Skip to main content
Download PDF

A comparative study on serum lipid levels in patients with thyroid dysfunction: a single-center experience in Ethiopia

BMC Endocrine Disorders volume 25, Article number: 47 (2025) Cite this article

Abstract

Background

Thyroid diseases are the most common endocrine disorders worldwide. Thyroid hormones are essential for lipid synthesis, metabolism, and mobilization. Lipid levels in the blood may be altered when there is thyroid dysfunction. Lipid changes are linked to hyperthyroidism and primarily involve total and low-density lipoprotein cholesterol. The serum lipid profile is negatively impacted by hypothyroidism, which may increase the risk of atherosclerotic disease development. Thus, hypothyroidism constitutes a significant cause of secondary dyslipidemia. However, the results obtained from different studies are inconsistent, and there are few data regarding lipid profiles in thyroid dysfunction patients in the study area. Therefore, this study aimed to assess the lipid profile of thyroid dysfunction patients at Wolaita Sodo University Comprehensive Specialized Hospital from May 1 to June 15, 2021.

Methods

A comparative cross-sectional study was conducted involving 200 participants (100 thyroid dysfunction patients and 100 age- and sex-matched controls). Socio-demographic and related data were collected from the study participants via a pretested structured questionnaire through face-to-face interviews. Independent sample T tests and Mann‒Whitney U tests were used for data analysis. P < 0.05 indicated statistical significance.

Results

Out of 200 study participants 40 (20%) hyperthyroid, 60 (30%) hypothyroidism, and 100 (50%) controls. In individuals with hyperthyroidism, the levels of triglycerides, total cholesterol, and low-density lipoprotein cholesterol were significantly lower than those in the control group. Compared to the control group, the hypothyroidism patients had significantly higher levels of triglycerides, low-density lipoprotein cholesterol, total cholesterol, and high-density lipoprotein cholesterol.

Conclusion

The lipid profile can change significantly as a result of thyroid dysfunction. Biochemical screening of lipid profiles is essential for improving patients with thyroid dysfunction with dyslipidemia.

Peer Review reports

Introduction

Thyroid hormones stimulate many aspects of carbohydrate metabolism, including quick uptake of glucose by cells, enhanced glycolysis, enhanced gluconeogenesis, and an accelerated rate of absorption from the gastrointestinal tract. Moreover, they enhance insulin production and consequently carbohydrate metabolism [1]. They also promote fat metabolism and stimulate protein synthesis. They cause quick mobilization of fat from fat tissues, increase plasma fatty acid concentrations and accelerate the oxidation of free fatty acids by cells [1, 2]. Additionally, they regulate important processes involved in thermogenesis and energy consumption [3, 4].

The majority of thyroid diseases are caused by abnormalities in the thyroid hormone production rate. Hyperthyroidism is a term for overactive tissue within the thyroid gland, resulting in overproduction and thus an excess of circulating free thyroid hormones: thyroxin (T4), triiodothyronine (T3), or both, whereas hypothyroidism is caused by insufficient production [5, 6]. Most hyperthyroid patients exhibit heat intolerance, tremor, palpitations, anxiety, weight loss despite a normal or increased appetite, increased frequency of bowel movements, and shortness of breath [4, 7, 8]. Common clinical manifestation of hypothyroidism include, fatigue, weight gain, trouble tolerating cold, joint and muscle pain, dry skin or dry, thinning hair, heavy or irregular menstrual periods or fertility problems, slowed heart rate, depression [9, 10].

Triiodothyronine (T3) and thyroxin (T4) are thyroid hormones that affect a variety of metabolic parameters. These hormones have a major impact on lipoprotein metabolism and a few cardiovascular disease (CVD) risk factors, thus influencing overall CDV risk (https://www.austincc.edu/ddingley/MLAB1331/LabManual/LabManual.htm) [11, 12]. In fact, it has been shown that rising thyroid-stimulating hormone (TSH) levels cause a linear increase in triglyceride, total cholesterol, and low-density lipoprotein cholesterol (LDL-C) levels as well as a linear decrease in high-density lipoprotein cholesterol (HDL-C) levels, even within the normal range of TSH levels [12, 13].

