Abstract
Thiamphenicol at the rate of 50 mg/kg/day given to female NZBxOUW F1 hybrid mice from weaning and continuing throughout life resulted in a considerable extension of lifespan, although this was less than in mice given the same drug dosage from first antinuclear antibody (ANA) positivity (Simpson, Aarons and Howie, 1979). Assessment of the changes in renal dysfunction and renal histology shows that thiamphenicol treatment did not prevent the development of immune complex glomerulonephritis although the rate of progression of the disease was slower than in untreated controls. Thiamphenicol failed to influence greatly the progressive anaemia which develops in these mice or to alter the pattern of ANA production. Although azotaemia developed in treated mice it was a terminal event. It was concluded that the action of thiamphenicol was to depress but not prevent immune complex formation possibly by impairing immunoglobulin formation although why immunofluorescent ANA formation remained unaffected is not understood.
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