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Table of Contents
ORIGINAL ARTICLE
Year : 2020  |  Volume : 3  |  Issue : 2  |  Page : 75-78

Prevalence of Thyroid Disorders in Patients with Type 2 Diabetes Mellitus


Department of Medicine, Sardar Patel Medical College, PBM Group of Hospitals, Bikaner, Rajasthan, India

Date of Submission16-Jul-2019
Date of Acceptance22-Dec-2019
Date of Web Publication12-Jan-2021

Correspondence Address:
Dr. Surendra Kumar Verma
Opposite Acharya Tulsi Cancer Hospital, PBM Hospital, Bikaner, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdep.jdep_12_19

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  Abstract 


Background and Objectives: Thyroid disorders are very common in the general population, and it is second only to diabetes as the most common condition to affect the endocrine system. In this study, we try to observe the prevalence of the type of thyroid dysfunction in patients with type 2 diabetes mellitus (T2DM). and its effect on glycemic parameters and the prevalence of autoimmune thyroid disorder in patients with T2DM. Settings and Design: This study included adults having T2DM. Patients were explained about the nature of the study and consent was obtained. Materials and Methods: Clearance was taken from the ethics committee. All participants who met the inclusion criteria were subjected to detailed clinical examination and relevant investigation. Statistical Analysis: Chi-square test was used for the analysis. Results: Two hundred and thirty-four patients (112 males and 122 females) were included in the study. The mean body mass index was high (26.21 ± 3.13 kg/m2). The mean hemoglobin (Hb) A1c was 8.81% ± 1.96%, whereas mean HbA1c in patients with both T2DM and thyroid dysfunction was 9.68% ± 1.35%. Thyroid dysfunction was found in 84 cases (35.8%), out of which the most common thyroid abnormality was overt hypothyroidism (61.9%) followed by subclinical hypothyroidism (27.3%). Out of 84 cases with thyroid dysfunction anti-thyroid peroxidase (TPO) was found positive in 45 cases (53.5%), and the most common thyroid dysfunction associated with positive anti-TPO was subclinical hypothyroidism (44%). Conclusions: The study shows a high prevalence of thyroid dysfunction among patients with T2DM and its association with poor glycemic control. The study also shows the prevalence of anti-TPO among patients and its significant correlation with thyroid dysfunction.

Keywords: Autoimmune thyroid disorder, diabetes, thyroid


How to cite this article:
Verma SK, Singhal V, Gupta H, Khan IA, Anil Kumar K R, Dara N. Prevalence of Thyroid Disorders in Patients with Type 2 Diabetes Mellitus. J Diabetes Endocr Pract 2020;3:75-8

How to cite this URL:
Verma SK, Singhal V, Gupta H, Khan IA, Anil Kumar K R, Dara N. Prevalence of Thyroid Disorders in Patients with Type 2 Diabetes Mellitus. J Diabetes Endocr Pract [serial online] 2020 [cited 2021 Jan 20];3:75-8. Available from: https://www.jdeponline.com/text.asp?2020/3/2/75/306765




  Introduction Top


Diabetes mellitus (DM) is a clinical syndrome characterized by hyperglycemia caused by absolute or relative deficiency of insulin. Lack of insulin affects the metabolism of carbohydrates, protein, and fat and can cause a significant decrease of water and electrolytes homeostasis.[1]

Diabesity is defined as obesity, and type 2 diabetes is likely to be the greatest epidemic in human history.[2] If the total number of diabetics in the world is to be collected in one country, it would be the third biggest country in the world.[2] In recent years, the prevalence of diabetes, as well as prediabetes, has significantly increased in India. A recent Indian Council of Medical Research sponsored study suggests the widespread seriousness of this condition across rural and urban areas with some areas showing prevalence as high as 13%.[3]

Thyroid disorders are also very common in the general population, and it is second only to diabetes as the most common condition to affect the endocrine system. Many thyroid abnormalities may coexist and interact with DM. DM affects thyroid functions at many sites, from hypothalamic control of thyroid-stimulating hormone (TSH) release to T3 production from T4 in the target tissues.

