Aggravation Of Esophageal Varices Research Articles

左胃静脈の発育形態からみたB-RTO後の食道静脈瘤出現・増悪の予測-超音波内視鏡による検討-

左胃静脈の発育形態からみたB-RTO後の食道静脈瘤出現・増悪の予測-超音波内視鏡による検討-

Clinical outcomes of balloon-occluded retrograde transvenous obliteration for the treatment of gastric variceal hemorrhage in Korean patients with liver cirrhosis: a retrospective multicenter study

Background/AimsThis study evaluated the clinical outcomes of balloon-occluded retrograde transvenous obliteration (BRTO) for the treatment of hemorrhage from gastric varices (GV) in Korean patients with liver cirrhosis (LC).MethodsWe retrospectively analyzed data from 183 LC patients who underwent BRTO for GV bleeding in 6 university-based hospitals between January 2001 and December 2010.ResultsOf the 183 enrolled patients, 49 patients had Child-Pugh (CP) class A LC, 105 had CP class B, and 30 had CP class C at the time of BRTO. BRTO was successfully performed in 177 patients (96.7%). Procedure-related complications (e.g., pulmonary thromboembolism and renal infarction) occurred in eight patients (4.4%). Among 151 patients who underwent follow-up examinations of GV, 79 patients (52.3%) achieved eradication of GV, and 110 patients (72.8%) exhibited marked shrinkage of the treated GV to grade 0 or I. Meanwhile, new-appearance or aggravation of esophageal varices (EV) occurred in 54 out of 136 patients who underwent follow-up endoscopy (41.2%). During the 36.0±29.2 months (mean±SD) of follow-up, 39 patients rebled (hemorrhage from GV in 7, EV in 18, nonvariceal origin in 4, and unknown in 10 patients). The estimated 3-year rebleeding-free rate was 74.8%, and multivariate analysis showed that CP class C was associated with rebleeding (odds ratio, 2.404; 95% confidence-interval, 1.013-5.704; P=0.047).ConclusionsBRTO can be performed safely and effectively for the treatment of GV bleeding. However, aggravation of EV or bleeding from EV is not uncommon after BRTO; thus, periodic endoscopy to follow-up of EV with or without prophylactic treatment might be necessary in LC patients undergoing BRTO.

Clinical outcome of esophageal varices after hepatic arterial infusion chemotherapy for advanced hepatocellular carcinoma with major portal vein tumor thrombus

To analyze the clinical outcome of esophageal varices (EV) after hepatic arterial infusion chemotherapy (HAIC) in patients with advanced hepatocellular carcinoma (HCC) and major portal vein tumor thrombus (Vp3/4). The study subjects were 45 consecutive patients who received HAIC for HCC with Vp3/4 between January 2005 and December 2009. HAIC comprised the combination therapy of intra-arterial 5-FU with interferon-α (5-FU/IFN) in 23 patients and low-dose cisplatin plus 5-FU (FP) in 22. Radiotherapy (RT) was also provided in 19 patients for portal vein tumor thrombosis. Aggravation rate for EV and overall survival rate were analyzed. The aggravation rates for EV were 47% and 64% at 12 and 24 months, respectively. The survival rates were 47% and 33% at 12 and 24 months, respectively. The response rates to 5-FU/IFN and FP were 35% and 41%, while the disease control rates in these two groups were 57% and 50%, respectively. There were no significant differences in the objective response and disease control between 5-FU/IFN and FP. Multivariate analysis identified size of EV (F2/F3) (HR = 7.554, P = 0.006) and HCC disease control (HR = 5.948, P = 0.015) as significant and independent determinants of aggravation of EV, and HCC disease control (HR = 12.233, P < 0.001), metastasis from HCC (HR = 11.469, P = 0.001), ascites (HR = 8.825, P = 0.003) and low serum albumin (HR = 4.953, P = 0.026) as determinants of overall survival. RT for portal vein tumor thrombosis tended to reduce the aggravation rate for EV in patients with these risk factors. Hepatocellular carcinoma disease control was the most significant and independent factor for aggravation of EV and overall survival in HCC patients with major portal vein tumor thrombosis treated with HAIC.

