Estrogen-induced pancreatitis in patients with previously covert familial Type V hyperlipoproteinemia☆
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Obesity, adiposity, and dyslipidemia: A consensus statement from the National Lipid Association
2013, Journal of Clinical LipidologyCitation 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
The interaction of familial and secondary causes of hypertriglyceridemia: Role in pancreatitis
2012, Journal of Clinical LipidologyHypertriglyceridemia-induced pancreatitis created by oral estrogen and in vitro fertilization ovulation induction
2008, Journal of Clinical LipidologyCitation 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 SciencesCitation 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
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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.