Autoimmunity has been implicated to be the major cause of thyroid-dysfunction associated DM. Autoimmunity in which circulating antibodies exist to numerous body tissue components destroy such tissues were stated to be the underlying mechanism behind the increased prevalence of thyroid disorders in type 1 (T1) DM, despite the fact, autoimmune thyroid diseases are known to be highly prevalent in all forms of the diabetes; no specific reason has been adduced for an increased prevalence of thyroid disorders in type 2 DM (T2DM). However, insulin, the hormone required for transporting glucose from plasma across cell membranes into the cytosol of many cells (including those of the skeletal muscle) is absolutely deficient in T1 diabetics and relatively deficient in T2 diabetics. Some authors have postulated that insulin treatment in T1 diabetics and insulin resistance with resultant high plasma insulin levels in T2 diabetes may equally predispose both groups to deranged thyroid function.


  Materials and Methods Top


The present study was conducted in the Department of Medicine, S.P. Medical College and Associated Group of PBM Hospitals, Bikaner. This study was a cross-sectional study. Participants were recruited from PBM Hospital and Associated Group of Hospitals, Bikaner. Ethical approval was obtained from the Institutional Research Ethics Committee, and written informed consent was taken from all participants. For each patient, the following data were collected as follows: age, sex, biochemical parameters (complete blood count including hemoglobin (Hb), total and differential leukocyte count, total platelet count, HbA1c, fasting plasma glucose, blood urea, serum creatinine, aspartate aminotransferase, alanine aminotransferase, total bilirubin, T3, T4, TSH, and anti-thyroid peroxidase (TPO) antibody.

Sample Size

A total of 234 patients of Medicine Department of S.P. Medical College and Associated group of PBM Hospital, Bikaner, during the study and who met the inclusion and exclusion criteria were included in this study.


  Results Top


  • General characteristic of patients [Table 1]
  • Table 1: General characteristic of patients

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    Age of the patients was varied from 40 to 85 years, with a maximum number of patients were observed in the age group of 51–60 years. The mean ages of the patients were 58.18 ± 10.08. One hundred and twelve patients were male and 122 patients were female. The mean body mass index (BMI) of T2DM cases was high (26.21 ± 3.13 kg/m2). The mean value of HbA1c was 8.81% ± 1.96%. The mean value of fetal bovine serum was 126.31 ± 29.76 mg/dl, and of postprandial blood sugar was 216.29 ± 52.82 mg/dl [Figure 1].
    Figure 1: Sugar level of diabetes type 2 patients

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  • Anti-TPO prevalence [Table 2]
  • Table 2: Anti TPO prevalence

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    In the present study, maximum (80.73%) cases of T2DM were anti-TPO negative, and only 19.23% of cases were anti-TPO positive.

  • Distribution of cases according to the thyroid hormone abnormality [Table 3]
  • Table 3: Distribution of cases, according to thyroid hormone abnormality

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    In the present study, maximum cases (64.10%) of T2DM were normal thyroid function, 22.22% cases were overt hypothyroidism, 9.83% cases were subclinical hypothyroidism, 1.28% cases secondary hypothyroidism, and 2.56% cases were hyperthyroidism.

  • Association between thyroid disorder and anti-TPO [Table 4]
  • Table 4: Association between thyroid disorder and anti TPO

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    In the present study, 20 of 23 cases of subclinical hyperthyroidism were anti-TPO positive, and three cases were anti-TPO negative. The association between thyroid disorder and anti-TPO was statistically significant.

  • The mean HbA1c was 8.81% ± 1.96%, whereas mean HbA1c in patients with both T2DM and thyroid dysfunction was 9.68% ± 1.35%.



