PRD 2016

LAS VEGAS – For patients with mild to moderate systemic lupus erythematosus, don’t go above six milligrams of prednisone daily, because the treatment is likely to be worse than the disease in the long run, said Michelle Petri, MD.

Speaking at the annual Perspectives in Rheumatic Diseases presented by Global Academy for Medical Education, Dr. Petri shared evidence-backed clinical pearls to help rheumatologists dial in good disease control for their systemic lupus erythematosus (SLE) patients without turning to too much prednisone.

Kari Oakes/Frontline Medical News

[email protected]

On Twitter @karioakes

LAS VEGAS – For patients with mild to moderate systemic lupus erythematosus, don’t go above six milligrams of prednisone daily, because the treatment is likely to be worse than the disease in the long run, said Michelle Petri, MD.

Speaking at the annual Perspectives in Rheumatic Diseases presented by Global Academy for Medical Education, Dr. Petri shared evidence-backed clinical pearls to help rheumatologists dial in good disease control for their systemic lupus erythematosus (SLE) patients without turning to too much prednisone.

Kari Oakes/Frontline Medical News

[email protected]

On Twitter @karioakes

LAS VEGAS – For patients with mild to moderate systemic lupus erythematosus, don’t go above six milligrams of prednisone daily, because the treatment is likely to be worse than the disease in the long run, said Michelle Petri, MD.

Speaking at the annual Perspectives in Rheumatic Diseases presented by Global Academy for Medical Education, Dr. Petri shared evidence-backed clinical pearls to help rheumatologists dial in good disease control for their systemic lupus erythematosus (SLE) patients without turning to too much prednisone.

Kari Oakes/Frontline Medical News

[email protected]

On Twitter @karioakes

LAS VEGAS – Patients with rheumatoid arthritis who have pulmonary symptoms and a restrictive pulmonary function test pattern have a high likelihood for a diagnosis of interstitial lung disease, making it necessary to put it high on the differential and to begin working collaboratively with pulmonologists, according to Jon T. Giles, MD.

Overall, 8%-15% of RA patients will develop clinically significant interstitial lung disease (ILD), although radiographic evidence of ILD can be seen in up to half of RA patients, and in one study about one in four patients had evidence of ILD on CT scanning within 2 years of RA diagnosis. The overall risk for RA patients to develop ILD has been shown to be nine times higher than for matched controls (Arthritis Rheum. 2010 Jun;62[6]:1583-91), Dr. Giles said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

An “alphabet soup” of ILD subtypes

Though there’s an “alphabet soup” of subtypes of ILD in RA, 90% of RA patients with ILD will have one of two conditions: usual interstitial pneumonitis (RA-UIP) or nonspecific interstitial pneumonitis (RA-NSIP). It’s not entirely clear whether one type of RA-ILD has a survival advantage over the other, Dr. Giles said.

Care for RA patients should include screening for ILD, said Dr. Giles. Physicians should ask about dry cough, dyspnea, and decreased exercise tolerance. Signs of ILD can include diminished oxygen saturation, a cardiac exam consistent with right heart disease, and rales. It’s not clear, he said, whether periodic chest radiographs or pulmonary function testing in asymptomatic RA patients is warranted.

Positive findings should prompt pulmonary function testing to include DLCO (diffusing capacity of lung for carbon monoxide), which may or may not be reduced in patients with clinically significant ILD. However, testing will show a restrictive pattern. A high-resolution chest CT should also be obtained.

Further evaluation should be done collaboratively with pulmonologists, and preferably with an ILD center, said Dr. Giles. A bronchoalveolar lavage and/or a lung biopsy may be considered.

Radiographic features of RA-UIP can include reticulation and honeycombing, predominantly seen in a subpleural and basilar distribution. Traction bronchiectasis may or may not be present. If a biopsy is performed, the histologic presentation of RA-UIP includes subpleural patches of dense fibrosis and honeycombing adjacent to healthy lung tissue; fibroblastic foci may be seen in the fibrotic regions.

In differentiating RA-UIP from interstitial pulmonary fibrosis (IPF), Dr. Giles said that lymphoid hyperplasia with germinal centers and peribronchial lesions are both more common in RA-UIP than in IPF. By contrast, fibroblastic foci are less common in RA-UIP than in IPF.

Sorting out the relationship between the use of disease-modifying antirheumatic drugs and ILD in RA is complicated by “complexities of attribution,” said Dr. Giles, since “RA patients with the most severe or refractory disease are more likely to both be exposed to a great number of RA therapies and higher doses and more combinations, and to have more risk factors for ILD.” Additionally, hypersensitivity pneumonitis can share some features with some subtypes of RA-ILD.

Treatment goals

Beyond maximizing smoking-cessation intervention, which should be done for all currently smoking ILD patients, treatment goals for RA-ILD are “a balancing act,” Dr. Giles said. Immunizations should be up to date for all RA-ILD patients, and any concomitant pulmonary conditions, such as asthma or chronic obstructive pulmonary disorder, should also be optimally treated. An early evaluation for lung transplant is warranted for RA-ILD as well, he said.

If patients are symptomatic, then the goal is symptom reduction, with the extent of radiographically or histologically documented involvement and the rate of decline to be factored into treatment decisions.

Immunosuppressive treatments for RA-ILD, Dr. Giles said, “are not supported by any randomized clinical trials.” However, corticosteroids are often effective for RA-NSIP; “UIP is often not steroid responsive,” he said. Other agents can include azathioprine, which can give a “double whammy” effect by addressing joint and lung disease. However, azathioprine should not be used concurrently with corticosteroids, he said.

Mycophenolate mofetil (CellCept) has known antifibrotic effects, and there have been case reports of improvement in RA-ILD. Cyclophosphamide is also occasionally used. A host of other treatments have been attempted, including the antifibrotics pirfenidone (Esbriet) and nintedanib (Ofev), although these have been studied only in interstitial pulmonary fibrosis, said Dr. Giles. “Treating symptomatic RA-ILD is always a challenge,” he said.

Dr. Giles has been a consultant to Roche/Genentech and Proximagen and has received grant funding from Pfizer.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Patients with rheumatoid arthritis who have pulmonary symptoms and a restrictive pulmonary function test pattern have a high likelihood for a diagnosis of interstitial lung disease, making it necessary to put it high on the differential and to begin working collaboratively with pulmonologists, according to Jon T. Giles, MD.

