PubMed · 1458411
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K Brown. 1992-12-15. Steroid therapy.. https://pubmed.ncbi.nlm.nih.gov/1458411/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
An outbreak of mainly extrapulmonary tuberculosis (TB) in a group of about 550 patients with rheumatoid arthritis (RA) is described. These patients had been attending the practice of a former general practitioner who treated cases of rheumatoid arthritis with phenylbutazone and steroids. The number of diagnosed TB cases was 55. Six cases had a contagious lung localisation. The possible sources of the outbreak were analysed. Both a visit on a same day as a sputum positive patient (chi 2-trend: 20.4; p < 0.001) and the administration of steroids (odds ratio (OR): 36.2; 95% confidence interval (CI): 8.8-313) were independent risk factors. There also appeared to be a relationship between TB and RA (OR: 4.4; 95%-BI: 2.2-9.1). Exogenous re(infection) and endogenous reactivation are possible causes of this outbreak.
We conducted a dual study of phenotype and function of natural killer cells (NK) using flow cytometry, this study being applied to renal transplantation. The CD 16 and CD 56 clusters correlated well with NK cytotoxicity, especially for CD 3 lymphocytes, whereas CD 57 should no longer be considered a NK marker. NK activity was determined on K 562 or Daudi cells, either spontaneously or after in vitro activation with r-interleukin 2 (LAK). Cytotoxicity was analyzed after labeling of target cells by carboxyfluoro-diacetate and measured by flow cytometry. We found that in renal transplant recipients NK cells were deficient in numbers and functions and showed that LAK activity was also diminished. Azathioprine appeared to be the main immunosuppressant impairing NK cells. Viral infections increased the numbers and functions of NK cells, whereas during malignancies they remain as low as in uncomplicated recipients. NK cells deficiency might be involved in the high incidence of de novo malignancies in renal transplant recipients.