Efficacy of endoscopic sclerotherapy on long-term management of oesophageal varices: a comparative study of results in patients with cirrhosis of the liver, non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal venous obstruction (EHO)

A prospective study was conducted to compare the results of long-term endoscopic variceal sclerotherapy in patients with different aetiologies of portal hypertension. A total of 404 consecutive patients were included. There were 234 patients with hepatic cirrhosis, 83 with non-cirrhotic portal fibrosis (NCPF) and 87 with extrahepatic portal venous obstruction (EHO). The mean follow-up for patients with cirrhosis, NCPF and EHO was 25, 37 and 28 months. A total of 73 (31%) patients with cirrhosis, 19 (23%) with NCPF and 10 (11.5%) with EHO rebled (P less than 0.05) on follow-up, prior to eradication of varices. Irrespective of the aetiology, 40 (17%) patients of Child's A class, 42 (33%) of Child's B and 20 (50%) of Child's C class rebled (P less than 0.01). The median bleeding free period (BFP) was longer (P less than 0.05) in patients with EHO than in cirrhotics. Patients in Child's A class had significantly longer BFP than those in Child's B, and the latter had a longer BFP than those in Child's C class (P less than 0.01). The probability of 7-year survival was also better with EHO (97.5%) and NCPF (73.6%) than cirrhotics (41%). Survivals in patients with EHO and NCPF were comparable (P less than 0.1). Similarly 7-year survival irrespective of aetiology in Child's A patients (90.7%) was longer than in Child's B (28.8%), and longer in Child's B than Child's C patients (0%). Success of eradication was greater (P less than 0.05) in EHO (92%) and NCPF (87%) than cirrhotic patients (75%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Non-cirrhotic portal fibrosis: current concepts and management

Non-cirrhotic portal hypertension (NCPH) comprises diseases having an increase in portal pressure (PP) due to intraheptic or prehepatic lesions, in the absence of cirrhosis. The lesions are generally vascular, either in the portal vein, its branches or in the perisinusoidal area. Because the wedged hepatic venous pressure is near normal, measurement of intravariceal or intrasplenic pressure is needed to assess PP. The majority of diseases included in the category of NCPH are well-characterized disease entities where portal hypertension (PHT) is a late manifestation and, hence, these are not discussed. Two diseases that present only with features of PHT and are common in developing countries are non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal vein obstruction (EHPVO). Non-cirrhotic portal fibrosis is a syndrome of obscure etiology, characterized by 'obliterative portovenopathy' leading to PHT, massive splenomegaly and well-tolerated episodes of variceal bleeding in young adults from low socioeconomic backgrounds, having near normal hepatic functions. In some parts of the world, NCPF is called idiopathic portal hypertension (IPH) or 'hepatoportal sclerosis'. Because 85-95% of patients with NCPF and EHPVO present with variceal bleeding, treatment involves management with endoscopic sclerotherapy (EST) or variceal ligation (EVL). These therapies are effective in approximately 90-95% of patients. Gastric varices are another common cause of upper gastrointestinal bleeding in these patients and these can be managed with cyanoacrylate glue injection or surgery. Other indications for surgery include failure of EST/EVL, and symptomatic hypersplenism. The prognosis of patients with NCPF is good and 5 years survival in patients in whom variceal bleeding can be controlled has been reported to be approximately 95-100%.     

Non-cirrhotic portal fibrosis (idiopathic portal hypertension): experience with 151 patients and a review of the literature