Overall, 8%-15% of RA patients will develop clinically significant interstitial lung disease (ILD), although radiographic evidence of ILD can be seen in up to half of RA patients, and in one study about one in four patients had evidence of ILD on CT scanning within 2 years of RA diagnosis. The overall risk for RA patients to develop ILD has been shown to be nine times higher than for matched controls (Arthritis Rheum. 2010 Jun;62[6]:1583-91), Dr. Giles said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

An “alphabet soup” of ILD subtypes

Though there’s an “alphabet soup” of subtypes of ILD in RA, 90% of RA patients with ILD will have one of two conditions: usual interstitial pneumonitis (RA-UIP) or nonspecific interstitial pneumonitis (RA-NSIP). It’s not entirely clear whether one type of RA-ILD has a survival advantage over the other, Dr. Giles said.

Care for RA patients should include screening for ILD, said Dr. Giles. Physicians should ask about dry cough, dyspnea, and decreased exercise tolerance. Signs of ILD can include diminished oxygen saturation, a cardiac exam consistent with right heart disease, and rales. It’s not clear, he said, whether periodic chest radiographs or pulmonary function testing in asymptomatic RA patients is warranted.

Positive findings should prompt pulmonary function testing to include DLCO (diffusing capacity of lung for carbon monoxide), which may or may not be reduced in patients with clinically significant ILD. However, testing will show a restrictive pattern. A high-resolution chest CT should also be obtained.

Further evaluation should be done collaboratively with pulmonologists, and preferably with an ILD center, said Dr. Giles. A bronchoalveolar lavage and/or a lung biopsy may be considered.

Radiographic features of RA-UIP can include reticulation and honeycombing, predominantly seen in a subpleural and basilar distribution. Traction bronchiectasis may or may not be present. If a biopsy is performed, the histologic presentation of RA-UIP includes subpleural patches of dense fibrosis and honeycombing adjacent to healthy lung tissue; fibroblastic foci may be seen in the fibrotic regions.

In differentiating RA-UIP from interstitial pulmonary fibrosis (IPF), Dr. Giles said that lymphoid hyperplasia with germinal centers and peribronchial lesions are both more common in RA-UIP than in IPF. By contrast, fibroblastic foci are less common in RA-UIP than in IPF.

Sorting out the relationship between the use of disease-modifying antirheumatic drugs and ILD in RA is complicated by “complexities of attribution,” said Dr. Giles, since “RA patients with the most severe or refractory disease are more likely to both be exposed to a great number of RA therapies and higher doses and more combinations, and to have more risk factors for ILD.” Additionally, hypersensitivity pneumonitis can share some features with some subtypes of RA-ILD.

Treatment goals

Beyond maximizing smoking-cessation intervention, which should be done for all currently smoking ILD patients, treatment goals for RA-ILD are “a balancing act,” Dr. Giles said. Immunizations should be up to date for all RA-ILD patients, and any concomitant pulmonary conditions, such as asthma or chronic obstructive pulmonary disorder, should also be optimally treated. An early evaluation for lung transplant is warranted for RA-ILD as well, he said.

If patients are symptomatic, then the goal is symptom reduction, with the extent of radiographically or histologically documented involvement and the rate of decline to be factored into treatment decisions.

Immunosuppressive treatments for RA-ILD, Dr. Giles said, “are not supported by any randomized clinical trials.” However, corticosteroids are often effective for RA-NSIP; “UIP is often not steroid responsive,” he said. Other agents can include azathioprine, which can give a “double whammy” effect by addressing joint and lung disease. However, azathioprine should not be used concurrently with corticosteroids, he said.

Mycophenolate mofetil (CellCept) has known antifibrotic effects, and there have been case reports of improvement in RA-ILD. Cyclophosphamide is also occasionally used. A host of other treatments have been attempted, including the antifibrotics pirfenidone (Esbriet) and nintedanib (Ofev), although these have been studied only in interstitial pulmonary fibrosis, said Dr. Giles. “Treating symptomatic RA-ILD is always a challenge,” he said.

Dr. Giles has been a consultant to Roche/Genentech and Proximagen and has received grant funding from Pfizer.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Patients with rheumatoid arthritis who have pulmonary symptoms and a restrictive pulmonary function test pattern have a high likelihood for a diagnosis of interstitial lung disease, making it necessary to put it high on the differential and to begin working collaboratively with pulmonologists, according to Jon T. Giles, MD.

Overall, 8%-15% of RA patients will develop clinically significant interstitial lung disease (ILD), although radiographic evidence of ILD can be seen in up to half of RA patients, and in one study about one in four patients had evidence of ILD on CT scanning within 2 years of RA diagnosis. The overall risk for RA patients to develop ILD has been shown to be nine times higher than for matched controls (Arthritis Rheum. 2010 Jun;62[6]:1583-91), Dr. Giles said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

An “alphabet soup” of ILD subtypes

Though there’s an “alphabet soup” of subtypes of ILD in RA, 90% of RA patients with ILD will have one of two conditions: usual interstitial pneumonitis (RA-UIP) or nonspecific interstitial pneumonitis (RA-NSIP). It’s not entirely clear whether one type of RA-ILD has a survival advantage over the other, Dr. Giles said.

Care for RA patients should include screening for ILD, said Dr. Giles. Physicians should ask about dry cough, dyspnea, and decreased exercise tolerance. Signs of ILD can include diminished oxygen saturation, a cardiac exam consistent with right heart disease, and rales. It’s not clear, he said, whether periodic chest radiographs or pulmonary function testing in asymptomatic RA patients is warranted.

Positive findings should prompt pulmonary function testing to include DLCO (diffusing capacity of lung for carbon monoxide), which may or may not be reduced in patients with clinically significant ILD. However, testing will show a restrictive pattern. A high-resolution chest CT should also be obtained.

Further evaluation should be done collaboratively with pulmonologists, and preferably with an ILD center, said Dr. Giles. A bronchoalveolar lavage and/or a lung biopsy may be considered.

Radiographic features of RA-UIP can include reticulation and honeycombing, predominantly seen in a subpleural and basilar distribution. Traction bronchiectasis may or may not be present. If a biopsy is performed, the histologic presentation of RA-UIP includes subpleural patches of dense fibrosis and honeycombing adjacent to healthy lung tissue; fibroblastic foci may be seen in the fibrotic regions.

In differentiating RA-UIP from interstitial pulmonary fibrosis (IPF), Dr. Giles said that lymphoid hyperplasia with germinal centers and peribronchial lesions are both more common in RA-UIP than in IPF. By contrast, fibroblastic foci are less common in RA-UIP than in IPF.

