

Data from the Mayo Clinic in Rochester, Minn., show that survival has improved significantly over the past decade. Research presented at the 2009 annual meeting of the American College of Rheumatology, but not yet published, indicated that survival was 70.7% among 147 RA patients who were followed in 1955–1994. In 1995–2007, survival increased to 79.5% in a group of 463 RA patients. Both patient groups were from the Olmsted County, Minn., cohort.

Earlier diagnosis and the use of methotrexate and biologic DMARDs may have contributed to this finding, Dr. Cush said.

Although many rheumatologists are enamored with the potential benefits of new biologics, they should remain resolute in their use of methotrexate, according to Dr. Cush. Findings from a recent meta-analysis suggest that the optimal methotrexate dosage may be achieved by starting at 15 mg/week orally, then escalating by 5 mg/month to a maximum dosage of 25–30 mg/week or the highest tolerable dose. In cases of insufficient response, the route of administration can be switched from oral to subcutaneous administration (Ann. Rheum. Dis. 2009;68:1094–9).

Several studies have compared methotrexate vs. tumor necrosis factor inhibitors with regard to efficacy and x-ray–protective effects. Methotrexate appears to be as potent as TNF inhibitors in terms of clinical outcomes. When x-ray outcomes are analyzed, however, the biologic has a margin of benefit over methotrexate that becomes more pronounced when the TNF inhibitor is combined with methotrexate.

Other data have documented the cost-effectiveness of therapy in early RA. Very early DMARD therapy is cost effective in reducing RA progression, but the cost-effectiveness of early biologics remains uncertain (Ann. Intern. Med. 2009;151:612–21).

If methotrexate monotherapy does not produce enough benefit, the recommended course is to add a biologic DMARD, usually a TNF inhibitor. The top five indications for the use of a TNF blocker in rheumatology are failure of methotrexate monotherapy, failure of multiple DMARDs, physician assessment of activity, presence of erosions on x-rays, and functional disability.

There is room for improvement in the treatment of RA. Remission is not common, Dr. Cush noted.

Disclosures: Dr. Cush reported being a clinical adviser, investigator, or consultant for numerous pharmaceutical companies. SDEF, Rheumatology News, and this newspaper are owned by Elsevier.

There continues to be room for improvement in rheumatoid arthritis therapy. Remission is not common.

Source DR. CUSH

SANTA MONICA, CALIF. — The treatment of rheumatoid arthritis has undergone a sea change, word of which has not reached beyond rheumatology in many cases.

Primary among the new rules of RA care is the admonition to use the best drug first and that “overtreatment” is good. Physicians should move more quickly to using combinations of agents, because the “data show we undertreat,” said Dr. John J. Cush, director of clinical rheumatology for the Baylor Research Institute and professor of medicine and rheumatology at Baylor University Medical Center at Dallas.

In addition to the aggressive use of disease-modifying antirheumatic drugs (DMARDs), optimal treatment of RA requires that physicians seize the opportunity to diagnose and manage cases of early disease. Many measures can be adopted to help achieve this goal, but Dr. Cush advocates the “promotion of practice policies to facilitate referral and [ensure] that every patient seeking an appointment for joint pain should be seen within 2 weeks or sooner.”

The integration of disease activity metrics can enhance outcomes by guiding treatment changes to achieve a specific goal. “Use of metrics yields a fourfold increase in remission rates,” Dr. Cush said at a meeting sponsored by

Word of the negative impact of comorbidities in RA has not spread far beyond rheumatology to primary care specialties. Given the cardiovascular disease (CVD) risks alone, physicians need to treat comorbidities in this population, he said.

RA patients develop CVD 10 years earlier than their unaffected peers, they have twice the malignancy rate of the general population, their rate of serious infection is six to nine times that of the general population, and their risk for both pulmonary disease and gastrointestinal bleeding is elevated. As a result, the life expectancy of RA patients is shorter than that of their age-matched peers (10 years shorter for women and 4 years shorter for men).

