As per the International Diabetes Federation, 422 million people are living with diabetes across the world, and it is expected to rise to a whooping figure of 592 million in 2035 of which 79.4 million diabetics will be from India.[1]

Thyroid hormones are essential for the normal development, differentiation, metabolic balance, and physiological function of virtually all tissues and thyroid function disorders are among the most common endocrine diseases. Hypothyroidism is the most common functional disorder of the thyroid gland. Pathology of the thyroid gland (primary hypothyroidism) accounts for over 99.5% of cases of thyroid gland failure and < 0.5% result from disorders of the pituitary gland or hypothalamus (central hypothyroidism).[2]

In the absence of thyroid hormones, anemia frequently develops and may be normocytic, hypochromic-microcytic, or macrocytic. Anemia is an uncommon finding in hyperthyroidism but when present may be morphologically similar to that observed in hypothyroidism.[3] Glycated hemoglobin has been routinely used to assess the glycemic control of the patients with diabetes mellitus. it is recognised as an excellent marker of glycemic control because its rate of formation is proportional to the blood glucose concnetration over the average RBC lifespan.[4]

One common endocrine condition that can affect erythropoiesis, plasma protein turnover, and glucose metabolism is hypothyroidism. Long-term glycemic management is often indicated by glycosylated hemoglobin (HbA1c). But in hypothyroid conditions, a longer erythrocyte lifespan and less red cell turnover might cause an unnaturally high HbA1c that is unrelated to blood glucose levels[5].

Thyroxine replacement therapy may regulate erythropoiesis and lower HbA1c by restoring euthyroidism. The purpose of the current study was to evaluate the change in HbA1c in non-diabetic patients with newly identified primary hypothyroidism after thyroxine treatment.

The main characteristic of the clinical condition known as hypothyroidism is decreased thyroid hormone production. About 99% of cases are primary hypothyroidism, which is caused by thyroid illness; less than 1% are caused by TSH insufficiency and are referred to as central hypothyroidism.

The thyroid hormone, which is crucial for controlling the body's general metabolic rate, affects glucose levels. The HbA1c readings show variations in the values of the glucose levels.

The quantity of research on HbA1c is currently rising. Numerous recommendations have been developed about the use of HbA1c in the diagnosis of diabetes, its significance in identifying patients at high risk for the disease, and its numerous "non-diabetic" applications[6]. The ADA recommendations from 2011 were the first to incorporate HbA1c as a diagnostic criterion, and it has since been a part of it. In the years that followed, these standards were examined and improved. Since then, the significance of measuring HbA1c using conventional tests has not diminished.

Study setting: Department of General Medicine at Sri Siddartha Instiute of Medical Sciences, T Begur, Nelamangla Taluk, Bangalore Rural on 100 cases. Newly diagnosed Hypothyroidism patients admitted or seen on OPD basis during the period of study.

Inclusion criteria:

• The patients who have given written and informed consent to participate in the study.
• Newly Diagnosed cases of Hypothyroidism.

Exclusion criteria:

• Diabetes mellitus (FBS>=126 mg/dl, PPBS: >=200 mg/dl).
• Impaired glucose tolerance ( 2h post 75g OGTT is between 140- 199 mg/dl).
• Hb< 10 g/dl.
• Known hemoglobinopathies.
• Renal or Liver diseases.
• Recent blood transfusions (< 3 months).
• Pregnant patients.

Method of collection of data:

All diagnosed cases of Hypothyroidism and underwent routine investigations will be considered for the study. Written and informed consent will be taken from the study subjects after explaining to them the plan and intention of the study in the language best known to them. Information is collected through structured proforma from each patient. All patients/their relatives will be interviewed as per the structured proforma. A detailed enquiry will be made about name, age, sex, address, history of diabetes, hypertension, liver disease, renal disease, treatment history. A detailed systemic examination will be done. Routine investigations will be collected, Glocosylated hemoglobin and TSH. Patients are followed up for a period of 3 months and HbA1C are levels are rechecked at the end of the three months of treatment with Thyroxine.

Data analysis:

Data will be entered in Microsoft Excel software and analyzed using the SPSS (Statistical Package for the Social Science) software. Analysis will be done using descriptive statistics like proportion, percentage, mean, and standard deviation, and inferential statistics like chi-square, t-test, and other suitable statistical tools will be applied.

