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Subclinical chronic pancreatitis in type I hyperlipoproteinemia

  • Ronald M. Krauss
    Correspondence
    Requests for reprints should be addressed to Dr. Ronald M. Krauss.
    Footnotes
    Affiliations
    Bethesda, Maryland USA
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  • Arnold G. Levy
    Footnotes
    Affiliations
    Bethesda, Maryland USA
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  • Author Footnotes
    1 From the Molecular Disease Branch of the National Heart and Lung Institute, and the Digestive Disease Branch of the National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Maryland.
    ∗ Present address: Donner Laboratory, University of California, Berkeley, California 94720.
    † Present address: Division of Gastroenterology, Department of Medicine, The George Washington University Medical Center, Washington, D.C. 20037.
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      Abstract

      Severe pancreatic exocrine insufficiency was demonstrated in a 41 year old man with familial type I hyperlipoproteinemia (fat-induced hyperlipemia). Plasma triglyceride concentration failed to increase significantly with increased dietary fat intake, and fecal fat excretion was markedly increased. Indices of intestinal function were normal. Pancreatic enzyme therapy resulted in reduced fat excretion and increased plasma triglyceride concentration. Secretin stimulation tests revealed impaired duodenal fluid volume, bicarbonate and pancreatic enzyme responses. Insulin-dependent diabetes mellitus had been diagnosed three years earlier. No attacks of acute pancreatitis had occurred in the preceding 20 years, and it is suggested that pancreatic damage may have resulted from repeated subclinical pancreatic insults due to elevated plasma lipid levels. This report is the first to indicate that pancreatic exocrine insufficiency may occur as a late complication of hyperlipemic disorders in the absence of recurrent acute pancreatitis. Steatorrhea may not be apparent because of therapeutic restriction of dietary fat, and the first manifestation of pancreatic exocrine disease may be an amelioration of fat-induced hyperlipemia.
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