  Discussion Top


Among the endocrinal disorders, diabetes occupies the major share. India is the diabetes capital of the world. DM is a complex multifactorial disease with varying etiologies, but in most of the cases, there is genetic predisposition. It has been associated with various physiologic changes in different organ systems of the human body. The varying complications are associated with the morbidity and mortality associated with diabetes. According to recent estimates, overall prevalence of T2DM was 4.3% in India.[4] In recent study, about 42 million people in India suffer from thyroid diseases. The prevalence of overt hypothyroidism in India is 3.9%. The prevalence of subclinical hypothyroidism is also high in our study, the value being 22.22%. The prevalence of subclinical and overt hyperthyroidism in India is 1.6% and 1.3%.[4] T2DM has an intersecting underlying pathology with thyroid dysfunction. Altered thyroid hormones have been described in patients with diabetes, especially those with poor glycemic control. In diabetic patients, the nocturnal TSH peak is blunted or abolished, and the TSH response to thyrotropin-releasing hormone is impaired. Reduced T3 levels have been observed in uncontrolled diabetic patients, and it becomes normal with improvement in glycemic control. This “low T3 state” could be explained by impairment in the peripheral conversion of T4–T3. The abnormal thyroid hormone level may also be the outcome of various medications that the diabetic patients received. For example, it is known that insulin, an anabolic hormone enhances the level of FT4 while it suppresses the level of T3 by inhibiting the hepatic conversion of T4 to T3. On the other hand, some of the oral hypoglycemic agents such as the phenylthioureas (sulfonylureas) are known to suppress the level of FT4 and T4 while causing raised levels of TSH.[4]

The most probable mechanism leading to hyperglycemia in thyroid dysfunction could be attributed to perturbed genetic expression of a constellation of genes along with physiological aberrations leading to impaired glucose utilization and disposal in muscles, overproduction of hepatic glucose output, and enhanced absorption of splanchnic glucose. These factors contribute to insulin resistance. Insulin resistance is also associated with thyroid dysfunction. Both hyperthyroidism and hypothyroidism have been associated with insulin resistance, which has been reported to be the major cause of impaired glucose metabolism in T2DM. The state-of-the-art evidence suggests a pivotal role of insulin resistance in underlining the relation between T2DM and thyroid dysfunction. A plethora of preclinical, molecular, and clinical studies has evidenced an undeniable role of thyroid malfunctioning as a comorbid disorder of T2DM.

In the present study, maxium cases (80.73%) of T2DM were anti-TPO negative, and only 19.23% of cases were anti-TPO positive.

A study conducted by Palma et al. in 2013, the prevalence of anti-TPO antibodies was 10.8%.[5]

In our study, maximum cases (64.10%) of T2DM were normal thyroid function, 22.22% cases were overt hypothyroidism, 9.83% cases were subhypothyroidism, 1.28% cases secondary hypothyroidism, and 2.56% cases were hyperthyroidism.

Kiran et al.[6] reported 28% of thyroid dysfunction in T2DM case with 13.2% having hypothyroidism, 8.8% having hyperthyroidism, and low T3 syndrome in 5.8%. Celani et al.[7] reported 31.4% of thyroid dysfunction in T2DM cases. Of these, subclinical hypothyroidism was most common (48.3%), followed by subclinical hyperthyroidism (24.2%) and by definite hypothyroidism (23.1%). Definite hyperthyroidism was found in 4 patients (4.4%).

