Vol. 2 Issue 1
On the cover: Official Journal of the Mexican Association of Hepatology
The major hepatological consequence of HCV infection is the progression to cirrhosis and its potential complications. Several factors have been clearly shown to be associated with fibrosis progression rate: duration of infection, age, male sex, consumption of alcohol, HIV coinfection and low CD4 count. As age and duration of infection increases, the risk of fibrosis increases and the impact of treatment (IFN) decreases. In conclusion, fibrosis progression has a progressive acceleration, sex, age and consumption of alcohol are strongly involved in this progression ; the possibility to assess with nonagressive biochemical markers the fibrosis stage will probably allow in the future to identify other factors related to fibrosis progression.
Hepatic encephalopathy and brain edema are important complications in the course of a patient with acute liver failure. Presumed unrelated for many years, increasing evidence suggests that an increase in brain water is seen in all forms of hepatic encephalopathy. Ammonia, traditionally linked to the pathogenesis of hepatic encephalopathy, plays an important role in the increase in brain water. In acute liver failure, an osmotic disturbance in the astrocyte, in combination with an alteration of cerebral blood flow results in overt brain edema and intracranial hypertension. In cirrhosis, magnetic resonance techniques indicate the presence of a brain osmotic disturbance. Several clinical factors modulate the development of brain swelling.
Hepatorenal syndrome is complication of advanced cirrhosis characterized by renal failure, changes in systemic blood pressure, and increased activity of endogenous vasoactive systems. Renal failure is due to severe renal vasoconstriction developing in the late stages of cirrhosis. The pathogenesis of hepatorenal syndrome is the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in the splanchnic circulation. This underfilling triggers a compensatory response with activation of vasoconstrictor systems. The diagnosis of hepatorenal syndrome is based on established diagnostic criteria aimed at excluding nonfunctional causes of renal failure. The prognosis of patients with hepatorenal syndrome is very poor. Liver transplantation is the best option in selected patients, but it is not always applicable due to the short survival expectancy and donor shortage. Pharmacological therapies based on the use of vasoconstrictor drugs (terlipressin, midodrine, octreotide or noradrenline) are the most promising in aims of successfully offering a bridge to liver transplantation. Prevention of hepatorenal syndrome with albumin infusion is recommended in patients with spontaneous bacterial peritonitis and with pentoxifylline in patients with acute alcoholic hepatitis.
Microlithiasis is the underlying cause in a significant proportion of patients with 'idiopathic' acute pancreatitis. The mechanism appears to be a relative deficiency of phosphatidylcholine in bile, with fast and extensive cholesterol crystallization as a result. Diagnosis of microlithiasis by microscopic detection of cholesterol crystals in bile is important and should lead to appropriate therapy (cholecystectomy, endoscopic sphincterotomy or ursodeoxycholic acid maintenance therapy).
Background & aims: The potential use of losartan, an angiotensin II type 1 receptor blocker, in the treatment of portal hypertension is still under debate. This randomized controlled trial compared the effects of losartan vs. propranolol on portal and systemic hemodynamics in patients with cirrhosis. Methods: Twenty-seven compensated patients were randomized to receive losartan 25 mg/day (n = 17) or propranolol (n = 10). Hepatic venous pressure gradient (HVPG), portal blood flow (Doppler duplex ultrasound) and systemic hemodynamics were measured at baseline and after 12-week treatment. Portal resistance was calculated as HVPG/portal blood flow. Results: Propranolol induced a reduction in cardiac output (p 0.002), heart rate (p 0.0001) and HVPG [from 16.4 (+ 4.1) to 13.1 (+ 3.6) mmHg (p 0.07)]; six patients showed a reduction equal or greater than 20% and were considered responders. Losartan caused a decrease in HVPG [from 15.6 (+ 4.2) to 11.8 (+ 3.5) mmHg (p 0.002)], without changes in portal blood flow and systemic hemodynamics. Changes in HVPG correlated with variations in portal resistance (r 0.88, p < 0.0001). Losartan induced a reduction in HVPG between 10 and 19% in 5/17 patients, and 20% or more in 8/17. Five out of eight patients who respond to losartan showed severe portal hypertension, with higher baseline HVPG (equal or greater than 16 mmHg). Conclusions: the administration of losartan in a doses of 25 mg per day may be effective in lowering portal pressure in patients with compensated cirrhosis, particularly in those with more severe portal hypertension.
Hepatic encephalopathy (HE) is a major sign of severe liver disease and the impact of associated bacterial infectious should be better evaluated. A retrospective cohort of 333 patients with cirrhosis and HE was analyzed in three periods of time, from 1984 to 1998. Variance analysis, Wilcoxon, Chi-square and Fisher's exact tests were used for statistical comparisons. Prevalence of bacterial infections decreased along the time (p = 0.0029). Spontaneous Bacterial Peritonitis -SBP- (37%) and urinary tract infection (30%) were the more frequent types of bacterial infections. Early death was significantly higher in HE with infection (46,47%) and the calculated RR was 2.047. Prognosis was worse in septicemia (79%) and respiratory tract infection (50%) and better in urinary tract infection (27%). SBP lethality was reduced from 70% to 38% (p = 0.062). In conclusion, lower prevalence of bacterial infections, in severe liver disease, was achieved in the last decade, but short-term prognosis remains bad, varying according to the type of bacterial infection.
We report a 53-year old Mexican female who developed liver dysfunction following a seven-day course of treatment with terbinafine for onychomycosis. She presented with jaundice and abdominal pain. Her serum bilirubin levels showed a peak value of 23.2 mg/dL seven weeks after discontinuing the medication. Infectious causes (hepatitis viruses A, B and C) were excluded. Imaging studies of the abdomen did not reveal any abnormalities. Serum iron and ceruloplasmin levels were normal. Autoantibodies were negative. A liver biopsy revealed necrosis and mononuclear infiltration of the parenchyma, mainly along the sinusoids and surrounding the portal spaces and biliary ducts. Eosinophil infiltration of the portal spaces was also noted. Treatment with ursodeoxycholic acid and ademethionine was started. Her liver tests normalized in the sixth months after stopping terbinafine.