Serum PAF-acetylhydrolase in severe renal or hepatic disease in man: relationship to circulating levels of PAF and effects of nephrectomy or transplantation.

(1) PAF-acetylhydrolases form a major pathway for the degradation of platelet-activating factor (PAF). Here we investigate the role of the kidney and the liver in the control of PAF-acetylhydrolase levels by comparing normal subjects to patients with abnormal liver or kidney function. These patients had either severe chronic liver disease, chronic renal failure or were anephric. In a few cases PAF was also measured. (2) In those patients where PAF was measured there was no evidence that circulating PAF levels determined PAF-acetylhydrolase release. (3) In anephric patients serum PAF-acetylhydrolase levels were normal or even raised. Therefore the kidney is unlikely to be the usual major source of serum PAF-acetylhydrolase in man. (4) Liver patients with chronic cholestasis had elevated serum PAF-acetylhydrolase especially in stage III or IV primary biliary cirrhosis, as well as in a patient with secondary biliary cirrhosis and one with cholangiocarcinoma. Since normalisation of liver function following liver transplantation was accompanied by a reduction to normal or near normal PAF-acetylhydrolase levels, it is likely that the liver can play an important role in regulating levels of this enzyme in serum.