Sorting out the relationship between the use of disease-modifying antirheumatic drugs and ILD in RA is complicated by “complexities of attribution,” said Dr. Giles, since “RA patients with the most severe or refractory disease are more likely to both be exposed to a great number of RA therapies and higher doses and more combinations, and to have more risk factors for ILD.” Additionally, hypersensitivity pneumonitis can share some features with some subtypes of RA-ILD.

Treatment goals

Beyond maximizing smoking-cessation intervention, which should be done for all currently smoking ILD patients, treatment goals for RA-ILD are “a balancing act,” Dr. Giles said. Immunizations should be up to date for all RA-ILD patients, and any concomitant pulmonary conditions, such as asthma or chronic obstructive pulmonary disorder, should also be optimally treated. An early evaluation for lung transplant is warranted for RA-ILD as well, he said.

If patients are symptomatic, then the goal is symptom reduction, with the extent of radiographically or histologically documented involvement and the rate of decline to be factored into treatment decisions.

Immunosuppressive treatments for RA-ILD, Dr. Giles said, “are not supported by any randomized clinical trials.” However, corticosteroids are often effective for RA-NSIP; “UIP is often not steroid responsive,” he said. Other agents can include azathioprine, which can give a “double whammy” effect by addressing joint and lung disease. However, azathioprine should not be used concurrently with corticosteroids, he said.

Mycophenolate mofetil (CellCept) has known antifibrotic effects, and there have been case reports of improvement in RA-ILD. Cyclophosphamide is also occasionally used. A host of other treatments have been attempted, including the antifibrotics pirfenidone (Esbriet) and nintedanib (Ofev), although these have been studied only in interstitial pulmonary fibrosis, said Dr. Giles. “Treating symptomatic RA-ILD is always a challenge,” he said.

Dr. Giles has been a consultant to Roche/Genentech and Proximagen and has received grant funding from Pfizer.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Patients with systemic sclerosis, mixed connective tissue disease, and Ehlers-Danlos syndrome who have a gastrointestinal symptom cluster that includes bloating, early satiety, and postprandial “brain fog” may be suffering from small intestine bacterial overgrowth, or SIBO.

This treatable condition occurs when enteric flora from the colon creep north into the small intestine, which is usually a relatively sterile environment. In addition to the bloating, dyspepsia, and nausea that SIBO can cause, patients may have an erratic bowel movement pattern, and can occasionally suffer from vitamin deficiencies and weight loss, Ali Rezaie, MD, said at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

“SIBO is not a primary disease,” said Dr. Rezaie, professor of gastroenterology at Cedars-Sinai Medical Center, Los Angeles, and lead author of a 2016 review on the diagnosis and treatment of SIBO (Curr Gastroenterol Rep. 2016 Feb;18[2]:8).

For patients with scleroderma or mixed connective tissue diseases as well as hypermobility disorders such as Ehlers-Danlos syndrome, the small bowel dysmotility associated with their conditions is often the primary disease. However, diabetes-associated gastroparesis and the presence of anti-vinculin and anti-CdtB antibodies in irritable bowel syndrome patients can also cause dysmotility, provoking SIBO.

Surgical procedures that can set patients up for SIBO include gastric bypass and ileocecal resection; medications such as opioids and anticholinergic or antidiarrheal medications also can be SIBO risk factors. Finally, chronic proton pump inhibitor use, autoimmune gastritis, and gastrectomy can all reduce gastric acid secretion, permitting bacterial overgrowth in the small intestine.

Normally, jejunal contents have around 100 colony-forming units (CFU) per mL, with Lactobacillus and Streptococcus predominating. However, in SIBO, there are more bacteria in the small intestine – greater than 1,000 CFU/mL – and enteric flora predominate.

Depending on the species predominating, an excess of hydrogen or methane may be produced during bacterial fermentation of food in the small intestine, Dr. Rezaie said. Though the preferred method for diagnosis is small-bowel aspiration, “this is an invasive, costly, and time-consuming procedure,” he said.

By contrast, breath testing is noninvasive and inexpensive, and detects excess levels of hydrogen or methane on the breath when performed at a fixed time after the patient is fed a bolus of lactulose or glucose. The test is diagnostic for SIBO because “the sole source of methane and hydrogen [as H₂] in our body is from the bacterial metabolism,” Dr. Rezaie said.

SIBO breath testing is considered positive if there are 10 or greater parts per million of methane at any time point, or if hydrogen levels rise by at least 20 parts per million within 90 minutes of the bolus feed.

The treatment for SIBO can be thought of in three phases, Dr. Rezaie said in an interview, referencing the consensus statement. The three treatment stages include induction of remission, maintenance of remission, and treatment of recurrence, should it recur.

Therapy for induction of remission is guided by the breath test results. If excessive methane production is not detected, then a broad-spectrum antibiotic such as amoxicillin, ciprofloxacin, trimethoprim-sulfamethoxazole, or rifaximin can be given for 14 days. If excess methane is detected, then the broad spectrum antibiotic should be combined with neomycin 500 mg by mouth for 14 days as well.

If a clinical response occurs, then a maintenance strategy can include restricting highly fermentable foods, using promotility drugs such as low-dose macrolides, tegaserod, or other 5HT₄ agonists, and ongoing vigilance for recurrent symptoms. If there’s a primary cause that can be remedied – for example, stopping a proton pump inhibitor or lysing identifiable intestinal lesions – then those factors can be addressed during remission as well.

For patients who can’t be brought into remission with one antibiotic course, another course of alternative antibiotics can be considered. Some patients may benefit from an elemental diet.

Managing recurrences involves further rounds of antibiotics together with optimizing motility and addressing other risk factors.

In terms of how SIBO affects management of the primary rheumatologic disease, patients should try to avoid frequent use of nonsteroidal anti-inflammatory drugs because of the potential for further untoward effects on a disrupted gut. However, there’s no reason to alter medical therapy otherwise, and biologic therapy “is generally well-tolerated in patients with small intestine bacterial overgrowth,” Dr. Rezaie said.

He pointed out that rheumatology patients can have so many medical issues that gastrointestinal symptoms may not rise to the surface, so a thorough review of systems should include careful questioning about digestive health. “Rheumatologists need to incorporate this knowledge into the management of their patients,” he said. “It’s a quality of life issue.”

Dr. Rezaie reported having received honoraria and consulted for Valeant Pharmaceuticals. Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Patients with systemic sclerosis, mixed connective tissue disease, and Ehlers-Danlos syndrome who have a gastrointestinal symptom cluster that includes bloating, early satiety, and postprandial “brain fog” may be suffering from small intestine bacterial overgrowth, or SIBO.

