madman
Super Moderator
Endocrine diseases may be associated with dyslipidaemia and may increase atherosclerotic cardiovascular disease (ASCVD) risk. This chapter describes changes in lipids and lipoproteins in diseases of the pituitary, thyroid, adrenal glands, ovaries, and testes, the mechanisms for these changes, ASCVD risk in these endocrine disorders, and whether treatment of the endocrine disorder improves the lipid profile and reduces ASCVD risk. Acromegaly, GH deficiency, Cushing syndrome, chronic glucocorticoid replacement, hypothyroidism, PCOS, and male hypogonadism can increase LDL-C and/or TG. Marked reductions in LDL-C are associated with hyperthyroidism, and extremely low HDL-C levels with testosterone and/or other anabolic steroid abuse. Acromegaly, GH deficiency, Cushing syndrome, and chronic glucocorticoid replacement are associated with increased ASCVD risk. Treatment of acromegaly, GH deficiency, hypothyroidism, Cushing syndrome, and testosterone deficiency reduces LDL-C, although statin therapy may still be needed. Effects on ASCVD are not known.
Hormones influence lipid and lipoprotein metabolism, and it is not surprising that endocrine diseases affect the lipid profile and may increase atherosclerotic cardiovascular disease (ASCVD) risk. Table 1 summarizes changes in low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG) and lipoprotein (a) [Lp (a)] in disorders of the pituitary, thyroid adrenal, and reproductive glands. This chapter describes changes in lipids in endocrine diseases, the underlying mechanisms for these changes, and the effect of treatment of the endocrine disease on dyslipidemia and ASCVD risk. This topic is the subject of the 2020 Endocrine Society Clinical Practice Guideline “Lipid Management in Patients with Endocrine Disorders.” [1].
Pituitary diseases
*Adult growth hormone (GH) deficiency
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
*Acromegaly
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Hypothyroidism and hyperthyroidism
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Adrenal disorders
*Cushing syndrome
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
*Chronic glucocorticoid therapy
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Menopause, and hormone replacement
*Pre-menopausal/Post-menopausal
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Polycystic ovary syndrome
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Male hypogonadism and testosterone replacement
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Testosterone and anabolic steroid abuse
-Lipid and lipoprotein alterations and mechanisms
-Management
Gender-affirming hormone therapy
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
Summary
Endocrine hormones affect lipid and lipoprotein metabolism. GH deficiency, acromegaly, Cushing syndrome, chronic glucocorticoid replacement, and hypothyroidism may elevate LDL-C and TG, and lower HDL-C. These diseases are associated with increased cardiovascular risk, which could be related to hormone abnormality and/or dyslipidemia. It is important to assess lipids in all these disorders. The increased risk of ASCVD in people with Cushing syndrome and chronic glucocorticoid replacement warrant treatment with statins if LDL-C is above 1.8 mmol/L (70 mg/dL). Treatment of endocrine diseases may reduce LDL-C and/or TG, although dyslipidemia may remain. Thyroid hormone treatment of overt and subclinical hypothyroidism reduces LDL-C. Treatment of hyperthyroidism raises LDLC. Therefore, in patients with hypo- or hyperthyroidism, the lipid profile should be repeated when thyroid function is normal.
Post-menopausal women as a group have increased ASCVD risk, compared to premenopausal women, although in postmenopausal women within 10 years after menopause, the risk of CHD may be unchanged or possibly decreased, while the risk of venous thromboembolism is increased. Several RCTs show that estrogen (and progestin) therapy in older women (more than 10 years after menopause), is associated with an increased risk of stroke, venous thromboembolism, and CHD. Male hypogonadism is associated with small changes in lipids and lipoproteins, which may improve with testosterone therapy; however, testosterone should be used for symptomatic hypogonadism and not for LDL-C reduction. Men, and women, who take supra-physiological doses of testosterone and/or other anabolic steroids (usually to build muscle and enhance athletic performance) have very low HDLC which should alert the endocrinologist to steroid abuse. Changes in lipids and lipoproteins associated with gender-affirming hormone therapy require further investigation.
Hormones influence lipid and lipoprotein metabolism, and it is not surprising that endocrine diseases affect the lipid profile and may increase atherosclerotic cardiovascular disease (ASCVD) risk. Table 1 summarizes changes in low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG) and lipoprotein (a) [Lp (a)] in disorders of the pituitary, thyroid adrenal, and reproductive glands. This chapter describes changes in lipids in endocrine diseases, the underlying mechanisms for these changes, and the effect of treatment of the endocrine disease on dyslipidemia and ASCVD risk. This topic is the subject of the 2020 Endocrine Society Clinical Practice Guideline “Lipid Management in Patients with Endocrine Disorders.” [1].
Pituitary diseases
*Adult growth hormone (GH) deficiency
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
*Acromegaly
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Hypothyroidism and hyperthyroidism
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Adrenal disorders
*Cushing syndrome
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
*Chronic glucocorticoid therapy
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Menopause, and hormone replacement
*Pre-menopausal/Post-menopausal
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Polycystic ovary syndrome
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Male hypogonadism and testosterone replacement
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
-Management
Testosterone and anabolic steroid abuse
-Lipid and lipoprotein alterations and mechanisms
-Management
Gender-affirming hormone therapy
-Lipid and lipoprotein alterations and mechanisms
-ASCVD risk
Summary
Endocrine hormones affect lipid and lipoprotein metabolism. GH deficiency, acromegaly, Cushing syndrome, chronic glucocorticoid replacement, and hypothyroidism may elevate LDL-C and TG, and lower HDL-C. These diseases are associated with increased cardiovascular risk, which could be related to hormone abnormality and/or dyslipidemia. It is important to assess lipids in all these disorders. The increased risk of ASCVD in people with Cushing syndrome and chronic glucocorticoid replacement warrant treatment with statins if LDL-C is above 1.8 mmol/L (70 mg/dL). Treatment of endocrine diseases may reduce LDL-C and/or TG, although dyslipidemia may remain. Thyroid hormone treatment of overt and subclinical hypothyroidism reduces LDL-C. Treatment of hyperthyroidism raises LDLC. Therefore, in patients with hypo- or hyperthyroidism, the lipid profile should be repeated when thyroid function is normal.
Post-menopausal women as a group have increased ASCVD risk, compared to premenopausal women, although in postmenopausal women within 10 years after menopause, the risk of CHD may be unchanged or possibly decreased, while the risk of venous thromboembolism is increased. Several RCTs show that estrogen (and progestin) therapy in older women (more than 10 years after menopause), is associated with an increased risk of stroke, venous thromboembolism, and CHD. Male hypogonadism is associated with small changes in lipids and lipoproteins, which may improve with testosterone therapy; however, testosterone should be used for symptomatic hypogonadism and not for LDL-C reduction. Men, and women, who take supra-physiological doses of testosterone and/or other anabolic steroids (usually to build muscle and enhance athletic performance) have very low HDLC which should alert the endocrinologist to steroid abuse. Changes in lipids and lipoproteins associated with gender-affirming hormone therapy require further investigation.
