Hypothyroidism & Hypercholesterolemia

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is there any relation between both, especially in subclinical hypothyroidism? and why?

looking forwards for answers, and thanks for your time.

Highlights from UTD:

"HYPOTHYROIDISM - Many hypothyroid patients have high serum concentrations of total cholesterol and low-density-lipoprotein (LDL) cholesterol, and some have high serum concentrations of triglycerides, intermediate-density lipoproteins, apoprotein A-1 and apoprotein B.

With respect to serum high-density-lipoprotein (HDL) cholesterol concentrations, high, normal or low values have been reported in different series.

The excess risk of coronary heart disease observed with hypothyroidism has been thought to be due, at least in part, to the characteristic lipid abnormalities (including high LDL).

Pathophysiology — The primary mechanism for hypercholesterolemia in hypothyroidism is accumulation of LDL cholesterol due to a reduction in the number of cell surface receptors for LDL, resulting in decreased catabolism of LDL. A decrease in LDL receptor activity has also been described.

Other mechanisms also may affect the serum cholesterol concentration in hypothyroidism:

•LDL oxidation is significantly increased in hypothyroid patients, the degree of which is directly related to the serum LDL cholesterol concentration.
•Diminished secretion of cholesterol into bile has been demonstrated in hypothyroid rats.
•Reduced cholesteryl ester transfer (the net transfer of cholesterol from HDL to LDL and very-low-density-lipoprotein [VLDL]) in hypothyroidism may minimize the increase in serum LDL cholesterol concentrations.

A different mechanism, reduced lipoprotein lipase activity, is responsible for the development of hypertriglyceridemia in hypothyroidism. The rate of synthesis of triglycerides is normal.

All patients with hypercholesterolemia (and hypertriglyceridemia) should be screened for hypothyroidism (and other secondary causes of hyperlipidemia) before being given specific lipid-lowering drug therapy. If hypothyroidism is present, the patient should be treated for three to four months with T4. If the serum lipid concentrations are not then normal, specific lipid-lowering therapy may be indicated. Patients in the latter group presumably have hypothyroidism superimposed upon primary hyperlipidemia.

SUBCLINICAL HYPOTHYROIDISM — Most patients with subclinical hypothyroidism have normal serum lipid concentrations. However, some have slightly high serum total and LDL cholesterol and lipoprotein (a) concentrations. Serum HDL cholesterol concentrations are low or normal in patients with subclinical hypothyroidism.

HYPERTHYROIDISM — Patients with hyperthyroidism have changes in lipid metabolism generally opposite to those described above for hypothyroidism. Serum total, LDL and HDL cholesterol concentrations tend to be low, as do serum apoprotein-B concentrations. Fatty acid clearance is increased, but lipolysis is increased even more, resulting in high serum fatty acid concentrations."
 
Highlights from UTD:

"HYPOTHYROIDISM - Many hypothyroid patients have high serum concentrations of total cholesterol and low-density-lipoprotein (LDL) cholesterol, and some have high serum concentrations of triglycerides, intermediate-density lipoproteins, apoprotein A-1 and apoprotein B.

With respect to serum high-density-lipoprotein (HDL) cholesterol concentrations, high, normal or low values have been reported in different series.

The excess risk of coronary heart disease observed with hypothyroidism has been thought to be due, at least in part, to the characteristic lipid abnormalities (including high LDL).

Pathophysiology — The primary mechanism for hypercholesterolemia in hypothyroidism is accumulation of LDL cholesterol due to a reduction in the number of cell surface receptors for LDL, resulting in decreased catabolism of LDL. A decrease in LDL receptor activity has also been described.

Other mechanisms also may affect the serum cholesterol concentration in hypothyroidism:

•LDL oxidation is significantly increased in hypothyroid patients, the degree of which is directly related to the serum LDL cholesterol concentration.
•Diminished secretion of cholesterol into bile has been demonstrated in hypothyroid rats.
•Reduced cholesteryl ester transfer (the net transfer of cholesterol from HDL to LDL and very-low-density-lipoprotein [VLDL]) in hypothyroidism may minimize the increase in serum LDL cholesterol concentrations.

A different mechanism, reduced lipoprotein lipase activity, is responsible for the development of hypertriglyceridemia in hypothyroidism. The rate of synthesis of triglycerides is normal.

All patients with hypercholesterolemia (and hypertriglyceridemia) should be screened for hypothyroidism (and other secondary causes of hyperlipidemia) before being given specific lipid-lowering drug therapy. If hypothyroidism is present, the patient should be treated for three to four months with T4. If the serum lipid concentrations are not then normal, specific lipid-lowering therapy may be indicated. Patients in the latter group presumably have hypothyroidism superimposed upon primary hyperlipidemia.

SUBCLINICAL HYPOTHYROIDISM — Most patients with subclinical hypothyroidism have normal serum lipid concentrations. However, some have slightly high serum total and LDL cholesterol and lipoprotein (a) concentrations. Serum HDL cholesterol concentrations are low or normal in patients with subclinical hypothyroidism.

HYPERTHYROIDISM — Patients with hyperthyroidism have changes in lipid metabolism generally opposite to those described above for hypothyroidism. Serum total, LDL and HDL cholesterol concentrations tend to be low, as do serum apoprotein-B concentrations. Fatty acid clearance is increased, but lipolysis is increased even more, resulting in high serum fatty acid concentrations."


Thanks a lot for the detailed reply. Could you tell me please what ''UTD'' stands for?
 
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