Interleukin (IL)-23, IL-31, and IL-33 Play a Role in the Course of Autoimmune Endocrine Diseases.

BACKGROUND: Interleukins (IL)-23, 31, and 33 are involved in the regulation of T helper 17 (Th17)/regulatory T (Treg) cells balance. The role of IL-23, 31 and 33 in non-endocrine autoimmune diseases has been confirmed. Data on the involvement of these cytokines in endocrine autoimmune diseases are limited. OBJECTIVE: This study aimed to determine the involvement of cytokines regulating the T helper 17 (Th17)/regulatory T (Treg) cells axis in the course of autoimmune endocrine diseases. METHODS: A total number of 80 participants were divided into 4 groups: the autoimmune polyendocrine syndrome (APS) group consisting of APS type 2 (APS-2) and type 3 (APS-3) subgroups, the Hashimoto's thyroiditis (HT) group, the Graves' disease (GD) group and the control (C) group. Fifteen cytokines related to Th17 and Treg lymphocytes were determined in the serum of all participants. RESULTS: Higher levels of IL-23 and IL-31 were found in the APS, GD, and HT groups compared to the C group. Higher levels of IL-23 and IL-31 were also observed in the APS-2 group, in contrast to the APS-3 group. Correlation analysis of variables in the groups showed a statistically significant correlation between the cytokines IL-23, IL-31, and IL-33 in the APS and APS-2 groups, but no correlation in the APS-3 and C groups. CONCLUSION: IL-23 and IL-31 are independent factors in the course of HT, GD, and APS-2, in contrast to APS-3. The positive correlation between IL-23 and IL-31, IL-23 and IL-33, and between IL-31 and IL-33 in the APS, APS-2 groups, but the lack of correlation in the APS-3 and C groups may further suggest the involvement of these cytokines in the course of Addison's disease.

[Multiple bone fractures caused by severe hypophosphatemia in the course of the mandible tumour].

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CD4+ cells in autoimmune thyroid disease.

The phenomenon of autoimmunity develops as a result of the triggering factor released by damaged cells. This leads to an infiltration of CD4+ cells involved in stimulating the effector cells cytotoxicity and stimulating the humoral response. One of the most common autoimmune disorders are autoimmune thyroid diseases, including Hashimoto's thyroiditis and Graves's diseases. Helper T lymphocytes, which are divided into Th1, Th2, Tregs, and the relatively new groups Th17, Th22, and Th9, are involved in the pathogenesis of AITD. CD4+ cell subtypes mature and differentiate by specific transcription factors and in a specific interleukin environment. Not only are Th1 and Th2 cells involved in the development of AITD, but also Th17, Th22, and Th9 lymphocytes and their correlation to Tregs lymphocytes. The plasticity of the CD4+ cells is very important, affecting the balance between these cells, as well the factors modulating their phenotypic variability. Patients with AITD have an increased percentage of Th17, Th22, and Th9 cells as well as defective function of Tregs lymphocytes. The balance between Th17 cells (and also other cytotoxic T cells) and Treg cells is also very important. Understanding the role of CD4 cells in the pathogenesis of AITD may be important not only for the development of the knowledge, but also for determining therapeutic targets.

Bilateral testicular infarction as a complication of acute cardiovascular diseases.

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Recurrent tetany in the course of metabolic alkalosis in patient with short bowel syndrome.

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Hypoglycaemia in endocrine, diabetic, and internal diseases [Hipoglikemia w schorzeniach endokrynologicznych, diabetologicznych i internistycznych].

Hypoglycemia is a decrease in blood glucose concentration below the physiological level. It occurs in healthy people and in people with various diseases with inadequate secretion of insulin by ß cells, or deficiency of counterregulatory hormones secreted at the moment of hypoglycemia. Hypoglycemia is also associated with diabetes therapy, regardless of whether behavioral therapy, oral hypoglycemic agents, or insulin are used. Distinguishing the causes of hypoglycemia is the basis for taking appropriate therapeutic actions that protect patients against subsequent episodes of lowering blood glucose and complications caused by hypoglycemia.

Vascular and cardiac function in young adults with classical congenital adrenal hyperplasia.

INTRODUCTION: Patients with classical congenital adrenal hyperplasia (CAH) have increased cardiovascular risk, but the vascular and cardiac function during longitudinal corticoids replacement therapy is not known thoroughly. MATERIAL AND METHODS: Cross-sectional study of 19 Caucasian adults with CAH (age 23.7 ± 3.8 years; twelve males) compared to 20 healthy volunteers matched for origin, sex, age, and body mass index (BMI). All of the participants were assessed for flow mediated dilatation of the brachial artery (FMD), intima-media thickness of the common carotid artery (cIMT) and common femoral artery (fIMT), standard echocardiography, and global longitudinal left ventricular function using two-dimensional speckle-tracking echocardiography (LSTE). RESULTS: The patients with CAH, compared with controls, had decreased FMD (9.4 ± 3.9 vs. 19.8 ± 5.2; p < 0.01), and the difference was still significant after correction for potential confounders. cIMT and fIMT were higher in the CAH group at baseline (for cIMT 0.47 ± 0.4 mm vs. 0.40 ± 0.03 mm; p < 0.01, for fIMT 0.47 ± 0.05 mm vs. 0.41 ± 0.04 mm; p < 0.01) but not after correction for potential confounders. The CAH subjects, compared with controls, had normal or similar left ventricular (LV) ejection fraction and LV mass index. The mean absolute value of LSTE differed in the CAH patients compared with controls (-20.5% ± 1.2 vs. -22.5% ± 1.7; p < 0.01), but it was still within the normal range. CONCLUSIONS: Young adults with CAH and glucocorticoid long-lasting treatment had impaired FMD, an insignificant increase of IMT, and subclinical changes in LV diastolic function in echocardiography.