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Nonalcoholic fatty liver disease (NAFLD) is a very common cause of chronic liver disease in United States. A large proportion of patients with NAFLD have co-existing metabolic syndrome which is a major risk factor for cardiovascular disease. A strong association between NAFLD and cardiovascular disease has been long suspected and recent studies have confirmed that cardiovascular disease is the single most important cause of mortality in these patient population. There is a suggestion that NAFLD may pose cardiovascular risk above and beyond that is conferred by traditional cardiovascular risk factors (e.g., dyslipidemia, diabetes and smoking). Health care providers managing patients with NAFLD should recognize this increased cardiovascular risk and should undertake early aggressive risk factor modification.

Anorectal varices are more common in patients with EHPVO, while portal hypertensive colopathy is more common in patients with cirrhosis. Large anorectal varices are also more common in patients with EHPVO than in patients with cirrhosis and there is an inverse relationship between anorectal varices and colopathy in both cirrhotic patients and patients with EHPVO.

SUMMARY Background Resistance to loop diuretics is common in patients with ascites. Diminished glomerular filtration rate (GFR) is thought to mediate resistance to loop diuretics. Midodrine, a commonly used alpha-1 agonist, has been shown to improve GFR in non-azotemic patients with cirrhosis. Aim To conduct a randomized, double-blind, placebo-controlled, cross-over study to test the hypothesis that midodrine significantly increases natriuretic response of IV furosemide in non-azotemic cirrhotics with ascites. Methods All subjects participated in both phases, which were (i) furosemide IV infusion + oral midodrine 15 mg administered 30 min before furosemide (ii) furosemide IV infusion + oral placebo administered 30 min before furosemide. Primary outcomes were 6-h urine sodium excretion and 6-h total urine volume. Results A total of 15 patients (men: 8; age: 52.7 ± 7.6 years; serum creatinine: 1.06 ± 0.2 mg/dL) were studied. Total 6-h urine sodium excretion was 109 ± 42 mmol in the furosemide + midodrine treatment phase and was not significantly different from that in the furosemide + placebo treatment phase (126 ± 69 mmol, P = 0.6). Similarly, mean 6-h total urine volume was not significantly different between two groups (1770 ± 262 mL vs. 1962 ± 170 mL, P = 0.25). Conclusions Oral midodrine does not increase the natriuretic response to furosemide in non-azotemic cirrhotic patients with ascites. Orally administered midodrine does not increase natriuretic response to furosemide in non-azotemic cirrhotic patients with ascites.

Background-A 58-year-old white man who was being followed by his hepatologist for nonalcoholic steatohepatitis-related liver cirrhosis and portal hypertension and who had been found to have a biopsy-proven hepatocellular carcinoma (HCC) on routine screening, self-referred to our center for a second opinion on the management of his HCC.