Background Nonalcoholic fatty liver disease (NAFLD) is indicated by liver steatosis without excessive alcohol use or other liver disease. Several studies have reported that metabolic syndromes such as obesity, type 2 diabetes mellitus, and dyslipidemia have a linear correlation associated with NAFLD pathophysiology. One of the characteristics of dyslipidemia in NAFLD is increase in serum triglycerides. This study aimed to develop a model of NAFLD characterized by an increase in serum triglyceride levels and histological profile of liver steatosis by high-fat diet in rats. Methods Twelve Wistar rats were fed with pellets enriched with 60% fat. They were housed individually, and the remaining pellets were weighted every day for intake evaluation. Blood samples were collected at day 0 and at the end of each trial period at days 7, 14, 21, and 28 for the measurement of triglyceride levels. Every animal from each group was also sacrificed for liver histopathological examination. Results This study has established developing the NAFLD animal model by induction of a high-fat diet. The levels of serum triglycerides were increased from baseline 80.41 ± 12.82 to 1152.00 ± 73.62, 493.66 ± 159.98, 556.00 ± 120.79, and 489.00 ± 156.75 mg/dL at days 7, 14, 21, and 28, respectively. Liver histology also showed liver steatosis development, inflammation, and hepatocellular ballooning, which were associated with the NAFLD state. Conclusions High-fat diet in rats induced hypertriglyceridemia along with NAFLD-like liver histopathology.

Aim: This study examines the effect of alpha-lipoic acid (ALA) on sodium valproate-induced liver injury through histological features of mice liver tissue. Materials and Methods: Mice were divided into three groups; (1) vehicle group, (2) sodium valproate group, and (3) sodium valproate-ALA group. The vehicle group was injected with saline intraperitoneal (i.p.) for 28 days. The sodium valproate group was injected with sodium valproate 300 mg/kg, i.p. daily for 2 weeks, after which the vehicle was administered daily until day 28. The sodium valproate-ALA group was injected with sodium valproate 300 mg/kg daily for 2 weeks before the administration of ALA 100 mg/kg i.p. until day 28. The mice were euthanized, and the liver was extracted for histopathological examination. Results: Histopathological examination of the liver section of the vehicle group showed a normal structure of the liver. Two weeks after the administration of sodium valproate, histopathological examination showed an abnormal structure of the liver, with necrotic appearance and inflammatory cells. Moreover, treatment with ALA after the administration of sodium valproate notably ameliorated hepatic histopathological lesions and the liver structure corresponded to a normal liver structure. Conclusion: ALA ameliorates sodium valproate-induced liver injury in mice.

Liver is one of the most vital organs that functions as a center for metabolism. One of the diseases that disrupt liver function with a high prevalence is NAFLD (Non Alcoholic Fatty Liver Disease). NAFLD is characterized by increased intracellular triglyceride accumulation. Increased lipid peroxidation can lead to Non Alcoholic Steato Hepatitis (NASH) and cirrhosis which induces proinflammatory cytokines. Alpha lipoic acid (ALA) is an antioxidant that has been widely used in treating metabolic syndrome. Based on several previous studies. ALA may be useful for the treatment of NAFLD by targeting various pathways in the development of NAFLD. The study divided animals into five groups as standard feed; high fat diet (HFD); HFD and ALA 100 mg/kg BW i.p .; HFD and ALA 100 mg/kg BW i.p also repaired -fed; HFD and repaired -fed. Based on the results of the study, it can be concluded that ALA as an antioxidant can improve liver cell histopathology in NAFLD rat induced high fat diet.

Drug-Related Problems (DRPs) are undesirable events and circumstances that affect the health outcomes of patients. These issues are mainly attributed to risk factors for hepatic cirrhosis. This study determines the risk factors for dominant hepatic cirrhosis against the incidence of DRPs and their influence in "X" hospital at Makassar. The research design was observational analytic with a cross-sectional study model using a medical record sample between January and June 2016. This study used 53 people as research samples that met the inclusion and exclusion criteria. The results showed that the number of DRPs were 91 in 43 patients (81.13%). The most risk factor for the occurrence of DRPs was a concomitant disease (52.67%). Additionally, spontaneous bacterial peritonitis, variceal bleeding, and cardiovascular diseases are the dominant risk factors. However, they do not have a significant influence on the incidence of DRPs in hepatic cirrhosis patients.