Non‐alcoholic fatty liver disease (NAFLD) is one of the most common causes of hepatic disorders. It represents a wide range of chronic liver diseases in patients with no history of significant alcohol consumption, starting with simple steatosis and progressing towards non‐alcoholic steatohepatitis, cirrhosis, and ultimately hepatocellular carcinoma. NAFLD is usually associated with type 2 diabetes mellitus, dyslipidemia, metabolic syndrome, and obesity. This disease has mostly been studied in obese individuals; however, it has been widely reported and studied among the lean/non‐obese population in recent years. The pathogenesis of NAFLD in non‐obese patients is associated with various genetic predispositions, particularly a patatin‐like phospholipase domain‐containing protein 3 G allele polymorphism, which results in the accumulation of triglyceride in the liver and resistance to insulin. Additionally, dietary factors such as high fructose consumption seem to play a substantial role in the pathology of non‐obese NAFLD. Although there is not enough evidence on the treatment of NAFLD in non‐obese patients, the standard approach is to advise altering one's lifestyle in order to diminish visceral adiposity. Dietary modification, weight loss, and increased physical activity are highly recommended. We aimed to review and summarize the existing information on the prevalence, pathogenesis, genetic predispositions, diagnosis, and treatment of NAFLD in non‐obese patients according to the latest literature.
Background Coronavirus Disease 2019 (Covid-19) is expanding worldwide. The characteristics of this infection in patients varies from country to country. To move forward, clinical data on infected patients are needed. Here, we report a comparison between fatalities and recovery of patients with severe Covid-19, based on demographic and clinical characteristics. Methods Between 5 March and 12 May 2020 in Mashhad, Iran, 1278 of 4000 suspected Covid-19 patients were confirmed positive by real-time reverse-transcriptase–polymerase-chain-reaction assay of upper respiratory specimens. We compared the demographic, exposure history and clinical symptoms of 925 survivors and 353 fatal cases with confirmed disease. Results Mean (SD) age for all confirmed patients was 56.9 (18.7) years, 67.1 (15.9) years in fatal cases and 53.0 (18.3) years in survivors. Multivariate logistic regression analysis showed that the outcome of patients was associated with age (odds ratio = 1.049, P = 0.0001, 95% CI = 1.040–1.057). Despite a high burden of Covid-19 infections in the 30–39 and 40–49 year age groups, most of these (89.6 and 87.2%, respectively) recovered. The median (IQR) duration of hospitalization was 9.0 (6.0–14.0) days. The most prevalent co-morbidities were cardiovascular disorders (21%) and diabetes (16.3%). Dyspnoea (72.7%), cough (68.1%) and fever (63.8%) were the most frequent clinical symptoms. Healthcare workers, of whom two (3%) died, comprised 5.2% of infected cases. Combination antiviral and antibiotic therapy was used in 43.0% of cases. Conclusions The characteristics of severe Covid-19 varied substantially between fatal cases and survivors, with diabetes and cardiovascular disorders the most prevalent co-morbidities. In contrast to other studies, there were a higher number of fatalities in younger patients in our setting.
Nutritional deficiencies and malnutrition are considered to be related to ulcerative colitis (UC); however, the association between serum levels of micronutrients and UC is not well known. This study aimed to evaluate the serum levels of micronutrients in UC patients and investigate their association with disease activity.This cross-sectional study was conducted on UC patients visiting the Department of Gastroenterology at 3 different teaching hospitals between January 2016 and January 2017. UC activity was measured based on Truelove and Witts’ severity index and guidelines for colonoscopy. A healthy gender- and age-matched group was also selected. Serum levels of zinc, copper, selenium, ceruloplasmin, albumin, and total protein were compared between the 2 groups of UC patients and healthy subjects using independent-samples t test. Also, the association between serum levels of micronutrients and UC activity was assessed by using Pearson and Spearman correlation coefficient tests. The data were analyzed by SPSS version 21, considering P ≤.05 as the statistical significance level.Overall, 112 (54 male and 58 female) individuals with the mean age of 34.6 years were studied in the 2 groups of UC patients (n = 56) and healthy subjects (n = 56). The 2 groups were homogeneous in terms of age, gender, marital status, place of residence, and educational level (P >.05). The serum levels of total protein (6.41 ± 1.1 vs 7.41 ± 0.4 g/dL; P = .0001), albumin (4.72 ± 1.1 vs 5.19 ± 0.28 g/dL; P = .0001), zinc (679 ± 62 vs 1055 ± 156 μg/L; P = .0001), and selenium (81.85 ± 6.4 vs 108.4 ± 12.98 micg/L; P = .0001) were significantly lower in the UC patients. The serum level of copper did not differ significantly between the 2 groups (P = .1).Considering the simultaneous reduction in nutritional criteria in the UC patient group, malnutrition appears to be a factor affecting micronutrient deficiency in patients with UC.
The DNA repair gene O⁶-methylguanine-DNA methyltransferase (MGMT) is frequently methylated in colorectal cancer (CRC). The aim of this study was to demonstrate that MGMT methylation may be one of the candidate mediators of field cancerization in the colon mucosa. Therefore, quantitative methylation-specific polymerase chain reaction was performed on tumor itself and additional samples of 5 and 10 cm away from the tumor in 40 CRC patients. Moreover, colon mucosa was examined from 30 cases with no evidence of cancer as a control. MGMT promoter methylation was present in 27.5% of colorectal tumor specimens. Tumors that showed MGMT promoter methylation had substantial MGMT promoter methylation in their normal adjacent mucosa. The methylation was also observed in 36.36% (4/11) of normal samples with MGMT promoter methylation in the adjacent tumors, in 20.79% (6/29) of samples without MGMT methylation in the adjacent tumors, and in 6.66% (2/30) of control samples (p<0.006 and p<0.001 respectively). Finally, the mean of MGMT methylation levels was significantly higher in the cancerous group than in the control group (6.25±1.702 vs. 0.086±0.036, p<0.001). Some CRCs arise from a field defect defined by epigenetic inactivation of MGMT. Detection of such abnormality may ultimately be useful in risk assessment for CRCs.
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