Data from the Mayo Clinic in Rochester, Minn., show that survival has improved significantly over the past decade. Research presented at the 2009 annual meeting of the American College of Rheumatology, but not yet published, indicated that survival was 70.7% among 147 RA patients who were followed in 1955–1994. In 1995–2007, survival increased to 79.5% in a group of 463 RA patients. Both patient groups were from the Olmsted County, Minn., cohort.

Earlier diagnosis and the use of methotrexate and biologic DMARDs may have contributed to this finding, Dr. Cush said.

Although many rheumatologists are enamored with the potential benefits of new biologics, they should remain resolute in their use of methotrexate, according to Dr. Cush. Findings from a recent meta-analysis suggest that the optimal methotrexate dosage may be achieved by starting at 15 mg/week orally, then escalating by 5 mg/month to a maximum dosage of 25–30 mg/week or the highest tolerable dose. In cases of insufficient response, the route of administration can be switched from oral to subcutaneous administration (Ann. Rheum. Dis. 2009;68:1094–9).

Several studies have compared methotrexate vs. tumor necrosis factor inhibitors with regard to efficacy and x-ray–protective effects. Methotrexate appears to be as potent as TNF inhibitors in terms of clinical outcomes. When x-ray outcomes are analyzed, however, the biologic has a margin of benefit over methotrexate that becomes more pronounced when the TNF inhibitor is combined with methotrexate.

Other data have documented the cost-effectiveness of therapy in early RA. Very early DMARD therapy is cost effective in reducing RA progression, but the cost-effectiveness of early biologics remains uncertain (Ann. Intern. Med. 2009;151:612–21).

If methotrexate monotherapy does not produce enough benefit, the recommended course is to add a biologic DMARD, usually a TNF inhibitor. The top five indications for the use of a TNF blocker in rheumatology are failure of methotrexate monotherapy, failure of multiple DMARDs, physician assessment of activity, presence of erosions on x-rays, and functional disability.

There is room for improvement in the treatment of RA. Remission is not common, Dr. Cush noted.

Disclosures: Dr. Cush reported being a clinical adviser, investigator, or consultant for numerous pharmaceutical companies. SDEF, Rheumatology News, and this newspaper are owned by Elsevier.

There continues to be room for improvement in rheumatoid arthritis therapy. Remission is not common.

Source DR. CUSH

SANTA MONICA, CALIF. — The treatment of rheumatoid arthritis has undergone a sea change, word of which has not reached beyond rheumatology in many cases.

Primary among the new rules of RA care is the admonition to use the best drug first and that “overtreatment” is good. Physicians should move more quickly to using combinations of agents, because the “data show we undertreat,” said Dr. John J. Cush, director of clinical rheumatology for the Baylor Research Institute and professor of medicine and rheumatology at Baylor University Medical Center at Dallas.

In addition to the aggressive use of disease-modifying antirheumatic drugs (DMARDs), optimal treatment of RA requires that physicians seize the opportunity to diagnose and manage cases of early disease. Many measures can be adopted to help achieve this goal, but Dr. Cush advocates the “promotion of practice policies to facilitate referral and [ensure] that every patient seeking an appointment for joint pain should be seen within 2 weeks or sooner.”

The integration of disease activity metrics can enhance outcomes by guiding treatment changes to achieve a specific goal. “Use of metrics yields a fourfold increase in remission rates,” Dr. Cush said at a meeting sponsored by

Word of the negative impact of comorbidities in RA has not spread far beyond rheumatology to primary care specialties. Given the cardiovascular disease (CVD) risks alone, physicians need to treat comorbidities in this population, he said.

RA patients develop CVD 10 years earlier than their unaffected peers, they have twice the malignancy rate of the general population, their rate of serious infection is six to nine times that of the general population, and their risk for both pulmonary disease and gastrointestinal bleeding is elevated. As a result, the life expectancy of RA patients is shorter than that of their age-matched peers (10 years shorter for women and 4 years shorter for men).

Data from the Mayo Clinic in Rochester, Minn., show that survival has improved significantly over the past decade. Research presented at the 2009 annual meeting of the American College of Rheumatology, but not yet published, indicated that survival was 70.7% among 147 RA patients who were followed in 1955–1994. In 1995–2007, survival increased to 79.5% in a group of 463 RA patients. Both patient groups were from the Olmsted County, Minn., cohort.