The findings of patients with thyroid dysfunctions clearly demonstrated the connection between thyroid hormones and lipid metabolism. Patients with overt hyperthyroidism exhibit decreased lipid levels, whereas patients with overt hypothyroidism exhibit elevated TG and cholesterol levels. These findings indicate that in addition to thyroid hormones, thyroid-stimulating hormone (TSH) has independent effects on lipid metabolism within the subclinical hypo-/hyperthyroid range [12, 14].

The overall incidence of hyperthyroidism is estimated to be about 0.05% to 1.3% with a predominant number being subclinical, this figure rises to between 4 and 5% among older women [15, 16]. In addition to other problems, liver biochemical dysfunctions affect 15–79% of patients with untreated hyperthyroidism; some of these patients experience substantial liver failure and impaired synthetic function [15]. The composition and transport of lipoproteins are strongly disrupted in thyroid diseases. The magnitude of change in plasma lipids varies from patient to patient [17]. The extent of these changes depends both on the severity and duration of thyroid dysfunction [2].

Along with several other cardiovascular risk factors, lipids are significantly impacted by thyroid dysfunction [12]. Research conducted in various nations on the lipid profile parameters of people with thyroid impairment has produced inconsistent findings. Several studies have shown that there are statistically significant differences in total cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and very low-density lipoprotein cholesterol levels between hyperthyroid and hypothyroid patients and healthy controls [18,19,20,21,22]. However, another study showed that the levels of total cholesterol, triglycerides, and low-density lipoprotein cholesterol remained unchanged in hyperthyroid patients compared to those in the normal group [23]. Another study indicated that there was an increase in cholesterol and LDL-L levels in hyperthyroid patients compared with those in healthy controls [24]. There was no statistically significant difference observed between hypothyroid patients and controls in terms of lipid profile parameters, specifically cholesterol, triglycerides, HDL-cholesterol, and LDL-cholesterol [25]. Moreover, information on Ethiopia, particularly in the study area, is limited.

Results obtained from clinical chemistry analyses can reveal changes in lipid profiles, such as total cholesterol, triglyceride, high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and very low-density lipoprotein-cholesterol (VLDL) levels [26,27,28]. Analysis of these parameters will definitely help in the early detection of lipid abnormalities in patients with hypothyroidism and hyperthyroidism, hence decreasing the associated mortality and morbidity rates. Therefore, this study aimed to compare the lipid profiles of dysfunction patients and controls at Wolaita Sodo University Comprehensive Specialized Hospital from May 1 to June 15, 2021.

Methods and materials

Study design, period and area

A hospital-based comparative cross-sectional study was conducted from May 1, 2021, to June 15, 2021, at the comprehensive specialized Hospital of Wolaita Sodo University from outpatient department. The hospital also serves outpatient services such as diabetic clinics, hypertension clinics, TB clinics, ART clinics, and maternity and pediatric facilities.

Inclusion criteria

Patients with TSH levels < 0.6 (mIU/L), T4 levels are (> 1.1 ng/dl) and FT3 levels > 3.07 (nmol/L) were included as hyperthyroidism. Additionally TSH levels (> 4.1 mIU/L) and FT4 levels (< 7.0 mcg/dl) were included in the hypothyroid patient group. Hospital staff members who were age and sex matched and had normal thyroid function were included as control participants.

Exclusion criteria

Study subjects and controls receiving medications known to alter lipid metabolism as well as those with neoplasms, kidney illness, liver disease, history of smokers, diabetes mellitus, or familial hypercholesterolemia were not allowed to participate in the study.

Study participants and controls with previous history of hyperthyroidism or hypothyroidism who are taking medicine were excluded from the study.

Data collection and laboratory methods

Socio-demographic, behavioral, and related data were collected through face-to-face interviews using a pretested structured questionnaire. Following the interview, a laboratory technician used a standard procedure to collect five millilitres of venous blood in ethylenediaminetetraacetic acid (EDTA) tubes, which were then carefully transferred into a clean tube. The blood was allowed to clot at room temperature and then centrifuged at 3000 rpm for 5 min. The serum was carefully separated from the red cells using a Pasteur pipette into a sample bottle and analyzed for free thyroid hormone and lipid levels as routine practice. Thyroid function tests were analyzed using the Cobas-e-411 electrochemiluminescence (ECL) analyzer. And the total cholesterol, HDL-C, triglycerides and lipoprotein A was estimated by COBAS INTEGRA 400 random access full automated auto analyzer and LDL-C concentration was calculated by Sampson equation. Triglycerides and total cholesterol was evaluated with enzymatic colorimetric method and HDL-C was analyzed by homogenous enzymatic colorimetric method.

