The Effect of Endocrine Disorders on Lipids and Lipoproteins

Review
In: Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000.
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Excerpt

Endocrine disorders and the administration of various hormones can alter lipid metabolism and plasma lipid levels, which may increase or decrease the risk of atherosclerotic cardiovascular disease. In many instances the literature is not consistent with various studies reporting different results. These differences may be due to a variety of factors such as the differences in the severity of the disease state, differences in the duration of the disease, underlying genetic factors that differ between individuals and populations, differences in environmental factors such as diet, the presence of other abnormalities that can alter lipid metabolism such as obesity or diabetes, and other unrecognized factors that could influence the expression and manifestation of various endocrine disorders on lipid parameters. Prolactinomas are associated with an increase in total and LDL-C levels. GH deficient patients often have an increase in total cholesterol, LDL-C, and triglyceride levels and a decrease in HDL-C levels, whereas GH therapy decreases total cholesterol and LDL-C but increases Lp(a) levels. Acromegaly is associated with an increase in Lp(a) levels as seen in GH therapy, but paradoxically similar to GH deficiency, acromegaly is accompanied by an increase in plasma triglycerides and a decrease in HDL-C levels. Hypothyroidism leads to an increase in total cholesterol, LDL-C, and Lp(a) levels and normal or increased triglycerides and HDL-C. In contrast, hyperthyroidism is characterized by decreases in total cholesterol, LDL-C, and Lp(a) levels, as well as HDL-C levels. Patients with endogenous Cushing’s syndrome typically display an increase in total cholesterol and LDL-C, and triglycerides, while the administration of glucocorticoids frequently also increases HDL-C levels. Men with low testosterone levels may have high LDL-C and triglyceride levels and decreased HDL-C levels, although this relationship is confounded by obesity and the metabolic syndrome, a common cause of male hypogonadism. Androgen deprivation therapy results in an increase in LDL-C, triglycerides, and Lp(a) and a decrease in HDL-C. The effect of testosterone replacement therapy on plasma lipids and lipoproteins is modest and variable but high dose androgen therapy used by athletes can markedly decrease HDL-C and also reduce Lp(a) levels. The loss of estrogens (postmenopausal females) is associated with a modest increase in LDL-C with either no change or a small decrease in HDL-C. Estrogen administration decreases LDL-C and Lp(a) levels while increasing triglycerides and HDL-C levels but these effects are dependent on the dose and route of administration (transdermal has smaller effects than oral). Concurrent progesterone treatment has little or no effect on the decrease in LDL-C induced by estrogen administration but may blunt the estrogen effect on HDL-C and triglyceride levels depending on the androgenicity of the progesterone. The polycystic ovarian syndrome is associated with increases in LDL-C, triglycerides, and Lp(a) and decreases in HDL-C. The dyslipidemia that occurs with prolactinomas, GH deficiency, hypothyroidism, Cushing’s syndrome, male hypogonadism, androgen deprivation therapy, polycystic ovarian syndrome, and the loss of estrogens may contribute to an increased risk of atherosclerotic cardiovascular disease. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.

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