Dysregulated glucose disposal and metabolism in adipocytes, muscles, and liver, along with impaired insulin secretion by the pancreatic beta-cells, constitute the four major organ system abnormalities, which play a definitive role in the pathogenesis of T2DM. It is worth considering that insulin resistance has been a proven condition in hyperthyroidism as well as hypothyroidism.[8]

Insulin resistance has been shown to be caused in hypothyroidism in various in vitro and preclinical studies where it was found that peripheral muscles became less responsive in hypothyroid conditions. A possible role of dysregulated metabolism of leptin has been implicated for such pathology.[8]

The pathological features of T2DM include increased intestinal glucose absorption, reduced insulin secretion, and change in the cell mass. Furthermore, symptoms also include increased insulin degradation, increased glucagon secretion, increased hepatic glucose production, enhanced catecholamines, and insulin resistance. These factors have been investigated to be an integral part of hyperthyroidism as well. Hence, an intersection of pathological basis occurs which gives us cue to an array of physiological aberrations, which are common in hyperthyroidism and T2DM.[8]

Insulin resistance and cell function are inversely correlated with TSH which may be explained by insulin-antagonistic effects of thyroid hormones along with an increase in TSH. The higher serum TSH usually corresponds to lower thyroid hormones through negative feedback mechanism. As TSH increased, thyroid hormones decreased, and insulin-antagonistic effects are weakened. These observations demonstrate that insulin imbalance is closely associated with thyroid dysfunction, and the phenomenon is mediated through cell dysfunction (T2DM).[8]

Both T2DM and hypothyroidism are associated with high BMI and insulin resistance, whereas hyperthyroidism is mostly associated with low BMI because of the high metabolic rate. Hence because of common pathophysiology, T2DM is more commonly associated with hypothyroidism compared to hyperthyroidism.

Hence, it is evident from the above discussion that thyroid dysfunction was more common in T2DM than nondiabetics. The results of the present study are more or less correlated with the various national and international studies.


  Conclusion Top


Thyroid disorders were more commonly found in female. Most common thyroid disorder associated with T2DM was overt hypothyroidism followed by subclinical hypothyroidism. Interestingly majority of patients with subclinical hypothyroidism had Anti-TPO Antibody positive, indicating autoimmunity. We also found that patients with both T2DM and thyroid disorder had poor glycemic control, thus requiring strict glycemic control.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Frier BM, Fisher M. Diabetes mellitus. In: Colledge NR, Walker BR, Ralston SH, editors. Davidson's Principals Practice of Medicine. 21sted., Ch. 21. Edinburgh: Churchill Livingstone Elsevier; 2010. p. 798.  Back to cited text no. 1
    
2.
Zimmet PZ. Diabetes and its drivers: The largest epidemic in human history? Clin Diabetes Endocrinol 2017;3:1.  Back to cited text no. 2
    
3.
Anjana RM, Deepa M, Pradeepa R, Mahanta J, Narain K, Das HK, et al. Prevalence of diabetes and prediabetes in 15 states of India: Results from the ICMR-INDIAB population-based cross-sectional study. Lancet Diabetes Endocrinol 2017;5:585-96.  Back to cited text no. 3
    
4.
Basu G, Mohapatra A. Interactions between thyroid disorders and kidney disease. Indian J Endocrinol Metab 2012;16:204-13.  Back to cited text no. 4
    
5.
Palma CC, Pavesi M, Nogueira VG, Clemente EL, Vasconcellos Mde F, Pereira LC Júnior, et al. Prevalence of thyroid dysfunction in patients with diabetes mellitus. Diabetol Metab Syndr 2013;5:58.  Back to cited text no. 5
    
6.
Kiran N, Amin P, Tayebeh S, Pegah E. Prevalence of thyroid dysfunction and its management in diabetic patients attending outpatient clinic of KIMS hospital. Int Res J Pharmacy 2013;4:132-5.  Back to cited text no. 6
    
7.
Celani MF, Bonati ME, Stucci N. Prevalence of abnormal thyrotropin concentrations measured by a sensitive assay in patients with type 2 diabetes mellitus. Diabetes Res 1994;27:15-25.  Back to cited text no. 7
    
8.
Wang C. The Relationship between Type 2 Diabetes Mellitus and Related Thyroid Diseases. J Diabetes Res 2013;2013:390534. doi: 10.1155/2013/390534. Epub 2013 Apr 4. PMID: 23671867; PMCID: PMC3647563.  Back to cited text no. 8
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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