Data quality assurance and management

Data quality was ensured by implementing all quality assurance programs. For accuracy and consistency, the English version of the questionnaire was translated into Wolaitisa, the native tongue, and then back into English. Again, 5% of the sample was pretested at the hospital before actual data collection, and training was given to the data collectors. The collected blood samples were kept cool in a humidified refrigerator until the time of measurement to prevent any impact from ambient temperature. During the sampling and experimentation processes, the manufacturer's instructions and normal operating procedures were closely adhered to. Background checks, automated clinical chemistry analyzers, and repeated analyses of randomly chosen samples were used to determine reproducibility; randomly chosen samples were confirmed using another clinical chemistry machine of a similar type; and hospital laboratories assessed device performance using whole-blood quality control as part of the testing procedure.

Statistical analysis and interpretation

The data were checked for completeness and consistency. Then, the data were imported into Epi-data version 3.1 (Epi-Data, Odense, Denmark) and exported into the Statistical Package for Social Science (SPSS) version 20 (SPSS, Chicago, USA) statistical software for Windows. Prior to conducting any appropriate statistical analysis, the collected data were tested for normality by the Shapiro‒Wilk test. Lipid profiles were compared between dysfunction patients and controls using an independent-samples T -test for normally distributed data and the Mann‒Whitney U test for non-normally distributed data. Additionally, independent-T test was used to compare lipid profiles between hyperthyroid and hypothyroid patients. The Pearson coefficient test was used to test the correlation between free thyroid hormone levels and lipid profiles. The level of statistical significance was defined as a p value ≤ 0.05 and a confidence interval of 95.

Results

Socio-demographic characteristics of the study participants

A total of 200 participants were included in the study; 60 patients had hypothyroidism (hypothyroid group), 40 patients had hyperthyroidism (hyperthyroid group), and 100 had a normal thyroid level (control group). In both the hypothyroid and hyperthyroid groups, more than 75% of the participants were female. More than 52.5% of the hyperthyroid patients were aged > 40 years. The mean ages of the hypothyroid and hyperthyroid patients were 30 ± 2.3 and 41 ± 5.2 years, respectively (Table 1).

Table 1 Baseline characteristics of study participants
Full size table

Comparison of lipid profiles between the hyperthyroid patients and the control group

Statistically significant differences were observed in the median total cholesterol (TC) level (P = 0.001) and mean ± SD of triglyceride level (P = 0.01) between the hyperthyroid patients and the control group. Patients with hyperthyroidism had significantly lower mean values of low-density lipoprotein cholesterol (P = 0.039) and median values of total cholesterol (P = 0.001) than did the control individuals. Other lipid levels, such as VLDL-C, the LDL-C/HDL-C ratio, and HDL-C levels, did not differ substantially across the groups, as described in Table 2.

Table 2 Comparison of lipid profile of the hyperthyroid patients with control group
Full size table

Comparison of lipid profiles between hypothyroid patients and control individuals

The hypothyroid group's mean serum triglyceride level and median total serum cholesterol level were considerably greater than those of the control group. When comparing the hypothyroid group to the control group, statistically significant decreases were observed in the levels of very low density lipoprotein (VLDL-C) and high density lipoprotein (HDL-C) (Table 3).

Table 3 Comparison of lipid profile of the hypothyroid patients with control group
Full size table

Correlations between serum thyroid hormone levels and lipid profiles in patients with thyroid dysfunction

Table 4 shows the relationship between serum thyroid hormone levels and lipid levels in hyperthyroid and hypothyroid patients. The results in this table show that there were negative and significant correlations between TSH and TC (r = −0.38, P = 0.01), between TSH and LDL-C (r = .−0.32, P = 0.004), and between T4 and LDL-C (r = −0.12, P = 0.0001) in hyperthyroid patients. as described in Table 4.