This treatable condition occurs when enteric flora from the colon creep north into the small intestine, which is usually a relatively sterile environment. In addition to the bloating, dyspepsia, and nausea that SIBO can cause, patients may have an erratic bowel movement pattern, and can occasionally suffer from vitamin deficiencies and weight loss, Ali Rezaie, MD, said at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

“SIBO is not a primary disease,” said Dr. Rezaie, professor of gastroenterology at Cedars-Sinai Medical Center, Los Angeles, and lead author of a 2016 review on the diagnosis and treatment of SIBO (Curr Gastroenterol Rep. 2016 Feb;18[2]:8).

For patients with scleroderma or mixed connective tissue diseases as well as hypermobility disorders such as Ehlers-Danlos syndrome, the small bowel dysmotility associated with their conditions is often the primary disease. However, diabetes-associated gastroparesis and the presence of anti-vinculin and anti-CdtB antibodies in irritable bowel syndrome patients can also cause dysmotility, provoking SIBO.

Surgical procedures that can set patients up for SIBO include gastric bypass and ileocecal resection; medications such as opioids and anticholinergic or antidiarrheal medications also can be SIBO risk factors. Finally, chronic proton pump inhibitor use, autoimmune gastritis, and gastrectomy can all reduce gastric acid secretion, permitting bacterial overgrowth in the small intestine.

Normally, jejunal contents have around 100 colony-forming units (CFU) per mL, with Lactobacillus and Streptococcus predominating. However, in SIBO, there are more bacteria in the small intestine – greater than 1,000 CFU/mL – and enteric flora predominate.

Depending on the species predominating, an excess of hydrogen or methane may be produced during bacterial fermentation of food in the small intestine, Dr. Rezaie said. Though the preferred method for diagnosis is small-bowel aspiration, “this is an invasive, costly, and time-consuming procedure,” he said.

By contrast, breath testing is noninvasive and inexpensive, and detects excess levels of hydrogen or methane on the breath when performed at a fixed time after the patient is fed a bolus of lactulose or glucose. The test is diagnostic for SIBO because “the sole source of methane and hydrogen [as H₂] in our body is from the bacterial metabolism,” Dr. Rezaie said.

SIBO breath testing is considered positive if there are 10 or greater parts per million of methane at any time point, or if hydrogen levels rise by at least 20 parts per million within 90 minutes of the bolus feed.

The treatment for SIBO can be thought of in three phases, Dr. Rezaie said in an interview, referencing the consensus statement. The three treatment stages include induction of remission, maintenance of remission, and treatment of recurrence, should it recur.

Therapy for induction of remission is guided by the breath test results. If excessive methane production is not detected, then a broad-spectrum antibiotic such as amoxicillin, ciprofloxacin, trimethoprim-sulfamethoxazole, or rifaximin can be given for 14 days. If excess methane is detected, then the broad spectrum antibiotic should be combined with neomycin 500 mg by mouth for 14 days as well.

If a clinical response occurs, then a maintenance strategy can include restricting highly fermentable foods, using promotility drugs such as low-dose macrolides, tegaserod, or other 5HT₄ agonists, and ongoing vigilance for recurrent symptoms. If there’s a primary cause that can be remedied – for example, stopping a proton pump inhibitor or lysing identifiable intestinal lesions – then those factors can be addressed during remission as well.

For patients who can’t be brought into remission with one antibiotic course, another course of alternative antibiotics can be considered. Some patients may benefit from an elemental diet.

Managing recurrences involves further rounds of antibiotics together with optimizing motility and addressing other risk factors.

In terms of how SIBO affects management of the primary rheumatologic disease, patients should try to avoid frequent use of nonsteroidal anti-inflammatory drugs because of the potential for further untoward effects on a disrupted gut. However, there’s no reason to alter medical therapy otherwise, and biologic therapy “is generally well-tolerated in patients with small intestine bacterial overgrowth,” Dr. Rezaie said.

He pointed out that rheumatology patients can have so many medical issues that gastrointestinal symptoms may not rise to the surface, so a thorough review of systems should include careful questioning about digestive health. “Rheumatologists need to incorporate this knowledge into the management of their patients,” he said. “It’s a quality of life issue.”

Dr. Rezaie reported having received honoraria and consulted for Valeant Pharmaceuticals. Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Patients with systemic sclerosis, mixed connective tissue disease, and Ehlers-Danlos syndrome who have a gastrointestinal symptom cluster that includes bloating, early satiety, and postprandial “brain fog” may be suffering from small intestine bacterial overgrowth, or SIBO.

This treatable condition occurs when enteric flora from the colon creep north into the small intestine, which is usually a relatively sterile environment. In addition to the bloating, dyspepsia, and nausea that SIBO can cause, patients may have an erratic bowel movement pattern, and can occasionally suffer from vitamin deficiencies and weight loss, Ali Rezaie, MD, said at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

“SIBO is not a primary disease,” said Dr. Rezaie, professor of gastroenterology at Cedars-Sinai Medical Center, Los Angeles, and lead author of a 2016 review on the diagnosis and treatment of SIBO (Curr Gastroenterol Rep. 2016 Feb;18[2]:8).

For patients with scleroderma or mixed connective tissue diseases as well as hypermobility disorders such as Ehlers-Danlos syndrome, the small bowel dysmotility associated with their conditions is often the primary disease. However, diabetes-associated gastroparesis and the presence of anti-vinculin and anti-CdtB antibodies in irritable bowel syndrome patients can also cause dysmotility, provoking SIBO.

Surgical procedures that can set patients up for SIBO include gastric bypass and ileocecal resection; medications such as opioids and anticholinergic or antidiarrheal medications also can be SIBO risk factors. Finally, chronic proton pump inhibitor use, autoimmune gastritis, and gastrectomy can all reduce gastric acid secretion, permitting bacterial overgrowth in the small intestine.

Normally, jejunal contents have around 100 colony-forming units (CFU) per mL, with Lactobacillus and Streptococcus predominating. However, in SIBO, there are more bacteria in the small intestine – greater than 1,000 CFU/mL – and enteric flora predominate.

Depending on the species predominating, an excess of hydrogen or methane may be produced during bacterial fermentation of food in the small intestine, Dr. Rezaie said. Though the preferred method for diagnosis is small-bowel aspiration, “this is an invasive, costly, and time-consuming procedure,” he said.

By contrast, breath testing is noninvasive and inexpensive, and detects excess levels of hydrogen or methane on the breath when performed at a fixed time after the patient is fed a bolus of lactulose or glucose. The test is diagnostic for SIBO because “the sole source of methane and hydrogen [as H₂] in our body is from the bacterial metabolism,” Dr. Rezaie said.