Earlier diagnosis and the use of methotrexate and biologic DMARDs may have contributed to this finding, Dr. Cush said.

Although many rheumatologists are enamored with the potential benefits of new biologics, they should remain resolute in their use of methotrexate, according to Dr. Cush. Findings from a recent meta-analysis suggest that the optimal methotrexate dosage may be achieved by starting at 15 mg/week orally, then escalating by 5 mg/month to a maximum dosage of 25–30 mg/week or the highest tolerable dose. In cases of insufficient response, the route of administration can be switched from oral to subcutaneous administration (Ann. Rheum. Dis. 2009;68:1094–9).

Several studies have compared methotrexate vs. tumor necrosis factor inhibitors with regard to efficacy and x-ray–protective effects. Methotrexate appears to be as potent as TNF inhibitors in terms of clinical outcomes. When x-ray outcomes are analyzed, however, the biologic has a margin of benefit over methotrexate that becomes more pronounced when the TNF inhibitor is combined with methotrexate.

Other data have documented the cost-effectiveness of therapy in early RA. Very early DMARD therapy is cost effective in reducing RA progression, but the cost-effectiveness of early biologics remains uncertain (Ann. Intern. Med. 2009;151:612–21).

If methotrexate monotherapy does not produce enough benefit, the recommended course is to add a biologic DMARD, usually a TNF inhibitor. The top five indications for the use of a TNF blocker in rheumatology are failure of methotrexate monotherapy, failure of multiple DMARDs, physician assessment of activity, presence of erosions on x-rays, and functional disability.

There is room for improvement in the treatment of RA. Remission is not common, Dr. Cush noted.

Disclosures: Dr. Cush reported being a clinical adviser, investigator, or consultant for numerous pharmaceutical companies. SDEF, Rheumatology News, and this newspaper are owned by Elsevier.

There continues to be room for improvement in rheumatoid arthritis therapy. Remission is not common.

Source DR. CUSH

New guidelines issued by the European League Against Rheumatism on the monitoring of patients with systemic lupus erythematosus offer advice for clinicians and recommendations for the design of observational studies.

The document includes recommendations on 10 components of patient monitoring. An appendix to the document contains a core set of data to be collected in routine clinical practice. Having such standardized data would be a significant help to research, according to Dr. Marta Mosca of the University of Pisa (Italy) and her fellow authors. The panel included dermatologists, rheumatologists, internists, and a nephrologist. They arrived at the following recommendations after a systematic literature review and numerous consultations:

▸ Patient assessment. Every visit should include assessments of the patient's disease activity, using a validated index; quality of life, determined either by history alone or in addition to a patient-completed measure such as a 0-10 visual analog scale; and comorbidities and drug toxicity. Organ damage should be assessed yearly.

▸ Cardiovascular risk factors. Cardiovascular disease (CVD), including related factors such as smoking, vascular events, physical activity level, oral contraceptive use, hormone therapies, and family history of CVD, should be assessed at baseline and monitored at least once a year thereafter. Similarly, lupus patients also need yearly blood tests for blood cholesterol and glucose levels as well as blood pressure measurement and determination of either body mass index or waist circumference. Patients on glucocorticoids and other lupus patients at particularly high risk for CVD may require more frequent assessment.

▸ Other comorbidities. All patients with SLE should be assessed for osteoporosis risk factors, including adequate calcium and vitamin D intake, regular exercise, and smoking habit. They should be screened and followed for osteoporosis according to either of two existing sets of guidelines: those for postmenopausal women or those for patients on glucocorticoids or other medications that reduce bone mass, such as methotrexate. Cancer screening (including Pap smears) is recommended according to guidelines for the general population.

▸ Infection risk. Lupus patients should be screened for HIV, hepatitis C virus, and hepatitis B virus, especially before the start of immunosuppressive drugs; for tuberculosis, according to local guidelines and especially before the initiation of immunosuppressive drugs; and for cytomegalovirus. Lupus patients should receive inactivated vaccines for influenza and pneumococcus in accordance with guidelines for immunosuppressed patients issued by the Centers for Disease Control and Prevention. It is ideal to do the immunization when the lupus is inactive. The use of other vaccines should be considered on a case-by-case basis. For the exact risk of infection to be determined, lupus patients should be monitored for neutropenia, severe lymphopenia, and low IgG.

