Fasting glucose levels and immunoglobulins were also assessed in NASH patients and random glucose levels in control subjects. In addition, a drug history, recording of height and weight for calculation of body mass index, and bloods for triglyceride and cholesterol levels were obtained for all NASH patients and control subjects. They were made up of volunteers and ambulatory outpatients with minor gastrointestinal complaints. All control subjects had normal liver function tests and no history of liver disease. No patient had antimitochondrial antibody or significantly elevated titres of antinuclear or antismooth muscle antibody.Ĭontrol subjects were age and sex matched with NASH patients. All patients were negative for hepatitis B surface antigen and antibody to hepatitis C. The third criterion was the absence of other relevant liver diseases. The mean alcohol consumption of NASH patients was 14 g per week 12 of the 22 patients drank no alcohol. Patients with detectable blood alcohol on a fasting morning specimen or an elevated mean corpuscular volume were excluded.
Alcohol history was taken by two physicians on two different occasions and confirmed with family members where possible. The second inclusion criterion was no significant alcohol consumption, defined as no greater than 20 g of alcohol per day. These patients had fatty infiltration on ultrasound or CT scan of the liver, abnormal liver function tests, and otherwise fulfilled the other inclusion criteria. Three patients did not consent to liver biopsy. Hepatic fibrosis and Mallory's bodies were not considered essential for the diagnosis. The minima histological criteria were the presence of macrovesicular steatosis and inflammation. Histological sections from each liver biopsy were stained with haematoxylin-eosin, Perls' Prussian blue, and Gordon and Sweet's reticulin and were interpreted by a single experienced histopathologist (RBD). Firstly, histological diagnosis was made with liver biopsy. Three diagnostic criteria were used for patient inclusion. They were consecutive cases diagnosed in our gastroenterology clinic between 19. Twenty two patients with NASH were studied.
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The aim of this study therefore was to determine the prevalence of SIBO in a series of NASH patients and to assess if this is accompanied by increased intestinal permeability or elevated serum levels of endotoxin and TNF-α. To our knowledge however no human study of NASH patients has measured intestinal permeability, endotoxin, or TNF-α levels. 10 It seems plausible therefore that gut derived endotoxin, perhaps from SIBO, is important in the pathogenesis of NASH via Kupffer cell stimulation and TNF-α production.
8, 9 Yang and coworkers have suggested that systemic endotoxaemia contributes to TNF-α production and steatohepatitis in genetically obese rats. In alcoholic liver disease, which shares histological similarities to NASH, endotoxin induced stimulation of Kupffer cells has been proposed as an important initiating event leading to the production of proinflammatory cytokines and oxygen free radicals. Considerable evidence already exists demonstrating that endotoxin can induce steatohepatitis, mediated chiefly via the cytokine tumour necrosis factor α (TNF-α). SIBO could increase intestinal permeability and absorption of endotoxin. 6, 7 Despite these observations the prevalence of SIBO has not been investigated in patients with NASH. 3 Finally, various rat models of SIBO have been associated with liver lesions similar to NASH 4, 5 that improved following antibiotics. 2 Thirdly, NASH has been reported in one individual with jejunal diverticulosis and SIBO diagnosed by a 14CO 2 bile acid breath test. 1 Secondly, several patients with jejunoileal bypass associated NASH required liver transplantation and NASH recurred rapidly following transplantation, particularly in patients who did not have the jejunoileal bypass reversed at the time of transplantation. Firstly, NASH was encountered as a common complication of jejunoileal bypass surgery for morbid obesity during the 1980s and could be reversed by treatment with metronidazole. Several observations have suggested that small intestinal bacterial overgrowth (SIBO) may play a role in NASH.
The pathogenesis of non-alcoholic steatohepatitis (NASH) remains unclear.
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