Table 4 Correlation between hypothyroidism, hyperthyroidism, and lipid profile in thyroid dysfunction patients
Full size table

Discussion

Thyroid dysfunction is more common among endocrine illnesses. The majority of thyroid illnesses are caused by abnormalities in the thyroid hormone production rate [29]. This study was conducted in three groups of subjects, that is, in the normal control group, hypothyroid group, and hyperthyroid group, with a predominance of female patients (77.5% in the hyperthyroid group and 78.3% in the hypothyroid group).

The present study showed that the mean level of serum triglycerides in hypothyroid patients was significantly greater than that in healthy controls. These findings are similar to the results of other studies [30,31,32]. Lipoprotein lipase enzyme activity may have decreased in the hypothyroid group, which could account for their higher triglyceride levels [33]. Conversely, in research conducted in Libya [24], these differences may be the result of racial and sex differences [27].

The hypothyroid patient median total cholesterol level was considerably greater in this study than in the control group. This result aligns with research carried out across many regions of the world [34,35,36,37]. Hormone deficiency and changes in hepatic lipase and lipoprotein lipase enzyme activity could also be causes [33, 38]. The primary factor contributing to elevated total cholesterol in hypothyroid individuals is a reduction in the expression of the low-density lipoprotein receptor gene in fibroblasts, hepatocytes, and other organs [39]. The low-density lipoprotein receptor is a protein that sits on the surface of the liver, and its main purpose is to identify and absorb lipoproteins or specific cholesterol particles and eliminate them from the bloodstream [40]. Thyroid hormones (T3 and T4) serve to increase the expression of these receptors [41]. However, the thyroid hormone level is decreased in patients with hypothyroidism.

In our study, the high-density lipoprotein cholesterol level was significantly lower in hypothyroid patients than in the controls. These findings are similar to those of a study conducted in India [32]. The mean LDL-C level in hypothyroid patients was significantly greater than that in control individuals. The increased levels of low-density lipoprotein cholesterol could be due to a decreased fractional clearance of low-density lipoprotein. Consequently, a decreased quantity of low-density lipoprotein cholesterol receptors in the liver may be the cause of this elevation [40]. These findings were in accordance with those of the study performed by Benny PD [32].

The findings of the current study showed a significant reduction in total cholesterol, triglycerides, and low-density lipoprotein cholesterol in hyperthyroid patients compared to those in the control group. This was in line with the results of other research projects carried out globally [42, 43]. The increased activity of the HMG-CoA reductase enzyme may be the source of the reduction, and elevated biliary excretion of cholesterol combined with higher receptor-mediated LDL particle catabolism is generally associated with elevated cholesterol levels [17].

In contrast, there were no significant differences in the total cholesterol triglyceride or low-density lipoprotein cholesterol levels between the hyperthyroid and control groups [23]. The reason might be the outcome of the treatment. According to several investigators, the lipid profile values of individuals with hyperthyroidism were found to be low and were adjusted to within normal ranges following treatment [44]. The levels of HDL-C and VLDL-C and the LDL-C/HDL-C ratio were not significantly different between the hyperthyroid group and the control group, which disagrees with the findings of another study [32]. These differences may be due to sample size variations [24].

In hyperthyroid patients, strong negative correlations were found between TSH and total cholesterol, between TSH and LDL-C, and between T3 and LDL-C with respect to the associations between lipid profile parameters and thyroid hormones. These findings disagree with those of a study conducted in Sudan [27]. Additionally, a positive and significant correlation was found between TSH and LDL-C and between TSH and TC in hypothyroid patients. These results align with those of another study carried out in Nepal, which demonstrated a positive connection between TSH and total cholesterol (TC) and between TSH and LDL hypothyroid individuals [45]. In the present study, there were no significant correlations between T3, TSH or T4 and HDL-C in either the hyperthyroid or hypothyroid patients, in contrast to the findings of other studies [21, 27].

Conclusion and recommendation

This study showed that, compared with those in the control group, most lipid profile parameters in thyroid dysfunction patients (hyperthyroid and hypothyroid) were altered. The levels of the serum lipid profile parameters TC, TG, and LDL-C were significantly lower in the hyperthyroid patients. Finally, there was also a negative and significant correlation between the serum TSH concentration and the levels of several lipids (TC and TG) in hyperthyroid patients. Biochemical screening for thyroid dysfunction is critical in all dyslipidemia patients as well as in all patients with unexpected improvement or worsening of their lipid profile [23, 46]. Periodic medical check-ups of the lipid profile of thyroid dysfunction patients should be considered before the development of cardiac and other diseases.

