Coronavirus as a Trigger Of Graves' Disease.

Context: SARS-CoV-2 infection was declared a pandemic in 2020 and affected millions of people worldwide. Angiotensin-converting enzyme-2 receptors, through which coronavirus enters the cells of different organs, have been detected in the thyroid gland. The most common cause of thyrotoxicosis is Graves' disease in which thyroid-receptors antibodies (TRAb) stimulate the TSH receptor, increasing thyroid hormone production and release. Case presentation: A 22-year-old woman had symptoms of palpitation, tremor, muscle weakness, anxiety and sleep disturbance. 3 weeks before the onset of these symptoms, the patient suffered from COVID-19, which lasted 14 days and was characterized by a course of moderate severity with fever up to 38°C, general weakness without shortness of breath. The patient had no pre-existing thyroid problems. Her TSH was <0.01 mU/L, FT4, FT3 and TRAb were increased. Antithyroid drugs, glucocorticosteroids and ß-blockers were prescribed. During 3 months of treatment doses of methimazole, methylprednisolone and bisoprolol were gradually reduced due to the improvement of the patient's condition and thyroid tests normalization. Conclusions: COVID-19 infection can cause Graves' disease and thyrotoxicosis. The onset of this disease after SARS-CoV-2 does not depend on the presence of pre-existing thyroid pathology and requires the appointment of glucocortisteroids.

Selected CNR1 polymorphisms and hyperandrogenemia as well as fat mass and fat distribution in women with polycystic ovary syndrome.

The endocannabinoid system is postulated to play an important role in the etiology of obesity, insulin resistance, fat distribution and metabolic disorders. Insulin resistance associated with abdominal obesity plays a leading role in the etiology of hyperandrogenism and other clinical features of the polycystic ovary syndrome (PCOS). A total of 174 women 16-38 years old, diagnosed with PCOS according to the Rotterdam criteria are recruited. Control group consisted of 125 healthy women 18-45 years old. Medical history, physical examination, anthropometric parameters and metabolic parameters were carried out. Six CNR1 gene polymorphisms were diagnosed. We observed a significantly three times higher risk of GG genotype in the polymorphism rs12720071 in women with PCOS versus the control group (p = 0.0344, OR = 3.01). A similar, significant 8-fold higher risk (p = 0.0176, OR = 8.81) was demonstrated for genotype CC polymorphism rs806368 associated with PCOS. We observed a 3.6-fold increased risk of hyperandrogenemia (free androgen index - FAI > 7) in patients with GG genotype in the rs12720071 polymorphism and AA genotype in the polymorphism rs1049353 (OR = 2.7). Our study may indicate a role of the endocannabinoid system in the occurrence of a specific hyperandrogenemia phenotype of PCOS.

[The blood leptin and the activity of the system inflammatory response in patients with diabetes mellitus type 2 with different body weight and disease duration].

Recent studies focused on the adipose tissue hormones role, especially leptin as one of the basic and generalized nonspecific inflammation markers among them. Some of the major markers are IL-2, IL -6 and TNF-alpha in the pathogenesis of diabetes (DM) and its complications. It is established that patients with type 2 diabetes lasting from 5 to 10 years represent the highest leptin and cytokines levels, and during this period cardiovascular complications of type 2 diabetes are formed. Also it is found that the leptin level was significantly lower in patients with normal body weight, while the levels of IL-6 and TNF-a are the highest in these patients. Obviously, the increased level of these cytokines helps to maintain a normal body weight in these patients. Despite the fact that type 2 diabetes is considered a non-autoimmune disease, it is known that for a long glucose toxicity and lipotoxicity metabolic immunosuppression occurs, which causes changes in T-cell immunity, and consequently to autoimmunity.

Effects of nitrosative stress and reactive oxygen-scavenging systems in esophageal physiopathy under streptozotocin-induced experimental hyperglycemia.

Experimental and clinical gastrointestinal data reported that nitrosative stress development involved in impaired barrier function, altered motility and a lowered threshold to noxious stimuli, but its pathogenetic role in diabetic esophagopathy remains unexplored. We tested the hypothesis that an imbalance in nonenzymatic glycation and glycooxidation, enhanced peroxynitrite formation, may play an important role in development esophageal mucosa (EM) lesions during streptozotocin-induced experimental hyperglycemia (EHG). To understand the biological significance of EM resistance in vivo used a glycomic approach to identification of lectin receptors glycosylation pattern. Were enrolled rat groups without/with EHG & modification of NO/NOS activity by L-arginine (L-arg) and indomethacin pre-treatment. Survival rate, destruction occurrence ratio, the size of EM lesions, and the number of EM lesions was investigated. To access the oligosaccharide residues the peroxidase conjugated lectin (HPA, SNA, WGA, PNA)-diaminobenzidine procedure was performed to EM sections. EHG was monitored daily by glucometer. Content of NO (NO(n)) was determinated by Griess reagent and reactive oxygen-scavenging systems (ROSS) activity - generally accepted biochemical methods. In EHG and L-arg pretreatment group reduced NO(n) and EM injury with markedly rise ROSS activity significantly vs to control; in the group with indomethacin pretreatment existed different ROSS activity. Presence of heterogeneous glycosylation pattern in different layers of EM was shown. In EHG staining with PNA and SNA were strongly positive. NS and ROSS play a critical role in esophagoprotection induced by EHG, because both involved increases in iNOS expression. These results indicate the usefulness of glycomic approach as multifunctional substrate of early evaluation of NS in esophageal physiopathy.