Thyroid dysfunction and diabetes mellitus are among the most ubiquitous endocrine disorders worldwide, frequently coexisting and reciprocally influencing metabolic regulation. Autoimmune overlap in type 1 diabetes mellitus (T1DM) predisposes patients to thyroid autoimmunity—with Hashimoto’s and Graves’ disease affecting up to ~20% of individuals with T1DM in some cohorts [1]. In type 2 diabetes mellitus (T2DM), pooled prevalence estimates reveal thyroid dysfunction in approximately 20–30%, markedly higher than non‑diabetic populations (≈6–9%) [2-5]. A recent meta‑analysis in India noted rates of 23.8% among diabetic patients, with subclinical hypothyroidism comprising nearly half of cases [6].

The pathophysiological interplay between thyroid hormones and glucose metabolism is increasingly elucidated. Thyroid hormones modulate hepatic gluconeogenesis, insulin secretion, and peripheral glucose uptake, while exerting significant effects on lipid metabolism and insulin resistance [7]. A 2024 Mendelian randomization study linked genetic variations in thyroid pathways to altered insulin sensitivity [8], and a meta-analysis reported that each unit rise in TSH or FT4 increased T2DM risk—though the relationship may be non‑linear [9]. Mechanistically, hypothyroidism exacerbates hyperglycaemia by reducing glucose disposal and enhancing insulin resistance, while hyperthyroidism accelerates carbohydrate turnover, destabilizing glycaemic control [10].

Emerging clinical evidence links thyroid dysfunction with worsened diabetic outcomes. A 2025 retrospective Indian study showed hypothyroidism in 20.9% of T2DM patients—with a predilection for longer disease duration and female sex, though no direct HbA1c association [11]. Another 2025 cross-sectional study from a tertiary Indian centre reported thyroid dysfunction in ~26.5% of T2DM patients; hypothyroidism was independently associated with higher rates of retinopathy, nephropathy, neuropathy, and peripheral arterial disease [12]. Furthermore, a narrative review in 2025 emphasized the bidirectional relationship and recommended integrated screening and management strategies [13].

Despite robust evidence of the metabolic impact of thyroid disorders in diabetes, region-specific data—particularly within Indian clinical settings—remain scarce. We, therefore, aimed to determine thyroid dysfunction prevalence in T1DM and T2DM, and to quantify its influence on FBG, PPBG, and HbA1c in our cohort.

Study Design and Setting

This was a hospital-based, cross-sectional observational study conducted in the Endocrinology Outpatient Department (OPD) of a tertiary care teaching hospital in India between January 2023 and May 2024. The study adhered to the principles of the Declaration of Helsinki and Good Clinical Practice (GCP) guidelines [14]. Ethical clearance was obtained from the Institutional Ethics Committee prior to initiation (Approval No.: IEC/2023/Biochem/019). All participants provided written informed consent.

Study Population

A total of 180 patients with a confirmed diagnosis of diabetes mellitus were recruited using non-probability purposive sampling. Of these, 60 patients had T1DM and 120 had T2DM. Diagnosis was established in accordance with the American Diabetes Association (ADA) 2024 criteria, which define T1DM based on clinical presentation and low or absent C-peptide levels, and T2DM by hyperglycaemia in the context of insulin resistance without autoimmune markers [14].

Inclusion Criteria

• Adults aged ≥18 years and ≤65 years.
• Confirmed diagnosis of T1DM or T2DM for at least one year to ensure stability of metabolic parameters [15].
• Willingness to participate and provide informed written consent.
• Exclusion Criteria
• Pre-existing thyroid disorders diagnosed before the onset of diabetes.
• Use of medications known to alter thyroid function (e.g., amiodarone, lithium, glucocorticoids) [16].
• Pregnant or lactating women, as pregnancy induces physiological changes in thyroid function [17].
• Patients with severe systemic comorbidities (advanced renal or liver disease, malignancy, chronic infections) which could confound metabolic parameters.

