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].

Not required for Clinical Vignette.

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.

Not required for Clinical Vignette.

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.

Endocrine diseases as causes of secondary hyperlipidemia.

Cardiovascular diseases are among the leading causes of increased morbidity and mortality in developed and developing countries. One of the most important risk factors responsible for atherosclerosis and subsequent cardiovascular diseases is hyperlipidaemia. Currently, hyperlipidaemias are divided into several clinical entities. The greatest risk is associated with hypercholesterolaemia. As a result, modern guidelines for the treatment and prevention of atherosclerosis focus predominantly on the reduction of LDL-cholesterol. Hypertriglyceridaemia and atherogenic dyslipidaemia, which are responsible for a less significant increase in the cardiovascular risk, are nowadays secondary targets of the treatment. During the work-up for hyperlipidaemia one of the essential actions is the exclusion of secondary causes of the lipid abnormalities. Those include, among others, endocrine diseases, diabetes, drugs, nephrotic syndrome, and pregnancy. Data regarding the impact of endocrine disease and diabetes on the lipid profile are scattered. In this review, the authors aimed to perform a thorough analysis of the available publications regarding the topic and the preparation of a comprehensive review dealing with the incidence, clinical features, and the therapy of hyperlipidaemias in patients with endocrine disease.