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Biomedical subjects

E S Weiner

Publications and source records attributed to E S Weiner.

10 recordsLinked to original sources
PubMed1993

Reduction of acute-phase proteins with tenidap sodium, a cytokine-modulating anti-rheumatic drug.

Four independent studies have investigated and compared the effects of tenidap sodium, naproxen and placebo on CRP in patients with active RA. One of these studies also investigated the effects of tenidap and naproxen on serum amyloid A (SAA) concentrations and ESR. The duration of the four studies ranged between 2 weeks and 24 weeks, and depending on the study, tenidap sodium was administered orally in doses of 40-120 mg/day and naproxen in doses of 1000 mg/day. In all four studies serum CRP concentrations in tenidap-treated patients had decreased significantly from baseline at the time of final assessment. The decrease in CRP concentration in tenidap-treated patients was observed as early as 1 week after initiation of therapy and was sustained for up to 6 months, the last assessment timepoint. CRP concentrations in naproxen-treated and placebo patients were essentially unchanged. The decreases from baseline observed in tenidap-treated patients were significantly greater than the changes observed in naproxen-treated or placebo patients. After 24 weeks of tenidap treatment the decrease in CRP was paralleled by significant decreases in SAA concentration and ESR. The finding that tenidap sodium rapidly, consistently and significantly lowered CRP serum concentrations differentiates tenidap sodium from the NSAID, naproxen. This could possibly have important therapeutic implications given that other long-term investigations have shown that reducing serum CRP and SAA concentrations correlates with a reduction in radiographically-assessed disease progression.

Acute-Phase Proteins↗
PubMed1991

Prognostic significance of anticentromere antibodies and anti-topoisomerase I antibodies in Raynaud's disease. A prospective study.

Seventy-seven patients with Raynaud's disease were studied for a mean of 4 years (range 1-11 years) to determine the relationship between autoantibodies and long-term clinical outcome. Anticentromere antibodies (ACA) were assayed by indirect immunofluorescence and by immunoblotting of HeLa cell chromosome extracts. Antibodies to topoisomerase I (anti-topo I) were assayed by immunodiffusion and immunoblotting. Antibodies to the major centromeric protein, CENP-B, and anti-topo I were studied by enzyme-linked immunosorbent assay (ELISA). Eight patients developed telangiectasias, 4 developed skin tightening, and 4 developed a connective tissue disease other than scleroderma. The presence of ACA at the start of the study was associated with the development of telangiectasias (P less than 0.003). An initial 100-kd band on immunoblot in conjunction with a positive anti-topo I ELISA result was associated with the development of tight skin (P less than 0.0025), while a 100-kd band with a negative anti-topo I ELISA result was associated with the subsequent development of a connective tissue disease other than scleroderma (P less than 0.0073). Patients who were initially ACA positive, had the 100-kd band on immunoblot, or had positive ELISA results for anti-topo I or for anti-CENP-B were 63-fold more likely to develop signs of connective tissue disease by the end of the study (P less than 0.000009). The presence of any of these autoantibodies was more sensitive (100%), although less specific (75%), than were findings from nailfold capillaroscopy (sensitivity 67% and specificity 95%) in predicting subsequent clinical progression. We conclude that findings of assays for anti-topo I and ACA complement the findings from nailfold capillaroscopy in providing useful prognostic information in Raynaud's disease.

Antibodies↗
PubMed1991

Idiotypic analysis of human anticentromere autoantibodies.

The idiotypes (Ids) of anticentromere antibodies (ACA) have been studied using a fusion protein obtained from cloned cDNA of the major centromere antigen, CENP-B, for isolation of the autoantibodies. IgG-ACA were affinity purified from 4 patient sera and anti-Ids prepared in rabbits. Analysis revealed the existence of two distinct types of immunodominant Ids. One Id is near the antibody combining site and one is framework associated. A longterm longitudinal study of Id expression in a patient who seroconverted from ACA (-) to ACA (+) when she developed Raynaud's phenomenon showed a close correlation between Id expression and ACA titers (r = 0.94). These results may be interpreted as evidence for an autoantigen driven process in the anticentromere immune response.

Adult↗
PubMed1990

Autoantibodies to topoisomerase I (Scl-70): analysis by gel diffusion, immunoblot, and enzyme-linked immunosorbent assay.

Anti-topoisomerase I autoantibodies (anti-topo I, anti-Scl-70) are associated with proximal scleroderma and are of prognostic significance in patients with Raynaud's disease. To establish a highly sensitive and specific system for the detection of anti-topo I, we have investigated sera from 409 patients and controls by Ouchterlony gel diffusion, Western immunoblot on chromosome proteins, and solid-phase enzyme-linked immunosorbent assay (ELISA) with purified topoisomerase I as antigen. The ELISA was more sensitive than the gel diffusion technique and was more specific than the Western immunoblot, while the immunoblot may identify additional autoantibodies.

Autoantibodies↗
PubMed1989

Aseptic necrosis and glucocorticosteroids in systemic lupus erythematosus: a reevaluation.

To reassess predisposing factors in patients with systemic lupus erythematosus (SLE) who develop aseptic necrosis of bone, we studied 172 patients with SLE seen at our institution between 1975 and 1987 followed for longer than 1 year. Twenty-eight (16.3%) of these patients developed clinically apparent aseptic necrosis. In 12 of these 28 the continuous glucocorticosteroid dose was known. These 12 patients were compared to 15 controls with SLE followed for a minimum of 4.5 years for whom continuous glucocorticosteroid dosage was also known. We were unable to find any significant differences between patients with aseptic necrosis and controls in prevalence of specific lupus organ system involvement, Raynaud's phenomenon, or abnormal serological or hematological variables. Overall disease activity at the time of maximal glucocorticosteroid dosage did not differ significantly between the 2 groups but was slightly greater at the time SLE was diagnosed in the group with aseptic necrosis. Glucocorticosteroid intake during the first 1.5 years after diagnosis of SLE and during the third year after diagnosis was significantly greater for the patients with aseptic necrosis than for the control patients, as was glucocorticosteroid intake during the maximal 1, 3 and 6 months of therapy. We conclude that glucocorticosteroid intake is the major factor predisposing to aseptic necrosis in patients with SLE.

Adolescent↗
PubMed1988

Clinical associations of anticentromere antibodies and antibodies to topoisomerase I. A study of 355 patients.

Anticentromere antibodies (ACA) and anti-topoisomerase I (anti-topo I) were assayed in serum samples from 355 patients: 89 with proximal scleroderma; 54 with CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias), without proximal scleroderma; 154 with primary and secondary Raynaud's disease; and 58 with other rheumatic diseases, without Raynaud's disease. Sera from healthy control subjects were also assayed. Using immunoblotting techniques, anti-topo I was detected in 28% of the patients with proximal scleroderma; using immunodiffusion techniques, this antibody was found in only 20% of the same group of patients. Anti-topo I and ACA were found primarily in patients with scleroderma, CREST syndrome, and Raynaud's phenomenon. ACA identified patients with less severe disease, whereas anti-topo I identified patients with skin and cardiac involvement and patients with malignancies.

Adult↗