BACKGROUND: Non-cirrhotic portal fibrosis (NCPF), the equivalent of idiopathic portal hypertension in Japan and hepatoportal sclerosis in the United States of America, is a common cause of portal hypertension in India. The clinical features, portographic and histological findings, and management of 151 patients with non-cirrhotic portal fibrosis are presented. METHODS: The disease is diagnosed by the presence of unequivocal evidence of portal hypertension in the definite absence of liver cirrhosis and extrahepatic portal vein obstruction (EHPVO). Retrospective analysis of records of 151 patients with NCPF was analyzed for the clinical presentation, physical findings, laboratory tests, radiological and histological findings, and for the outcome of treatment. RESULTS: The disease is characterized by massive splenomegaly with anemia, preserved liver function and benign prognosis in a majority of patients. Splenoportovenography (SPV) showed massive dilatation of the portal and splenic veins, and the presence of collaterals. Twenty-four (15.9%) patients showed evidence of natural/spontaneous shunts (splenorenal 15, umbilical nine) on SPV; these patients had a lower incidence of variceal bleeding. Liver histology demonstrated maintained lobular architecture, portal fibrosis of variable degree, sclerosis and obliteration of small-sized portal vein radicles, and subcapsular scarring with the collapse of the underlying parenchyma. Piecemeal or hepatocytic necrosis was absent in all histology specimens. Three patients showed nodular transformation along with abnormal liver functions, and may represent late manifestation of NCPF where features are similar to those seen in patients with incomplete septal cirrhosis. In the initial part of the study, surgery (side-to-side lieno-renal shunt) was the preferred modality of treatment, however, endoscopic sclerotherapy or variceal ligation has now become the preferred first line of management of variceal bleeding. CONCLUSIONS: The epidemiological and clinical features of NCPF have more similarity to IPH than has previously been documented. The development of spontaneous shunts tends to protect these patients from variceal bleeding.     

Non-cirrhotic portal fibrosis

Non-cirrhotic portal hypertension (NCPH) comprises of diseases having an increase in portal pressure (PP) due to intraheptic or prehepatic lesions, in the absence of cirrhosis. The lesions are generally vascular, either in the portal vein, its branches or in the perisinusoidal area. Because the wedged hepatic venous pressure (WHVP) is near normal, measurement of intravariceal or intrasplenic pressure is needed to assess portal pressure. The majority of the diseases included in the category of NCPH are well characterized disease entities where portal hypertension (PHT) is a late manifestation and hence, these are not discussed. Two diseases which present only with features of PHT and are common in developing countries are NCPF and extra-hepatic portal vein obstruction (EHPVO). Non-cirrhotic portal fibrosis is a syndrome of obscure etiology, characterized by 'Obliterative portovenopathy' leading to PHT, massive splenomegaly, repeated well tolerated episodes of variceal bleeding and anemia in young adults from low socio-economic strata of life. The hepatic parenchymal functions are nearly normal. Jaundice, ascites and hepatic encephalopathy are rare. Management of variceal bleeding remains the main concern as nearly 85% of patients with NCPF present with variceal bleeding. Endoscopic variceal ligation or sclerotherapy are equally effective in about 90-95% of the patients. Gastric varices are seen in about 25% patients and a bleed from them can be managed with cyanoacrylate glue injection or surgery. Other indications for surgery include failure of endoscopic therapy to control acute bleed and symptomatic hypersplenism. The prognosis of patients with NCPF is good and 5-years survival rates in patients in whom variceal bleeding can be controlled is about > 95%.     

Non-cirrhotic portal hypertension versus idiopathic portal hypertension

Portal hypertension occurs in a number of disorders other than cirrhosis and they are collectively called non-cirrhotic portal hypertension (NCPH). The common causes of NCPH include idiopathic portal hypertension (IPH), non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal venous thrombosis (EHPVT). Other causes include schistosomiasis, hepatic venous outflow tract obstruction, veno-occlusive disease and congenital hepatic fibrosis. Patients with IPH and EHPVT present with upper gastrointestinal bleeding, splenomegaly, ascites after gastrointestinal bleeding, features of hypersplenism, growth retardation and jaundice due to portal biliopathy. The diagnosis is usually made by abdominal ultrasound, upper gastrointestinal endoscopy, normal liver function tests and normal liver histology. Variceal bleeding in NCPH has lower mortality as compared with cirrhosis because of better liver functions in NCPH. Treatment for NCPH includes primary prophylaxis for variceal bleeding and prevention of repeat bleeding using drugs like beta-blockers, endoscopic sclerotherapy and endoscopic band ligation of varices. In patients with uncontrolled variceal bleeding or symptomatic hypersplenism, porto-systemic shunt surgery or splenectomy are required.     

