GI, Liver & Pancreas Pathology
Farid Kosari; Raika Jamali; Tayeb Ramim; Ebrahim Musavi Jahan Abad
Abstract
Background & Objective: The aim of this present study was to assess the relationship between serum zinc levels and liver histopathological findings in non-alcoholic steatohepatitis (NASH) patients.Methods: This case-control study was performed in consecutively selected NASH patients who had been ...
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Background & Objective: The aim of this present study was to assess the relationship between serum zinc levels and liver histopathological findings in non-alcoholic steatohepatitis (NASH) patients.Methods: This case-control study was performed in consecutively selected NASH patients who had been referred to a general hospital. The control group consisted of age and sex-matched individuals with normal physical examinations, laboratory findings, and liver ultrasounds. Serum zinc level was measured using atomic absorption spectrophotometry. Liver histopathological findings were determined based on non-alcoholic fatty liver activity score.Results: A cohort of eighty biopsy-proven NASH patients and eighty controls were enrolled in the study. The mean serum zinc level was significantly lower in the NASH group compared with the controls. The mean serum zinc concentration was significantly lower in moderate and severe lobular inflammation groups than the mild group. After multiple adjustments for potential contributing variables, serum zinc level was associated with the severity of lobular inflammation. Nonetheless, it was not associated with liver steatosis and fibrosis. A serum zinc value of 89 (µg/dl) yielded a sensitivity and specificity of 93% and 86%, respectively, characterizing patients with lobular inflammation of less than two inflammatory foci per high-power field (HPF) from more advanced groups. Furthermore, a value of 79.55 (µg/dl) yielded a sensitivity and specificity of 87% and 100%, respectively, distinguishing those with a lobular inflammation grade of less than four foci per HPF from more advanced cases. Conclusion: Serum zinc level might be associated with the severity of lobular inflammation in NASH.
Ali Zare-Mirzaie; Behrang Kazeminezhad; Mona Akbari Ghouchani
Abstract
Background& Objective: Increase in intra- and extracellular glucose levels can cause oxidative stress, and the prolonged imbalance between prooxidants and antioxidantscan lead to cell damage and the associated complications in patients with diabetes. Vitamin D acts as a strong antioxidant in ...
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Background& Objective: Increase in intra- and extracellular glucose levels can cause oxidative stress, and the prolonged imbalance between prooxidants and antioxidantscan lead to cell damage and the associated complications in patients with diabetes. Vitamin D acts as a strong antioxidant in the body and several studies emphasized on its important role to prevent oxidative stress in prediabetic and diabetic subjects. The current study aimed at determining and comparing the total antioxidant capacity (TAC) in individuals with hemoglobin A1c (HbA1c) below and above 6.5%, and its correlation with vitamin D levels. Methods: The current cross sectional study was conducted on a total of 107 patients with diabetes (HbA1c >6.5%) and 107 non-diabetic subjects (HbA1c <6.5%) referred to Rassool Akram Hospital, Tehran, Iran from 2015 to 2016, as the sample population. The two groups were compared regarding their TAC and vitamin D serum levels and the association between vitamin D concentration and TAC was evaluated. Results: Age and body mass index (BMI)were significantly higher in patients with diabetes, compared with the serum levels of vitamin D and TAC (P P=0.003). In multivariate regression model, the duration of diabetes was also significantly associated with TAC level (beta coefficient=-0.82, P <0.001). Conclusion: The low serum levels of TAC and vitamin D in patients with diabetes could be indicative of oxidative stress in the presence of high blood glucose levels. Supplementation of vitamin D in patients with diabetes might be effective to control the negative impacts of the disease and decrease cells’ exposure to oxidative environment in prediabetes.
