Journal of Research in Medical Sciences
Volume:21 Issue: 10, 2016 Oct

The aim of this study was to assess the atheromatous plaque, in the abdominopelvic arteries as a marker of cardiac risk in patients with or without gallstone disease (GD).
A total of 136 patients were enrolled in this cross‑sectional study. Forty‑eight patients had GD and the remaining 88 patients did not. The presence or absence of gallstones was noted during abdominal ultrasonography while vascular risk factors such as plaque formation, intima‑media thickness, plaque calcification, mural thrombus, stenosis, aneurysm, and inflammation were recorded during an abdominopelvic computed tomography scan. In addition, percentage of the abdominopelvic aorta surface covered by atheromatous plaque was calculated.
The mean age of patients with GD and without GD was 50.81 ± 16.20 and 50.40 ± 12.43, respectively. Patients with GD were more likely to have diabetes mellitus, a higher body mass index (BMI) (P  We demonstrated a direct relationship between GD and abdominopelvic atheromatous plaque, which is a marker for increased cardiovascular risk, for the first time in the literature. Patients with GD exhibit greater abdominopelvic atherosclerosis and therefore, have a higher risk of cardiovascular disease.

Endometriosis is a multifactorial hormonally related complex disease with unknown etiology. Epidemiologic data were suggested the possible effects of endocrine disrupting chemicals such as bisphenol A (BPA) on endometriosis. BPA is similar to endogenous estrogen and has the ability to interact with estrogen receptors and stimulate estrogen production. Our aim was to evaluate the relationship between urinary BPA concentrations in women with endometrioma.
This case–control study consisted of fifty women who have been referred to gynecology and infertility center with endometrioma and were candidates for operative laparoscopy and ovarian cystectomy as cases. Fifty women who had not any evidence of endometrioma in clinical and ultrasound evaluation and came to the same clinic for routine check-up were selected as controls. One-time urine sample was collected after receiving informed consent before surgery and medical intervention. Total BPA in urine was measured with high-performance liquid chromatography method and detection limit was 0.33 ng/mL.
Percentage of urine samples containing BPA was 86% of cases and 82.4% of control. Urinary BPA showed a right-skewed distribution. The mean concentration of BPA was 5.53 ± 3.47 ng/mL and 1.43 ± 1.57 ng/mL in endometriosis and control group, respectively (P This study showed a positive association between urinary BPA concentrations and endometrioma. However, further large-scale studies are needed to confirm this hypothesis.

The aim of the current trial was to investigate the effect of Vitamin D treatment on metabolic markers in people with Vitamin D deficiency and thyroid autoimmunity.
In this double‑blind, randomized, placebo‑controlled clinical trial, 65 Vitamin D deficient euthyroid or hypothyroid patients with positive TPO‑Ab were enrolled. They randomly allocated into two groups to receive oral Vitamin D3 (50000 IU weekly) and placebo for 12 weeks. Serum concentration of calcium, phosphorus, albumin, C‑reactive protein, blood urea nitrogen, creatinine, glycated hemoglobin (HbA1c), insulin, fasting plasma glucose (FPG), triglyceride (TG), total cholesterol, and high‑density lipoprotein were measured in both groups before and after the trial. Homeostasis model assessment estimates of beta cell function (HOMA‑B) and HOMA‑insulin resistance (HOMA‑IR) were calculated before and after trial in both groups.
Thirty‑three and thirty‑two participants were allocated to Vitamin D‑treated and placebo‑treated groups, respectively. Mean (standard error) level of Vitamin D increased significantly in Vitamin D‑treated group (45.53 [1.84] ng/mL vs. 12.76 [0.74] ng/mL, P = 0.001). The mean of HbA1c and insulin was increased significantly both in Vitamin D‑treated and placebo‑treated groups (P  Our findings showed that weekly 50000 IU oral Vitamin D3 for 12 weeks did not improve metabolic markers, IR, or insulin secretion in Vitamin D deficient patients with Hashimoto thyroiditis.

The aim of this study was to check the effectiveness of Vitamin D supplementation on the disease activity of Vitamin D-deficient systemic lupus erythematosus (SLE) patients.
In this randomized, double-blind, placebo-controlled trial, 45 Vitamin D-deficient SLE patients were studied in two groups, namely interventional and placebo groups. The interventional group patients were treated with Vitamin D (50,000 unit/weekly Vitamin D for 12 weeks and then 50,000 unit/monthly for 3 months) and placebo group patients were only administered the placebo. The level of Vitamin D and the level of disease activity using SLE disease activity index (SLEDAI) were measured before and after intervention period in each group, and for intra- and between-groups comparison, we used t-test and repeated measure ANOVA.
A total of 90 patients were enrolled in this study. The mean of Vitamin D was increased significantly after therapy in interventional group (17.36 ± 4.26 ng/ml vs. 37.69 ± 5.92 ng/ml, P  According to our study, it is suggested that using Vitamin D in patients with SLE could not have better outcomes in this regard. However, there are many unknown environmental or biological factors which are associated with the disease activity of SLE and have not been identified yet.

The present study was performed to develop a scoring system for predicting cure status in patients with cutaneous leishmaniasis (CL).
This study included 199 patients with CL from Skin Diseases and Leishmaniasis Research Center (Isfahan, Iran). Data were collected as longitudinal in each visit of patients. We applied ordinal logistic generalized estimating equation regression to predict score on this correlated data. To evaluate the fitted model, split sample validation method was applied. SPSS software was used for data analysis.
The regression coefficients of the fitted model were used to calculate score for cure status. Based on split-sample validation method, overall correct classification rate was 82%.
This study suggested a scoring system predict cure status in CL patients based on clinical characteristics. Using this method, score for a CL patient is easily obtained by physicians or health workers.

Mitochondrial dysfunction is one of the main causative factors in a wide variety of complications such as neurodegenerative disorders, ischemia/reperfusion, aging process, and septic shock. Decrease in respiratory complex activity, increase in free radical production,
increase in mitochondrial synthase activity, increase in nitric oxide production, and impair in electron transport system and/or mitochondrial permeability are considered as the main factors responsible for mitochondrial dysfunction. Melatonin, the pineal gland hormone, is selectively taken up by mitochondria and acts as a powerful antioxidant, regulating the mitochondrial bioenergetic function. Melatonin increases the permeability of membranes and is the stimulator of antioxidant enzymes including superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase. It also acts as an inhibitor of lipoxygenase. Melatonin can cause resistance to oxidation damage by fixing the microsomal membranes. Melatonin has been shown to retard aging and inhibit neurodegenerative disorders, ischemia/reperfusion, septic shock, diabetes, cancer, and other complications related to oxidative stress.
The purpose of the current study, other than introducing melatonin, was to present the recent findings on clinical effects in diseases related to mitochondrial dysfunction including diabetes, cancer, gastrointestinal diseases, and diseases related to brain function.