▸ Frequency of assessments. Assessment every 6-12 months is adequate in patients with no disease activity, no organ damage, and no comorbidities. Preventive measures should be stressed during these visits. The committee found no data to suggest an optimal frequency of clinical and laboratory assessment in patients with lupus.

▸ Laboratory assessment. The committee recommended that baseline lab assessment include monitoring antinuclear antibody, anti–double-stranded DNA, anti-Ro, anti-La, anti-RNP, anti-Sm, antiphospholipid, C3, and C4. Reevaluation of antiphospholipid antibodies is necessary in previously negative patients prior to pregnancy, surgery, transplant, and estrogen-containing treatments, or in the presence of a new neurologic or vascular event. Before pregnancy, anti-Ro and anti-La antibodies also should be monitored. Remeasurement of anti-dsDNA and low levels of C3 or C4 may support evidence of disease activity or remission.

At 6- to 12-month intervals, patients with inactive disease should have the following lab tests: complete blood count, erythrocyte sedimentation rate, C-reactive protein, serum albumin, serum creatinine (or EGFR), urinalysis, and urine protein:creatinine ratio. Any patient on a specific drug treatment should have that drug monitored as well.

▸ Mucocutaneous involvement. Cutaneous manifestations include lupus erythematosus (LE)–specific lesions, including acute cutaneous LE (CLE), subacute CLE, chronic CLE, and intermittent CLE lesions, and LE-nonspecific lesions. Many conditions may mimic LE and therefore may require an evaluation by an experienced dermatologist as well as a skin biopsy for histologic analysis. Follow-up rebiopsy is recommended if there is a change in the clinical morphology of the lesions, or if there is a lack of response to treatment.

▸ Kidney. Patients with a persistently abnormal urinalysis or raised serum creatinine should have urine protein:creatinine ratio tests, urine microscopy, and renal ultrasound, and should be considered for biopsy referral. Patients with established nephropathy should have protein:creatinine ratio and immunologic tests, urine microscopy, and blood pressure evaluations at least every 3 months for the first 2-3 years. Patients with established chronic renal disease should be followed according to the National Kidney Foundation guidelines for chronic kidney disease (www.kidney.org).

▸ Neuropsychiatric manifestations. Neurologic involvement (central, peripheral, or autonomic) occurs frequently in SLE. The most frequent syndromes observed are headache, mood disorders, seizures, cognitive impairment, and cerebrovascular disease. The assessment of neurologic symptoms is difficult and no specific instrument has been evaluated in clinical practice. Therefore, the guidelines recommend that patients should be monitored by clinical history. Cognitive impairment may be assessed by evaluating memory, attention, concentration, and word-finding difficulties (Ann. Rheum. Dis. 2009 Nov. 5 [doi:10.1136/ard.2009.117200]).

▸ Eye assessment. The incidence of retinopathy among SLE patients who are treated with antimalarial drugs is low (0.5%). Risk factors are age older than 60 years, presence of macular degeneration, retinal dystrophy, obesity, liver disease, renal insufficiency, duration of therapy longer than 5 years, daily dose of hydroxychloroquine greater than 6.5 mg/kg, or chloroquine greater than 3 mg/kg. Recommendations on screening for antimalarial retinopathy include a baseline eye assessment according to published guidelines (Ophthalmology 2002;109:1377-82).

Thereafter, in low-risk patients, no further testing is required for the next 5 years; after the first 5 years of treatment, eye assessment is recommended yearly. In high-risk patients, an eye assessment is recommended yearly. In addition, an eye assessment may be required if there are symptoms suggesting eye involvement by lupus.

In most cases, anything left out of these recommendations should be considered part of standard good clinical practice. In some cases, items were not addressed because of contradictory evidence, wrote the authors, who also included an agenda for future research.