SIBO breath testing is considered positive if there are 10 or greater parts per million of methane at any time point, or if hydrogen levels rise by at least 20 parts per million within 90 minutes of the bolus feed.

The treatment for SIBO can be thought of in three phases, Dr. Rezaie said in an interview, referencing the consensus statement. The three treatment stages include induction of remission, maintenance of remission, and treatment of recurrence, should it recur.

Therapy for induction of remission is guided by the breath test results. If excessive methane production is not detected, then a broad-spectrum antibiotic such as amoxicillin, ciprofloxacin, trimethoprim-sulfamethoxazole, or rifaximin can be given for 14 days. If excess methane is detected, then the broad spectrum antibiotic should be combined with neomycin 500 mg by mouth for 14 days as well.

If a clinical response occurs, then a maintenance strategy can include restricting highly fermentable foods, using promotility drugs such as low-dose macrolides, tegaserod, or other 5HT₄ agonists, and ongoing vigilance for recurrent symptoms. If there’s a primary cause that can be remedied – for example, stopping a proton pump inhibitor or lysing identifiable intestinal lesions – then those factors can be addressed during remission as well.

For patients who can’t be brought into remission with one antibiotic course, another course of alternative antibiotics can be considered. Some patients may benefit from an elemental diet.

Managing recurrences involves further rounds of antibiotics together with optimizing motility and addressing other risk factors.

In terms of how SIBO affects management of the primary rheumatologic disease, patients should try to avoid frequent use of nonsteroidal anti-inflammatory drugs because of the potential for further untoward effects on a disrupted gut. However, there’s no reason to alter medical therapy otherwise, and biologic therapy “is generally well-tolerated in patients with small intestine bacterial overgrowth,” Dr. Rezaie said.

He pointed out that rheumatology patients can have so many medical issues that gastrointestinal symptoms may not rise to the surface, so a thorough review of systems should include careful questioning about digestive health. “Rheumatologists need to incorporate this knowledge into the management of their patients,” he said. “It’s a quality of life issue.”

Dr. Rezaie reported having received honoraria and consulted for Valeant Pharmaceuticals. Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Pay attention to GI symptoms in your scleroderma patients. Gut involvement in scleroderma, a result of vasculopathy and fibrosis affecting the GI tract, is common and can be debilitating, said Daniel Furst, MD.

Speaking at the annual Perspectives in Rheumatologic Diseases presented by the Global Academy for Medical Education, Dr. Furst said that the progression often begins at the mouth and esophagus, and progresses through the digestive system, eventually reaching the rectum and anus.

“You think about motility issues early on, in the esophagus,” and early oral symptoms can include mouth dryness, said Dr. Furst, who is associated with the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence (Italy).

As scleroderma begins to affect the midgut, Dr. Furst said that the secondary results of the decrease in motility are symptoms such as heartburn, nausea, vomiting, and early satiety.

“When you have a decrease in motility, then the normal ... housekeeping waves of the midgut and the colon are decreased,” he said. Bacteria from the colon can then invade the small bowel, causing overgrowth of the midgut by species not normally seen there. Not only gas, but also malnutrition can eventually result, he said.

When scleroderma affects the lower gut, patients can have bloating, diarrhea, and constipation, and finally, incontinence of the bowel, a condition with often devastating psychosocial consequences.

The choice of promotility agents depends on the area affected; erythromycin and metoclopramide help in the upper GI tract, while tegaserod can be helpful in the lower gut.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Pay attention to GI symptoms in your scleroderma patients. Gut involvement in scleroderma, a result of vasculopathy and fibrosis affecting the GI tract, is common and can be debilitating, said Daniel Furst, MD.

Speaking at the annual Perspectives in Rheumatologic Diseases presented by the Global Academy for Medical Education, Dr. Furst said that the progression often begins at the mouth and esophagus, and progresses through the digestive system, eventually reaching the rectum and anus.

“You think about motility issues early on, in the esophagus,” and early oral symptoms can include mouth dryness, said Dr. Furst, who is associated with the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence (Italy).

As scleroderma begins to affect the midgut, Dr. Furst said that the secondary results of the decrease in motility are symptoms such as heartburn, nausea, vomiting, and early satiety.

“When you have a decrease in motility, then the normal ... housekeeping waves of the midgut and the colon are decreased,” he said. Bacteria from the colon can then invade the small bowel, causing overgrowth of the midgut by species not normally seen there. Not only gas, but also malnutrition can eventually result, he said.

When scleroderma affects the lower gut, patients can have bloating, diarrhea, and constipation, and finally, incontinence of the bowel, a condition with often devastating psychosocial consequences.

The choice of promotility agents depends on the area affected; erythromycin and metoclopramide help in the upper GI tract, while tegaserod can be helpful in the lower gut.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Pay attention to GI symptoms in your scleroderma patients. Gut involvement in scleroderma, a result of vasculopathy and fibrosis affecting the GI tract, is common and can be debilitating, said Daniel Furst, MD.

Speaking at the annual Perspectives in Rheumatologic Diseases presented by the Global Academy for Medical Education, Dr. Furst said that the progression often begins at the mouth and esophagus, and progresses through the digestive system, eventually reaching the rectum and anus.

“You think about motility issues early on, in the esophagus,” and early oral symptoms can include mouth dryness, said Dr. Furst, who is associated with the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence (Italy).

As scleroderma begins to affect the midgut, Dr. Furst said that the secondary results of the decrease in motility are symptoms such as heartburn, nausea, vomiting, and early satiety.

“When you have a decrease in motility, then the normal ... housekeeping waves of the midgut and the colon are decreased,” he said. Bacteria from the colon can then invade the small bowel, causing overgrowth of the midgut by species not normally seen there. Not only gas, but also malnutrition can eventually result, he said.

When scleroderma affects the lower gut, patients can have bloating, diarrhea, and constipation, and finally, incontinence of the bowel, a condition with often devastating psychosocial consequences.

The choice of promotility agents depends on the area affected; erythromycin and metoclopramide help in the upper GI tract, while tegaserod can be helpful in the lower gut.

Global Academy for Medical Education and this news organization are owned by the same parent company.

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On Twitter @karioakes

LAS VEGAS – Dermatologists need to be alert for amyotrophic dermatomyositis in patients with rash where lupus might be considered, because of the need for vigilant surveillance for cancer and lung disease in this population.