Patient Recruitment and Clinical Assessment

Eligible patients attending the Endocrinology OPD were screened for inclusion and exclusion criteria. After obtaining informed consent, a detailed clinical history was recorded, including age, sex, duration of diabetes, family history of thyroid disease, smoking status, and current anti-diabetic medications. A thorough physical examination was conducted, with emphasis on signs suggestive of thyroid dysfunction (e.g., goitre, weight change, dry skin).

Anthropometric and Blood Pressure Measurement

Height was measured to the nearest 0.1 cm using a stadiometer, and weight to the nearest 0.1 kg using a digital scale, with patients in light clothing and without shoes. Body Mass Index (BMI) was calculated as weight (kg) divided by height squared (m²) and categorised as per World Health Organization (WHO) Asian BMI guidelines [18]. Blood pressure was measured in the right arm, in a seated position, using a calibrated mercury sphygmomanometer; two readings five minutes apart were averaged.

Laboratory Investigations

All biochemical tests were performed in the hospital’s NABL-accredited central laboratory using standardised protocols to ensure validity and reproducibility.

• Fasting Blood Glucose (FBG): After an overnight fast of 8–12 hours.
• Postprandial Blood Glucose (PPBG): Measured two hours after a standardised carbohydrate-rich meal to minimise inter-individual variation [19].
• Glycated Hemoglobin (HbA1c): Assessed by High-Performance Liquid Chromatography (HPLC) using a certified NGSP and IFCC traceable method, considered the gold standard for long-term glycaemic control [20].
• Thyroid Function Tests: Serum Thyroid Stimulating Hormone (TSH) and Free Thyroxine (FT4) were measured by Chemiluminescence Immunoassay (CLIA) using an automated analyser (e.g., Roche Cobas e411) with intra-assay and inter-assay coefficient of variation (CV) <5% [21].

All samples were collected under aseptic precautions and processed within two hours of collection.

Classification of Thyroid Status

Based on test results, patients were categorised as follows [22, 23]:

• Euthyroid: Normal TSH and FT4 levels.
• Subclinical Hypothyroidism: Elevated TSH with normal FT4.
• Overt Hypothyroidism: Elevated TSH with low FT4.
• Subclinical Hyperthyroidism: Suppressed TSH with normal FT4.
• Overt Hyperthyroidism: Suppressed TSH with elevated FT4.

Statistical Analysis

Data were entered and cleaned using Microsoft Excel 2019 and analysed with IBM SPSS Statistics version 26.0 (IBM Corp., Armonk, NY, USA). Continuous variables were tested for normality using the Shapiro-Wilk test. Normally distributed variables were expressed as mean ± standard deviation (SD), while categorical variables were presented as frequency and percentage.

Student’s t-test was employed to compare mean FBG, PPBG, and HbA1c levels between euthyroid and thyroid dysfunction groups within T1DM and T2DM categories. The Chi-square test (or Fisher’s exact test where appropriate) was used to assess associations between categorical variables. A p-value <0.05 was considered statistically significant [24].

Demographic and Clinical Characteristics

A total of 180 patients were included: 60 with T1DM and 120 with T2DM. The mean age was significantly lower in T1DM patients (28.4 ± 6.2 years) compared to T2DM patients (52.7 ± 8.3 years). Female patients slightly outnumbered males in both groups. Mean BMI was within the normal range for T1DM but higher among T2DM patients.

Table 1: Demographic and Clinical Characteristics

Prevalence of Thyroid Dysfunction

In this study, thyroid dysfunction was identified in a substantial proportion of both diabetes cohorts. Specifically, 32% (19 out of 60) of patients with T1DM were found to have some form of thyroid abnormality, whereas among T2DM patients, the prevalence was slightly lower at 28% (34 out of 120)

A closer analysis of the types of dysfunction revealed that subclinical hypothyroidism emerged as the predominant abnormality across both groups. This condition, characterised by elevated serum TSH levels with normal circulating FT4 concentrations, accounted for the majority of cases detected. Subclinical hypothyroidism is clinically significant because, although often asymptomatic, it can progressively impair metabolic regulation and exacerbate insulin resistance if left unaddressed.