Outcome of injection sclerotherapy using absolute alcohol in patients with cirrhosis, non-cirrhotic portal fibrosis, and extrahepatic portal venous obstruction

In order to assess the comparative efficacy and safety of endoscopic injection sclerotherapy in patients with portal hypertension of different etiology, i.e., cirrhosis, non-cirrhotic portal fibrosis, and extrahepatic portal venous obstruction, 87 patients with variceal bleeding were initiated on sclerotherapy using absolute alcohol. There was no significant difference in the success rate of sclerotherapy as well as in the number of sessions and volume of alcohol required for variceal obliteration between the three groups. Major complications included esophageal ulcers (30.0%), symptomatic strictures (18.6%), and interval re-bleed (17.1%) with similar complication rates for the three groups (p greater than 0.05). There was no difference between patients with Child's class A cirrhosis compared with classes B and C together with respect to efficacy and complications of sclerotherapy. Fifty patients (25 cirrhosis, 11 non-cirrhotic portal fibrosis, and 14 extrahepatic portal venous obstruction) with complete variceal obliteration were followed up for a mean period of 16.5 months. Sixteen patients (32%) had variceal recurrence, but bleeding due to recurrent varices occurred in only one case. There was no difference among the three groups for overall variceal recurrence, although recurrence tended to be somewhat later in extrahepatic portal venous obstruction (9.4 +/- 4.0 months) compared with that in cirrhosis (5.1 +/- 3.6 months) and non-cirrhotic portal fibrosis (4.8 +/- 2.6 months).     

Factors influencing development of portal hypertensive gastropathy in patients with portal hypertension.

Portal hypertensive gastropathy (PGP) is an important cause of bleeding in portal hypertension patients. Although hyperdynamic congestion seems to be the underlying mechanism, the factors that influence the development of PGP are not understood. To investigate these, 107 patients [cirrhosis, 35; noncirrhotic portal fibrosis (NCPF), 24; extrahepatic portal vein obstruction (EHPVO), 46; Budd-Chiari syndrome, 2] were prospectively studied. Eighty-three patients had Child's A, 17 had Child's B, and 7 had Child's C liver disease. Before sclerotherapy, although intravariceal pressure was similar, 4 cirrhosis patients (3.7%) but no NCPF or EHPVO patients had PGP. After sclerotherapy, 21 additional patients (20.3%) developed PGP during a follow-up of 23.2 +/- 3.4 months (range, 1-52). The incidence of PGP was higher in cirrhotic patients (37.1%) than in NCPF (16.7%; P less than 0.05) or EHPVO (8.7%; P less than 0.01) patients. The probability of developing PGP among all patients at the end of 52 months of follow-up was 30%, more in cirrhosis than in EHPVO (55% vs. 15%; P less than 0.005). Only 2 patients bled from PGP during follow-up. Development of PGP correlated with severity of liver disease, being more common in Child's C than Child's A patients (87% vs. 13%; P less than 0.001). PGP was seen more often in patients with gastroesophageal varices than in patients with esophageal varices alone (42% vs. 11%; P less than 0.01). In conclusion, the results show that development of PGP is significantly influenced by sclerotherapy, severity of liver disease, etiology of portal hypertension, coexisting gastric varices and is not directly correlated with intravariceal pressure.     

Endoscopic sclerotherapy using absolute alcohol.

To assess the efficacy of absolute alcohol as a sclerosant, endoscopic sclerotherapy was carried out using a conventional endoscope and an indigenously designed injector. Forty three patients with portal hypertension who had presented with history of variceal bleeding were included in the study. Portal hypertension was caused by cirrhosis in 30 (69.8%), non-cirrhotic portal fibrosis in eight (18.6%) and extra-hepatic obstruction in five (11.8%). Acute bleeding was successfully controlled in all 11 patients, seven with a fresh bleed and four who rebled while on endoscopic sclerotherapy regimen. All patients with fresh, recent, or old bleeding were treated with a weekly endoscopic sclerotherapy schedule. Reduction in variceal size of two or more grades was achieved in all 20 patients who had completed at least four endoscopic sclerotherapy courses with total eradication of varices in 16 (80%). The mean (+/- SD) number of endoscopic sclerotherapy courses and time required for variceal eradication was 6.06 (+/- 1.87) and 9.1 (+/- 4.69) weeks respectively. None of these patients has shown appearance of fresh varices in a follow up of 18.47 +/- 8.50 weeks (range six to 38 weeks). Six patients died; all deaths were caused by progressive hepatic encephalopathy. Complications usually seen were dysphagia, retrosternal pain and fever; these were mild and easily tolerated by the patients. Rebleeding occurred in four patients who had received less than four endoscopic sclerotherapy courses. Absolute alcohol appears to be an effective, safe, economical, and freely available sclerosant. advocate endoscopic sclerotherapy as the first line of treatment for acute variceal bleeding and recommend a weekly schedule for the early eradication of varices.     

