[A case of severe hyperparathyroidism in clinical practice. Case report].

Disorders of the mineral balance often determine the symptoms, the severity of the course and the prognosis of many diseases. Primary hyperparathyroidism (PHPT) is a common endocrine disease caused by increased secretion of parathyroid hormone as a result of primary damage to the parathyroid glands. Diagnosis of PHPT is often difficult. Clinical signs of PHPT appear months or years after the onset of the disease, however, the presence of hypercalcemia serves as an early indication of the disease of the thyroid gland. Often, patients are observed for a long time by related specialists (rheumatologists, traumatologists-orthopedists, oncologists), which gives rise to a lot of problems consisting in the lack of adequate treatment and its result, the progression of the disease, disability, and a decrease in the quality of life. Often, patients are observed for a long time by related specialists (rheumatologists, orthopedic traumatologists, oncologists) under the "masks" of various pathologies (osteoporosis, recurrent urolithiasis, etc.), which gives rise to a lot of problems, consisting in an erroneous diagnosis, lack of adequate treatment and its result, progression of the disease, disability, and a decrease in the quality of life. Late diagnosis of PHPT leads to the development of severe complications (osteoporetic fractures, renal failure) and an increased risk of premature death. A clinical case of late diagnosis of PHPT at the stage of pronounced bone complications of the disease, which proceeded under the guise of osteoarthritis, is considered. According to the results of laboratory and instrumental studies, the following were revealed: hypercalcemia, a significant increase in the concentration of PTH, adenoma of the left lower parathyroid gland, hyperparathyroid osteodystrophy, and a decrease in bone mineral density. Surgical treatment was performed - selective parathyroidectomy with the development of hypocalcemia in the early postoperative period, which was stopped by taking calcium supplements and active vitamin D metabolites and is designed to help practitioners of various specialties to understand the issues of diagnosis of PHPT and effective care for patients.

[Efficacy of metformin in abdominal obesity].

AIM: To study the effect of metformin on metabolic parameters, body weight (BW), and waist circumference (WC) in patients with abdominal obesity (AO). SUBJECTS AND METHODS: The results of using metformin 2000 mg daily for 3 months in 46 patients with AO. The comparison group consisted of 50 people. BW, WC, and blood pressure (BP) were measured; lipid profile parameters and blood insulin concentrations were determined; and Homeostasis Model Assessment (HOMA) estimates were calculated. Metabolic syndrome (MS) and AO were judged by the 2005 International Diabetes Federation (IDF) criteria. RESULTS: The study and comparison groups showed were reductions in BW by 4.2 and 1.7 kg and in WC by 4.2 and 1.1 cm, respectively. Metformin used in the patients with AO contributed to a more significant improvement in the lipid profile than in those who received no medication. A decrease in the HOMA index was observed only in the metformin group. The effects of the drug were more pronounced in MS and insulin resistance. The use of metformin in the patients with AO decreased lower BW and HOMA index and improved lipid metabolism even in the absence of MS. CONCLUSION: The trial has demonstrated that the people with AO may take metformin could be used in to reduce BW and WC and to treat and prevent MS.

[Affection of myocardium in diabetes mellitus]. / Porazheniia miokarda pri sakharnom diabete.

Echocardiography was performed in 67 patients with compensated diabetes mellitus (DM) type I and II. No signs of cardiovascular failure were noted. 20 patients have undergone myocardial scintigraphy. The patients were found to have hyperkinetic central hemodynamics resultant in DM type I from tachycardia, high rate of circulatory shortening of myocardial fibers, in DM type II from compensatory myocardial hypertrophy. In both diabetic types the function of myocardial relaxation was deteriorated as indicated by increased end diastolic volume and slow left ventricular relaxation. This evidences for initial cardiac failure. Myocardial scintigraphy registered perfusion defects in all the examinees, more profound in diabetes mellitus type II. The above findings explain the existence of marked coronarogenic and metabolic myocardial defects in DM.