hepatic 25-hydroxylation of vitamin D and that alcohol, while having no effect on 25 OH D production in adult livers, inhibits synthesis in pup livers. Alcohol-mediated decreases in pup hepatic 25 OH D production as well as decreases in 25 OH D transport from mother to fetus (13) Printed in U. S. A. Fatty Acid Abnormalities in Cystic Fibrosis PHILIP M. FARRELL, ELAINE H. MISCHLER, MICHAEL J. ENGLE, D. JEANNETTE BROWN, AND SZE-ME1 LAU Departments of Pediatrics and Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53792ABSTRACT. Fatty acids were measured by gas chromatography in lipid extracts of plasma and tissues obtained from three categories of 46 patients with cystic fibrosis. Low levels of the major essential fatty acid linoleate were found in plasma total lipids of patients who had malabsorption but not in those without evidence of steatorrhea. Circulating arachidonic acid was only slightly decreased, and the unusual triene reflecting pathologically altered fatty acid metabolism (20:3w9) was generally not detected, nor was the trieneltetraene ratio abnormal except for in Received February 1, 1984; accepted August 24, 1984 of malabsorption, namely plasma carotene (r = 0.64) and fecal fat excretion (r = 0.76). Our data therefore indicate that the abnormality in linoleate is associated with (secondary to) malabsorption of dietary fat despite pancreatic enzyme replacement therapy and consumption of a regular diet. The frequency of this alteration was determined to be quite high in 40 patients with steatorrhea, 85% of whom showed values below the lower limit of normal for plasma linoleate. It was of interest to find markedly decreased levels of linoleate in adipose tissue, cardiac muscle, and lung and lesser reductions in liver and psoas muscle taken at autopsies. Tissue arachidonic acid percentage was normal, however, and 20:3w9 was rarely present. Thus, the physiological significance of this common abnormality in

The discrepancy between the presence of necrosis and the occurrence of MOF favors association but not cause in AP. A complex, systems-based, pleiotropic inflammatory network with a common root, in which the extent of pancreatic necrosis influences the severity of MOF in certain individuals and MOF exacerbates the development of pancreatic necrosis in others, seems more likely.

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