Balloon Occlusion Retrograde Transvenous Obliteration for Inferior Mesenteric Vein–Systemic Shunt

Two cases of portosystemic encephalopathy caused by an inferior mesenteric vein (IMV)–internal iliac vein shunt and an IMV–renal vein shunt are presented. IMV and systemic varicosity consisted of a first functional segment, a stagnant segment, and a second functional segment. Both patients underwent balloon occlusion retrograde transvenous obliteration (BRTO), using a microcatheter, to occlude the stagnant segment selectively. Although transient portal vein thrombosis was observed in case 1 and aggravation of esophageal varices was observed in case 2, these complications were tolerable. Following BRTO, the portosystemic encephalopathy in both cases resolved, and serum ammonia levels, although elevated, remained within the normal range.

Changes in Portal Systemic Pressure Gradient After Balloon-Occluded Retrograde Transvenous Obliteration of Gastric Varices and Aggravation of Esophageal Varices

Changes in Portal Systemic Pressure Gradient After Balloon-Occluded Retrograde Transvenous Obliteration of Gastric Varices and Aggravation of Esophageal Varices

Changes in Portal Systemic Pressure Gradient After Balloon-Occluded Retrograde Transvenous Obliteration of Gastric Varices and Aggravation of Esophageal Varices

The purpose of this study was to evaluate change in the portal systemic pressure gradient (PSPG) following balloon-occluded retrograde transvenous obliteration (BRTO) and the aggravation of esophageal varices. The PSPG was monitored before and after BRTO in 19 patients. PSPG changes were obtained by subtracting the PSPG before BRTO from that after BRTO. The development of outflow vessels (e.g., left inferior phrenic vein) was classified into two grades: Grade 1, BRTO alone; and Grade 2, coil embolization plus BRTO. After confirming demonstration of the whole gastric varices on angiography and computed tomography, BRTO was conducted using a 5% ethanolamine-iopamidol mixture. Endoscopy was performed to evaluate gastric and esophageal varices before, within 1 month, and 3-6 months after BRTO. Eradication of gastric varices was obtained in all patients and aggravation of esophageal varices was seen in 11 patients. The PSPG was significantly elevated by BRTO (p=0.0362). The PSPG was significantly elevated in patients with Grade 2 compared with those with Grade 1 (7.7+/-3.7 vs. 3.3+/-4.3 mmHg, respectively; p=0.0314) and in those with esophageal varices before treatment compared with those without (7.4+/-4.0 vs. 3.2+/-3.9 mmHg, respectively; p=0.0482). The cumulative aggravation rate of esophageal varices was significantly higher in 11 patients with a PSPG elevation>5 mmHg than in 8 patients with one of <or=5 mmHg (p=0.0105). In conclusion, BRTO induced a significant elevation in PSPG, with the degree of elevation influencing the aggravation of esophageal varices following BRTO.

What are the risk factors for aggravation of esophageal varices in patients with hepatocellular carcinoma?

The risk factors for aggravation of esophageal varices (EV) in patients with hepatocellular carcinoma (HCC) are poorly understood. The aim of this study was to evaluate the effects of HCC on the appearance of the red color (RC) sign on EV and also investigate whether risk factors for the appearance of the RC sign differed between patients with and without HCC. A total of 243 patients with cirrhosis (127 with HCC, 116 without HCC) without the RC sign, with no previous variceal hemorrhage, and not on prophylactic treatment for EV were enrolled. The endpoint was defined as being either when the RC sign was first noted, or when variceal bleeding occurred. In patients without HCC, follow-up was discontinued if HCC was discovered. The risk factors were analyzed by Cox proportional hazards regression. In patients with HCC, portal vein tumor thrombus was a statistically independent risk factor (risk ratio [RR] 4.58, 95% confidence interval [CI] 1.32-15.86), although the presence of HCC was not. A large HCC (> or =50 mm) tended to be a risk factor, but this was not statistically significant (RR 2.50, 95%CI 0.98-6.39). Child-Pugh classification and low platelet count were common risk factors regardless of whether HCC was present or not. Portal vein tumor thrombus, but not the presence of HCC, was a significant risk factor for aggravation of EV in patients with HCC. Cirrhotic patients with portal vein tumor thrombus should receive more aggressive management of portal hypertension to prevent aggravation of EV.