New guidelines issued by the European League Against Rheumatism on the monitoring of patients with systemic lupus erythematosus offer advice for clinicians and recommendations for the design of observational studies.

The document includes recommendations on 10 components of patient monitoring. An appendix to the document contains a core set of data to be collected in routine clinical practice. Having such standardized data would be a significant help to research, according to Dr. Marta Mosca of the University of Pisa (Italy) and her fellow authors. The panel included dermatologists, rheumatologists, internists, and a nephrologist. They arrived at the following recommendations after a systematic literature review and numerous consultations:

▸ Patient assessment. Every visit should include assessments of the patient's disease activity, using a validated index; quality of life, determined either by history alone or in addition to a patient-completed measure such as a 0-10 visual analog scale; and comorbidities and drug toxicity. Organ damage should be assessed yearly.

▸ Cardiovascular risk factors. Cardiovascular disease (CVD), including related factors such as smoking, vascular events, physical activity level, oral contraceptive use, hormone therapies, and family history of CVD, should be assessed at baseline and monitored at least once a year thereafter. Similarly, lupus patients also need yearly blood tests for blood cholesterol and glucose levels as well as blood pressure measurement and determination of either body mass index or waist circumference. Patients on glucocorticoids and other lupus patients at particularly high risk for CVD may require more frequent assessment.

▸ Other comorbidities. All patients with SLE should be assessed for osteoporosis risk factors, including adequate calcium and vitamin D intake, regular exercise, and smoking habit. They should be screened and followed for osteoporosis according to either of two existing sets of guidelines: those for postmenopausal women or those for patients on glucocorticoids or other medications that reduce bone mass, such as methotrexate. Cancer screening (including Pap smears) is recommended according to guidelines for the general population.

▸ Infection risk. Lupus patients should be screened for HIV, hepatitis C virus, and hepatitis B virus, especially before the start of immunosuppressive drugs; for tuberculosis, according to local guidelines and especially before the initiation of immunosuppressive drugs; and for cytomegalovirus. Lupus patients should receive inactivated vaccines for influenza and pneumococcus in accordance with guidelines for immunosuppressed patients issued by the Centers for Disease Control and Prevention. It is ideal to do the immunization when the lupus is inactive. The use of other vaccines should be considered on a case-by-case basis. For the exact risk of infection to be determined, lupus patients should be monitored for neutropenia, severe lymphopenia, and low IgG.

▸ Frequency of assessments. Assessment every 6-12 months is adequate in patients with no disease activity, no organ damage, and no comorbidities. Preventive measures should be stressed during these visits. The committee found no data to suggest an optimal frequency of clinical and laboratory assessment in patients with lupus.

▸ Laboratory assessment. The committee recommended that baseline lab assessment include monitoring antinuclear antibody, anti–double-stranded DNA, anti-Ro, anti-La, anti-RNP, anti-Sm, antiphospholipid, C3, and C4. Reevaluation of antiphospholipid antibodies is necessary in previously negative patients prior to pregnancy, surgery, transplant, and estrogen-containing treatments, or in the presence of a new neurologic or vascular event. Before pregnancy, anti-Ro and anti-La antibodies also should be monitored. Remeasurement of anti-dsDNA and low levels of C3 or C4 may support evidence of disease activity or remission.

At 6- to 12-month intervals, patients with inactive disease should have the following lab tests: complete blood count, erythrocyte sedimentation rate, C-reactive protein, serum albumin, serum creatinine (or EGFR), urinalysis, and urine protein:creatinine ratio. Any patient on a specific drug treatment should have that drug monitored as well.

▸ Mucocutaneous involvement. Cutaneous manifestations include lupus erythematosus (LE)–specific lesions, including acute cutaneous LE (CLE), subacute CLE, chronic CLE, and intermittent CLE lesions, and LE-nonspecific lesions. Many conditions may mimic LE and therefore may require an evaluation by an experienced dermatologist as well as a skin biopsy for histologic analysis. Follow-up rebiopsy is recommended if there is a change in the clinical morphology of the lesions, or if there is a lack of response to treatment.