Data availability

The data set supporting the conclusion of this article are incorporated in this manuscript.

References

  1. Guyton AC. Text book of medical physiology: China: Elsevier Saunders; 2006.

  2. Diekman M, Anghelescu N, Endert E, Bakker O, Wiersinga WJJCEM. Changes in plasma LDL and HDL cholesterol in hypo and hyperthyroid patients are related to changes in free thyroxine, not to polymorphisms in LDL receptor or cholesterol ester transfer protein genes. J Clin Endocrinol Metab. 2000;85:1857–62.

  3. Iwen KA, Oelkrug R. Brabant GJJoME. Effects of thyroid hormones on thermogenesis and energy partitioning. J Mol Endocrinol. 2018;60(3):R157–70.

  4. Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiol Rev. 2014;94(2):355–82.

  5. Mohamedali M, Reddy Maddika S, Vyas A, Iyer V, Cheriyath PJIjon. Thyroid disorders and chronic kidney disease. Int J Nephrol. 2014;2014.

  6. Altahir WH, Abdella MA, Ahemd E, Ismail AJJoS, Technology. Assessment of lipids profile in hyperthyroidism sudanese patients in North Kordofan State, Sudan. J Sci Technol. 2013;14(1).

  7. Goichot B, Caron P, Landron F. Bouée SJCe. Clinical presentation of hyperthyroidism in a large representative sample of outpatients in France: relationships with age, aetiology and hormonal parameters. Clin Endocrinol. 2016;84(3):445–51.

  8. Biondi B, Palmieri EA, Klain M, Schlumberger M, Filetti S. Lombardi GJEJoE. Subclinical hyperthyroidism: clinical features and treatment options. Eur J Endocrinol. 2005;152(1):1–9.

  9. Drake MT, editor Hypothyroidism in clinical practice. Mayo Clin Proc. 2018;93(9):1169–72.

  10. Surks MI, Ross D, Mulder JJUW, MA. Clinical manifestations of hypothyroidism. 2012. Retrieved from http://www.uptodate.com.

  11. Kumar DV, Mathur DS, Tuteja DRKJIJMBS. Effects of thyroid dysfunction on lipid profile. IJMBS. 2019;3:76–80.

  12. Rizos C, Elisaf M. Liberopoulos EJTocmj. Effects of thyroid dysfunction on lipid profile. Open Cardiovasc Med J. 2011;5:76.

  13. Sun X, Sun Y, Li W-C, Chen C-Y, Chiu Y-H, Chien H-Y, et al. Association of thyroid-stimulating hormone and cardiovascular risk factors. Intern Med. 2015;54(20):2537–44.

  14. Peppa M, Betsi G, Dimitriadis GJJol. Lipid abnormalities and cardiometabolic risk in patients with overt and subclinical thyroid disease. Intern Med. 2011;2011.

  15. Yorke EJCMIE, Diabetes. Hyperthyroidism and liver dysfunction: a review of a common comorbidity. J Lipids. 2022;15:11795514221074672.

  16. Opoku‐Akyeampong NAAS, Agyei‐Nkansah A, Yorke EJCCR. Liver dysfunction associated with hyperthyroidism: Lessons from 2 Case reports. Clin Med Insights Endocrinol Diabetes. 2021;9(6):e04067.

  17. Duntas LHJT. Thyroid disease and lipids. Clin Case Rep. 2002;12(4):287–93.

  18. Ball M, Griffiths D. Thorogood MJJotRSoM. Asymptomatic hypothyroidism and hypercholesterolemia. Thyroid. 1991;84(9):527–9.

  19. Hollowell JG, Staehling NW, Flanders WD, Hannon WH, Gunter EW, Spencer CA, et al. Serum TSH, T4, and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). R Soc Med. 2002;87(2):489–99.

  20. Gharib H, Tuttle RM, Baskin HJ, Fish LH, Singer PA,McDermott MTJTjoce, et al. Subclinical thyroid dysfunction: a joint statement on management from the American Association of Clinical Endocrinologists, the American Thyroid Association, and the Endocrine Society. J Clin Endocrinol Metab. 2005;90(1):581–5.

