Impact of propranolol on preventing renal dysfunction in patients with cirrhosis

Background: One of the earliest diagnostic signs of hepatorenal syndrome in patients suffering from liver cirrhosis is an increase in the renal vascular resistive index [RI]. In this study, the impact of propranolol on decreasing this index and to postpone the probability of hepatorenal syndrome has been investigated

Methods: In the current research, 30 patients with liver cirrhosis with different age and sexes have been enrolled. Demographic data and complete medical history have been collected using a specific questionnaire. At first, renal artery Doppler ultrasonography was performed to determine the RI. The patients were then treated with propranolol, and under supervision, the dose of the drug was increased gradually every 3 to 5 days to reach the target of 25% decrease in resting heart rate. One month after reaching the target dose of the medicine, Doppler ultrasonography was repeated for the patients and the second RI was compared with the pretreatment ones

Results: According to our results after treatment with propranolol, a significant decrease of RI was observed [p < 0.01]. However, there was no significant difference in the glomerular filtration rate [GFR] before and after treatment with propranolol [p = 0.290]. In our study, we found that administering propranolol was associated with significant changes in RI and GFR between the patients with compensated and decompensated cirrhosis [mean change: -0.005 +/- 0.017 vs. -0.058 +/- 0.045; p < 0.01 for RI and -4.226 +/- 17.440 vs. 13.486 +/- 12.047; p < 0.01 for GFR in patients with compensated and decompensated cirrhosis, respectively]

Conclusion: Propranolol reduces renal vascular RI in patients with cirrhosis. The response rates in the patients with decompensating cirrhosis were significantly higher than the patients with compensating cirrhosis

Fulminate hepatic failure as an initial presentation of non-hodgkin lymphoma: a case report

Viral hepatitis and toxins comprise most common causes of fulminate hepatic failure that are often diagnosed with standard laboratory tests. Herein we discuss a rare, difficult to diagnosis etiology of acute liver failure [ALF]

A 62-year-old man presented with a two-week history of fever and fatigue. At four days before admission he became lethargic

His past medical and drug histories were unremarkable

Physical examination revealed generalized jaundice, fever and loss of consciousness. Laboratory tests showed elevated liver transaminases with direct hyper-bilirubinemia

Abdominal ultrasonography and CT scan showed hepatosplenomegaly and para-aortic abdominal lymph-adenopathy

A further work-up included liver biopsy

The histopathology and imunohistochemistry was compatible with diffuse large B-cell lymphoma. He underwent high dose glucocorticoid therapy but his condition deteriorated rapidly and he died eight days after admission

ALF as an initial manifestation of malignant hepatic infiltration is extremely rare yet should be considered in all patients with unknown hepatic failure that are highly suspicious for malignant neoplasm