Effect of Thyroid Function on LDL Oxidation in Hypothyroidism and Hyperthyroidism

Abstract

Oxidized low-density lipoproteins (LDL) are highly suspected of initiating the atherosclerosis process. Hypothyroidism is frequently associated with hypercholesterolemia and carries increased risk for atherosclerosis. In contrast to hypothyroidism, hyperthyroidism is not associated with increased LDL cholesterol, but is associated with increased oxidized LDL. This study was designed to evaluate the changes in LDL oxidation in subjects with hypothyroidism or hyperthyroidism, and to reveal the effects of treatment in hypothyroidism and hyperthyroidism on LDL oxidation and lipid profiles. Thirty-two patients with hypothyroidism and 16 patients with hyperthyroidism were studied before the therapy and thereafter, when they were euthyroid with appropriate treatment. Plasma lipids and lipoproteins, and the oxidizability of LDL by determining the levels of malonaldehyde bis (dimethyacetyl) (MDA) and diene conjugation, were determined at baseline and after the patients were rendered euthyroid. The actual content of dienes in LDL particles was increased in hypothyroidism, with a decrease after T4 supplementation (p < .001). Dienes in LDL particles were increased in hyperthyroidism, with a decrease after treatment (p < .05). In hypothyroid patients, the lag phase was shorter in the pretreatment period than in the euthyroid period (p > .05). The lag phase of hyperthyroid patients was shorter in the pretreatment period than in the euthyroid period and hypothyroid state (p < .001). The Cu2+-catalyzed dienes of LDL and MDA oxidation in the hypothyroid state and the subsequent euthyroid states were decreased (p < .001). The Cu2+-catalyzed dienes of LDL (p < .01) and MDA oxidation (p < .001) in hyperthyroid patients after treatment were decreased. The enhanced LDL oxidation may play a role in the cardiac disease process in both hypothyroidism and hyperthyroidism.

Metabolic and cardiovascular risk in patients with a history of differentiated thyroid carcinoma: A case-controlled cohort study

“…While L-T4 treatment can improve dyslipidemia, the long-term effect of the L-T4 load on cardiovascular risk is unknown [ 33 , 34 ]. Overt hyperthyroidism is associated with reduced total- and HDL-cholesterol concentrations [ 35 , 36 ], which normalize after remission of hyperthyroidism [ 37 ]. Several studies have found no difference in lipid profiles in sub-clinical hyperthyroidism [ 38 , 39 ], though reduced cholesterol levels have sometimes been reported in subjects older than 55 years [ 40 ].…”

Glucose tolerance and lipid profile in longterm exogenous subclinical hyperthyroidism and the effects of restoration of euthyroidism, a randomised controlled trial

“…Regarding lipid metabolism, overt hyperthyroidism is associated with decreased plasma concentrations of total and/or LDL cholesterol, 3,[12][13][14][15][16] that normalize after correction of hyperthyroidism ( Table 2). [17][18][19] Subclinical hyperthyroidism is a state, in which the patient has a suppressed thyrotrophin (TSH) level (below 0·4 mU/l), although the free T4 level is within the normal range. This condition affects several organ systems, including bone [20][21][22][23] and the cardiovascular system.…”

“…Regarding lipid metabolism, overt hyperthyroidism is associated with decreased plasma concentrations of total and/or LDL cholesterol, 3,12–16 that normalize after correction of hyperthyroidism (Table 2). 17–19 …”

The Pathological Links between Adiposity and the Carpal Tunnel Syndrome

“…On the other side, the oxidation of the LDL-receptor increases, favoring inflammation and oxidative stress as described above [ 80 ]. The lipoprotein lipase activity is also impaired in hypothyroidism with a reduction in the TG clearance and an increase in the circulating VLDL particles [ 87 ]. The synthesis of endogenous cholesterol is not increased but the amount of available cholesterol in the liver is maintained or is even higher because the cholesterol absorption is increased and beta-oxidation in hepatocytes is decreased; the overall effect is a higher VLDL output from the liver [ 88 ].…”