▸ Kidney. Patients with a persistently abnormal urinalysis or raised serum creatinine should have urine protein:creatinine ratio tests, urine microscopy, and renal ultrasound, and should be considered for biopsy referral. Patients with established nephropathy should have protein:creatinine ratio and immunologic tests, urine microscopy, and blood pressure evaluations at least every 3 months for the first 2-3 years. Patients with established chronic renal disease should be followed according to the National Kidney Foundation guidelines for chronic kidney disease (www.kidney.org).

▸ Neuropsychiatric manifestations. Neurologic involvement (central, peripheral, or autonomic) occurs frequently in SLE. The most frequent syndromes observed are headache, mood disorders, seizures, cognitive impairment, and cerebrovascular disease. The assessment of neurologic symptoms is difficult and no specific instrument has been evaluated in clinical practice. Therefore, the guidelines recommend that patients should be monitored by clinical history. Cognitive impairment may be assessed by evaluating memory, attention, concentration, and word-finding difficulties (Ann. Rheum. Dis. 2009 Nov. 5 [doi:10.1136/ard.2009.117200]).

▸ Eye assessment. The incidence of retinopathy among SLE patients who are treated with antimalarial drugs is low (0.5%). Risk factors are age older than 60 years, presence of macular degeneration, retinal dystrophy, obesity, liver disease, renal insufficiency, duration of therapy longer than 5 years, daily dose of hydroxychloroquine greater than 6.5 mg/kg, or chloroquine greater than 3 mg/kg. Recommendations on screening for antimalarial retinopathy include a baseline eye assessment according to published guidelines (Ophthalmology 2002;109:1377-82).

Thereafter, in low-risk patients, no further testing is required for the next 5 years; after the first 5 years of treatment, eye assessment is recommended yearly. In high-risk patients, an eye assessment is recommended yearly. In addition, an eye assessment may be required if there are symptoms suggesting eye involvement by lupus.

In most cases, anything left out of these recommendations should be considered part of standard good clinical practice. In some cases, items were not addressed because of contradictory evidence, wrote the authors, who also included an agenda for future research.

New guidelines issued by the European League Against Rheumatism on the monitoring of patients with systemic lupus erythematosus offer advice for clinicians and recommendations for the design of observational studies.

The document includes recommendations on 10 components of patient monitoring. An appendix to the document contains a core set of data to be collected in routine clinical practice. Having such standardized data would be a significant help to research, according to Dr. Marta Mosca of the University of Pisa (Italy) and her fellow authors. The panel included dermatologists, rheumatologists, internists, and a nephrologist. They arrived at the following recommendations after a systematic literature review and numerous consultations:

▸ Patient assessment. Every visit should include assessments of the patient's disease activity, using a validated index; quality of life, determined either by history alone or in addition to a patient-completed measure such as a 0-10 visual analog scale; and comorbidities and drug toxicity. Organ damage should be assessed yearly.

▸ Cardiovascular risk factors. Cardiovascular disease (CVD), including related factors such as smoking, vascular events, physical activity level, oral contraceptive use, hormone therapies, and family history of CVD, should be assessed at baseline and monitored at least once a year thereafter. Similarly, lupus patients also need yearly blood tests for blood cholesterol and glucose levels as well as blood pressure measurement and determination of either body mass index or waist circumference. Patients on glucocorticoids and other lupus patients at particularly high risk for CVD may require more frequent assessment.

▸ Other comorbidities. All patients with SLE should be assessed for osteoporosis risk factors, including adequate calcium and vitamin D intake, regular exercise, and smoking habit. They should be screened and followed for osteoporosis according to either of two existing sets of guidelines: those for postmenopausal women or those for patients on glucocorticoids or other medications that reduce bone mass, such as methotrexate. Cancer screening (including Pap smears) is recommended according to guidelines for the general population.