  21. Walsh JP, Bremner AP, Bulsara MK,O’leary P, Leedman PJ, Feddema P, et al. Thyroid dysfunction and serum lipids: a community-based study. J Clin Endocrinol Metab. 2005;63(6):670–5.

  22. Tunbridge WM, Evered DC, Hall R, Appleton D, Brewis M, Clark F, Evans JG, Young E, Bird T, Smith PA. Lipidprofiles and cardiovascular disease in the Whickham area with particular reference to thyroid failure. Clin Endocrinol. 1977;7(6):495–508.

  23. Mohammed S, Abd Alrahman Abd Alla AA, Siddeg AN. Evaluation of serum lipid profile in Sudanese patient with thyroid dysfunction. Clin Endocrinol (Oxf).

  24. Alsalmi WM, Shaglouf LHF, Azab AEJCMJ. Correlation between hypothyroidism, hyperthyroidism, and lipid profile in thyroid dysfunction patients. SJAMS. 2018;4(2):6–14.

  25. Davchevska MJ, Ivanovska VM, Stefanovska VVJAMJ. Hypothyroidism and its association with changes in the lipid profile. Clin Med J. 2021;1(2):89–99.

  26. Sharma A, Kaur J, Kaur A, Uppal N. Kaur MJIJoCB, Research. Evaluation of serum lipid profile in patients with hyperthyroidism. Acad Med J. 2017;4(2):126–8.

  27. Yousif AM, Ataelfadeal KA, Dafalla AM, Khalafalla AS, Faisal S, Abdorabo AA, et al. Serum Lipid Profile among Sudanese Patients Diagnosed with Hyperthyroidism. Muthanna Med J. 2022;6(2):176–84.

  28. Altaher WH, Ahemd EM, Ismail A. Assessment of lipids profile in hyperthyroidism sudanese patients in North Kordofan State, Sudan. 2013.

  29. Ganie MA, Zargar AHJIJoE, Metabolism. Scenario of endocrinology in South Asia. Medknow; 2007. p. 1–2.

  30. Bhattacharya S, Kalra S. South Asian Endocrinology: Challenges and Concerns, Collaboration and Consolidation. Indian J Endocrinol Metab. 2023;27(5):373–6.

  31. Bell RJ, Rivera‐Woll L, Davison SL, Topliss DJ, Donath S, Davis SRJCe. Well‐being, health‐related quality of life and cardiovascular disease risk profile in women with subclinical thyroid disease–a community‐based study. J Nepal Health Res Counc. 2007;66(4):548–56.

  32. Benny P, Maliekkal J, Geetha N, VH ANJNJoP, Pharmacy, Pharmacology. A study on lipid profile in thyroid dysfunction. 2023;13(6):1174-.

  33. Valdemarsson S, Hansson P, Hedner P. Nilsson-Ehle PJEJoE. Relations between thyroid function, hepatic and lipoprotein lipase activities, and plasma lipoprotein concentrations. Natl J Physiol Pharm Pharmacol. 1983;104(1):50–6.

  34. Mansfield BS, Bhana S. Raal FJJJoC, Endocrinology T. Dyslipidemia in South African patients with hypothyroidism. Acta Endocrinol. 2022;29: 100302.

  35. Bianco AC. Taylor PJNRE. Levothyroxine treatment and cholesterol in hypothyroidism. J Clin Transl Endocrinol. 2020;16(4):193–4.

  36. Deschampheleire M, Luyckx F. Scheen AJRMdL. Thyroid disorders and dyslipidemias. Nat Rev Endocrinol. 1999;54(9):746–50.

  37. Genéz Yeza EN, Mir CN, Ares RM, Pedrozo WR, Bonneau GA. Prevalence of thyroid dysfunction and its relationship with the lipid profile in patients in hospital from Encarnación. Rev Med Liege.

  38. Găleşanu C, Lisnic N, Teslaru R, Apostu L, Zbranca EJRm-caSdMsNdI. Lipids profile in a group of hypothyroid patients vs. treated hypothyroid patients. 2004;108(3):554–60.

