Carotid intima-media thickness as a marker of atherosclerosis in hemodialysis patients.

Atherosclerotic changes in carotid arteries of hemodialysis (HD) patients reflect global atherosclerotic changes in vasculature. Carotid intima-media thickness (CIMT) can be used for atherosclerosis prediction and assessment of cardiovascular risks in HD patients, and thus screening high-risk patients. In this cross-sectional study, CIMT was measured using ultrasonography (B-mode with 5-10-MHz multifrequency linear probe) in HD patients in our hospitals. Additionally, we assessed the relationship between their CIMT and some cardiovascular risk factors. A total of 62 HD patients (64.5% male) were included. Age, body mass index, low-density lipoprotein, fasting blood sugar, history of diabetes mellitus and cardiovascular disease, serum albumin, and duration and adequacy of HD in study patients had significant association with their CIMT. There were no significant relationships between CIMT and patient's gender, smoking, serum calcium, phosphate, calcium x phosphate product, hemoglobin, and uric acid level. More diagnostic modalities must be performed for detecting the impact of atherosclerosis on HD patients with high CIMT.

The serum levels of adiponectin and leptin in mustard lung patients.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) due to sulfur mustard (SM), known as mustard lung, is an important late pulmonary complication of SM poisoning. Due to the possible role of systemic inflammation in mustard lung, we evaluated the serum levels of adiponectin and leptin in these patients. MATERIALS AND METHODS: Thirty nonsmoker mustard lung patients in stable phase were enrolled into this study. Also, 30 COPD and 21 healthy participants were entered as control groups. Complete lung function tests were performed in the participants. The serum levels of adiponectin and leptin were measured in all groups. RESULTS: There were no statistically significant differences in mean adiponectin and leptin levels among the groups (p = 0.38 and p = 0.35, respectively). There was a downward trend in leptin to adiponectin ratio from lower to higher stages of global initiative for chronic obstructive lung disease guidelines in mustard lung patients, which was not statistically significant (p = 0.8). CONCLUSION: Our results showed that there is no difference in mean adipokine levels in stable mustard lung patients compared with control groups. There was a foot-point in the alterations of serum adipokines regarding the severity of COPD, which needs to be documented by larger sample group.