Impact of Subclinical Hypothyroidism on Liver Enzymes and Lipid Profile

Subclinical Hypothyroidism

subclinical hypothyroidism on liver enzymes and lipid profile

the goal of the randomized controlled observational study is to observe the effect of subclinical hypothyroidism on liver enzymes and lipid profile

Subclinical hypothyroidism (SCH) is a prevalent endocrine disorder defined by elevated levels of thyroid-stimulating hormone (TSH) with normal concentrations of free thyroxine (T4) \[1\]. Despite its often-asymptomatic nature, SCH has been increasingly recognized for its association with a variety of metabolic abnormalities, with lipid profile disturbances being particularly notable\[2\]. The thyroid gland is one of the primary endocrine glands in human body and is in charge of the hormones triiodothyronine (T3) and thyroxine (T4). These hormones influence hepatic functions by regulating all cells' baseline metabolic rates, including hepatocytes. Therefore, any thyroid condition may impair liver function\[3\] . sub clinical hypothyroidism is indicated by a moderate rise in TSH levels (TSH \> 4 mIU/l), along with normal thyroid hormone levels. Approximately 3% of the general population is affected by overt hypothyroidism. However, sub clinical hypothyroidism is found in 5-10% of the global population, as well as 8-10% of individuals aged over 65 years \[4\]. It should be noted that thyroid hormones have a crucial impact on multiple organs, especially the liver\[5\]. SCH is more common in women, the elderly, and individuals with a family history of diabetes and thyroid diseases (6, 7)SCH patients had significantly higher triglyceride (TG) levels (1.69 ± 1.9 vs. 1.45 ± 1.4) than the healthy population \[8\]. Another study by Sindhu and Vijay (9) suggested that SCH patients had more significant dyslipidemia than the euthyroid population, including total cholesterol(TC),very low-density lipoprotein cholesterol (VLDL-C), and low-density lipoprotein cholesterol (LDL-C). Subclinical hypothyroidism (SCH) contributes to the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) through several mechanisms \[10-12\]. One significant mechanism involves the activity of thyroid-stimulating hormone (TSH) on the cell membrane of hepatocytes, which disrupts triglyceride metabolism in the liver. Additionally, atherogenic dyslipidemia is commonly observed in patients with hypothyroidism. The primary cause of hyperlipidemia associated with hypothyroidism is a decrease in cholesterol excretion and a significant rise in apoB lipoproteins. This is mainly due to insufficient breakdown and turnover of cholesterol, stemming from a reduction in the number of low-density lipoprotein (LDL) receptors present on the surface of hepatocytes

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