Parvovirus arthropathy outbreak in southwestern United States.

OBJECTIVE: We describe an outbreak of parvovirus (PV) arthropathy that was detected in a rheumatology clinic in San Antonio, Texas, during the winter of 1994. Parvovirus B19 causes acute symmetric polyarthritis (ASPA) in adults. In the US, the majority of cases described are from the northern US. METHODS: An outbreak of PV arthropathy was monitored in a San Antonio area rheumatology clinic. RESULTS: Of the 16 affected patients, 69% were female, ages ranging from 23 to 60 years; 75% had close contact with children, 58% of whom were exposed to children with clinical PV. All patients noted an acute arthritis except for 2 patients with polyarthralgias. The most common presentation was ASPA (9/16), with 10/16 complaining of viral prodrome, and 5/16 having a nonspecific rash, but none with the typical "slapped cheek" appearance. Eleven patients had an ASPA at some time in their illness. Of these, 3 had a true migratory arthritis that developed into an ASPA and another 2 were additive. Two additional patients had persistent asymmetric polyarthritis. The most common joints involved were the metacarpophalangeals, proximal interphalangeals, wrists, and knees. Most patients' syndromes lasted < 6 weeks, but 3 patients had symptoms that lasted longer than 6 months. Eight of 10 had elevated erythrocyte sedimentation rate. Rheumatoid factor was detected in 3 patients and antinuclear antibody in 2. All patients were treated symptomatically with nonsteroidal antiinflammatory drugs and a few also received low dose corticosteroids. Because of suspicious clinical presentations, 2 patients were presumed to have gonococcal arthritis before PV titers were available. CONCLUSION: This is the first large series on adults with PV arthropathy reported in the southern US. In contrast to the usual features of ASPA, the outbreak appears unique in that almost 40% of cases presented with a true migratory arthritis.

Azathioprine hepatotoxicity is uncommon in patients with Rheumatic diseases.

At present, there is no consensus regarding the utility of liver enzyme monitoring in rheumatology patients undergoing treatment with azathioprine (AZA). To further investigate this issue, we retrospectively reviewed for current or past use of AZA all patient records in our Disease Modifying Antirheumatic Drug (DMARD) clinic from May 1986 through September 1996. Information available from individual DMARD charts included AZA data (dates initiated, dose, indication for changing dose or stopping AZA), co-administered DMARDs, and aspartate aminotransferase (AST) serum values. In patients followed in the clinic through February 1994, serum alkaline phosphatase (AP) values additionally were available. Published reports of AZA hepatotoxicity in rheumatoid arthritis (RA) patients were found by a MEDLINE search, supplemented by a manual search of reference lists.We screened 429 patient records, and all patients who had received AZA at any time during the study period (n = 56) were identified for further review. The mean daily AZA dose was 96 mg (median = 100 mg/ day, range = 25-200 mg/day). All of the 56 patients had undergone routine periodic monitoring of serum AST while taking AZA (mean interval = 26 days); 30 of these patients additionally underwent monitoring of serum AP (mean interval = 24 days). Twenty-three (41%) of the patients had at least one episode of an abnormally elevated serum AST and/or AP while taking AZA. Only 1 of these 2 laboratory values was abnormal in 12 patients. The average time from AZA initiation to first appearance of an abnormal AST and/or AP value was 27 days (range = 7-62 days). During observation alone, all abnormal laboratory test results became normalized in 20 of 23 patients (87%) during the study period. There were no interventions in response to an abnormal laboratory value, and no patient experienced an adverse clinical outcome attributable to AZA hepatotoxicity during the 10-year study period.AZA use for rheumatic conditions may be associated with elevations in both the serum AST and/or AP values. Most of these elevations were transient, and none were clinically significant in our patient population. This study supports current American College of Rheumatology guidelines, which do not recommend routine periodic monitoring with liver enzyme tests in RA patients taking AZA. Furthermore, this study suggests that the utility of the baseline liver enzyme test in these patients is not well established.

Quantitative measurement of erosion growth and joint space loss in rheumatoid arthritis hand radiographs.

OBJECTIVE: To evaluate the performance of simple, inexpensive quantitative techniques for measuring erosion growth and joint space loss in serial hand radiographs of patients with rheumatoid arthritis (RA). METHODS: Erosions were measured using a plastic overlay template of sample erosion sizes. Joint spaces were measured with a hand held measuring micrometer. In the first phase of testing, a spectrum of individual erosions and joint spaces was measured to determine intra and interobserver correlations and variability. In the 2nd phase, the tools were used to measure serial changes in RA hand radiographs. Observer correlations and the ability to discriminate serial changes were determined and compared to the scoring method of Sharp. RESULTS: Measurements of individual erosion areas and joint spaces were highly reproducible. Intra and interobserver correlations were significant (p < 0.05) for serial erosion growth and joint space loss measurements, as well as changes in Sharp scores. Quantitative measurements correlated highly with the corresponding Sharp score changes. Of all measurements or scores recorded, quantitative joint space loss measurements were statistically superior in discriminating serial change in RA hand radiographs. Quantitatively measured joint space loss correlated well with both erosion growth measurements and serial change in total Sharp scores. CONCLUSION: Quantitative measurement of erosion growth and joint space loss is possible with simple inexpensive techniques. Further study is needed to confirm our data, which suggest that quantitative measurement of joint space narrowing may be the most useful discriminator of serial changes in RA hand radiographs.

McArdle's disease presenting as treatment resistant polymyositis.

The broad spectrum and often incomplete presentation of polymyositis frequently confound its distinction from other myopathies. In 18 months of screening for myophosphorylase in all muscle biopsy specimens at our institution, 2 cases of McArdle's disease were discovered in patients previously thought to have refractory PM. Given the important treatment implications of this distinction, all patients with "refractory PM" in whom the diagnosis has not been firmly established should be screened for myophosphorylase deficiency.

A novel pathway of human T lymphocyte activation. Identification by a monoclonal antibody generated against a rheumatoid synovial T cell line.

Substantial evidence indicates that compartmentalized infiltrates of T lymphocytes are central to the pathogenesis of autoimmune diseases such as rheumatoid arthritis, but the mechanisms by which such cells become activated remain unknown. To define surface components of activation pathways important in the function of these cells, we have generated mAb against a rheumatoid synovial T cell line. One such antibody, termed anti-UM4D4, reacts with an Ag, termed UM4D4, which is strongly expressed on most rheumatoid synovial T cell lines and clones, and on a subset of peripheral blood T cells, resting or activated. Anti-UM4D4 is mitogenic in soluble form for PBMC and certain T cell clones, and is comitogenic with the phorbol ester PMA for purified resting T lymphocytes. These functional effects are similar to those previously observed with antibodies to epitopes of CD2 and CD3, surface Ag involved in two well defined pathways of human T cell activation. Binding of anti-UM4D4 to T cells is not, however, blocked by antibodies directed at various epitopes of CD2 and CD3. Moreover, UM4D4 does not comodulate with CD3, and is expressed on a T cell line that lacks CD2, CD3, and CD28. The data, therefore, indicate that anti-UM4D4 identifies a T cell activation pathway, distinct from those previously described, that could play a role in the pathogenesis of T cell-mediated autoimmune diseases.