Accelerated hypertension in a patient with mixed connective tissue disease.
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Biomedical subjects
Publications and source records attributed to M Kuwana.
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Using plasmids containing the genes for thymidine kinase (tk) and neomycin resistance (neo), we have shown that DNA-mediated genotypic transformation of L and Chinese hamster ovary (CHO) cells is increased several-fold by the presence of the sterol-binding polyene antibiotic, amphotericin. Transformation into the same host cells, using genomic DNA, was also enhanced by amphotericin. Phenotypic expression of beta-galactosidase activity of a plasmid containing the gene for the enzyme was also markedly elevated when the antibiotic was added at transfection. Other sterol-binding polyene antibiotics also showed activity in these DNA-mediated gene transfer assays.
OBJECTIVE: The clinical and laboratory features of seven Japanese patients with anti-aminoacyl-tRNA synthetase (ARS) autoantibodies against PL-7 (anti-threonyl-tRNA synthetase) were analyzed and compared with previously published findings. METHODS: Serum samples from 1,135 Japanese patients with various autoimmune diseases were screened for anti-PL-7 antibodies using RNA and protein immunoprecipitation assays. The patients whose sera contained anti-PL-7 antibodies were assessed regarding clinical symptoms and clinical course. RESULTS: Sera from seven patients were found to have anti-PL-7 antibodies. These autoantibodies were associated with polymyositis/dermatomyositis (PM/DM) and/or interstitial lung disease (ILD). The clinical diagnoses of these seven patients were PM - systemic sclerosis (SSc) overlap (5 patients), DM (1 patient) and idiopathic pulmonary fibrosis (IPF) (1 patient). All patients had ILD with a chronic course and six also had arthritis (85%) and five sclerodactyly (71%). CONCLUSIONS: These results indicate that anti-PL-7 autoantibodies are closely associated with PM-SSc overlap as well as ILD, arthritis and sclerodactyly in our series of Japanese patients.
OBJECTIVE: To determine whether elevated levels of antibodies to HCMV protein UL83 were present in patients with SSc and if their prevalence was associated with major SSc-associated autoantibodies. METHODS: The study population consisted of 253 Caucasian subjects (110 SSc patients and 143 controls). IgG antibodies to UL83 were measured by an enzyme-linked immunosorbent assay (ELISA). Antibodies to centromere and RNA polymerase (RNAP) were determined by indirect immunofluorescence and immnoprecipitation methods, respectively. RESULTS: The mean level of anti-UL83 antibodies in the sera of SSc patients as a whole was significantly higher than that in control subjects (14.75 vs 10.6 units/microl, p = 0.002). Both subgroups of patients contributed to this variation: compared to controls, anti-UL83 antibody levels were higher in diffuse (16.32 vs 10.6 units/microl, p = 0.012) as well as in those with the limited form of the disease (13.95 vs 10.6 units/microl, p = 0.015). Anti-UL83 antibodies were not associated with major SSc associated autoantibodies. CONCLUSION: Humoral immunity to HCMV protein UL83 may be relevant to the etiopathogenesis of scleroderma.
We report a patient with overlapping systemic sclerosis-systemic lupus erythematosus who developed refractory thrombocytopenia and recurrent thromboses. Coagulation and platelet labeling studies revealed that platelets were being consumed by the thrombus formation, and anticoagulation with warfarin dramatically increased the platelet count. This case report suggests that platelet consumption due to thrombus formation is one of the causes of thrombocytopenia in patients with rheumatic disease.