One of the most common types of endocrine abnormalities is thyroid diseases, and this is the case worldwide, including in India. These conditions distinguish themselves by unique characteristics like the ease of diagnosis, the viability of medical intervention, and the obvious visibility that even a small thyroid enlargement affords the attending physician. In order to effectively manage these disorders, prompt diagnosis and therapeutic intervention are essential [1]. The effects of variations in thyroid hormone levels ripple through several physiological domains, including oxygen intake, body temperature, growth, brain activity, and sensitivity to other hormones. Additionally, these hormones control how proteins, fats, carbs, vitamins, nucleic acids, and inorganic ions are metabolised [2]. An increase in basal metabolic rate is caused by the excretion of significant amounts of these substances. At the same time, the rate of nutrient uptake for energy production increases significantly, and protein synthesis increases as well. When taken together, these elements lead to a widespread increase in the functional activity of the body. Notably, thyroid hormones affect development processes in both general and targeted ways [3]. Thyroid hormones significantly alter the way that fats are metabolised. These hormones promote the mobilisation of fat deposits in adipose tissue, which raises plasma concentrations of fatty acids and encourages cells to oxidise free fatty acids more quickly. Together, thyroid disorders alter the makeup and movement of lipoproteins in plasma, resulting in unique changes in plasma lipid profiles, the degree of which depends on the type and severity of thyroid dysfunction [4]. There has been much discussion in the scientific community on a higher risk of coronary artery disease in hypothyroid patients due to changes in lipoprotein profiles that have atherogenic consequences [5]. Whereas hyperthyroidism results in increased cholesterol excretion and accelerated low-density lipoprotein (LDL) turnover, which lowers total cholesterol and LDL cholesterol levels, hypothyroidism lowers HDL-C [6,7]. Triglyceride turnover and chylomicron clearance are significantly impacted by thyroid hormones, which also affect hepatic lipogenesis in both hyperthyroidism and hypothyroidism. Through increased oxidation of nascent fatty acids and decreased re-esterification, thyroid hormones lower the formation of very low-density lipoproteins (VLDL) and hepatic total cholesterol. Increased hepatic VLDL secretion is seen in hypothyroid individuals [8]. Previous research has documented higher plasma triglyceride concentrations in hypothyroidism, which is consistent with current findings. The ratio of low-density lipoprotein (LDL) to high-density lipoprotein (HDL) is higher in hypothyroidism and lower in hyperthyroidism [9, 10]. The significance of this fat-laden discussion is highlighted by the proven link between high cholesterol levels and the risk of coronary artery disease [11]. Therefore, the goal of the current study is to explain the changes in lipid profiles that occur when thyroid dysfunction is present.

Aims & objectives: This project aims to provide information on how to identify lipid abnormalities in hypothyroid and hyperthyroid people early on, and relationship of lipid profile parameters with the thyroid dysfunctions.

This cross-sectional study was conducted in the collaboration of department of pathology and biochemistry in a tertiary care hospital, India. The study sample comprised of 120 participants attending out- patient and in-patient departments during the study period.

The participant pool were divided into three groups: forty patients with hypothyroidism (the hypothyroid group), forty patients with hyperthyroidism (the hyperthyroid group), and forty patients with normal thyroid function (the euthyroid group).

Inclusion Criteria:

• Patient’s ≥18 years of age with both genders
• Patients diagnosed with hypothyroidism, Hyperthyroid or euthyroid
• Patients with no history of thyroxine and hypolipidemic drugs
• Patients who provide written informed consent for the study

Exclusion Criteria:

• Patient’s less than 18 years of age
• Patients having diabetes mellitus, pregnancy, hypercortisolism or pituitary diseases
• History of drugs including; thyroxine, hypolipidemic, oral contraceptives, androgens, steroids, and immunosuppressant
• Patients who not provides written informed consent for the study

The personal information, medical and pharmacological history and personal habits were recorded for each participant. T3, T4 and TSH test was done by automated electro Chemiluminescence immunoassay. Participants were categorized according to the American Thyroid Association criteria into 3 groups [12]; euthyroid, when TSH between 0.4 and 4.5 mic IU/mL, SCH, when TSH >4.5 with normal level of FT4, and overt hypothyroidism, when TSH >4.5 with low level of FT4. At the same time, all three of the previously described groups had their levels of total cholesterol, triglycerides, high-density lipoprotein (HDL), very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and the LDL/HDL ratio estimated.