Ruth Ann Vleugels, MD, walked attendees through a series of dermatomyositis diagnostic pearls at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“When a patient has dermatomyositis but doesn’t have muscle disease, you really have to rely on the skin findings,” since you’re lacking the tipoff of muscle disease at presentation, Dr. Vleugels, professor of dermatology at Brigham and Women’s Hospital, Boston, said in an interview. This is especially true because, on biopsy, “the pathological findings are identical to that of lupus,” she said.

Dr. Vleugels emphasized that it’s important not to miss a more subtle, less violaceous heliotrope eruption, especially in lighter-skinned patients; similarly, Gottron’s papules are not always papular and limited to the knuckle pads, but can be more macular and linear, with psoriasiform scaling. Nail findings such as dilated capillary loops with dystrophic and hypertrophied cuticles are also a big clue. Photodistributed erythema – the “shawl sign” – can be subtle, but offers additional support for a dermatomyositis diagnosis.

Though the erythematous midface rash of lupus resembles a dermatomyositis rash in many ways, there’s a critical differentiator of the two rashes, Dr. Vleugels said. “In dermatomyositis patients, it very classically hugs, or involves, the nasolabial folds, whereas in our systemic lupus patients, the erythema of the cheeks spares the nasolabial folds.”

Global Academy for Medical Education and this news organization are owned by the same parent company.

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On Twitter @karioakes

LAS VEGAS – Dermatologists need to be alert for amyotrophic dermatomyositis in patients with rash where lupus might be considered, because of the need for vigilant surveillance for cancer and lung disease in this population.

Ruth Ann Vleugels, MD, walked attendees through a series of dermatomyositis diagnostic pearls at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“When a patient has dermatomyositis but doesn’t have muscle disease, you really have to rely on the skin findings,” since you’re lacking the tipoff of muscle disease at presentation, Dr. Vleugels, professor of dermatology at Brigham and Women’s Hospital, Boston, said in an interview. This is especially true because, on biopsy, “the pathological findings are identical to that of lupus,” she said.

Dr. Vleugels emphasized that it’s important not to miss a more subtle, less violaceous heliotrope eruption, especially in lighter-skinned patients; similarly, Gottron’s papules are not always papular and limited to the knuckle pads, but can be more macular and linear, with psoriasiform scaling. Nail findings such as dilated capillary loops with dystrophic and hypertrophied cuticles are also a big clue. Photodistributed erythema – the “shawl sign” – can be subtle, but offers additional support for a dermatomyositis diagnosis.

Though the erythematous midface rash of lupus resembles a dermatomyositis rash in many ways, there’s a critical differentiator of the two rashes, Dr. Vleugels said. “In dermatomyositis patients, it very classically hugs, or involves, the nasolabial folds, whereas in our systemic lupus patients, the erythema of the cheeks spares the nasolabial folds.”

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Dermatologists need to be alert for amyotrophic dermatomyositis in patients with rash where lupus might be considered, because of the need for vigilant surveillance for cancer and lung disease in this population.

Ruth Ann Vleugels, MD, walked attendees through a series of dermatomyositis diagnostic pearls at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“When a patient has dermatomyositis but doesn’t have muscle disease, you really have to rely on the skin findings,” since you’re lacking the tipoff of muscle disease at presentation, Dr. Vleugels, professor of dermatology at Brigham and Women’s Hospital, Boston, said in an interview. This is especially true because, on biopsy, “the pathological findings are identical to that of lupus,” she said.

Dr. Vleugels emphasized that it’s important not to miss a more subtle, less violaceous heliotrope eruption, especially in lighter-skinned patients; similarly, Gottron’s papules are not always papular and limited to the knuckle pads, but can be more macular and linear, with psoriasiform scaling. Nail findings such as dilated capillary loops with dystrophic and hypertrophied cuticles are also a big clue. Photodistributed erythema – the “shawl sign” – can be subtle, but offers additional support for a dermatomyositis diagnosis.

Though the erythematous midface rash of lupus resembles a dermatomyositis rash in many ways, there’s a critical differentiator of the two rashes, Dr. Vleugels said. “In dermatomyositis patients, it very classically hugs, or involves, the nasolabial folds, whereas in our systemic lupus patients, the erythema of the cheeks spares the nasolabial folds.”

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – When genetic risk and lifestyle risk factors collide with the baseline systemic inflammation of rheumatoid arthritis (RA), cardiovascular risk increases significantly. Helping patients to manage risk for cardiovascular disease (CVD) requires getting comfortable in making risk assessments and counseling patients about medication and lifestyle options, especially for patients who are not actively being managed by primary care physicians.

Jon Giles, MD, said that a large portion of the elevated risk for CVD in patients with RA is “driven by the fact that [RA] patients have more atherosclerosis.”

Dr. Giles, professor of medicine at Columbia University, New York, said that other CVD risk factors can boost the risk further. “If you have diabetes, smoking, high blood pressure, elevated lipids in your blood – if you have a combination of those plus inflammation, it makes that risk even higher,” Dr. Giles said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“There’s definitely a lot of data that suggests that, as rheumatologists, we’re not doing a very good job of screening and treating for cardiovascular disease and risk,” Dr. Giles said in an interview at the meeting. He suggests that his fellow rheumatologists become comfortable with screening and treatment guidelines for cardiovascular disease. For selected patients, coronary CT or carotid ultrasound may be valuable in guiding decision making, since very low LDL cholesterol may be correlated with an increased risk of CVD for some patients with RA.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – When genetic risk and lifestyle risk factors collide with the baseline systemic inflammation of rheumatoid arthritis (RA), cardiovascular risk increases significantly. Helping patients to manage risk for cardiovascular disease (CVD) requires getting comfortable in making risk assessments and counseling patients about medication and lifestyle options, especially for patients who are not actively being managed by primary care physicians.

Jon Giles, MD, said that a large portion of the elevated risk for CVD in patients with RA is “driven by the fact that [RA] patients have more atherosclerosis.”

Dr. Giles, professor of medicine at Columbia University, New York, said that other CVD risk factors can boost the risk further. “If you have diabetes, smoking, high blood pressure, elevated lipids in your blood – if you have a combination of those plus inflammation, it makes that risk even higher,” Dr. Giles said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“There’s definitely a lot of data that suggests that, as rheumatologists, we’re not doing a very good job of screening and treating for cardiovascular disease and risk,” Dr. Giles said in an interview at the meeting. He suggests that his fellow rheumatologists become comfortable with screening and treatment guidelines for cardiovascular disease. For selected patients, coronary CT or carotid ultrasound may be valuable in guiding decision making, since very low LDL cholesterol may be correlated with an increased risk of CVD for some patients with RA.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – When genetic risk and lifestyle risk factors collide with the baseline systemic inflammation of rheumatoid arthritis (RA), cardiovascular risk increases significantly. Helping patients to manage risk for cardiovascular disease (CVD) requires getting comfortable in making risk assessments and counseling patients about medication and lifestyle options, especially for patients who are not actively being managed by primary care physicians.