Table 1. Baseline clinical and biochemical characteristics.

Table 2. Changes in thyroid profile, HbA1c, and fasting glucose

Change in Thyroid Function and HbA1c after Treatment

.

Table 3. Lipid profile changes after 6 months of thyroxine therapy.

Table 4. Correlation between HbA1c and thyroid function parameters.

Although there was no discernible change in fasting glucose, this trial showed that non-diabetic hypothyroid patients' HbA1c significantly decreased after six months of thyroxine supplementation[7]. This lends credence to the idea that decreased glycemia, not a longer erythrocyte lifespan, is the cause of raised HbA1c in hypothyroidism. When euthyroidism is restored, red cell turnover returns to normal, which lowers HbA1c levels.

These results are consistent with earlier research that found comparable patterns. The changes in lipid profiles provide additional evidence of the metabolic advantages of thyroxine replacement. Clinically, this emphasizes that without glucose test confirmation, mildly raised HbA1c in untreated hypothyroidism should not be mistakenly regarded as prediabetes[8].

The data indicates that the prevalence of overt hypothyroidism decreased with age, which is inconsistent with the frequency in the general population, which is higher in the elderly, according to numerous research. Numerous investigations, like the Wickham survey and the Colorado thyroid disease prevalence research, have shown that the general population's prevalence of hypothyroidism rises with age[9-10].

Bilic EdinaTo learn more about how L-thyroxine medication affects glucose regulation in people with subclinical hypothyroidism, Komarica et al. undertook a study. Following a 6-month course of L thyroxine and physical activity, the patients' FBS, PPBS, HbA1c, fasting insulin, and lipid levels all significantly decreased, indicating that thyroxine treatment will improve blood sugar control by bringing TSH levels back to normal.

Insulin and HbA1c levels were correlated with thyroid hormones by Vibha Uppalet al., who also found a positive and significant correlation between HbA1c levels and TSH levels.

Thyroxine replacement significantly reduces HbA1c in non-diabetic hypothyroid patients independent of changes in glucose levels. Physicians should account for thyroid status when interpreting HbA1c results, especially in the context of borderline elevations.

1. International Diabetes Federation. IDF Diabetes Atlas Update Poster. 6^th Brussels,Belgium:International Diabetes Federation;2014.
2. Bashir H, Bhat MH, Farooq R, et al. Comparison of hematological parameters in untreated and treated subclinical hypothyroidism and primary hypothyroidism patients. Med J Islam Repub Iran. 2012;26(4):172-178.
3. Fein HG, Rivlin RS. Anemia in thyroid diseases. Med Clin North Am 1975;59:113345.
4. Mohan Kumar KM, Bobby Z, Selvaraj N, Kumar Das A, ChandraKoner B, Sen SK, et al. Possible link between glycated hemoglobinand lipid peroxidation in hyperthyroidism. Clin Chim Act a 2004;342:18792.
5. American Diabetes Association. Clinical practice recommendations 2012. Diabetes Care 2012;35:S1163.
6. Meena R , Choudhary S, Choudhary K R et al. Effect of Thyroid hormone on HbA1C levels in Patients with newly detected hypothyroidism. IJR 2020;9(1)
7. Kim MK, Kwon HS, Baek KH, Lee JH, Park WC, Sohn HS, et al.Effects othyroid hormone on A1C and glycated albumin levels in nondiabetic subjects with overt hypothyroidism. Diabetes Care 2010;33:25468.
8. Anantarapu S, Vaikkakara S, Sachan A, Phaneendra BV,Suchitra MM, Reddy AP, et al. Effects of thyroid hormonereplacement on glycated haemoglobin levels in non diabeticsubjects with overt hypothyroidism. Arch Endocrinol Metab 2015;59:495500.
9. Bhattacharjee R, Thukral A, Chakraborty PP, Roy A, Goswami S, Ghosh S, Mukhopadhyay P, Mukhopadhyay S, Chowdhury S, et al. Effects of thyroid status on glycated hemoglobin. Indian J Endocr Metab 2017;21:26-30
10. Deepika Sakthisekaran.repository tnmgrmu[internet].2019[updated 31 Aug 2019; cited 2019 Dec 5].Available from : http://repositorytnmgrmu. ac.in/11256/