Elsevier

Metabolism

Volume 21, Issue 7, July 1972, Pages 657-666
Metabolism

Estrogen-induced pancreatitis in patients with previously covert familial Type V hyperlipoproteinemia

https://doi.org/10.1016/0026-0495(72)90089-3Get rights and content

Abstract

Previously covert familial Type V hyperlipoproteinemia became overt in three women and one man, when pancreatitis followed postmenopausal and postprostatectomy estrogen administration. Exogenous and endogenous hypertriglyceridemia were severely exacerbated, carbohydrate tolerance worsened, and activity of postheparin lipolytic enzymes were depressed by estrogenic “therapy”. Amelioration of pancreatitis, decrements in hyperglyceridemia and hyperglycemia, and increments in postheparin lipolytic activities followed cessation of estrogens.

References (48)

  • M. Kekki et al.

    Plasma triglyceride turnover during use of oral contraceptives

    Metabolism

    (1971)
  • Z. Javier et al.

    Ovulatory suppressants, estrogens and carbohydrate metabolism

    Metabolism

    (1968)
  • I.B. Salans et al.

    Effect of insulin pretreatment on glucose and lipid metabolism of liver slices from normal rats

  • W.N. Spellacy et al.

    Glucose and insulin alterations after one year of combination type oral treatment

    Metabolism

    (1968)
  • W.N. Spellacy et al.

    Human growth hormone levels in normal subjects receiving an oral contraceptive

    JAMA

    (1967)
  • J. Slack

    Risks of ischaemic heart disease in familial hyperlipoprotaemic states

    Lancet

    (1969)
  • D.S. Fredrickson et al.

    Fat transport in lipoproteins. An integrated approach to mechanisms and disorders

    New Eng. J. Med.

    (1967)
    D.S. Fredrickson et al.

    Fat transport in lipoproteins. An integrated approach to mechanisms and disorders

    New Eng. J. Med.

    (1967)
    D.S. Fredrickson et al.

    Fat transport in lipoproteins. An integrated approach to mechanisms and disorders

    New Eng. J. Med.

    (1967)
    D.S. Fredrickson et al.

    Fat transport in lipoproteins. An integrated approach to mechanisms and disorders

    New Eng. J. Med.

    (1967)
    D.S. Fredrickson et al.

    Fat transport in lipoproteins. An integrated approach to mechanisms and disorders

    New Eng. J. Med.

    (1967)
  • C.J. Glueck et al.

    Norethindrone acetate, postheparin lipolytic activity and plasma triglycerides in patients with familial Types I, III, IV, and V hyperlipoproteinemia

    Ann. Intern. Med.

    (1971)
  • H.M.P. Poulsen

    Familial lipemia: A new form of lipidosis showing increase in neutral fats combined with attacks of acute pancreatitis

    Acta Med. Scand.

    (1950)
  • G. Klatskin et al.

    Relationship between relasping pancreatitis and essential hyperlipemia

    Amer. J. Med.

    (1952)
  • R.A. Joske

    Aetliologic factors in the pancreatic syndrome

    Brit. Med. J.

    (1955)
  • J.B. Gross et al.

    Chronic pancreatitis

    Amer. J. Med.

    (1956)
  • C. Wang et al.

    Serum lipids in acute pancreatitis

    Gastroenterology

    (1959)
  • N.J. Greenberger et al.

    Pancreatitis and hyperlipaemia: a study of serum lipid alterations in 25 patients with acute pancreatitis

    Medicine (Balt.)

    (1966)
  • Cited by (85)

    • Obesity, adiposity, and dyslipidemia: A consensus statement from the National Lipid Association

      2013, Journal of Clinical Lipidology
      Citation Excerpt :

      Very high TG levels characteristic of chylomicronemia lead to increased plasma viscosity and abnormal blood rheology,73,74 leading to flow disturbances and ischemia at the microvascular level. This mechanism has been postulated to be etiologic of TG-related pancreatitis, the most common clinical complication of severe hypertriglyceridemia and chylomicronemia.75,76 Disordered TG metabolism resulting in nonchylomicron hypertriglyceridemia is one of the five defining features of the metabolic syndrome.77

    • Hypertriglyceridemia-induced pancreatitis created by oral estrogen and in vitro fertilization ovulation induction

      2008, Journal of Clinical Lipidology
      Citation Excerpt :

      Because of these or other mechanisms, estrogen alone has been reported to induce pancreatitis without increased lipid levels.33 Estrogen-induced pancreatitis sometimes unmasks otherwise covert hyperlipoproteinemias.6 There is a report of a patient with type III hyperlipoproteinemia developing severe hypertriglyceridemia during pregnancy and after taking birth control pills.8

    • Clomiphene-induced acute pancreatitis without hypertriglyceridemia

      2007, American Journal of the Medical Sciences
      Citation Excerpt :

      Exogenous estrogens have been shown to increase the levels of both triglyceride and high-density lipoprotein. Estrogen replacement therapy or contraceptive therapy may bring about hypertriglyceridemia and pancreatitis.11–14 Tamoxifen, a nonsteroidal estrogen antagonist, also lowers the total and low-density lipoprotein cholesterol levels and increases the triglyceride and high-density lipoprotein cholesterol levels, which can be associated with pancreatitis.15–18

    • Lipids and Lipoproteins and Effects of Hormone Therapy

      2007, Treatment of the Postmenopausal Woman: Basic and Clinical Aspects, Third Edition
    View all citing articles on Scopus

    Supported in part by N.I.H. (NICHD) Grant 1 RO1 HD 04851, and by the General Clinical Research Center Grant RR-00068-10. A portion of this work was done during Dr. Glueck's tenure as an Established Investigator of the American Heart Association 1971–1976.

    1

    Charles J. Glueck, M.D.: Project Director, General Clinical Research Center, and Director, Lipoprotein Research Laboratory, University of Cincinnati College of Medicine, Department of Internal Medicine (Metabolism), Cincinnati General Hospital, Cincinnati, Ohio.

    2

    Deborah Scheel, B.A.: Research Assistant, General Clinical Research Center, University of Cincinnati College of Medicine, Department of Internal Medicine (Metabolism), Cincinnati General Hospital, Cincinnati, Ohio.

    3

    James Fishback, B.A.: Research Assistant, General Clinical Research Center, University of Cincinnati College of Medicine, Department of Internal Medicine (Metabolism), Cincinnati General Hospital, Cincinnati, Ohio.

    4

    Paula Steiner, B.A.: Master Technician, Lipoprotein Research Laboratory, General Clinical Research Center, University of Cincinnati College of Medicine, Department of Internal Medicine (Metabolism), Cincinnati General Hospital, Cincinnati, Ohio.

    View full text