Contact with rashes during pregnancy.
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Glomerulonephritis with proteinuria of sufficient degree to manifest the nephrotic syndrome followed aplastic crises induced by human parvovirus (B19) in seven patients with homozygous sickle-cell disease, within 7 days in five patients and 6-7 weeks in two. Segmental proliferative glomerulonephritis was found in all four patients who underwent acute renal biopsies and focal segmental glomerulosclerosis was found in the fifth patient who had a biopsy 4 months later. One patient recovered completely, one died in chronic renal failure after 3 months, and the others had impaired creatinine clearance, four with continuing proteinuria.
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The role of intrauterine transfusion for fetal hydrops arising from maternal paravirus B19 infection is unclear. 66 cases of fetal hydrops arising from B19 infection were reported in England and Wales between June, 1992, and September, 1994. In 29 cases the fetus was dead at the time of the first abnormal ultrasound or a therapeutic abortion as performed; 12 of the 38 alive at the first abnormal scan received intrauterine transfusions and 3 of the 12 died. 26 did not receive intrauterine transfusions and 13 died. After adjustment for the severity of the hydrops as assessed by the ultrasound and for gestational age, the odds of death among those who received an intrauterine transfusion was significantly less than among those who did not (odds ratio 0.14, 95% CI 0.02-0.96). These findings suggest that intrauterine transfusion will benefit some fetuses with hydrops arising from parvovirus B19 infection.
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This study was undertaken to assess the incidence and significance of autoantibody production following B19 infection, 53 patients with acute B19 infection (positive for serum anti-B19 IgM) were studied; symptoms were rash and arthralgia (n = 26), rash (n = 7), arthralgia (n = 16), aplastic crisis (n = 3), and intrauterine death (n = 1). These patients were followed for 26-85 months (mean 57 months) and re-assessed for persistent symptoms, serum anti-B19 antibodies, and serum autoantibodies. At follow-up, 14 test and two control patients had one or more serum autoantibodies (anti-nuclear antibody, anti-smooth muscle antibody, gastric parietal cell antibody, anti-reticulin antibody, anti-mitochondrial antibody, rheumatoid factor) at a titre of > or = 40 (P = 0.004). Seven test patients and no control patients had serum autoantibody at a titre > or = 160. Of these seven test patients, only one had persistent symptoms. At follow-up assessment, this woman was 48-year-old, had persistent arthralgia for 4 years following acute B19 infection, rheumatoid factor at a titre of 160 (1920 IU/ml), and had been independently diagnosed as having rheumatoid arthritis. In conclusion, results of the present study showed that low titre autoantibody production was common following symptomatic B19 infection, however, while interesting from a virological standpoint, this finding may be of little significance for future development of autoimmune disease.
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