Transcription factor 7-like 2 (TCF7L2) gene polymorphisms are strong predictors of type 2 diabetes among nonobese diabetics in the Turkish population

WOS: 000395632600003PubMed ID: 28263491Background/aim: Type 2 diabetes (T2D) is a multifactorial disease, determined by environmental and genetic factors. Currently, the transcription factor 7-like 2 (TCF7L2) gene shows the strongest association with T2D. In this study, we investigated whether TCF7L2 gene polymorphisms are associated with T2D in a Turkish population. Materials and methods: Using PCR-RFLP and PCR-SSCP, we genotyped six intronic polymorphisms in the TCF7L2 gene, commonly associated with T2D, in 169 individuals with diabetes and 119 healthy controls. Results: We found that rs7903146 C -> T substitution in intron 3 (OR: 1.9, P = 0.005) and rs12255372 G -> T substitution in intron 4 (OR: 2.1, P = 0.002) were significantly associated with T2D while other SNPs were not associated (P > 0.05). We determined no association between TCF7L2 gene polymorphisms and fasting glucose, fasting insulin, HbA1c, or HOMA-IR levels (P > 0.05), except for rs7903146 C -> T substitution, which was significantly associated with the fasting glucose level (P = 0.003). Conclusion: Our results indicate that, in the Turkish population, the T allele of the rs7903146 (C -> T) and rs12255372 (G -> T) polymorphisms in the TCF7L2 gene is an independent risk factor for the development of T2D.Selcuk University Research Foundation [09202048]We would like to thank Dr Hulya Ozdemir and Dr Suleyman Hilmi Ipekci for their assistance in this study. This study was supported by the Selcuk University Research Foundation (09202048)

Comparison of Salivary Cortisol, Serum Cortisol, Plasma ACTH and Urinary Free Cortisol Levels in Thyrotoxic and Hypothyroid Patients

Objective: Hypothalamo-pituitary-adrenal (HPA) axis is affected by thyroid hormones. The present study was designed to compare the level of salivary cortisol, serum cortisol, plasma adrenocorticotropic hormone (ACTH) and urinary free cortisol (UFC) levels in patients with subclinical and overt thyrotoxicosis and hypothyroidism. Material and Methods: We analyzed the salivary cortisol, serum cortisol, plasma ACTH and UFC levels in 123 patients with thyroid dysfunction. The patients were classified into four groups; overt thyrotoxicosis (n=32), subclinical thyrotoxicosis (n=29), overt hypothyroidism (n=28) and subclinical hypothyroidism (n=34). Results: There were no significant differences in terms of salivary cortisol, serum cortisol, plasma ACTH and UFC levels in patients with subclinical and overt thyrotcodcosis (p>0.05). Similarly, no significant differences could be detected in terms of salivary cortisol, serum cortisol, plasma ACTH and UFC levels in patients with subclinical and overt hypothyroidism (p>0.05). The comparison of patients with hypothyroidism and thyrotoxicosis also did not yield any significant difference in terms of salivary cortisol, serum conisol, plasma ACTH and UFC levels (p>0.05). Conclusion: Similar salivary cortisol, serum cortisol, plasma ACTH and UFC levels were detected in patients with hypothyroidism and thyrotoxicosis. Thus, we may suggest that thyroid hormone status does not play a role in the HPA axis. The major limitation of this study was the absence of a healthy control group. Further studies with large numbers of patients are required to clarify the association between thyroid hormone dysfunction and glucocorticoid levels

Hypothalamic-Pituitary Axis Function and Adrenal Insufficiency in COVID-19 Patients.

The outbreak of COVID-19 has affected more than half a billion people worldwide and caused more than 6 million deaths since 2019. The responsible virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily affects the lungs, but it has multisystemic effects. It is well known that dysfunction of multiple endocrine organs may occur during or after COVID-19. Impairment of hypothalamic-pituitary-adrenal (HPA) axis is of utmost importance as it may lead to death if went undiagnosed. SARS-CoV-2 may cause both primary and secondary adrenal insufficiencies (AI). The clinical manifestations of AI are generally non-specific and might be attributed to the complications caused by the infection itself. The underlying pathogenetic mechanisms were explained by the immunogenic, vascular effects of the infection or the direct effects of the virus. The diagnosis of AI in critically ill patients with COVID-19 is not straightforward. There is lack of consensus on the cut-off values of basal serum cortisol levels and stimulation tests during the disease. Here we review the literature with a special regard on the evaluation of HPA axis in patients with COVID-19. We conclude that the possibility of AI should always be kept in mind when dealing with patients with COVID-19, and repeated basal cortisol measurements and the ACTH stimulation test results could guide the clinician during the diagnostic process

Multiorgan dysfunction accompanied with metimazole and thyroid storm

A 41-year-old man with a history of hyperthyroidism had been treated with methimazole and propranolol for the past 2 months. He developed multiorgan dysfunction with acute liver failure, severe lactic acidosis, disseminated intravascular coagulation, heart failure and acute pulmonary edema with rapid deterioration of renal function. The patient had no history of alcoholism, drug abuse, blood transfusion, or exposure to hepatitis A, B, or C. Extrahepatic obstruction was ruled out with an abdominal ultrasonogram. Serologic studies and immunologic tests were negative. This case illustrates the sudden and abrupt deterioration of multiorgan dysfunction due to antithyroid drug administration and thyroid storm. The thyroid storm score of Burch and Wartofsky was 90/140. The multiorgan dysfunction was reversed by discontinuation of the methimazole and treat with hemodialysis, steroids, cholestyramine, nonselective beta-blocker, fresh frozen plasma infusion and supportive management in the intensive care unit. The patient was discharged from the hospital with normal coagulation parameters, renal and liver function tests. (C) 2012 Elsevier Ltd. All rights reserved

Plasma total oxidant and antioxidant status after oral glucose tolerance and mixed meal tests in patients with polycystic ovary syndrome

WOS: 000383571900007PubMed ID: 27300033Purpose Insulin resistance (IR) and increased oxidative stress (OS) are the characteristics of polycystic ovary syndrome (PCOS). In this study, we aimed to evaluate the effects of oral glucose tolerance (OGTT) and mixed meal tests (MMT) on plasma total oxidant (TOS) and total antioxidant status (TAS) in patients with PCOS and the relationship between these parameters and IR, calculated via homeostasis of model assessment-IR (HOMA-IR) and Matsuda's insulin sensitivity index (ISI) derived from OGTT and MMT. Methods Twenty-two patients with PCOS, and age- and body mass index (BMI)-matched 20 women as controls were enrolled into the study. Five-hour OGTT and MMT were performed on different days, and before and after these tests, plasma TOS and TAS levels were investigated. IR was calculated with HOMA-IR and Matsuda's ISI. Results HOMA-IR levels were higher in patients with PCOS, compared to controls, while Matsuda's ISI derived from OGTT and MMT was higher in controls. Plasma TOS levels before OGTT and MMT were higher in patients with PCOS than controls, while TAS levels were similar. After OGTT, plasma TOS levels became decreased at 5th hour, when compared to baseline values in PCOS group. Likewise, the same decrement was found in controls, but the decrement was not significant. After OGTT and MMT at 5th hour, no changes were observed in TAS levels, compared to baseline. Conclusion Matsuda's ISIs derived from OGTT and MMT can be used instead of each other, and interestingly, we found a decrease in TOS levels after OGTT in patients with PCOS.Konya Training and Research Hospital's Research FundThis study was supported by Konya Training and Research Hospital's Research Fund

Do We Need to Replace GH to Correct Anemia in Hypopituitarism?

WOS: 000209805102094