Research Report

Glucose Abnormalities in Hypothyroidism  

Said Azzoug1, 2 , Souad Chellali3 , Fatma Zohra Boudissa3 , El Hadj Ahmed Koceir3 , Djamila Meskine1, 2 , Farida Chentli4
1 Endocrine Diseases Department, Bologhine Hospital, Algiers, Algeria
2 Laboratory of Endocrinology and Metabolism, Algiers University, Algeria
3 Department of Biology, USTHB University, Algiers, Algeria
4 Endocrine Diseases Department, Bab El Oued Hospital, Algiers, Algeria
Author    Correspondence author
International Journal of Clinical Case Reports, 2018, Vol. 8, No. 3   doi: 10.5376/ijccr.2018.08.0003
Received: 12 Feb., 2018    Accepted: 21 Mar., 2018    Published: 13 Apr., 2018
© 2018 BioPublisher Publishing Platform
This is an open access article published under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Preferred citation for this article:

Azzoug S., Chellali S., Boudissa F.Z., Koceir E.H.A., Meskine D., and Chentli F., 2018, Glucose abnormalities in hypothyroidism, International Journal of Clinical Case Reports, 8(3): 10-13 (doi: 10.5376/ijccr.2018.08.0003)

Abstract

It is classically known that thyroid hormones excess or hyperthyroidism induce hyperglycemia. However, thyroid hormone deficiency or hypothyroidism can also induce glucose abnormalities through the development of abdominal obesity and insulin resistance. The aim of our study was to assess the frequency and predictive factors of glucose abnormalities during hypothyroidism. In this retrospective study, we included 425 patients (383 F/42 M) presenting with primary hypothyroidism. We investigated the presence of hyperglycemia, either fasting (≥100 mg/dl) and/or at 2 hours after an oral glucose tolerance test with 75 grams of glucose (≥140 mg/dl). Hyperglycemia was found in 37.6%. Subjects with hyperglycemia were older than those with normoglycemia (54.4±1.08 vs. 45.7±0.8 years), their Body Mass Index (BMI) was higher (31.5±0.53 vs. 28.7±0.37 kg/m2), they had higher blood pressure (54.3% vs. 21.5%) and a family history of diabetes (36.2% vs. 29.8%). We conclude that glucose abnormalities are frequent in hypothyroidism and are developed mostly in patients with risk factors for insulin resistance such as age, high blood pressure and a positive family history of type 2 diabetes.

Keywords
Hypothyroidism; Hyperglycemia; Insulin resistance

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.

 

 

Table 1 Comparison of patients with hyperglycemia and patients with normoglycemia

 

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.

 

 

Table 2 Comparison of patients who resumed normoglycemia and patients in whom hyperglycemia persisted

 

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.

 

 

Table 3 Eating habits and physical activity status in patients with hyperglycemia and patients with normal blood glucose

 

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.

 

References

Cettour-Rose P., Theander-Carrillo C., Asensio C., Klein M., Visser T.J., Burger A.G., Meier C.A., and Rohner-Jeanrenaud F., 2005, Hypothyroidism in rats decreases peripheral glucose utilization, a defect partially corrected by central leptin infusion, Diabetologia, 48:624-633

https://doi.org/10.1007/s00125-005-1696-4

PMid:15756538

 

Crunkhorn S., and Patti M.E., 2008, Links between thyroid hormone action, oxidative metabolism, and diabetes risk? Thyroid, 18: 227-237

https://doi.org/10.1089/thy.2007.0249

PMid:18279023

 

Dimitriadis G., Mitrou P., Lambadiari V., Boutati E., Maratou E., Panagiotakos D.B., Koukkou E., Tzanela M., Thalassinos N., and Raptis S.A., 2006, Insulin action in adipose tissue and muscle in hypothyroidism, J Clin Endocrinol Metab, 91: 4930-4937

https://doi.org/10.1210/jc.2006-0478

PMid:17003097

 

Dimitriadis G., Parry-Billings M., Bevan S., Leighton B., Krause U., Piva T., Tegos K., Challiss R.A., Wegener G., and Newsholme E.A., 1997, The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats, European Journal of Clinical Investigation, 27(6): 475-483

https://doi.org/10.1046/j.1365-2362.1997.1380688.x

 

