Background

Due to their ubiquitous actions, thyroid hormone deficiency can have clinical and metabolic consequences. It has been established that hypothyroidism can induce insulin resistance that predisposes to glucose abnormalities.

The aim of our study was to assess the frequency and predictive factors of glucose abnormalities during hypothyroidism.

1 Subjects and Methods

This is a retrospective study including 425 patients (383 F/42 M) presenting with primary hypothyroidism. We have investigated the presence of hyperglycemia in our patients, either fasting glycemia ≥ 100 mg/dl and/or glycemia after oral glucose tolerance test with 75 grams of glucose (OGTT) ≥ 140 mg/dl.

Thereafter, we have compared patients with hyperglycemia to patients with normoglycemia for a set of factors such as age, Body Mass Index (BMI), Free Thyroxine (FT4) level, triglyceride level, personal antecedent of High Blood Pressure (HBP) and positive family history of type 2 diabetes to look for predictive factors of hyperglycemia in hypothyroidism.

2 Results

Out of 425 patients, 36.7% had hyperglycemia. In order to search for predictive factors, we compared hypothyroid patients with hyperglycemia to hypothyroid patients with normal blood glucose levels as depicted in Table 1.

After treatment of hypothyroidism and normalization of thyroid hormones levels, patients who had hyperglycemia were reevaluated. Patients in whom hyperglycemia persisted were compared to patients who resumed normal blood glucose levels as depicted in Table 2.

We have also done an evaluation of eating habits and physical activity status and made a comparison between patients with hyperglycemia and patients with normal blood glucose levels as depicted in Table 3.

3 Discussion

Thyroid hormones modulate glucose metabolism through effects on insulin action, intracellular insulin signaling, ß-cell function, hepatic gluconeogenesis, lipolysis and lipid oxidation (Crunkhorn and Patti, 2008).

Hypothyroidism one of the most common endocrine disorders may predispose to hyperglycemia through development of insulin resistance and metabolic syndrome.

Experiments performed in muscle of hypothyroid rats and adipose tissue fragments isolated from patients with hypothyroidism showed that rates of glucose transport did not increase when insulin was increased within the physiological range (Pedersen et al., 1988; Cettour-Rose et al., 2005). Furthermore, observations in hypothyroid subjects using euglycemic hyperinsulinemic clamps have shown resistance of whole body glucose disposal to plasma insulin levels (Rochon et al., 2003; Maratou et al., 2009; Mitrou et al., 2010).

In Dimitriadis’ study, forearm and adipose tissue blood flow and glucose disposal rates in hypothyroid patients were significantly decreased at 60-90 min after the meal when plasma insulin levels reached their peak. Decrease in blood flow was postulated to be responsible for the defect in insulin-stimulated glucose disposal in the forearm and adipose tissue. Indeed, calculated fractional glucose extraction was not impaired, suggesting that the resistance of glucose disposal to insulin in hypothyroidism could be accounted for by the impairment of vasodilatation as a consequence of endothelial dysfunction and impairment of the sympathetic system action (Dimitriadis et al., 1997; Lekakis et al., 1997; Haluzik et al., 2002; Dimitriadis et al., 2006).

Many studies have shown a strong association between hypothyroidism and metabolic syndrome, thyroid function has been associated with individual components of metabolic syndrome. FT4 levels were associated with total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides levels (Roos et al., 2007).

In Shantha’s study, the prevalence of subclinical hypothyroidism was 21.9% and that of overt hypothyroidism was 7.4% in patients with metabolic syndrome, whereas in the control group, the prevalence of subclinical hypothyroidism was 6.6% and that of overt hypothyroidism was 2%. In this study, mean systolic pressure, diastolic pressure, waist circumference, fasting blood sugar, total cholesterol, LDL cholesterol, triglycerides and TSH values were significantly higher in the metabolic syndrome group compared to the control group (Shantha et al., 2009).

The study by Uzunlulu, had shown that the prevalence of subclinical hypothyroidism was 16.4% in patients with metabolic syndrome. The metabolic syndrome group had significantly higher levels of mean systolic pressure, diastolic pressure, waist circumference, body mass index, fasting blood sugar, total cholesterol, LDL cholesterol, triglycerides and TSH values. Subclinical hypothyroidism was significantly associated with metabolic syndrome (Uzunlulu et al., 2007).

In the study done by Ogbera, the prevalence of metabolic syndrome in patients with hypothyroidism was 40%. Hyperglycemia was the commonest occurring metabolic syndrome defining criterion. It was reported in 50% (Ogbera et al., 2012).

4 Conclusion

Carbohydrate abnormalities are frequent in patients with hypothyroidism. They occur in patients with risk factors for type 2 diabetes such as age, obesity, a family history of type 2 diabetes, and a personal history of high blood pressure and high triglyceride levels.

Furthermore, there is a negative correlation between FT4 levels and the risk of carbohydrate abnormalities, which supports the hypothesis that thyroid hormone deficiency is diabetogenic.

The modulating role of dietary factors and physical activity is important as demonstrated by the risk of hyperglycemia by poor eating habits and lack of physical activity.

Authors’ contributions

S.A., E.A.K., S.C. and F.Z.B. carried out the study and drafted the manuscript, D.M. and F.C. participated in the study. All authors read and approved the final manuscript.

Acknowledgments

The authors thank patients and all persons who participated in the carrying out of this study.

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