Beatriz Peñas

Development of hyperdynamic circulation and response to β-blockers in compensated cirrhosis with portal hypertension.

Nonselective β‐blockers are useful to prevent bleeding in patients with cirrhosis and large varices but not to prevent the development of varices in those with compensated cirrhosis and portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence the response to β‐blockers. To characterize the hemodynamic profile of each stage of PHT in compensated cirrhosis and the response to β‐blockers according to stage, we performed a prospective, multicenter (tertiary care setting), cross‐sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated cirrhosis before and after intravenous propranolol (0.15 mg/kg): 194 patients had an HVPG ≥10 mm Hg (clinically significant PHT [CSPH]), with either no varices (n = 80) or small varices (n = 114), and 79 had an HVPG >5 and <10 mm Hg (subclinical PHT). Patients with CSPH had higher liver stiffness (P < 0.001), worse Model for End‐Stage Liver Disease score (P < 0.001), more portosystemic collaterals (P = 0.01) and splenomegaly (P = 0.01) on ultrasound, and lower platelet count (P < 0.001) than those with subclinical PHT. Patients with CSPH had lower systemic vascular resistance (1336 ± 423 versus 1469 ± 335 dyne · s · cm‐5, P < 0.05) and higher cardiac index (3.3 ± 0.9 versus 2.8 ± 0.4 L/min/m2, P < 0.01). After propranolol, the HVPG decreased significantly in both groups, although the reduction was greater in those with CSPH (‐16 ± 12% versus ‐8 ± 9%, P < 0.01). The HVPG decreased ≥10% from baseline in 69% of patients with CSPH versus 35% with subclinical PHT (P < 0.001) and decreased ≥20% in 40% versus 13%, respectively (P = 0.001). Conclusion: Patients with subclinical PHT have less hyperdynamic circulation and significantly lower portal pressure reduction after acute β‐blockade than those with CSPH, suggesting that β‐blockers are more suitable to prevent decompensation of cirrhosis in patients with CSPH than in earlier stages. (Hepatology 2016;63:197–206)

Effects of Sapropterin on Portal and Systemic Hemodynamics in Patients With Cirrhosis and Portal Hypertension: A Bicentric Double-Blind Placebo-Controlled Study

OBJECTIVES:Tetrahydrobiopterin (BH4), a cofactor of nitric oxide synthase, might have a role in the treatment of portal hypertension (PHT) as its administration improves endothelial nitric oxide generation and hepatic endothelial dysfunction, and reduces portal pressure in experimental models of cirrhosis. Sapropterin is an oral synthetic analogue of BH4 recently approved for the treatment of phenylketonuria. This study evaluated the safety and effects of sapropterin on hepatic and systemic hemodynamics in patients with cirrhosis and PHT.METHODS:Forty patients with cirrhosis and PHT (hepatic venous pressure gradient (HVPG) ≥10 mm Hg) were randomly allocated to receive sapropterin (n=19) for 2 weeks (5 mg/kg/day increased to 10 at day 8) or placebo (n=21) in a double-blind multicenter clinical trial. Randomization was stratified according to concomitant treatment with β-adrenergic blockers. We studied at baseline and post-treatment splanchnic (HVPG and hepatic blood flow (HBF)) and systemic hemodynamics, endothelial dysfunction and oxidative stress markers (von Willebrand factor and malondialdehyde), liver function tests, and safety variables.RESULTS:HVPG was not modified by either sapropterin (16.0±4.4 vs. 15.8±4.7 mm Hg) or placebo (16.0±4.6 vs. 15.5±4.9 mm Hg). HBF, systemic hemodynamics, endothelial dysfunction markers, and liver function tests remained unchanged. Sapropterin was well tolerated (no patient required dose adjustment or withdrawal), and adverse events were mild and similar between groups.CONCLUSIONS:Sapropterin, an oral synthetic analogue of BH4, at the used dose did not reduce portal pressure in patients with cirrhosis. Sapropterin was safe and no serious adverse effects or deleterious systemic hemodynamic effects were observed.

Role of Endoscopy in Primary Prophylaxis for Esophageal Variceal Bleeding

Cirrhosis is the leading cause of portal hypertension in the Western world. From a clinical standpoint, the most significant consequence of portal hypertension is the development of esophageal varices. Despite the many advances in the management of variceal bleeding, it remains a life-threatening complication of portal hypertension. Primary prophylaxis to prevent the first bleeding episode in patients with cirrhosis and esophageal varices is therefore critically important in the management of patients with cirrhosis.

Tumor rectal de crecimiento lateral tipo no granular resecado mediante disección endoscópica submucosa pura: un tratamiento inusual para una lesión atípica

Consulta de Alto Riesgo de Cancer Colorrectal. Unidad de Endoscopia. Department of Gastroenterology. Hospital Universitario Ramon y Cajal. Madrid. Universidad de Alcala, IRYCIS. Madrid, Spain. Endoscopy Division. National Cancer Center Hospital. Tokyo, Japan. Department of Gastroenterology. Fujita Health University University School of Medicine. Aichi, Japan. Department of Gastroenterology. Hospital Virgen de la Arrixaca. Murcia, Spain. Department of Pathology. Hospital Universitario Ramon y Cajal. Madrid. Universidad de Alcala, IRYCIS. Madrid, Spain. Departmento of General and Digestive Surgery. Hospital Universitario Ramon y Cajal. Madrid. Universidad de Alcala, IRYCIS. Madrid, Spain PICTURES IN DIGESTIVE PATHOLOGY