  39. ARGENTINO TC, ENDOCRINOLÓGICAS SPJR. DISFUNCIÓN TIROIDEA SUBCLÍNICA DISFUNCIÓN TIROIDEA Y AMIODARONA. 2009;46(4).

  40. Pirahanchi Y, Sinawe H, Dimri M. Biochemistry, LDL Cholesterol. 2018.

  41. Shahid MA, Ashraf MA, Sharma S. Physiology, thyroid hormone. 2018.

  42. Nishitani H, Okamura K, Noguchi S, Inoue K, Morotomi Y, Fujishima M. serum lipid levels in thyroid dysfunction with special reference to transient elevation during treatment in hyperthyroid Graves' disease. Horm Metab Res. 1990;22(9):490–3.

  43. Musa RI, Akuyam AS. Evaluation of serum lipid profile among hyperthyroid patients in Aminu Kano Teaching Hospital, Kano. BJMLS. 2021;6(2):16–21.

  44. Hussain A, Bhat MH, Misgar RA, Bashir MI, Wani AI. A Study on Lipid Abnormalities in Hyperthyroidism and their Response to Antithyroid Drugs. 2021.

  45. Regmi A, Shah B, Rai B, Pandeya AJNMCJ. Serum lipid profile in patients with thyroid disorders in central Nepal. 2010;12(4):253–6.

  46. Teixeira PDFDS, Reuters VS, Ferreira MM, Almeida CP, Reis FAA, Buescu A, et al. Lipid profile in different degrees of hypothyroidism and effects of levothyroxine replacement in mild thyroid failure. Natl J Lab Med. 2008;151(4):224–31.

Download references

Acknowledgements

We express our sincere gratitude to Wolaita Sodo University for ethical sanctions for this study. Moreover, we place on record our wholehearted thanks to the heads and staff of chronic diseases clinics care, and laboratory staff, Wolaita Sodo University Comprehensive Specialized Hospital, and those who consented to participate in the study.

Funding

There is no funding to report.

Author information

Authors and Affiliations

  1. School of Medical Laboratory Sciences, College of Health Sciences and Medicine, Wolaita Sodo University, Wolaita Sodo, Ethiopia

    Tamirat Ersino Kebamo, Abinet Tantu & Getachew Alemu Walano

  2. School of Medical Laboratory Sciences, College of Health and Medical Sciences, Debre Tabor University, Debre Tabor, Ethiopia

    Yenealem Solomon

Authors
  1. Tamirat Ersino Kebamo
    View author publications

    You can also search for this author inPubMed Google Scholar

  2. Abinet Tantu
    View author publications

    You can also search for this author inPubMed Google Scholar

  3. Yenealem Solomon
    View author publications

    You can also search for this author inPubMed Google Scholar

  4. Getachew Alemu Walano
    View author publications

    You can also search for this author inPubMed Google Scholar

Contributions

TEK is the principal investigator and is involved in the design of the study, data analysis, and interpretation of the findings, report writing, and manuscript preparation. GA, YS, and participated by advising and supervising the research process and gave constructive comments to increase the quality of the study, TEK and AT commented, edited, and approved the final manuscript of the research.

Corresponding author

Correspondence to Tamirat Ersino Kebamo.

Ethics declarations

Ethics approval and consent to participate

Ethical clearance was obtained from the Ethical Review Committee of Wolaita Sodo University, College of Health Science and Medicine (reference number: CSHM/ER/01/21). Written informed consent was obtained from each study participant after the objective and procedures of the study were explained. Written consent to participate was obtained from the parents/guardians of the minors included in this study (minors are considered anyone under the age of 16). To ensure data confidentiality, study participants were identified by codes rather than names or other identifiers, and data collection was prevented from being accessed by unauthorized parties. Above all, the Committee on Publication Ethics and the Declaration of Helsinki ethical guidelines for medical research involving human beings were strictly followed during the entire study.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Kebamo, T.E., Tantu, A., Solomon, Y. et al. A comparative study on serum lipid levels in patients with thyroid dysfunction: a single-center experience in Ethiopia. BMC Endocr Disord 25, 47 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12902-025-01851-1

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12902-025-01851-1

Keywords

BMC Endocrine Disorders

ISSN: 1472-6823

Contact us