Haluzik M., Nedvikova J., Bartak V., Dostalova I., Vlcek P., Racek P., Taus M., Svacina S., Alesci S., and Pacak K., Effects of hypo- and hyperthyroidism on noradrenergic activity and glycerol concentrations in human subcutaneous abdominal adipose tissue assessed with microdialysis, J Clin Endocrinol Metab, 88:5605-5608

https://doi.org/10.1210/jc.2003-030576

PMid:14671140

 

Lekakis J., Papamichael C., Alevizaki M., Piperingos G., Marafelia P., Mantzos J., Stamatelopoulos S., and Koutras D.A., 1997, Flow-mediated, endothelium-dependent vasodilatation is impaired in subjects with hypothyroidism, borderline hypothyroidism and high-normal serum thyrotropin levels, Thyroid, 7:411-414

https://doi.org/10.1089/thy.1997.7.411

PMid:9226212

 

Maratou E., Hadjidakis D.J., Kollias A., Tsegka K., Peppa M., Alevizaki M., Mitrou P., Lambadiari V., Boutati E., Nikzas D., Tountas N., Economopoulos T., Raptis S.A., Dimitriadis G., Maratou E., Hadjidakis D.J., Kollias A., Tsegka K., Peppa M., Alevizaki M., Mitrou P., Lambadiari V., Boutati E., Nikzas D., Tountas N., Economopoulos T., Raptis S.A., and Dimitriadis G., 2009, Studies of insulin resistance in patients with clinical and subclinical hypothyroidism, European Journal of Endocrinology, 160(5): 785-790

https://doi.org/10.1530/EJE-08-0797

PMid:19141606

 

Mitrou P., Raptis S.A., and Dimitriadis G., 2010, Insulin action in hyperthyroidism: a focus on muscle and adipose tissue, Endocrine Reviews, 31(5): 663-679

https://doi.org/10.1210/er.2009-0046

PMid:20519325

 

Ogbera A.O., Kuku S., and Dada O., 2012, The metabolic syndrome in thyroid disease: A report from Nigeria, Indian J Endocrinol Metab, 16(3): 417-422

https://doi.org/10.4103/2230-8210.95688

PMid:22629511 PMCid:PMC3354852

 

Pedersen O., Richelsen B., Bak J., Arnfred J., Weeke J., and Schmitz O., Characterization of the insulin resistance of glucose utilization in adipocytes from patients with hyper- and hypothyroidism, Acta Endocrinol, 119:228-234

https://doi.org/10.1530/acta.0.1190228

 

Rochon C., Tauveron I., Dejax C., Benoits P., Capitan P., Fabricio A., Berry C., Champedon C., Thieblot P., and Grizard J., 2003, Response of glucose disposal to hyperinsulinemia in human hypothyroidism and hyperthyroidism, Clin Sci., 104:7-15

https://doi.org/10.1042/cs1040007

PMid:12519082

 

Roos A.R., Bakker S.J.L., Links T.P., Gans R.O.B., and Wolffenbuttel B.H.R., 2007, Thyroid Function Is Associated with Components of the Metabolic Syndrome in Euthyroid Subjects, J Clin Endocrinol Metab, 92:491-496

https://doi.org/10.1210/jc.2006-1718

PMid:17090642

 

Shantha G.P., Kumar A.A., Jeyachandran V., Rajamanickam D., Rajkumar K., Salim S. et al., 2009, Association between primary hypothyroidism and metabolic syndrome and the role of C reactive protein: A cross sectional study from South India, Thyroid Res, 2:2

https://doi.org/10.1186/1756-6614-2-2

PMid:19272156 PMCid:PMC2655275

 

Uzunlulu M., Yorulmaz E., and Oguz A., 2007, Prevalence of subclinical hypothyroidism in patients with metabolic syndrome, Endocr J, 54:71-76

https://doi.org/10.1507/endocrj.K06-124

PMid:17102569

International Journal of Clinical Case Reports
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