Patients with diabetes mellitus (DM) have an increased risk of osteoporotic fractures, which is associated with a bone fragility.

Accumulation of advanced glycation end products, hyperhomocysteinemia causes increased apoptosis of osteocytes, decreased bone formation and bone remodeling in DM. Adiponectin stimulates osteocalcin expression and osteoblast differentiation through the activation of AMPK. AMPK-activation stimulates differentiation and mineralization of osteoblasts. Hypoadiponectinemia, which is often observed in obesity and diabetes, can causes bone fragility.

Diabetes mellitus is a state of low bone turnover, which is confirmed by decreased markers of bone formation (osteocalcin, P1NP), decreased markers of bone resorption (CTX, TRAP), increased regulatory markers of bone remodeling (OPG, sclerostin).

Thus, the study of the pathophysiology of bone metabolism, the level of bone metabolism markers in patients with diabetes mellitus gives broad prospects in understanding the mechanisms of osteoporosis as complication of diabetes mellitus, the selection of targeted therapy and the improvement of early diagnosis of the disease.

Since the discovery of vitamin D, interest in role of vitamin D in human body is consistently growing, and there is increasing evidence that vitamin D is not only essential to bone health but may also be involved in physiology of many other tissues. Thus understanding of its aspects in particular tissues appears to be important because of possible contribution to pathophysiologic processes. Intracrine regulatory systems associated with widely expressed vitamin D metabolizing enzymes, ways of cellular intake and signal pathways involved are of particular interest. Association of local effects with vitamin D level in blood is under investigation on animal models as well as in clinical studies; values of vitamin D level that mediate extraskeletal effects should be determined. In this review, we discuss impact of vitamin D on immune function and its association with skin, nervous system, cardiovascular system, obesity and diabetes mellitus, cancer, reproductive function, prevention of falls and quality of life improvement.

Gastroesophageal reflux disease (GERD) is a gastrointestinal motility disorder that results from the reflux of stomach contents into the esophagus resulting in symptoms or complications. GERD is now widely prevalent around the world, with clear evidence of increasing prevalence in many developing countries. Treatment for most people with GERD includes lifestyle changes and medication. Proton pump inhibitors (PPIs) are a mainstay therapy for all gastric acid-related diseases. Long-term use of PPIs is associated with hypomagnesaemia, hypokalemia, hypocalcaemia, osteoporosis and bone fractures, chronic renal disease, acute renal disease, and other. Clinical concerns arise from a small but growing number of case reports presenting PPI-induced hypomagnesaemia. In 2011 the U.S. Food and Drug Administration is informing the public that prescription PPI may cause low serum magnesium levels if taken for prolonged periods of time.

In this article, we present the case of a 56-year-old patient with muscle cramps, violation of cardiac rhythm, lethargy and other caused by hypomagnesaemia, hypocalcaemia and hypokalemia with a low parathyroid hormone level while using a PPI. After magnesium repletion abnormalities resolved. A causal relation with PPI use was supported by the recurrence of hypomagnesaemia after re-challenge.

In this article, we discuss difficulties in parathyroid localization modalities in diagnosis of primary hyperparathyroidism. Most often, superior parathyroid glands are located on the posteromedial surface of the right and left lobes of the thyroid gland, however, they also could be found at the carotid bifurcation, behind pharynx and esophagus, as well as inside thyroid gland. Location of the inferior parathyroid glands is more variable: on the side or back surface, or below the lower pole of the thyroid gland, as well as in thymus, posterior or anterior mediastinum, or inside thyroid. Localization modalities of primary hyperparathyroidism are based on neck ultrasonography, scintigraphy with sestamibi, computed tomography of neck and mediastinum. In cases with combination of multinodal goitre and an intrathyroid location of the parathyroid gland, there might be additional difficulties in verification of various patterns (thyroid nodules or parathyroid glands). In this article, we present two clinical cases of intrathyroid location of parathyroid glands. The algorithm of parathyroid adenoma localization is shown. Determination of PTH level in washing liquid after fine-needle aspiration biopsy from necessary punctures of the nodule formations, which can be either intrathyroid parathyroid glands or thyroid nodules, can also help to avoid diagnostic mistakes.

The article presents a review of the clinical guidelines of 2017 American College of Rheumatology for prevention and treatment of glucocorticoid-induced osteoporosis. The guidelines i contain fracture risk gradation not only for people over 40 years , based on the measurement of bone mineral density, 10-year probability of fractures by FRAX and prior osteoporotic fractures, but also for people under 40 years. The guidelines present , recommendations for initial and follow-up treatment for prevention of glucocorticoid-induced osteoporosis according the level of risk of fractures in different age groups of adults, and in children from 4 years of age, in patients with organ transplant and patients older than 30 years, receiving very high-dose of glucocorticoids . Oral bisphosphonates were recommended as first line treatment due to safety, cost, and because of lack of evidence for superior antifracture benefits from other OP medications. Oral bisohosphonates could be switched to another medication in case of intolerance. The issues of applicability of these recommendations in national clinical practice are being discussed.