Statistical analysis: All statistical analyses of data were performed using the Statistical Package for the Social Sciences (SPSS) version 20.0 for windows (IBM Corp.) and Microsoft Excel 2010. Differences in mean ± SD values were analyzed for statistical significance using one-way ANOVA test and chi-square test. P<0.05 was considered as statistically significant.

In the present study, 120 patients with thyroid disorders were recruited. Among patient’s majority of them (39.2%) were 41-50 years age group, with female predominance (61.8%). Most of them (59.2%) were residing at urban area and 45% belong to middle socio-economic class. 35.8% patients were obese (Table I).

Tables 1: The outcomes of the current study are displayed in

Results of lipid assays (Table.2) mean serum levels of TC, TG VLDL, LDL cholesterol and LDL/HDL ratio indicated significantly higher among hypothyroid group as compared to euthyroid group (p<0.05), whereas mean HDL level were significantly lower in hypothyroid group as compared to euthyroid group (p<0.05).

Table 2: Lipid profile parameters in hypothyroid and euthyroid group

Mean serum levels of TC, TG, VLDL, LDL cholesterol and LDL/HDL ratio were significantly lower among hyperthyroid group as compared to euthyroid group (p<0.05), whereas mean HDL level were significantly higher in hyperthyroid group as compared to euthyroid group (p<0.05).

Table 3: Lipid profile parameters in hyperthyroid and euthyroid group

Dyslipidemia, a common finding in patients with thyroid disease, is predominantly due to the influence of thyroid hormones on almost all aspects of lipid metabolism.

In our study majority of the subjects were 41-50 years age group, predominantly females; concordance findings also reported by Al‑odat et al [13].

During the current investigation, the hypothyroid group's average serum total cholesterol levels were statistically significantly higher than those of the Euthyroid group. Prior research done by Rizos, et al [14] and Upadhyay P, et al [15] have documented a similar increase in total cholesterol. One possible explanation for this increase is the odified hepaticlipase activity. Notably, hypothyroidism has been linked to a decrease in lipoprotein lipase activity.

Compared to the normal euthyroid group, the hypothyroid group's average serum triglyceride level was shown to be considerably greater. Similar patterns were noted in other studies; Chaudhuri, et al [16] and Zhenjiang H, et al [17]. The elevated triglyceride levels in the hypothyroid group are thought to be caused by decreased lipoprotein lipase activity. Plasma triglyceride production is unaffected in hypothyroidism patients, but fractional clearance of endogenous and exogenous triglycerides is significantly reduced. It seems that this change plays a role in the development of hypertriglyceridemia in these people [18].

In this study, the hypothyroid group's HDL levels significantly decreased when compared to the control group Jawzal K, et al. [19] and Madhura NS et al. [20] reported similar results. The decreased synthesis, mobilisation, and breakdown of lipids that frequently occur in the setting of hypothyroidism may be the cause of the decrease in HDL levels. On the other hand, participants in the hypothyroid group did not have significantly greater VLDL levels than those in the control group. These results are consistent with Tarboush et al [21] findings; Generally speaking, VLDL catabolism slows down in hypothyroidism. In addition to structural changes within the VLDL particles themselves, these changes in VLDL dynamics are closely associated with changes in the activity of lipoprotein lipase and hepatic lipase.

The hypothyroid group's mean LDL readings were statistically significantly higher than those of the control group. Reduced fractional clearance of LDL particles may be the cause of this. A lower number of LDL receptors in the liver may be the cause of this attenuation. These results are consistent with the findings of the Alamdari S et al. study [22]. Additionally, it was discovered that the hypothyroid group's mean LDL-C/HDL-C ratio was much higher than the euthyroid group's. These outcomes are consistent with what Sharma A, et al. [23].

When compared to the euthyroid group, the hyperthyroid group's mean LDL: HDL ratio value showed a statistically significant decrease. The hyperthyroid group showed a significant decline in this ratio. These results are in line with what James SR et al. [24].

A significant relationship between thyroid dysfunction and dyslipidemia was noticed. It is possible for dysregulated thyroid function to result in significant changes to the lipid profile, which is a significant risk factor for cardiovascular disorders. Thus; thyroid dysfunction can have an important effect on lipid profile. Screening for thyroid dysfunction is critical in all dyslipidemic patients, as well as in all patients with unexpected improvement or worsening of their lipid profile.

Conflicts of interest: none

Source of funding: none

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