Therapeutic exercise in rheumatoid arthritis and osteoarthritis may be useful in improving aerobic capacity, strengthening muscles, improving endurance and increasing flexibility. This article reviews the major studies of exercise in these conditions and summarizes the authors recommendations regarding the use of therapeutic exercise in the treatment of rheumatoid arthritis osteoarthritis.

Whether palisading granuloma formation occurs with leukocytoclastic vasculitis in rheumatoid nodules and in histopathologically similar conditions is debatable. Patients with high titers for rheumatoid factor and severe erosive rheumatoid arthritis are at risk for both rheumatoid vasculitis and rheumatoid nodules. A patient with all of these features developed a papular eruption. These papules showed clinicopathologic features both of leukocytoclastic vasculitis and of early palisading granuloma. Lesions resolved slowly with low-dose oral corticosteroid therapy. It is proposed that these lesions be called rheumatoid papules and that they may represent a link between vasculitis and the palisaded granulomatous reaction seen in rheumatoid nodules.

Prostaglandins are long-chain, saturated, oxygenated fatty acids. Relatively large quantities of prostaglandins have been found in gut mucosa, suggesting that these substances play an important role in gastrointestinal physiology. Non-steroidal anti-inflammatory drugs (NSAIDs) cause damage to the gastric, intestinal, and colonic mucosa in experimental animals and in humans. Prostaglandins protect the gastric mucosa against injury induced by NSAIDs, and this property has been labelled cytoprotection. The mechanisms of cytoprotection have been extensively evaluated and are probably multifactorial, including effects on the gastric mucosal barrier, gastric blood flow, mucus, bicarbonate, and fluid section, ionic transport, cyclic AMP, and surface-active phospholipids. Prostaglandins may also prevent NSAID-induced injury in the small intestine and colon. The mechanisms responsible for prostaglandin protection in the lower gut against injurious agents are unknown. Further studies of the role of prostaglandins in the gut and their relationship to the effects of NSAIDs are needed. The results of these investigations may lead to a better understanding of the importance of prostaglandins in the physiology of the gastrointestinal tract, and may provide information regarding actions of NSAIDs on the functional integrity of the gastric, intestinal, and colonic mucosa.

Although oral medication induced esophageal injury (OMIEI), is a well-known and preventable condition, many cases are still missed, particularly in the elderly patients.To determine the frequency and outcome of oral medication-induced esophageal injury in elderly patients.Records of 390 patients aged over 65 years, with diagnoses of dysphagia, odynophagia, and noncardiac chest pain, over the period of 11 years, were selected for a retrospective review. Patients who had barium studies only, in whom endoscopy was not done or was unsuccessful, and those with incomplete data were excluded, leaving 250 patients for further review.Diagnosis of OMIEI was made in 27% (68 of 250) patients. Fifty-one of 68 (75%) patients with OMIEI responded to conservative management, including H2 blockers, proton pump inhibitors, antacids, or sucralfate. The remaining 17 patients (25%) developed esophageal strictures requiring dilation.A high index of clinical suspicion and low threshold for empiric treatment and diagnostic measures (endoscopy, barium swallow study), may be helpful, if indicated, for early diagnosis and prompt therapy of OMIEI.

Arthritis & RheumatismVolume 29, Issue 2 p. 286-291 Brief ReportFree to Read Light and electron microscopic findings in poems, or Japanese multisystem syndrome Elliott L. Semble MD, Elliott L. Semble MD Assistant Professor of Medicine Departments of Medicine (Rheumatology) and Pathology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North CarolinaSearch for more papers by this authorDr. Venkata R. Challa MD, Corresponding Author Dr. Venkata R. Challa MD Associate Professor of Pathology Departments of Medicine (Rheumatology) and Pathology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North CarolinaDepartment of Pathology, Bowman Gray School of Medicine, 300 S. Hawthorne Road, Winston-Salem, NC 27103Search for more papers by this authorDavid A. Holt MD, David A. Holt MD Fellow in Rheumatology Departments of Medicine (Rheumatology) and Pathology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North CarolinaSearch for more papers by this authorEdward J. Pisko MD, Edward J. Pisko MD Associate Professor of Medicine (Rheumatology) Departments of Medicine (Rheumatology) and Pathology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North CarolinaSearch for more papers by this author Elliott L. Semble MD, Elliott L. Semble MD Assistant Professor of Medicine Departments of Medicine (Rheumatology) and Pathology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North CarolinaSearch for more papers by this authorDr. Venkata R. Challa MD, Corresponding Author Dr. Venkata R. Challa MD Associate Professor of Pathology Departments of Medicine (Rheumatology) and Pathology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North CarolinaDepartment of Pathology, Bowman Gray School of Medicine, 300 S. Hawthorne Road, Winston-Salem, NC 27103Search for more papers by this authorDavid A. Holt MD, David A. Holt MD Fellow in Rheumatology Departments of Medicine (Rheumatology) and Pathology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North CarolinaSearch for more papers by this authorEdward J. Pisko MD, Edward J. Pisko MD Associate Professor of Medicine (Rheumatology) Departments of Medicine (Rheumatology) and Pathology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North CarolinaSearch for more papers by this author First published: February 1986 https://doi.org/10.1002/art.1780290218Citations: 22AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume29, Issue2February 1986Pages 286-291 RelatedInformation

The pathognomonic triad of a rheumatoid pleural effusion (round multinucleated inflammatory giant cells, large elongated cells and a background of granular material) has only rarely been reported, with only one case examined by electron microscopy. This paper present an additional case with emphasis on its ultrastructural features and immunochemical characteristics. Our data support an origin of the components of the effusions in the pleural rheumatoid nodules.

Clinical, laboratory, genetic, and radiologic studies were evaluated for 18 patients with rheumatoid arthritis who were treated for a mean of 16.6 months with a regimen involving supplementary aspirin and piroxicam, an investigational, nonsteroidal antiinflammatory agent. Although improvement in disease activity was seen, progression was evident on successive radiographs. Disease activity was not associated with the presence of any of the genetic markers. Peptic ulcers developed in 33% of patients, all of whom had type O blood. ABO blood typing may therefore be useful in patients with rheumatoid arthritis before consideration of therapy with potentially ulcerogenic drugs.