Year : 2013 | Volume
: 10 | Issue : 4 | Page : 1--2
Hypothyroidism and metabolic syndrome
Rohinivilasam V Jayakumar
Department of Endocrinology, AIMS School of Medicine, Cochin, India
Rohinivilasam V Jayakumar
Department of Endocrinology, AIMS School of Medicine, P. O. Ponekkara, Cochin-682041
|How to cite this article:|
Jayakumar RV. Hypothyroidism and metabolic syndrome.Thyroid Res Pract 2013;10:1-2
|How to cite this URL:|
Jayakumar RV. Hypothyroidism and metabolic syndrome. Thyroid Res Pract [serial online] 2013 [cited 2020 Jun 5 ];10:1-2
Available from: http://www.thetrp.net/text.asp?2013/10/4/1/106800
Metabolic Syndrome refers to a cluster of cardiovascular risk factors, whose underlying pathophysiology is thought to be related to Insulin Resistance (IR). The components include dyslipidemia, hypertension, abdominal obesity, and hyperglycemia. Though Reaven Banting had baptized this syndrome in 1988, this entity has seen ups and downs in the medical field in getting acceptance for designation as a syndrome over the decades. In today's discussion, let us look at the association between hypothyroidism and metabolic syndrome. To understand the topic, let us look at some of the known facts about Metabolic Syndrome.
Though there are many diagnostic criteria put forwade by organizations like American Heart Association (AHA) and World Health Organization (WHO), the National Cholesterol Education Programe Adult Treatment panel-III (NCEP-ATP-III) guidelines are widely accepted as it is very easy to diagnose, but whether it over estimates, is still a concern. According to WHO criteria, glucose abnormality is a must and, hence, it is thought to be biased towards diabetics. Microalbuminuria is listed in WHO criteria and not in NCEP-ATP III. Prevalence of this syndrome varies up to 24% between the two definitions as shown in Framingham Offspring study by Meigs et al. McLaughlin et al. found that 78% of those with Metabolic Syndrome are insulin resistant, but only 48% of those with IR had metabolic syndrome. C - reactive protein has been found to be an independent cardiovascular disease (CVD) risk factor and marker of insulin resistance, but it is not included as a criteria. Adiponectin, a marker, which correlates well with insulin resistance, hypertension, and hyperlipidemia, is a strong inverse risk factor for CVD and has to be considered as a component of metabolic syndrome. Other markers like Plasminogen Activator Inhibitor and fibrinogen with good predictive values for CVD also contend for a seat in the Metabolic Syndrome bandwagon. There are still many other unidentified factors which contribute to the IR and, hence, metabolic syndrome. Is thyroid dysfunction, as documented by elevated Thyroid-stimulating hormone (TSH), one among them?
My experience  with the thyroid status in Metabolic Syndrome is as follows. One twenty patients from those who attended my endocrine clinic, who were diagnosed to have metabolic syndrome, based on NCEP ATP-III criteria, between age groups of 10 and 60 years were taken into the study. Out of the 120, 42 were males and 78 were females. Highest number (32) of the total patients (120) belonged to the age group of 10-20 years. Thirty patients were in the 31-40 years age group. Obesity or increased waist circumference was observed in all 120 patients, high-density lipoprotein (HDL) abnormality in 75, triglycerides (TG) abnormality in 67, hypertension in 69, and fetal bovine serum (FBS) > 110 mg in 47 patients. Thyroid functions were normal in 48 patients. Eighteen patients had hypothyroidism, 52 had subclinical hypothyroidism, and two had subclinical hyperthyroidism. Among patients who had thyroid dysfunction, 12 had history suggestive of thyroid dysfunction, six had diffuse grade1 goitre, two had multinodular goiter (MNG), and one had single adenoma. Physical findings of hypothyroidism were present in only seven cases. Hypothyroidism and subclinical hypothyroidism were present in 60% of patients with metabolic syndrome.
Looking into the available literature on the subject, it is obvious that high normal TSH was associated with greater degree of IR than low normal TSH and also this was correlated with low-density lipoprotein (LDL) level. Chubb, et al. showed that the estimated 10 yr cardiovascular (CV) risk of a insulin resistant patient at a TSH of 1 mIU/L was almost half of that of TSH 5 mIU/L. In Rotterdam study, women with subclinical hypothyroidism and normal lipids had higher ischemic heart disease (IHDs) and aortic atherosclerosis. Taddei et al. showed that endothelial dysfunction can occur with subclinical hypothyroidism. Sat Byul has shown that there is a relationship between thyroid function and CV risk factors and higher levels of TSH may predict the Metabolic Syndrome in Koreans (Journal of Korean Medical Science. 2011 April). Metabolic syndrome occurs in one in every four persons with thyroid disorders as shown by Anthonia (Indian Journal of Endocrinology and Metabolism (IJEM)-2012 Vol. 16). Higher TSH levels and subclinical hypothyroidism with a TSH > 10 mIU/l are associated with increased odds of prevalent but not incident Metabolic Syndrome.  In a study from South India, Shantha et al. has shown that overt and subclinical hypothyroidism is significantly associated with Metabolic Syndrome patients, and females have an increased risk of this association. She has also shown that these patients have increased signs of systemic inflammation as evidenced by higher levels of high-sensitivity C-reactive protein (HsCRP). Whether these patients will benefit from thyroxine therapy is not clear. A recent study from Amsterdam looked at the relationship between serum TSH and Metabolic Syndrome in older population. Their conclusion was that subjects with high normal TSH have a higher prevalence of Metabolic Syndrome compared to those with a serum TSH in the low normal range. 
Many studies looking at the association of Metabolic Syndrome with thyroid dysfunction has found more subclinical hypothyroidism, rather than overt hypothyroidism. The elevated TSH in Metabolic Syndrome may be due to inflammatory mediators and hormones from fatty tissue, like leptin, resistin, or adiponectin, acting at the hypothalamo-pituitary level. The TSH alone is elevated with normal T3 and T4, suggesting the possibility of thyroid TSH receptor resistance to TSH. One of the previous studies has shown mutation of Deiodinase-2 gene associated with IR. This mutation can reduce the intracellular production of T3, which can result in higher TSH production due to inefficient T3 feedback at the pituitary level. Recent studies by Chugh et al. (IJEM, 2012), attribute the elevated TSH in Metabolic Syndrome as a consequence of a metabolic syndrome, rather than a state of subclinical hypothyroidism.
Metabolic Syndrome, a clinical entity has to be clearly defined with more risk factors with proven predicting capacity. There is an increased incidence of thyroid dysfunction, especially elevated TSH with normal T3 and T4, in Metabolic Syndrome. Hence, it is justifiable to order for TSH and T4 in all patients with this syndrome. Also, it seems that elevated TSH may be included in the list of criteria for diagnosing metabolic syndrome. More randomized, controlled studies are needed to study the relationship between the IR and thyroid dysfunction.
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