Jon Giles, MD, said that a large portion of the elevated risk for CVD in patients with RA is “driven by the fact that [RA] patients have more atherosclerosis.”

Dr. Giles, professor of medicine at Columbia University, New York, said that other CVD risk factors can boost the risk further. “If you have diabetes, smoking, high blood pressure, elevated lipids in your blood – if you have a combination of those plus inflammation, it makes that risk even higher,” Dr. Giles said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

“There’s definitely a lot of data that suggests that, as rheumatologists, we’re not doing a very good job of screening and treating for cardiovascular disease and risk,” Dr. Giles said in an interview at the meeting. He suggests that his fellow rheumatologists become comfortable with screening and treatment guidelines for cardiovascular disease. For selected patients, coronary CT or carotid ultrasound may be valuable in guiding decision making, since very low LDL cholesterol may be correlated with an increased risk of CVD for some patients with RA.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Change in federal reimbursement for physicians is coming. Though the change is inevitable, physicians still have to weigh choices about when they might want to jump in with both feet, since entry into the full incentive payment system will be optional – for a time.

The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) is “basically a reorganization of all of these disparate reward and penalty systems” that have existed within the federal health care reimbursement landscape, said Joseph S. Eastern, MD. “The idea was to collect them all within one system.”

The new system is called the Medicare Incentive Payment System, or MIPS. Physicians are already familiar with many MIPS components, including meaningful use of the electronic health record, “which everybody thought was going away, but it isn’t,” said Dr. Eastern, a dermatologist in private practice in Belleville, N.J., who’s affiliated with Seton Hall University, South Orange, N.J. Also included are the Physician Quality Reimbursement System (PQRS) and the value-based modifier system.

MIPS is designed so that “you’ll either get a reward or a penalty depending on how well you do, compared with other physicians,” said Dr. Eastern, speaking at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

The alternative, he said, is to opt for one of the Alternative Payment Models, or APMs. However, details about APMs are “really up in the air, because a lot of them have either not been doing very well, or have not been very well defined,” so that physicians often don’t currently have enough data to make an informed choice. He expects the APM landscape to sort out over the next year or two.

Opting not to comply and take the 1%-3% cut in Medicare reimbursement associated with noncompliance might make sense for just a few physicians, though it might seem tempting, Dr. Eastern said in a video interview. Since the penalties will escalate significantly over the next few years, he feels that only physicians who are considering retiring soon or selling their practices should consider opting out.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Change in federal reimbursement for physicians is coming. Though the change is inevitable, physicians still have to weigh choices about when they might want to jump in with both feet, since entry into the full incentive payment system will be optional – for a time.

The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) is “basically a reorganization of all of these disparate reward and penalty systems” that have existed within the federal health care reimbursement landscape, said Joseph S. Eastern, MD. “The idea was to collect them all within one system.”

The new system is called the Medicare Incentive Payment System, or MIPS. Physicians are already familiar with many MIPS components, including meaningful use of the electronic health record, “which everybody thought was going away, but it isn’t,” said Dr. Eastern, a dermatologist in private practice in Belleville, N.J., who’s affiliated with Seton Hall University, South Orange, N.J. Also included are the Physician Quality Reimbursement System (PQRS) and the value-based modifier system.

MIPS is designed so that “you’ll either get a reward or a penalty depending on how well you do, compared with other physicians,” said Dr. Eastern, speaking at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

The alternative, he said, is to opt for one of the Alternative Payment Models, or APMs. However, details about APMs are “really up in the air, because a lot of them have either not been doing very well, or have not been very well defined,” so that physicians often don’t currently have enough data to make an informed choice. He expects the APM landscape to sort out over the next year or two.

Opting not to comply and take the 1%-3% cut in Medicare reimbursement associated with noncompliance might make sense for just a few physicians, though it might seem tempting, Dr. Eastern said in a video interview. Since the penalties will escalate significantly over the next few years, he feels that only physicians who are considering retiring soon or selling their practices should consider opting out.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Change in federal reimbursement for physicians is coming. Though the change is inevitable, physicians still have to weigh choices about when they might want to jump in with both feet, since entry into the full incentive payment system will be optional – for a time.

The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) is “basically a reorganization of all of these disparate reward and penalty systems” that have existed within the federal health care reimbursement landscape, said Joseph S. Eastern, MD. “The idea was to collect them all within one system.”

The new system is called the Medicare Incentive Payment System, or MIPS. Physicians are already familiar with many MIPS components, including meaningful use of the electronic health record, “which everybody thought was going away, but it isn’t,” said Dr. Eastern, a dermatologist in private practice in Belleville, N.J., who’s affiliated with Seton Hall University, South Orange, N.J. Also included are the Physician Quality Reimbursement System (PQRS) and the value-based modifier system.

MIPS is designed so that “you’ll either get a reward or a penalty depending on how well you do, compared with other physicians,” said Dr. Eastern, speaking at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

The alternative, he said, is to opt for one of the Alternative Payment Models, or APMs. However, details about APMs are “really up in the air, because a lot of them have either not been doing very well, or have not been very well defined,” so that physicians often don’t currently have enough data to make an informed choice. He expects the APM landscape to sort out over the next year or two.

Opting not to comply and take the 1%-3% cut in Medicare reimbursement associated with noncompliance might make sense for just a few physicians, though it might seem tempting, Dr. Eastern said in a video interview. Since the penalties will escalate significantly over the next few years, he feels that only physicians who are considering retiring soon or selling their practices should consider opting out.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Although biologics have transformed treatment of many rheumatologic disorders, their structure and mechanism of action can come with immunogenic baggage. “They’re proteins; consequently, one can expect immunogenicity,” said Daniel Furst, MD, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Immunogenicity can increase clearance of drugs; it can also interfere with the function of the drug. Although physicians may be tempted to think that developing an antidrug antibody to a specific drug is the principal cause for lack of efficacy in an individual patient, “in fact, it’s not that simple,” said Dr. Furst. “There are comorbidities, other drugs, which can affect the immunogenicity itself; there’s even the specific epitope that’s being affected by the drug antibody, which may or may not result in neutralization and an effect.”

In the broad class of tumor necrosis factor inhibitors (TNFIs), about 30% of patients taking adalimumab or infliximab will develop autoantibodies. This is higher than the 10% rate of autoantibody development for other TNFIs.

