Antiresorptive agents are widely used to treat osteoporosis. Both reduction in bone turnover and increase in BMD may be necessary to decrease the fracture risk. The aim of the study was to evaluate the effects of aledronate on bone turnover markers and bone mineral density in postmenopausal women with osteoporosis. The study involved a group of 56 postmenopausal women with osteoporosis treated with alendronate (70 mg) weekly at the Institute of Nuclear Medicine Clinical Center University of Sarajevo during a 12-months period. Bone mineral density (BMD) at lumbar spine and proximal femur and bone turnover markers (serum β-CrossLaps, urinary N-telopeptides of type I collagen (NTx), total serum alkaline phosphatase (AP) and serum osteocalcin) were measured at baseline and after 12 months of the treatment with aledronate. BMD values significantly increased both at lumbar spine by 13.46% and proximal femur by 21.96% during the study period (-3.12±0.24 vs. -2.7±0.19 and -2.55±0.2 vs. -1.99±0.19 respectively; p<0.001). Bone turnover markers significantly decreased during the study period; C-terminal telopeptides of type I collagen fragment (β-CrossLaps) 49.0% (0.51±0.05 vs.0.26±0.028 ng/mL), NTX 33.4% (48.3±4.9 vs.32.15±3.25 nMBCE/mM Cr), AP 24.3% (81.1±5.2 to 61.43±5.2 IU/L) and serum osteocalcin by 29.7% (34.3±2.65 to 24.1±1.36 ng/mL)(p<0.001). Alendronate treatment increased BMD and reduced the level of bone turnover markers. Therefore, the treatment with aledronate during 12 months period can be recommended in postmenopausal women with osteoporosis.

The aim of this study was to assess echocardiographic changes in female patients with untreated dysfunctional thyroid states and whether the therapy aimed to normalize the thyroid dysfunction could lead to improvement in cardiac systolic and diastolic function. The study included 90 female subjects who performed control of thyroid hormonal status at the Institute of Nuclear Medicine at the University of Sarajevo Clinics Centre and who previously were untreated for the thyroid functional disorders. The study sample was divided in three groups based on the thyroid hormones levels: a) hyperthyroid group (n= 30) b) hypothyroid group (n=30) and c) euthyroid (control). Echocardiography measurements were performed on commercially available Toshiba, SSH 140. Before the therapy no statistically significant differences in the peak early and late mitral inflow velocities (E/A) values between the study groups was observed, but the mean left ventricular ejection fraction (LVEF) in hypothyroid group was significantly lower (58.30+/-1.05) compared to control (64.96+/-0.71) and hyperthyroid group (64.69+/-1.31) (p<0.001). In hypothyroid group we found significant increase in mean LVEF (58.30+/-1.05 vs. 64.95+/-0.86, p<0.01) and E/A (1.06+/-0.07 vs. 1.17+/-0.08; p=0.01) values after the normalization of thyroid hormone status.Thyroid dysfunctional states were not associated with impaired diastolic function, probably due to the short duration of thyroid dysfunction and timely and successful conversion therapy. Systolic function however was significantly reduced in hypothyroid patients but subsequently improved after the adequate therapy. Early diagnostic approach in patients with thyroid dysfunctional states is important for avoidance of cardiac complications that accompany these disorders.

The metabolic syndrome (MS) is a multi-factorial disorder which includes a main risk factors associated with the development of cardiovascular, neurologic, renal and endocrine diseases, especially type 2 diabetes. This study has been conducted to estimate the prevalence of the MS in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) and its association with cardiovascular morbidity. The study included 37 patients (25 type 2 diabetic patients and 12 non-diabetic patients), who had been on peritoneal dialysis for > 3 months. At the beginning of CAPD treatment (baseline) and at the end of follow-up, we measured: body mass index (BMI), blood pressure, fasting blood glucose, triglycerides and high-density lipoprotein cholesterol (HDLC) and defined the prevalence of the MS using the modified National Cholesterol Education Program (NCEP; Adult Treatment Panel III) for peritoneal dialysis patients. The overall prevalence of the MS was 89.2%. The metabolic syndrome was estimated in all (100%) type 2 diabetic patients (vs. 60% patients on the beginning of CAPD treatment). In non-diabetic peritoneal patients, the MS was estimated in 50% cases, according to 33.3% at the beginning CAPD treatment. Development of the MS was significantly higher in the type 2 diabetic patients in compared with non-diabetic patients until the end of follow-up examination (p=0.0005). The prevalence of LVH in type 2 diabetic patients with the MS was significantly higher (p=0.002) than in non-diabetic peritoneal patients with the MS. We didn't found statistical significantly difference in the prevalence of ischemic heart disease between this two category of peritoneal dialysis patients (p=0.076). The results indicate that the metabolic syndrome is presented in high percentage in peritoneal dialysis patients, and it's also important risk factor of high cardiovascular morbidity rate in these patients, especially in type 2 diabetic patients.

The evolution of homocysteine (Hcy) changes after acute myocardial infarction is still not elucidated. Serum Hcy concentration has been shown to increase between acute and convalescent period after myocardial infarction and stroke. Also a decrease in serum Hcy during acute phase was observed. It is still not clear whether the Hcy is a culprit or an innocent bystander in cardiovascular diseases. Addressing the discrepancies in Hcy changes in patients with acute myocardial infarction might give insight in Hcy role in cardiovascular diseases and offer implications both for the clinical interpretation and patients risk stratification. The aim of the study was to evaluate serum Hcy concentration changes during early post myocardial infarction. The study included 55 patients with AMI from the Clinics for Heart Diseases and Rheumatism at University of Sarajevo Clinics Centre. For Hcy analysis blood was collected on day 2 and 5 after the AMI onset. Serum Hcy concentration was determined quantitatively with fluorescent polarisation immunoassay on AxSYM system. Cluster analysis revealed two groups of AMI patients with different trends of serum Hcy changes. Increase in serum Hcy concentration was observed in 33 (60,0%) patients (AMI 1 group), while in 22 (40,0%) patients a decrease was observed (AMI 2 group). On day 2, patients in AMI 2 group had significantly higher mean Hcy concentration compared to AMI 1 group of patients (15,27+/-0,96 and 11,59+/-0,61 micromol/L p<0,05). On day 5, no significant difference in mean Hcy level between AMI 1 and AMI 2 group of patients was observed (14,86+/-1,1 vs. 12,75+/-0,74 micromol/L respectively). Significant differences between AMI 1 and AMI 2 patients were observed in VLDLC levels and CK-MB activity on day 2. Patients in AMI 1 group had significant increase in platelets count from day 2 to day 5 (230,1+/-11,6 vs. 244,2+/-11,0; p<0,05). Our study of serial Hcy changes in patients with AMI revealed two different patterns of Hcy changes in early post infarction period which might reflect two distinct populations of AMI patients. Although further research is necessary, possible explanation for the observed findings could be a different genetic background, vitamin and oxidative status of patients with AMI.

The present study was carried out to evaluate the renoprotective antioxidant effect of Spirulina platensis on gentamicin-induced acute tubular necrosis in rats. Albino-Wistar rats, (9male and 9 female), weighing approximately 250 g, were used for this study. Rats were randomly assigned to three equal groups. Control group received 0,9 % sodium chloride intraperitoneally for 7 days at the same volume as gentamicin group. Gentamicin group was treated intraperitoneally with gentamicin, 80 mg/kg daily for 7 days. Gentamicin+spirulina group received Spirulina platensis 1000 mg/kg orally 2 days before and 7 days concurrently with gentamicin (80 mg/kg i.p.). Nephrotoxicity was assessed by measuring plasma nitrite concentration, stabile metabolic product of nitric oxide with oxygen. Plasma nitrite concentration was determined by colorimetric method using Griess reaction. For histological analysis kidney specimens were stained with hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) stain. Plasma nitrite concentration and the level of kidney damage were significantly higher in gentamicin group in comparison both to the control and gentamicin+spirulina group. Spirulina platensis significantly lowered the plasma nitrite level and attenuated histomorphological changes related to renal injury caused by gentamicin. Thus, the results from present study suggest that Spirulina platensis has renoprotective potential in gentamicin-induced acute tubular necrosis possibly due to its antioxidant properties.

The aim of this study was to investigate the role of inducible nitric oxide synthase (iNOS) in gentamicin-induced acute tubular necrosis in rats using the iNOS inhibitor L-N6-(1-iminoethyl) lysine (L-NIL). Wistar rats, both sexes (n=18), were equally divided into three groups. Gentamicin group received intraperitoneally (i.p.) gentamicin in 0.9 % NaCl at a dose of 80 mg/kg/day for five consecutive days. L-NIL+gentamicin group received L-NIL at a dose of 3 mg/kg i.p. 36, 24 and 12 h before first dose of gentamicin. Control group received 0.9 % NaCl i.p. for five consecutive days at the equal volume as gentamicin group. Griess reaction was used for determination plasma level of NO. Semiquantitative histological analysis was used for the evaluation of kidney damage level. The plasma NO level and the level of kidney damage were statistically higher in gentamicin group in comparison to the control group (p=0.046). Application of L-NIL prior to gentamicin led to certain decrease in the plasma level of NO as well as in the level of kidney damage. Application of L-NIL, prior to gentamicin administration, did not provide complete protective effects of L-NIL on the kidney, which was demonstrated on kidney sections. The lack of anticipated protective effect of L-NIL on kidney tissue might be explained with the fact that we have used L-NIL prior but not during/after gentamicin administration. It would be necessary to examine the effects of L-NIL administration not only before, but as well during and possibly after the administration of gentamicin.