Role of Non-Selective Beta Blockers in Hepatocellular Carcinoma: An Analysis in Patients with Cirrhosis and Portal Hypertension

There are many different biochemical processes responsible for the hepatocelluar carcinoma (HCC) development that can be targeted for the prevention or halt progression of the HCC. Non-selective betablockers (NSBB) affects a multitude of intracellular biochemical and signaling pathways involved in carcinogenesis. Aim: To determine if NSBB may be protective for HCC in patients with cirrhosis and portal hypertension. Methods: We retrospectively enrolled 200 patients from medical records diagnosed with cirrhosis and portal hypertension between January 2001 and December 2013. Eighteen patients were excluded (taking selective beta-blocker and/or unavailable medical records). The etiology of cirrhosis, use of NSBB, demographics and the presence of HCC was collected. Result: There were 140 males and 42 females. The mean age for portal hypertension with cirrhosis without HCC was 53.5 ± 11.4 & with HCC was 62.2 ± 9.5 years. Univariate analysis of the association of NSBB with HCC yielded OR = 0. 11 (95% CI: 0.04 to 0.25); p \u3c 0.0001, suggesting a protective effect of NSBB. Multivariable analysis suggests virtually no change when the Odds ratio (OR) was adjusted for diabetes mellitus (DM), alcohol use, Hepatitis B virus (HBV) status, Black race and age ≥ 53. There was a slight increase in the OR adjusted for statin use. Conclusion: This study highlights association of NSBB use in the patients with liver cirrhosis and portal hypertension for prevention of HCC

Role of Non-Selective Beta Blockers in Hepatocellular Carcinoma: An Analysis in Patients with Cirrhosis and Portal Hypertension

There are many different biochemical processes responsible for the hepatocelluar carcinoma (HCC) development that can be targeted for the prevention or halt progression of the HCC. Non-selective beta-blockers (NSBB) affects a multitude of intracellular biochemical and signaling pathways involved in carcinogenesis. Aim: To determine if NSBB may be protective for HCC in patients with cirrhosis and portal hypertension. Methods: We retrospectively enrolled 200 patients from medical records diagnosed with cirrhosis and portal hypertension between January 2001 and December 2013. Eighteen patients were excluded (taking selective beta-blocker and/or unavailable medical records). The etiology of cirrhosis, use of NSBB, demographics and the presence of HCC was collected. Result: There were 140 males and 42 females. The mean age for portal hypertension with cirrhosis without HCC was 53.5 ± 11.4 & with HCC was 62.2 ± 9.5 years. Univariate analysis of the association of NSBB with HCC yielded OR = 0. 11 (95% CI: 0.04 to 0.25); p \u3c 0.0001, suggesting a protective effect of NSBB. Multivariable analysis suggests virtually no change when the Odds ratio (OR) was adjusted for diabetes mellitus (DM), alcohol use, Hepatitis B virus (HBV) status, Black race and age ≥ 53. There was a slight increase in the OR adjusted for statin use. Conclusion: This study highlights association of NSBB use in the patients with liver cirrhosis and portal hypertension for prevention of HCC

Prevalence and risk factors for hypertensive crisis in a predominantly African American inner-city community

Purpose: A 3-year case control study was conducted to determine the prevalence of hypertensive crisis and its subtypes, hypertensive emergency and hypertensive urgency. The secondary objectives were to identify risk factors for hypertensive emergencies and to determine the odds of developing acute target organ damage among predominantly African American patients with a confirmed diagnosis of hypertension. Materials and methods: Using emergency department medical records, patients with a confirmed diagnosis of hypertension were identified. From the pool of hypertensive patients, cases and controls were selected and matched 1:1 for age, gender and race. Cases were hypertensive patients with hypertensive crisis, defined as BP ≥ 200/120 mmHg. Controls had a diagnosis of hypertension and BP < 200/120 mmHg. Cases and controls, as well as cases with hypertensive emergencies and hypertensive urgencies were compared based on important demographic and clinical variables. Results: Almost 90% of study population were African Americans. The prevalence of hypertensive crisis was 11.4% and hypertensive emergencies was 3.2%. Hypertensive emergencies accounted for 28% of patients with crisis. The predictors for hypertensive emergencies were older age (p = .002), male gender (p < .007), anemia (p < .0001), history of coronary artery disease (p < .001), congestive heart failure (p < .001) and chronic renal insufficiency (p < .001). Having healthcare insurance and access to medical care did not reduce the odds of developing hypertensive emergencies. Race was not a significant risk factor in the progression from hypertensive crisis to hypertensive emergencies (p = .47). Conclusions: The study highlights the high prevalence of hypertensive crisis and hypertensive emergencies in the predominantly African American urban population, which is 5 times the United States average. However, race is not a predictor of development of hypertensive emergencies and acute target organ damage in patients with already severely elevated blood pressure