For non-TNFIs, including abatacept, tocilizumab, and rituximab, “the incidence of immunogenicity is significantly lower,” on the order of 1%-5%, said Dr. Furst, who has appointments at the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence, Italy.

Still, “there’s reasonable evidence that antidrug antibodies to TNFIs decrease efficacy and increase toxicity, particularly skin reactions,” he said.

Global Academy for Medical Education and this organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Although biologics have transformed treatment of many rheumatologic disorders, their structure and mechanism of action can come with immunogenic baggage. “They’re proteins; consequently, one can expect immunogenicity,” said Daniel Furst, MD, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Immunogenicity can increase clearance of drugs; it can also interfere with the function of the drug. Although physicians may be tempted to think that developing an antidrug antibody to a specific drug is the principal cause for lack of efficacy in an individual patient, “in fact, it’s not that simple,” said Dr. Furst. “There are comorbidities, other drugs, which can affect the immunogenicity itself; there’s even the specific epitope that’s being affected by the drug antibody, which may or may not result in neutralization and an effect.”

In the broad class of tumor necrosis factor inhibitors (TNFIs), about 30% of patients taking adalimumab or infliximab will develop autoantibodies. This is higher than the 10% rate of autoantibody development for other TNFIs.

For non-TNFIs, including abatacept, tocilizumab, and rituximab, “the incidence of immunogenicity is significantly lower,” on the order of 1%-5%, said Dr. Furst, who has appointments at the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence, Italy.

Still, “there’s reasonable evidence that antidrug antibodies to TNFIs decrease efficacy and increase toxicity, particularly skin reactions,” he said.

Global Academy for Medical Education and this organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Although biologics have transformed treatment of many rheumatologic disorders, their structure and mechanism of action can come with immunogenic baggage. “They’re proteins; consequently, one can expect immunogenicity,” said Daniel Furst, MD, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Immunogenicity can increase clearance of drugs; it can also interfere with the function of the drug. Although physicians may be tempted to think that developing an antidrug antibody to a specific drug is the principal cause for lack of efficacy in an individual patient, “in fact, it’s not that simple,” said Dr. Furst. “There are comorbidities, other drugs, which can affect the immunogenicity itself; there’s even the specific epitope that’s being affected by the drug antibody, which may or may not result in neutralization and an effect.”

In the broad class of tumor necrosis factor inhibitors (TNFIs), about 30% of patients taking adalimumab or infliximab will develop autoantibodies. This is higher than the 10% rate of autoantibody development for other TNFIs.

For non-TNFIs, including abatacept, tocilizumab, and rituximab, “the incidence of immunogenicity is significantly lower,” on the order of 1%-5%, said Dr. Furst, who has appointments at the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence, Italy.

Still, “there’s reasonable evidence that antidrug antibodies to TNFIs decrease efficacy and increase toxicity, particularly skin reactions,” he said.

Global Academy for Medical Education and this organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – When rheumatologists consider a differential diagnosis that includes seronegative rheumatoid arthritis, they should also consider chikungunya, according to Len Calabrese, DO.

The patient who presents with weeks to months of unexplained arthralgia and perhaps arthritis and a negative autoimmune panel deserves consideration of chikungunya or another arbovirus, said Dr. Calabrese, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Among the mosquito-borne arboviruses now in play in the Western Hemisphere, chikungunya is particularly likely to cause long-lasting and sometimes debilitating joint pain weeks and even months after initial infection.

An alphavirus, chikungunya virus makes most affected individuals quite ill, and serum IgG and IgM titers persist long after infection. Testing is straightforward, as long as the virus is a candidate diagnosis, Dr. Calabrese said.

In addition to obtaining an accurate travel history, said Dr. Calabrese, physicians should consider the possibility of autochthonous transmission, which occurs when an infected individual who returns from an endemic area is bitten by mosquitoes once home. Flares of autochthonous transmission can result in pockets of locally heavy transmission far from the zones where chikungunya usually resides.

Dr. Calabrese is chair of clinical immunology and chair of osteopathic research and education at the Cleveland Clinic, and he reported no relevant financial disclosures.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – When rheumatologists consider a differential diagnosis that includes seronegative rheumatoid arthritis, they should also consider chikungunya, according to Len Calabrese, DO.

The patient who presents with weeks to months of unexplained arthralgia and perhaps arthritis and a negative autoimmune panel deserves consideration of chikungunya or another arbovirus, said Dr. Calabrese, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Among the mosquito-borne arboviruses now in play in the Western Hemisphere, chikungunya is particularly likely to cause long-lasting and sometimes debilitating joint pain weeks and even months after initial infection.

An alphavirus, chikungunya virus makes most affected individuals quite ill, and serum IgG and IgM titers persist long after infection. Testing is straightforward, as long as the virus is a candidate diagnosis, Dr. Calabrese said.

In addition to obtaining an accurate travel history, said Dr. Calabrese, physicians should consider the possibility of autochthonous transmission, which occurs when an infected individual who returns from an endemic area is bitten by mosquitoes once home. Flares of autochthonous transmission can result in pockets of locally heavy transmission far from the zones where chikungunya usually resides.

Dr. Calabrese is chair of clinical immunology and chair of osteopathic research and education at the Cleveland Clinic, and he reported no relevant financial disclosures.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – When rheumatologists consider a differential diagnosis that includes seronegative rheumatoid arthritis, they should also consider chikungunya, according to Len Calabrese, DO.

The patient who presents with weeks to months of unexplained arthralgia and perhaps arthritis and a negative autoimmune panel deserves consideration of chikungunya or another arbovirus, said Dr. Calabrese, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Among the mosquito-borne arboviruses now in play in the Western Hemisphere, chikungunya is particularly likely to cause long-lasting and sometimes debilitating joint pain weeks and even months after initial infection.

An alphavirus, chikungunya virus makes most affected individuals quite ill, and serum IgG and IgM titers persist long after infection. Testing is straightforward, as long as the virus is a candidate diagnosis, Dr. Calabrese said.

In addition to obtaining an accurate travel history, said Dr. Calabrese, physicians should consider the possibility of autochthonous transmission, which occurs when an infected individual who returns from an endemic area is bitten by mosquitoes once home. Flares of autochthonous transmission can result in pockets of locally heavy transmission far from the zones where chikungunya usually resides.

Dr. Calabrese is chair of clinical immunology and chair of osteopathic research and education at the Cleveland Clinic, and he reported no relevant financial disclosures.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes