No abstract

Psoriasis is a common inflammatory skin disease, and conflicting data have been published about osteoporosis and bone turnover markers in patients with psoriatic arthritis. The aim of this study was to assess bone mineral density (BMD) and bone turnover markers in psoriatic patients with and without peripheral arthritis and to investigate the relationship between clinical parameters and markers of bone turnover. Forty-seven patients (24 women, 23 men) with psoriasis were included to the study. Demographic data and clinical characteristics were recorded. Erythrocyte sedimentation rate and C-reactive protein were assessed as disease activity parameters. BMD was determined for lumbar spine and total hip by dual X-ray absorptiometry (DXA). Serum Ca, P, alkalen phosphatase (ALP), and serum type I collagen cross-linked C telopeptide (CTX) were measured as bone turnover markers in all patients. The patients were divided into two groups according to their peripheral arthritis status. The clinical and laboratory variables, as well as bone mass status of the groups, were compared with each other. Eighteen patients had peripheral arthritis. All the female patients were premenopausal. None of the patients had radiologically assessed axial involvement. There was no significant difference between the BMD levels of psoriatic patients with and without arthropathy. One patient (5%) had osteoporosis, and nine (50%) patients had osteopenia in arthritic group, while eight (27.5%) patients had osteopenia in patients without arthritis. Serum CTX, ALP, Ca, and P levels were not significantly different in arthritic than in non-arthritic patients (p > 0.05). In patients with psoriatic arthritis, the duration of arthritis was negatively correlated with BMD values of lumbar spine and total femur and serum CTX levels, suggesting an association of increased demineralization with the duration of joint disease. In conclusion, psoriatic patients with peripheral arthritis with longer duration of joint disease may be at a risk for osteoporosis, which can require preventative treatment efforts.

Hypercholesterolemia is a major risk factor for atherosclerosis. Dysregulation of adipokines contribute to atherosclerotic diseases. Apelin has recently been shown to be secreted by the adipose tissue in association with hyperinsulinemia and inflammation. We searched plasma apelin levels in patients with elevated low density lipoprotein (LDL)-cholesterol having no additional disorder. Thirty-three patients with hypercholesterolemia and 50 age-, sex-, and body mass index-matched healthy controls were evaluated for their apelin, adiponectin and high sensitivity C-reactive protein (hsCRP) levels, and homeostasis model assessment (HOMA) indexes. Plasma apelin-12 and adiponectin were determined by ELISA and RIA, respectively. Plasma apelin levels were lower in patients with elevated LDL-cholesterol compared to healthy controls (p<0.001). Plasma adiponectin concentration was also lower in the dyslipidemic patients (p<0.001). hsCRP levels were similar in the two groups. Fasting plasma glucose was normal in both groups. HOMA indexes in the dyslipidemic group were higher than the controls (p=0.005). A mild to moderate negative correlation with HOMA and positive correlation with high density lipoprotein cholesterol of apelin was found in the dyslipidemic group. Plasma apelin is decreased in non-obese, non-diabetic and normotensive patients with elevated LDL-cholesterol. Low apelin levels in hypercholesterolemia seem associated with insulin resistance, which needs to be investigated in larger populations as well as in other atherosclerotic conditions.

Hcy levels are elevated in patients on Iso treatment for CA. It may be due to either the inhibition of cystathionine-beta-synthase, an enzyme required in the metabolism of Hcy, by the drug and/or the liver dysfunction. Daily supplementation with vitamin B12 and folate, which are the cofactors of the enzymatic reactions involved in Hcy metabolism, can lower plasma levels of Hcy, so it is recommended to take these vitamins in case of deficiency along with Iso to prevent premature occlusive vascular disease.

Background/Aims: Adiponectin seems to be an important modulator for metabolic and vascular diseases. A case study was designed to measure plasma adiponectin levels and to investigate the effects of angiotensin-converting enzyme inhibitors on adiponectin levels in type-2 diabetic patients with proteinuria. Methods: Forty-nine patients (28 males, 21 females) and 23 healthy volunteers (13 males, 10 females) were included in the case study. Patients with proteinuria were treated with 5 mg/day ramipril (n = 21) for 4 weeks. Results: Adiponectin levels of patients were significantly lower than those of healthy volunteers (p < 0.001). There were significant negative correlations between adiponectin concentrations and insulin levels as well as the homeostasis model assessment (HOMA) index in the patient group (r = –0.655, p < 0.001; r = –0.469, p = 0.001, respectively). There was also a significant negative correlation between plasma adiponectin concentrations and the degree of proteinuria (r = –0.912, p < 0.001). Plasma adiponectin levels in patients with proteinuria (n = 21; 4.81 ± 3.17 µg/ml) were significantly lower than those without proteinuria (n = 28; 10.25 ± 2.03 µg/ml; p < 0.001). After the treatment period, adiponectin levels significantly increased (p < 0.001) and proteinuria, plasma insulin, and HOMA indexes significantly decreased in the treatment group (p < 0.001, p < 0.001, p = 0.002, respectively). Conclusions: The results suggest that adiponectin is inversely correlated with proteinuria and treatment with ramipril both corrects proteinuria and increases the low adiponectin levels in diabetic patients.