Furthermore, a few patients in both groups exhibited overt hypothyroidism—manifested by raised TSH accompanied by decreased FT4—and a smaller number had subclinical or overt hyperthyroidism, though these were comparatively rare. These findings align with previous reports indicating that the risk of developing thyroid dysfunction, particularly subclinical hypothyroidism, is higher in individuals with diabetes due to complex autoimmune and metabolic interactions.

Overall, these results underscore the importance of routine screening for thyroid dysfunction in diabetic patients to enable early detection and timely intervention, which is critical for optimising metabolic control and minimising the risk of long-term complications.

Impact on Glycaemic Parameters

Among patients with T1DM, the presence of thyroid dysfunction (TD) was associated with significantly poorer glycaemic control. Specifically, individuals with thyroid dysfunction exhibited a markedly higher mean FBG level (168.5 ± 23.4 mg/dL) compared to their euthyroid counterparts (145.2 ± 20.1 mg/dL; p < 0.001). Similarly, PPBG readings were elevated in the thyroid dysfunction subgroup (245.6 ± 32.8 mg/dL) relative to the euthyroid group (218.3 ± 29.7 mg/dL; p = 0.002). In addition, mean HbA1c was substantially higher in patients with thyroid dysfunction (9.2 ± 1.1%) than in euthyroid patients (8.1 ± 0.9%; p < 0.001), indicating sustained hyperglycaemia over the preceding three months.

A comparable trend was observed among patients with T2DM. Those with coexisting thyroid dysfunction had significantly increased mean FBG (162.7 ± 21.5 mg/dL vs 139.8 ± 18.6 mg/dL; p < 0.001), PPBG (238.9 ± 35.1 mg/dL vs 205.4 ± 27.8 mg/dL; p < 0.001), and HbA1c levels (8.7 ± 0.8% vs 7.5 ± 0.7%; p < 0.001) compared to euthyroid T2DM patients. These findings underscore the adverse impact of thyroid dysfunction on glycaemic control in both forms of diabetes, highlighting the need for routine thyroid screening and timely intervention to optimise metabolic outcomes.

Table 2: Comparison of Glycaemic Parameters

Figure 2: Comparison of mean FBG, PPBG, and HbA1c in ET1DM, TDT1DM, ET2DM, and TDT2DM groups. TDT1DM and TDT2DM subgroups show higher levels compared to ET1DM and ET2DM, indicating the impact of TD on glycaemic control. Abbreviations:  FBG (Fasting Blood Glucose), PPBG (Postprandial Blood Glucose), and HbA1c (Glycated Hemoglobin). ET1DM: Euthyroid T1 DM; TDT1DM: Thyroid Dysfunction T1DM

In T1DM, mean HbA1c was 8.1% (95% CI: 7.82–8.38) in the euthyroid subgroup and 9.2% (95% CI: 8.67–9.73) in those with thyroid dysfunction. Similarly, in T2DM, mean HbA1c was 7.5% (95% CI: 7.35–7.65) in euthyroid patients and 8.7% (95% CI: 8.42–8.98) in those with thyroid dysfunction (Table 3). All between-group differences were statistically significant (p < 0.001, independent sample t-test).

Table 3: HbA1c with 95% Confidence Intervals

The present study examined the prevalence of thyroid dysfunction among patients with type 1 and type 2 diabetes mellitus and assessed its impact on key glycaemic parameters, including FBG, PPBG, and HbA1c. Our findings indicate a substantial burden of thyroid dysfunction in both T1DM and T2DM populations, with a prevalence of 32% and 28%, respectively. Subclinical hypothyroidism emerged as the most prevalent form of thyroid abnormality, consistent with previous reports [25–27].

