[Diabetic osteopathy].

INTRODUCTION: The aim of this study was to point out some dilemmas about the existence and pathogenesis of primary diabetic osteopathy as a separate entity, based on currently available studies. Expert disagreements are present not only about the occurrence of generalized osteopathy with diabetic disease, but also about direct relationship between metabolic diabetes control and bone metabolism and influence of disease duration and sex on bone changes. PATHOGENESIS OF DIABETIC OSTEOPATHY: Decreased bone formation is the basic mechanism leading to decreased bone mass. Biochemical markers showed no clear connection with bone density measurement. Insulin and insulin-like growth facotr (IGF) affect bone metabolism. OSTEOPATHY IN PATIENTS WITH DIABETIC DISEASE-TYPE1: Some clinical studies have shown that patients with diabetic disease-type have a mild decrease in bone mass, while others have not presented such results. OSTEOPATHY IN PATIENTS WITH DIABETIC DISEASE-TYPE2: In patients with diabetic disease-type 2 the risk for osteopathy is even less defined. Patients treated with oral hypoglycemics present with higher decrease of bone mass has than patients treated with insulin therapy. This could partly be explained by anabolic effects of insulin on bones. BONE FRACTURES IN PATIENTS WITH DIABETIC DISEASE: Literature data are contradictory concerning the occurrence of bone fractures in diabetic patients. A survey of bone fracture occurrence in diabetic patients was performed in "Veljko Vlahovic Medical Center" in Vrbas and it included a group of 100 patients with diabetic disease. The results show that 12 patients had some fractures: mostly females in postmenopause, aged and with secondary insulin-dependent diabetes and most frequently arm fractures. Considering contradictory literature data, further longitudinal studies are necessary.

[Effects of alendronate on the markers of bone metabolic activity in postmenopausal women with osteoporosis].

INTRODUCTION: Bisphosphonates are synthetic compounds used in treatment of osteoporosis and inhibition of bone resorption. MATERIAL AND METHODS: The research included a group of 30 postmenopausal women with osteoporosis, treated with alendronate (70 mg per week--Fosamax tablets in combination with calcium and active vitamin D--Alpha D3 0.25mcg). The control group included 20 women with osteoporosis treated with hormone substitution therapy (HST), calcitonin and deca duraboline. Bone metabolic activity, was evaluated using osteocalcin for bone formation and cross-laps for bone resorption. Blood samples were taken before therapy and 6-8 weeks after. RESULTS: The serum levels of osteocalcin and cross-laps during application of alendronate were statistically significantly lower comparing to those in pre-therapy. The serum levels of osteocalcin and cross-laps during the therapy applied in the control group were statistically insignificantly lower than values in pre-therapy. Osteocalcin has a tendency of decreasing in both groups, and it was slightly more evident in alendronate group. Cross-laps demontrated the same tendency of decreasing in both groups, and it was more evident in alendronate group. DISCUSSION: Our results have shown the efficacy of alendronate in preventing bone loss, which was highly statistically significant. They have also shown its suppressive effect on bone formation and resorption, but the effects were statistically less significant. CONCLUSION: Alendronate significantly reduces the level of bone resorption in postmenopausal women with osteoporosis. Its effects on bone formation are less expressed Alendronate's effects on bone metabolism become evident not later than 6-8 weeks after therapy application. Parameters of bone metabolic activity are very useful diagnostic means in evaluation of alendronate effect on bone metabolic activity and in the prognosis of bone mass loss.

[Effects of hyperthyroidism on bone mass in women of reproductive age]. / Uticaj hipertiroidizma na masu kosti zena u generativnom periodu zivota.

INTRODUCTION: Hyperthyroidism is one of the most frequent endocrinopathies in women of reproductive age. Consequently, increased risk of osteoporosis may be expected. MATERIAL AND METHODS: The research has included a group of 30 hyperthyroid women and a control group of 30 healthy women of reproductive age. Age and some clinical characteristics were analyzed, as well as some anthropometric parameters. Bone mass parameters were determined by measuring bone mineral density using ultrasound devices (SAHARA-Hologic). RESULTS: Bone mass parameters in hyperthyroid women are significantly lower than in controls (BUA: 63.25+/-12.17; 69.73+/-10.02 dB/MHz respectively; SOS: 1523.90+/-24.47; 1540.19+/-26.59 m/s respec. QUI/STIFF 79.78+/-13.95; 89.09+/-13.99% respec.) Duration of hyperthyroidism affects bone density and reduces it. DISCUSSION: Obtained results were expected, having in mind that hyperthyroidism is a condition characterized by increased bone catabolic rate. Also, negative correlation between the duration of hyperthyroidism and bone mass parameters (BUA, SOS) was expected, because it is logical that consolidation of bone mass in adult life cannot be maintained in circumstances in which metabolic rate is increased. During hyperthyroidism, bone loss is expected. In order to confirm this, future studies of bone markers are necessary. CONCLUSION: Based on results obtained in the study, the following conclusions were made: hyperthyroidism is accompanied by decreased values of bone mass parameters; this effect depends on duration of hyperthyroidism. We confirmed that hyperthyroidism may be the cause of decrease in bone mass, particularly if it lasts more than a year. To prevent osteoporosis in women of reproductive age with hyperthyroidism and involutional osteoporosis later in life, early diagnosis and effective therapy of hyperthyroidism is imperative.