Thromboelastographic evaluation of coagulation in patients with extrahepatic portal vein thrombosis and non‐cirrhotic portal fibrosis: A pilot study

Background and Aims: Non‐cirrhotic portal hypertension due to extrahepatic portal vein thrombosis (EHO) and non‐cirrhotic portal fibrosis (NCPF) is a major cause of upper gastrointestinal hemorrhage in India. Hypercoagulability has been proposed to explain the thrombosis in the portal vein in EHO and intrahepatic portal vein radicals in NCPF. However, some authors have reported hypocoagulability in these patients. Thromboelastography (TEG), which gives a dynamic assessment of coagulation, has potential for evaluating coagulation in these patients but has not been used so far. It was the aim of this study to evaluate the coagulation status in patients of EHO and NCPF using TEG. Methods: Thirty patients with EHO and 19 patients with NCPF were studied. TEG was done in all patients. R (reaction time), K (constant), α (angle), MA (maximal amplitude), A 60 (width of tracing after 60 min) were recorded and TEG index calculated and compared to controls. Results: Seven patients (23.3%) in the EHO group and eight (42.1%) in the NCPF group had severe thrombocytopenia (platlets, < 50 000 cells/dL). TEG showed significantly shorter R, higher MA and larger A in both EHO and NCPF compared to controls (P < 0.01). Thrombocytopenia normalized A but R continued to be significantly shorter in EHO and NCPF. Overt hypercoagulability (TEG index, > +2.5) was seen in two patients with EHO and one patient with NCPF. Conclusion: A latent hypercoagulable state exists in patients with EHO and NCPF which is partially masked by the thrombocytopenia secondary to splenomegaly and hypersplenism.     

Non-cirrhotic portal fibrosis in children.

BACKGROUND AND OBJECTIVES: Non-cirrhotic portal fibrosis (NCPF) is an infrequent cause of portal hypertension in children. We report 11 children with NCPF, from among 338 with portal hypertension, seen over 6.5 years. METHODS: The diagnosis was based on patent splenoportal axis on ultrasonography and/or splenoportal venography and liver biopsy showing no evidence of cirrhosis or other diagnosis, in children with portal hypertension. Those with variceal bleed were managed with endoscopic sclerotherapy and/or shunt surgery. RESULTS: The median age was 11 years (range 5 to 14), and 8 were boys. Presentation was with variceal bleed in 6, lump in left upper abdomen in 5 (though all children had splenomegaly) and esophageal varices on endoscopy. The median spleen enlargement was 8.5 cm; 8 also had hepatomegaly. Hypersplenism was present in 7, and two had developed ascites after bleed. Of 6 children presenting with bleed, variceal obliteration was achieved on sclerotherapy (average 5.6 sessions) in 4 while two underwent shunt surgery for associated hypersplenism. After median follow up of 57.5 months (range 12-78) all are alive and well. CONCLUSION: NCPF is an uncommon cause of portal hypertension in Indian children. Presentation with variceal bleed is less common than in adults; sclerotherapy is effective.     

Etiological spectrum of esophageal varices due to portal hypertension in Indian children: Is it different from the West?

