Osteoarthritis Treatment in the Veteran Population.

Patients with osteoarthritis benefit most from a comprehensive treatment strategy, including education, exercise, analgesia, and in severe cases, surgery.

Etanercept-induced Henoch-Schönlein purpura in a patient with ankylosing spondylitis.

Ankylosing spondylitis (AS) is a chronic inflammatory disease that primarily affects the axial skeleton. Extra-articular manifestations are less common relative to other rheumatic diseases, and vasculitic complications typically involve the ascending aorta and aortic valve. The use of tumor necrosis factor inhibitors is efficacious in the treatment of patients with AS. Since their routine use, however, tumor necrosis factor inhibitors have been associated with the development of drug-induced complications including the induction of lupus and both cutaneous and systemic vasculitis. In this report, we describe a patient with severe longstanding AS, who developed Henoch-Schönlein purpura after commencing therapy with etanercept. Tumor necrosis factor inhibitor-induced Henoch-Schönlein purpura has been very rarely reported and has been mostly recognized in patients with rheumatoid arthritis.

Treatment of adult inflammatory myositis with rituximab: an emerging therapy for refractory patients.

BACKGROUND: Rituximab is a genetically engineered chimeric, murine/human monoclonal antibody directed against the CD20 antigen on B-cells. Recent studies of inflammatory myopathy have shown that B-cells are important in the etiopathogenesis of these diseases, and therefore suggest a role for B-cell depletion therapy in idiopathic inflammatory myopathy. The few case reports and small series that have been published suggest that anti-B-cell therapy is effective for the clinical manifestations of inflammatory myopathy. OBJECTIVES: To report our experience using rituximab to treat 3 patients with refractory idiopathic inflammatory myopathy (IIM), and to review and discuss the available literature regarding reported experience using rituximab in treating IIM. METHODS: We describe the clinical courses of 3 patients with IIM treated by us with rituximab after unsatisfactory responses to conventional therapy. We performed a search of the English language literature utilizing PubMed, and identified 8 articles that also described the use of rituximab for treatment of IIM. RESULTS: Improvement in our patients was manifested by an increase in muscle strength and decline in creatinine kinase levels in all 3 patients. Recurrent muscle weakness and elevated muscle enzymes occurred in 2 patients postinfusion; retreatment with rituximab resulted in similar clinical improvement. Our experience, and that 20 of 21 patients described in 8 cited reports demonstrate a favorable clinical response in patients treated with B-cell depletion therapy for IIM. CONCLUSIONS: Early uncontrolled clinical experience indicates that rituximab may be a valuable therapeutic agent for treatment of refractory IIM. Further investigation regarding the optimal dosing regimen, treatment length, and long-term safety profile of rituximab therapy for IIM is warranted.

Drug-induced lupus due to anti-tumor necrosis factor alpha agents.

PURPOSE: To evaluate the reported cases of drug-induced lupus erythematosus (DILE) due to anti-tumor necrosis factor (TNF) alpha therapy and to compare "classic" DILE with DILE secondary to anti-TNFalpha therapy. We also add 3 case reports related to 3 different anti-TNFalpha drugs to the literature. METHODS: We searched the Medline database for cases published in English and evaluated 53 cases in 27 papers purported to be TNFalpha-induced DILE. We compared the clinical and laboratory features of cases that fulfilled our criteria for TNFalpha DILE to those of DILE due to non-TNFalpha drugs as found in standard texts. We also report the clinical and laboratory findings of our 3 patients with drug-induced lupus related to anti-TNFalpha drugs, 1 each in patients treated with adalimumab, etanercept, and infliximab. RESULTS: Of the 53 purported cases of DILE due to anti-TNFalpha therapy, we excluded 17 with cutaneous manifestations alone and 3 with overlap syndromes and mixed connective tissue disease. In the 33 cases that met our criteria for systemic DILE, 21 cases were due to infliximab, 10 cases were due to etanercept, and only 2 cases were related to adalimumab. TNFalpha-blocker-induced DILE cases had a higher prevalence of antibodies to double-stranded DNA, rash, and hypocomplementemia than DILE due to other drugs. Fever is common in both types of DILE. Renal disease, which is rare in classic DILE, has been reported in cases of TNFalpha DILE. CONCLUSIONS: TNFalpha DILE has significant clinical and laboratory manifestations which distinguish it from DILE due to drugs other than anti-TNF agents and may be difficult to diagnose in patients treated for autoimmune diseases. It is appropriate to consider whether all patients who are begun on anti-TNF therapy should have pretreatment serologic evaluation for systemic lupus erythematosus.

