Severe Endogenous Hypertriglyceridemia During Treatment with Estrogen and Oral Contraceptives<sup>1</sup>

Zorrilla, E; Hulse, Mildred; Hernandez, A; Gershberg, Herbert

doi:10.1210/jcem-28-12-1793

Cited by 67 publications

(9 citation statements)

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“…Estrogens and estrogen-containing oral contraceptives elevate triglyceride (TG)1 levels in normal women (1) and may also aggravate pre-existing hypertriglyceridemia, sometimes producing marked hyperlipidemia (2) and, occasionally, a complication of hypertriglyceridemia such as pancreatitis (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

“…Subcutaneous buttock adipose tissue biopsy was performed by the method of Hirsch and Goldrick (25) and fat cell diameter was measured from a fixed frozen section of adipose tissue by 2 Using specific antisera kindly given by Doctors Christian Ehnholm, Jussi Huttunen, and Esko Nikkila. Goldrick (27) and fat cell weight was obtained by multiplying the cell volumne by the specific gravity of triglyceride.…”

Section: Introductionmentioning

confidence: 99%

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Effect of estrogen on post-heparin lipolytic activity. Selective decline in hepatic triglyceride lipase.

Applebaum¹,

Goldberg²,

Pykälistö³

et al. 1977

J. Clin. Invest.

200

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A B S T R A C T The rise in plasma triglyceride (TG) levels associated with estrogen administration has been thought to arise from impaired clearance because of the uniform suppression of post-heparin lipolytic activity (PHLA). Recently PHLA has been shown to consist of two activities: hepatic TG lipase and extrahepatic lipoprotein lipase (LPL). To determine whether estrogen might induce a selective decline in one of these activities, both hepatic TG lipase and extrahepatic LPL were measured in postheparin plasma from 13 normal women before and after 2 wk of treatment with ethinyl estradiol (1 ,ug/kg per day). Hepatic TG lipase and extrahepatic LPL were determined by two techniques: (a) separation by heparin-Sepharose column chromatography, and (b) selective inhibition with specific antibodies to post-heparin hepatic TG lipase and milk LPL. Estrogen uniformly depressed hepatic TG lipase as measured by affinity column (-68±12%, mean±SD, P < 0.001) or antibody inhibition (-63±11%, P < 0.001). Extrahepatic LPL was not significantly changed by affinity column (-22±40%) or antibody inhibition (-3+42%). Direct measurement of adipose tissue LPL from buttock fat biopsies also showed no systematic change in the activated form of LPL measured as heparin-elutable LPL (+64+164%) or in the tissue form of LPL measured in extracts of acetone-ether powders (+21±77%). The change in hepatic TG lipase correlated with the change in PHLA (r = 0.969, P < 0.01). However, neither the change in PHLA nor hepatic TG lipase correlated with the in-

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of estrogen on post-heparin lipolytic activity. Selective decline in hepatic triglyceride lipase.

Applebaum¹,

Goldberg²,

Pykälistö³

et al. 1977

J. Clin. Invest.

200

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“…Common estrogen-containing treatments and conditions include birth control pills, hormone replacement therapy for menopause, tamoxifen treatment, clomiphene treatment for polycystic ovary syndrome, and pregnancy. [1][2][3][4][5] In male patients, hypertriglyceridemia was reported in postprostatectomy estrogen therapy 6 and in high-dose estrogen therapy as a preparatory step for sex-change surgery. 7 Estrogen-induced severe hypertriglyceridemia can sometimes lead to severe pancreatitis.…”

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confidence: 99%

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

Lee

Goldberg

2008

Journal of Clinical Lipidology

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Hypertriglyceridemia is one of the known causes of pancreatitis. Estrogen treatment can aggravate hypertriglyceridemia by increasing very low density lipoprotein secretion and reducing hepatic triglyceride lipase. In this paper, we present 3 patients who developed severe hypertriglyceridemia with conditions that increased estrogen. Two patients were found to have genetic lipoprotein lipase deficiency and were treated with birth control pills. The third was a patient with polycystic ovary disease who was receiving ovulation induction therapy for in vitro fertilization.

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“…These increments largely or entirely disappeared if therapy was stopped but were still present at the twenty-second to twenty-fourth month if treatment continued. 1 The group of work-ers headed by Zorilla 18 also reported increased serum triglycerides, pre-beta lipoproteins, and cholesterol during sequential therapy with mestranol and mestranol chlormadinone acetate (Table IV).…”

Section: Discussionmentioning

confidence: 98%

Serum lipids during oral contraceptive exposure

Corredor

Mendelsohn

Sabeh

et al. 1970

Clin Pharma and Therapeutics

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The serum total cholesterol did not change significantly du ring 6 to 60 months of exposure to an oral contraceptive steroid combination (mestranol and norethynodrel). It has been indicated that the use of oral contraceptive steroids is associated with increases or no change in serum cholesterol/' 2, 3, 6, 8, 11, 13, 17 triglycerides,1,2 3, 6, 8, 11, 17 phospholipids,2' 3 beta lipoproteins,13 and low density and very low density lipoproteins. 1 , 2, 17 The studies cited vary in the particular steroids used, their dosages, and the duration of exposure to the contraceptives. Also, in some of the studies,s, 8, 17 pre-exposure observations were not available, and deductions concerning possible lipid effects of the oral contraceptive agent or agents were based on comparisons with untreated controls.The data herein presented are based on studies in women using only one pair of steroids, namely, mestranol and norethynodrel (Enovid) in one of three dosage combinations for contraception.Aided by grants from the Addison H. Gibson Foundation, the Western Pennsylvania Arthritis Foundation, and the Commonwealth of Pennsylvania.Received for publication Aug. 11, 1969. Accepted for publication Oct. 7, 1969. 188 Materials and methodsSerum total and alpha and beta lipoprotein cholesterol 9 , 12, 15 and total triglycerides 16 were measured at intervals of 6 months or less in 25 women (totalling 28 treatment periods ) in the fasting state prior to and during ingestion of mestranol and ethynodrel on Days 5 through 26 of the menstrual cyde. Enovid-E (mestranol 0.1 mg., norethynodrel 2.5 mg.), Enovid-5 (mestranol 0.075 mg., norethynodrel 5 mg.), and Enovid-10 (mestranol 1.15 mg., norethynodrel 10 mg.) were taken by 19, 8, and 1 of the women, respectively.Body weight was recorded at each visit. Our da ta are based on a minimum of 6 months of therapy or multiples thereof. When multiple measurements of serum lipids were performed in a patient prior to or within the initial or sueceeding 6 month period of observation, these were averaged and treated as one determination within that interval. The same procedure was followed with the body weight data. The statistical significance of any

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Severe Endogenous Hypertriglyceridemia During Treatment with Estrogen and Oral Contraceptives¹

Cited by 67 publications

References 0 publications

Effect of estrogen on post-heparin lipolytic activity. Selective decline in hepatic triglyceride lipase.

Effect of estrogen on post-heparin lipolytic activity. Selective decline in hepatic triglyceride lipase.

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

Serum lipids during oral contraceptive exposure

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Severe Endogenous Hypertriglyceridemia During Treatment with Estrogen and Oral Contraceptives1

Cited by 67 publications

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Effect of estrogen on post-heparin lipolytic activity. Selective decline in hepatic triglyceride lipase.

Effect of estrogen on post-heparin lipolytic activity. Selective decline in hepatic triglyceride lipase.

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

Serum lipids during oral contraceptive exposure

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Severe Endogenous Hypertriglyceridemia During Treatment with Estrogen and Oral Contraceptives¹