Hipertensión portal secundaria a sarcoidosis hepática

The etiology of hepatic granulomas varies depending on the epidemiology. In developed countries, primary biliary chol­angitis (PBC) is the main cause followed by sarcoidosis. In developing countries, it is tuberculosis. We present the case of a patient with chronic liver disease, whose anatomo­pathological diagnosis was compatible with sarcoidosis. It was a 55-year-old woman, with a history of type 2 diabe­tes (DBT), insulin-requiring and overweight. Her disease debuted with SAE, subsequently presenting HDA of vari­ceal origin. She was referred to our institution for study. Physical examination has hepatosplenomegaly and in the laboratory FAL and yGT augmented with non-reactive anti-LKM and AMA. Ultrasonography of the abdomen showed hepatosplenomegaly, without focal images. Hepatic biopsy puncture was performed, which reported numerous portal-site granulomas. The ECA dose was increased. The diagnosis of sarcoidosis was established and treatment with deflazacort was started. She presented an upper gastrointes­tinal bleeding causing her death.

EVALUATION OF PROGRESSION OF HEPATIC FIBROSIS IN A GROUP OF PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE ACCOMPANIED FOR 10 YEARS

ABSTRACT BACKGROUND: Non-alcoholic fatty liver disease has been progressively diagnosed in the general population as a consequence of the increased prevalence of obesity and type 2 diabetes mellitus, its main risk factors. It is characterized by accumulation of fat in the hepatocytes associated with lobular inflammation and balonization, which can lead to cirrhosis and hepatocarcinoma. Thus, a characterization and follow-up of a progression of the fibrosis level of these patients becomes important, being that the transient hepatic elastography is a reliable method for this evaluation with a measure of the kapa index. OBJECTIVE: To evaluate the progression of hepatic fibrosis through elastography in patients with non-alcoholic fatty liver disease. METHODS: Patients who had previously performed hepatic biopsy and noninvasive scores for non-alcoholic steatohepatitis (NASH) and fibrosis were included in the study. These same subjects were then submitted to current clinical evaluation, laboratory and liver elastography tests, defining the level of liver fibrosis, about 10 years after the first evaluation. RESULTS: Data were analyzed for 66 patients previously submitted to liver biopsy. Of these, 16 were not found, four could not participate because they were debilitated due to hepatic cirrhosis, two had died from an automobile accident and five from complications of cirrhosis of the liver. Therefore, of the 50 patients with a known history, 9 (18%) had died of cirrhosis or were unable to attend the examination because of their liver disease. The remaining population was predominantly female (61.5%), mean age of 63 years, being overweight, dyslipidemia (76.9%), disorders of the glycemic profile (76.9%), and metabolic syndrome (82.1%). Of the 39 cases evaluated, 35% had the same degree of fibrosis at the initial evaluation (biopsy) and at the current evaluation (elastography), 33% had an increase in the degree of fibrosis and another 30% had a decrease in the degree of fibrosis. Twenty-eight patients had NASH at baseline. Regarding these patients, it was observed in the current evaluation, that 25% remained stable in the degree of fibrosis, 39% progressed, and 35% regressed. CONCLUSION: Despite some limitations of our study, such as the small number of patients, and the use of two different methods of evaluation (biopsy and elastography), the data obtained allow us to conclude that of the 39 evaluated cases, 33% (13) presented progression of fibrosis and the total group of 50 patients, 42% had cirrhosis or died due to liver disease. The presence of NASH on hepatic biopsy did not prove to be, in our study, a predictive of the evolution of hepatic fibrosis in the patients.