The high coexistence of thyroid disorders in diabetic patients is attributed to the well-established pathophysiological interplay between thyroid hormones and glucose metabolism [28]. Thyroid hormones significantly modulate hepatic gluconeogenesis, insulin secretion, and peripheral glucose uptake. Hypothyroidism, whether overt or subclinical, is known to exacerbate insulin resistance, reduce glucose disposal, and impair lipid metabolism [29]. Conversely, hyperthyroidism can cause increased hepatic glucose output and enhanced intestinal glucose absorption, leading to greater glycaemic variability and higher insulin requirements [30]. These mechanistic links are supported by multiple epidemiological and clinical studies demonstrating increased odds of thyroid dysfunction in patients with both T1DM and T2DM compared to the general population [26, 31].

Our study further revealed that thyroid dysfunction, particularly hypothyroid states, was associated with significantly higher mean FBG, PPBG, and HbA1c values in both T1DM and T2DM groups. These results align with prior studies reporting poorer glycaemic control and increased insulin resistance in diabetic patients with concurrent thyroid dysfunction [32, 33]. For instance, Biondi et al. (2010) highlighted that even mild thyroid failure adversely impacts metabolic control and cardiovascular risk factors in diabetes [29]. Similarly, a meta-analysis by Han et al. found that subclinical hypothyroidism significantly worsens HbA1c levels in T2DM patients [34].

The prevalence rates observed in our cohort are slightly higher than those reported in some Western studies but are comparable to rates seen in similar Indian and Asian contexts [35, 36]. Possible reasons for this variation include genetic predisposition, dietary iodine sufficiency, and regional differences in autoimmune thyroiditis prevalence [37]. The slightly higher prevalence in T1DM compared to T2DM is expected due to the autoimmune nature of both conditions, which share common immunological pathways [26, 28].

These findings have important clinical implications. First, they underscore the need for routine thyroid function screening in patients with diabetes, as recommended by the ADA and other expert groups [14]. Early detection and appropriate management of thyroid dysfunction can help optimise insulin dosing, improve glycaemic stability, and potentially reduce the risk of diabetes-related complications [15]. Secondly, physicians should maintain a high index of suspicion for thyroid disorders, particularly in patients with unexplained deterioration in glycaemic control, fluctuating blood glucose levels, or resistant dyslipidaemia [16, 38].

The strengths of this study include a well-defined cohort, standardised laboratory measurements, and robust statistical analysis, including the calculation of confidence intervals and appropriate tests of significance. However, it has some limitations. Being a cross-sectional study, it cannot establish causality between thyroid dysfunction and poor glycaemic outcomes. Longitudinal studies are warranted to evaluate whether treating subclinical hypothyroidism in diabetic patients leads to sustained improvements in glycaemic indices and reduces cardiovascular risk [38, 39]. Additionally, the sample size, while adequate, may limit the generalisability to larger diverse populations.

In conclusion, our study highlights a high burden of thyroid dysfunction among T1DM and T2DM patients in our setting and demonstrates its significant adverse impact on glycaemic control. Regular screening and timely treatment of thyroid dysfunction should be integrated into diabetes care protocols to achieve optimal metabolic outcomes and prevent complications.

This study highlights a significant prevalence of thyroid dysfunction among both T1DM and T2DM patients in our cohort, with subclinical hypothyroidism being the most frequent abnormality. The presence of thyroid dysfunction was associated with consistently higher fasting blood glucose, postprandial blood glucose, and HbA1c levels, indicating a clear adverse impact on glycaemic control. These findings underscore the importance of routine thyroid screening in patients with diabetes and suggest that early identification and appropriate management of thyroid dysfunction may contribute to optimised glycaemic targets, reduced insulin resistance, and prevention of long-term metabolic complications. Further prospective studies are warranted to assess the benefits of timely thyroid hormone replacement therapy in improving diabetes outcomes.

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