[Update 2016] [OA] Md KF, Brinton EA, Grunfeld C. The Effect of Endocrine Disorders on Lipids and Lipoproteins. 2000. The Effect of Endocrine Disorders on Lipids and Lipoproteins - Endotext - NCBI Bookshelf
A variety of endocrine disorders can alter lipid metabolism resulting in changes in plasma lipid and lipoprotein levels. There is a not always a perfect correlation between the changes in hormone deficiency and hormone excess or their therapy.
Prolactinomas are associated with an increase in total and LDL cholesterol levels.
Growth hormone deficient patients often have an increase in total cholesterol, LDL cholesterol, and triglyceride levels and a decrease in HDL cholesterol levels, whereas growth hormone therapy decreases total cholesterol and LDL cholesterol but increases Lp(a) levels.
Acromegaly is associated with an increase in Lp(a) levels as seen in growth hormone therapy, but paradoxically similar to growth hormone deficiency, acromegaly is accompanied by increased an increase in plasma triglycerides and a decrease in HDL cholesterol levels.
Hypothyroidism leads to an increase in total cholesterol, LDL cholesterol, and Lp(a) levels and normal or increased triglycerides and HDL cholesterol. In contrast, hyperthyroidism is characterized by decreases in total cholesterol, LDL cholesterol, and Lp(a) levels, as well as HDL cholesterol levels.
Patients with endogenous Cushing's syndrome typically display an increase in total and LDL cholesterol, and triglycerides, while the administration of glucocorticoids frequently increases HDL cholesterol levels.
Men with low testosterone levels may have high LDL cholesterol and triglyceride levels and decreased HDL cholesterol 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 cholesterol, triglycerides, and Lp(a) and a decrease in HDL cholesterol.
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 cholesterol and also reduce Lp(a) levels.
The loss of estrogens (postmenopausal females) is associated with a modest increase in LDL cholesterol with either no change or a small decrease in HDL cholesterol. Estrogen administration decreases LDL cholesterol and Lp(a) levels while increasing triglycerides and HDL cholesterol 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 cholesterol induced by estrogen administration but may blunt the estrogen effect on HDL cholesterol and triglyceride levels depending on the androgenicity of the progesterone. The polycystic ovarian syndrome is associated with increases in LDL cholesterol, triglycerides, and Lp(a) and decreases in HDL cholesterol.
The dyslipidemia that occurs with prolactinomas, growth hormone deficiency, 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
A variety of endocrine disorders can alter lipid metabolism resulting in changes in plasma lipid and lipoprotein levels. There is a not always a perfect correlation between the changes in hormone deficiency and hormone excess or their therapy.
Prolactinomas are associated with an increase in total and LDL cholesterol levels.
Growth hormone deficient patients often have an increase in total cholesterol, LDL cholesterol, and triglyceride levels and a decrease in HDL cholesterol levels, whereas growth hormone therapy decreases total cholesterol and LDL cholesterol but increases Lp(a) levels.
Acromegaly is associated with an increase in Lp(a) levels as seen in growth hormone therapy, but paradoxically similar to growth hormone deficiency, acromegaly is accompanied by increased an increase in plasma triglycerides and a decrease in HDL cholesterol levels.
Hypothyroidism leads to an increase in total cholesterol, LDL cholesterol, and Lp(a) levels and normal or increased triglycerides and HDL cholesterol. In contrast, hyperthyroidism is characterized by decreases in total cholesterol, LDL cholesterol, and Lp(a) levels, as well as HDL cholesterol levels.
Patients with endogenous Cushing's syndrome typically display an increase in total and LDL cholesterol, and triglycerides, while the administration of glucocorticoids frequently increases HDL cholesterol levels.
Men with low testosterone levels may have high LDL cholesterol and triglyceride levels and decreased HDL cholesterol 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 cholesterol, triglycerides, and Lp(a) and a decrease in HDL cholesterol.
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 cholesterol and also reduce Lp(a) levels.
The loss of estrogens (postmenopausal females) is associated with a modest increase in LDL cholesterol with either no change or a small decrease in HDL cholesterol. Estrogen administration decreases LDL cholesterol and Lp(a) levels while increasing triglycerides and HDL cholesterol 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 cholesterol induced by estrogen administration but may blunt the estrogen effect on HDL cholesterol and triglyceride levels depending on the androgenicity of the progesterone. The polycystic ovarian syndrome is associated with increases in LDL cholesterol, triglycerides, and Lp(a) and decreases in HDL cholesterol.
The dyslipidemia that occurs with prolactinomas, growth hormone deficiency, 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
