Autoimunska tireoidna bolest i poliglandularne autoimunske bolesti

Autoimmune polyglandular syndrome (APS) involves dysfunction of two or more endocrine glands, which is based on the autoimmune mechanism. Many authors in addition to the two main APS syndrome, involves the third stand in which autoimmune thyroid disease (ATD) is associated with other autoimmune diseases. APS type 1 occurs less frequently, starting in early childhood and the key is mutation in autoimmune regulator gene. Three major components characterize this syndrome: hypoparathyroidism, autoimmune adrenal insufficiency and mucocutaneous candidiasis. APS type 2 is associated with the HLA antigen system and basically is a disorder of CD4+ and CD25+ regulatory T-cells. The main components of the syndrome are: Addison's disease, ATD and type 1 diabetes mellitus. An important feature of APS is that the expression of components occurs in different time intervals, with each other long periods. ATD is more common than other autoimmune endocrine diseases and include Graves' disease, chronic autoimmune thyroiditis and postpartum thyroiditis. ATD associated with HLA class II genes and polymorphism of cytotoxic T-lymphocytes antigen 4. In basic there is disorder of cellular and humoral immunity, with auto-antibodies targeting tissue specific antigen and and present infiltration of mononuclear cells, predominantly lymphocytes in the affected tissue. The most common antibodies are thyroid peroxidase, thyroglobulin and TSH receptor antibodies. ATD is often associated with other endocrine (diabetes mellitus type 1, Addison's disease, autoimmune pituitary disease, hypoparathyreoidism, premature ovarian failure) and non-endocrine autoimmune diseases. Given the frequency of ATD is a legitimate screening of ATD in other autoimmune diseases, and not vice versa. Testing involves the determination of TPO antibodies and TSH to separate those with high risk of developing ATD and forecasts for further screening

Osteoporosis reversibility in a patient with celiac disease and primary autoimmune hypothyroidism on gluten free diet: A case report

Introduction. Secondary osteoporosis occurs in many diseases. Celiac disease-induced osteoporosis is the consequence of secondary hyperparathyroidism. Biochemical bone markers show predominance of bone resorption, thus making the bisphosphonates the first line therapy option. Intestinal mucosal changes are reversible on gluten-free diet. Osteoporosis reversibility is also possible, provided postmenopausal osteoporosis risk factors independent from celiac disease are not present. Case report. We presented a postmenopausal woman with at least a 10-year history of celiac disease prior to diagnosis, which had overt secondary hyperparathyroidism with insufficient status of vitamin D and a significant bone mass reduction. At the time of diagnosis of celiac disease the patient was receiving 250 g of levothyroxine daily without achieving optimal substitution. Three years after the initiation of gluten-free diet the patient was without any signs and symptoms of the disease. All laboratory findings were within normal range. It was decided to treat the underlying disease and to supplement calcium and vitamin D without the initiation of bisphosponate therapy. Conclusion. Osteoporosis regression justified this therapeutic approach. The presence of primary autoimmune hypothyroidism makes this case specific, since the inability for optimal substitution therapy with a high daily dose of levothyroxine provoked the suspicion of celiac disease

Physical activity and bone turnover in women with osteopenia

Background/Aim. Osteoporosis is a systemic disease of the skeleton characterized by a decrease in bone mass and changes in the bone structure. An increased tendency of the bone tissue for fractures occurs as a consequence of these changes. The initial phase of physiological aging of the bones that gradually leads to osteoporosis is osteopenia. This paper tracks the effects of a specific kind of physical exercise program in women with osteopenia. The aim was to quantify the impact of this program on: the concentration of bone metabolism blood markers, muscle strength, aerobic capacity, and physical dimensions. Methods. The sample consisted of 26 women in postmenopause (age 46–58) divided into two groups – experimental group (n = 15) and control group (n = 11). A combined program of exercise consisting of aerobic activities and strength training was applied in the experimental group, while the control group did not join in the exercise program. The program lasted for 7 weeks, three times a week with a break day between the trainings. The intensity of the aerobic training was in the span of 60% to 70% of heart rate reserve (HRR), and the intensity of the strength training was in the span of 60% to 85% of one repetitive maximum (1RM). Osteopenia was diagnosed prior to the experiment by applying a dual energy X-ray absorptiometry of the lumbar spine and the hip. The following was measured before and after the experiment: the level of biochemical markers in the serum [Beta-aspartic acid β-cross laps (CTx), total procollagen type 1 N-terminal peptide (tP1NP) and bone isoenzyme of alkaline phosphatase (ALP), 1RM of leg extensors, maximum oxygen consumption (VO2 max), bodily height and mass, and a calculated Body Mass Index (BMI). Results. Significant changes were determined only in the experimental group. During the experimental period, there was a significant increase of muscle strength and VO2 max, with a decrease of Beta-CTx concentration. No statistically significant changes were recorded in the control group. Conclusion. A 7- week period of systematic exercise showed to be sufficient to increase muscle strength and VO2 max, partially also to decrease bone resorption, but insufficient to alter bone volume, bodily mass, and BMI

The impact of currently used oral antihyperglycemic drugs on dysfunctional adipose tissue

Obesity is a disease with pandemic frequency, often accompanied by chronic metabolic and organic complications. Type 2 diabetes mellitus (T2DM) is among the most common metabolic complications of obesity. The first step in the treatment of T2DM is medical nutrition therapy combined with moderate physical activity and with advice to patients to reduce their body weight. Pharmacotherapy starts with metformin, and in the case of inadequate therapeutic response, another antihyperglycemic agent should be added. The most clinical experience exists with sulfonylurea agents, but their use is limited due to high incidence of hypoglycemia and increase in body weight. Based on the fact that dysfunction of adipose tissue can lead to the development of chronic degenerative complications, precise use of drugs with a favorable effect on the functionality of adipose tissue represents an imperative of modern T2DM treatment. Antihyperglycemic drugs of choice in obese individuals are those which cause maturation of adipocytes, improvement of secretion of protective adipokines, and redistribution of fat mass from visceral to subcutaneous depots. Oral antihyperglycemic agents that can affect the functionality of adipose tissue are metformin, SGLT-2 inhibitors, DPP-4 inhibitors, and thiazolidinediones