Spondyloarthropathy: an independent risk factor for kidney stones.

PURPOSE: To better stratify risk and to verify previous prevalence reports, we conducted a retrospective cohort study comparing the lifetime incidence of nephrolithiasis in patients with spondyloarthropathies (SpA) and rheumatoid arthritis (RA). PATIENTS AND METHODS: Patients with SpA or rheumatoid factor-positive RA were identified from the rheumatology clinics of two Veterans Affairs hospitals and the University of Minnesota. Among them, 168 were confirmed to meet the American College of Rheumatology criteria and gave informed consent to participation. They were sent a survey regarding their rheumatologic diagnosis, coexistent conditions, medications, and history of kidney stones. Of the total, 143 patients responded and met the criteria for analysis. Rheumatoid arthritis patients were age and sex matched with SpA patients as controls. RESULTS: Populations were similar in all categories except that RA patients were more likely to have used prednisone (P < 0.001), bisphosphonates (P < 0.001), and calcium supplementation (P = 0.03). Kidney stones were reported by 23 (29.11%) of the 79 SpA patients compared with 8 (12.5%) of the 64 RA patients (chi (2) = 5.75; P = 0.025). Subgroup analysis of self-reporting stone history in 85 patients was found to be reliable on imaging review (sensitivity 82%; specificity 100%). CONCLUSIONS: Self-reporting of kidney stones by patients is a reliable measure. Despite adjusting for medication use and matching two similar arthritic populations, patients with SpA had a higher incidence of kidney stones than those with RA. This finding suggests that SpA is an independent risk factor for nephrolithiasis. Future studies will evaluate urinary risk factors and polymorphisms in the ANKH gene that may predispose to stone formation in this high-risk group.

Amelogenin, a major structural protein in mineralizing enamel, is also expressed in soft tissues: brain and cells of the hematopoietic system.

The amelogenin protein is considered as the major molecular marker of developing and mineralizing ectodermal enamel. It regulates the shape, size, and direction of growth of the enamel mineral crystallite. Recent data suggest other roles for amelogenin beyond regulation of enamel mineral crystal growth. The present study describes our recent discovery of amelogenin expression in soft tissues: in brain and in cells of the hematopoietic system, such as macrophages, megakaryocytes and in some of the hematopoietic stem cells. Reverse transcription-polymerase chain reaction (RT-PCR) followed by cDNA sequencing revealed, in mouse brain, two amelogenin mRNA isoforms: the full-length amelogenin including exon 4, and the isoform lacking exon 4. Immunohistochemistry revealed amelogenin expression in brain glial cells. Mouse macrophages were found to express the full-length amelogenin sequence lacking exon 4. Confocal microscopy revealed colocalization of amelogenin and CD41 (a megakaryocyte marker), as well as amelogenin and CD34 (a hematopoietic stem cell marker) in some of the bone marrow cells. The expression of amelogenin, a major structural protein of the mineralizing extracellular enamel matrix, also in cells of non-mineralizing soft tissues, suggests that amelogenin is multifunctional. Several different potential functions of amelogenin are discussed.

Rheumatologic conditions of the foot.

Podiatric physicians are frequently the first clinicians with the opportunity to diagnose a rheumatologic disease. Awareness of the multisystem nature of the more common rheumatologic conditions will assist podiatrists in making the appropriate diagnosis. The specific joints affected, the temporal pattern of joint involvement, and the distribution of affected joints give clues to the diagnosis. Knowledge of the current treatment for rheumatic diseases as well as early referral for evaluation by a medical physician is essential for the appropriate care of patients with systemic arthritis.