This trial is evaluating whether Treatment will improve 1 primary outcome and 5 secondary outcomes in patients with Nonalcoholic Steatohepatitis. Measurement will happen over the course of Month 0, Month 12.
This trial requires 12 total participants across 1 different treatment groups
This trial involves a single treatment. Treatment is the primary treatment being studied. Participants will all receive the same treatment. There is no placebo group. The treatments being tested are not being studied for commercial purposes.
About 23,000 cases of NAFLD develop annually in the United States. Because 25% of people with NAFLD develop non-alcoholic steatohepatitis, they are at high risk of progression to liver cancer if they do not undergo liver transplantation.
Although the physical presentation and correlation of histological features of NASH with clinical presentation are different, the major histological feature of NASH and a marker for histological features of steatohepatitis are the presence of a steatosis of more than 5 percent of liver weight and >10 percent of triglyceride in a person's blood.
There is no clear cause of nonalcoholic steatohepatitis, but the exact contribution from the environment is undefined. Patients with nonalcoholic steatohepatitis are at risk for the development of steatohepatitis and hepatocellular carcinoma, and thus have an increased risk of liver-related death.
Given the low likelihood of spontaneous resolution of NASH, the possibility of remission should be considered if histological criteria for NASH are validated as a separate clinicopathologic entity.
Nonalcoholic steatohepatitis is a syndrome characterized by a marked, unexplained inflammatory process of the liver with histologically documented fat malabsorption that occurs in otherwise healthy people who do not consume excessively alcoholic beverages. Patients will often present with clinical features of fatigue, weight loss, and ascites.\n
The current treatments for NASH are targeted towards the reduction of liver damage and the risk of progression to liver cirrhosis or hepatocellular carcinoma. There is also uncertainty in the knowledge regarding the benefits of lifestyle modification. Some studies suggest that exercise plus a healthy diet are better methods of preventing the development of NASH than non-pharmaceutical-based approaches. There is also a high rate of comorbidity of this disease with diabetes but more research is needed in these groups to formulate recommendations.
The incidence of mild side effects (i.e. diarrhea or skin reactions) was minimal (approximately 6%, or 5% if severe side effects were excluded). Serious side effects, although rare, include worsening of liver enzymes, pancreatitis, pancreatitis-related death, heart problems, chest pain, and coma. It is not surprising that the drug has not been approved by the FDA for certain applications.
In this patient population, NASH and cirrhosis had a similar prevalence rate, but NASH had higher stage III fibrosis and a higher mortality rate. In clinical practice, NASH should be considered by general practitioners and clinicians when patients present with imaging abnormalities of the liver and/or their risk factors.
The incidence of cirrhosis and primary sclerosing cholangitis is increasing. Primary sclerosing cholangitis is associated with diabetes mellitus, and cholestasis of unknown cause seems to be linked to obesity and tobacco usage. In the absence of reliable markers or a specific cause, NASH is considered secondary to systemic factors.
The combination of UDCA with statins was predominant in both treatment groups. Combination of UDCA, and statins with azathioprine was typically used only in patients with diabetes.
Patients with NASH have higher levels of distress in several medical and quality-of-life domains. Furthermore, baseline distress contributes significantly to improvement of medical and psychosocial outcomes.
In our meta-analysis, in patients with NASH who had histologically proven fibrosis and/or inflammation (histologic stage F3), the only treatment found to have proven superiority to a placebo was UDCA, showing statistically significant improvement of both MELD score change and fibrosis progression. Patients that did not have signs of inflammation showed a trend toward improved clinical outcomes with UDCA treatment. In the absence of histological evidence of fibrosis (and thus inflammation) the patients' improvement following UDCA treatment was not statistically significant. Thus, it cannot be excluded that other variables in our meta-analysis may have contributed to the lack of significant improvement compared to a placebo for these patients.