▸ Infection risk. Lupus patients should be screened for HIV, hepatitis C virus, and hepatitis B virus, especially before the start of immunosuppressive drugs; for tuberculosis, according to local guidelines and especially before the initiation of immunosuppressive drugs; and for cytomegalovirus. Lupus patients should receive inactivated vaccines for influenza and pneumococcus in accordance with guidelines for immunosuppressed patients issued by the Centers for Disease Control and Prevention. It is ideal to do the immunization when the lupus is inactive. The use of other vaccines should be considered on a case-by-case basis. For the exact risk of infection to be determined, lupus patients should be monitored for neutropenia, severe lymphopenia, and low IgG.

▸ Frequency of assessments. Assessment every 6-12 months is adequate in patients with no disease activity, no organ damage, and no comorbidities. Preventive measures should be stressed during these visits. The committee found no data to suggest an optimal frequency of clinical and laboratory assessment in patients with lupus.

▸ Laboratory assessment. The committee recommended that baseline lab assessment include monitoring antinuclear antibody, anti–double-stranded DNA, anti-Ro, anti-La, anti-RNP, anti-Sm, antiphospholipid, C3, and C4. Reevaluation of antiphospholipid antibodies is necessary in previously negative patients prior to pregnancy, surgery, transplant, and estrogen-containing treatments, or in the presence of a new neurologic or vascular event. Before pregnancy, anti-Ro and anti-La antibodies also should be monitored. Remeasurement of anti-dsDNA and low levels of C3 or C4 may support evidence of disease activity or remission.

At 6- to 12-month intervals, patients with inactive disease should have the following lab tests: complete blood count, erythrocyte sedimentation rate, C-reactive protein, serum albumin, serum creatinine (or EGFR), urinalysis, and urine protein:creatinine ratio. Any patient on a specific drug treatment should have that drug monitored as well.

▸ Mucocutaneous involvement. Cutaneous manifestations include lupus erythematosus (LE)–specific lesions, including acute cutaneous LE (CLE), subacute CLE, chronic CLE, and intermittent CLE lesions, and LE-nonspecific lesions. Many conditions may mimic LE and therefore may require an evaluation by an experienced dermatologist as well as a skin biopsy for histologic analysis. Follow-up rebiopsy is recommended if there is a change in the clinical morphology of the lesions, or if there is a lack of response to treatment.

▸ Kidney. Patients with a persistently abnormal urinalysis or raised serum creatinine should have urine protein:creatinine ratio tests, urine microscopy, and renal ultrasound, and should be considered for biopsy referral. Patients with established nephropathy should have protein:creatinine ratio and immunologic tests, urine microscopy, and blood pressure evaluations at least every 3 months for the first 2-3 years. Patients with established chronic renal disease should be followed according to the National Kidney Foundation guidelines for chronic kidney disease (www.kidney.org).

▸ Neuropsychiatric manifestations. Neurologic involvement (central, peripheral, or autonomic) occurs frequently in SLE. The most frequent syndromes observed are headache, mood disorders, seizures, cognitive impairment, and cerebrovascular disease. The assessment of neurologic symptoms is difficult and no specific instrument has been evaluated in clinical practice. Therefore, the guidelines recommend that patients should be monitored by clinical history. Cognitive impairment may be assessed by evaluating memory, attention, concentration, and word-finding difficulties (Ann. Rheum. Dis. 2009 Nov. 5 [doi:10.1136/ard.2009.117200]).

▸ Eye assessment. The incidence of retinopathy among SLE patients who are treated with antimalarial drugs is low (0.5%). Risk factors are age older than 60 years, presence of macular degeneration, retinal dystrophy, obesity, liver disease, renal insufficiency, duration of therapy longer than 5 years, daily dose of hydroxychloroquine greater than 6.5 mg/kg, or chloroquine greater than 3 mg/kg. Recommendations on screening for antimalarial retinopathy include a baseline eye assessment according to published guidelines (Ophthalmology 2002;109:1377-82).

Thereafter, in low-risk patients, no further testing is required for the next 5 years; after the first 5 years of treatment, eye assessment is recommended yearly. In high-risk patients, an eye assessment is recommended yearly. In addition, an eye assessment may be required if there are symptoms suggesting eye involvement by lupus.

In most cases, anything left out of these recommendations should be considered part of standard good clinical practice. In some cases, items were not addressed because of contradictory evidence, wrote the authors, who also included an agenda for future research.