Background and Aim:  Information about portal hypertension (PHT) in children is meagre. We therefore studied the spectrum and outcome of PHT in children (≤14 years of age) over a period of 9 years.
Methods:  PHT was diagnosed on endoscopy (presence of varices) in 517 cases during the study period. The diagnosis of extrahepatic portal venous obstruction (EHPVO) and Budd–Chiari Syndrome (BCS) were made on the basis of ultrasound examination. Cirrhosis was diagnosed on the basis of clinical, biochemical, ultrasound, and liver biopsy (whenever feasible). Noncirrhotic portal fibrosis (NCPF) and congenital hepatic fibrosis (CHF) were diagnosed on liver biopsy. Endoscopic sclerotherapy (EST) was done in all the patients who presented with variceal bleeding and surgery was performed whenever indicated.
Results:  Causes of PHT included EHPVO in 54%, cirrhosis in 39%, CHF in 3%, NCPF in 2%, and BCS in 2%. Of these, 279 (54%) patients presented with upper gastrointestinal bleeding and this group comprised of EHPVO in 85%, cirrhosis in 10%, CHF in 2.5%, NCPF in 2%, and BCS in 1%. Bleeding was the presenting feature in 85% of EHPVO cases and in 13% of cirrhosis cases. In EHPVO cases, variceal eradication was achieved in 95% of cases with a mean 5 ± 2.4 EST sessions. Surgery was required in 24 cases of EHPVO. Mortality due to bleeding was 1.7% in EHPVO and 30% in cirrhosis.
Conclusions:  EHPVO and cirrhosis are the two major causes of PHT in children. However, predominant cause of variceal bleeding is EHPVO. EST is an effective method of treatment in EHPVO.     

Sclerotherapy after Variceal Hemorrhage in Noncirrhotic Portal Fibrosis

Sixty patients with variceal bleeding due to noncirrhotic portal fibrosis were treated by repeated endoscopic injection sclerotherapy. During each session, the varices were injected with a mean volume of 14.4 ml of 1% polidocanol intravariceally. This decreased rebleeding, as evidenced by a reduction in mean bleeding risk factor and transfusion requirement. Difference between pre- and post-sclerotherapy parameters were significant (p less than 0.001). Variceal obliteration was achieved in 53 (88%) patients. The mean sclerotherapy sessions required for eradication were 8.43 (SD = 2.41). Minor complications related to the procedure occurred in 12% of patients. Cumulative survival for 5 yr was 86%. Survival was significantly related to Child's status, being 97.5% for Child's A and 64% for Child's B patients. Recurrence of varices occurred in 15% of patients after a mean interval of 19 months. We conclude that endoscopic sclerotherapy is an effective method of treatment for variceal bleeding due to non-cirrhotic portal fibrosis, and is a reasonable alternative to surgery.     

Pediatric non-cirrhotic portal hypertension:Endoscopic outcome and perspectives from developing nations

Non-cirrhotic portal hypertension(NCPH) forms an important subset of portal hypertension in children. Variceal bleed and splenomegaly are their predominant presentation. Laboratory features show cytopenias(hypersplenism) and preserved hepatic synthetic functions. Repeated sessions of endoscopic variceal ligation or endoscopic sclerotherapy eradicate esophageal varices in almost all cases. After variceal eradication, there is an increased risk of other complications like secondary gastric varices, cholangiopathy, colopathy, growth failure,especially in extra-hepatic portal vein obstruction(EHPVO). Massive splenomegaly-related pain and early satiety cause poor quality of life(QoL). Meso-Rex bypass is the definitive therapy when the procedure is anatomically feasible in EHPVO. Other portosystemic shunt surgeries with splenectomy are indicated when patients present late and spleen-related issues predominate. Shunt surgeries prevent rebleed, improve growth and QoL. Non-cirrhotic portal fibrosis(NCPF) is a less common cause of portal hypertension in children in developing nations.Presentation in the second decade, massive splenomegaly and patent portal vein are discriminating features of NCPF. Shunt surgery is required in severe cases when endotherapy is insufficient for the varices. Congenital hepatic fibrosis(CHF)presents with firm palpable liver and splenomegaly. Ductal plate malformation forms the histological hallmark of CHF. CHF is commonly associated with Caroli's disease, renal cysts, and syndromes associated with neurological defects.Isolated CHF has a favourable prognosis requiring endotherapy. Liver transplanta-tion is required when there is decompensation or recurrent cholangitis, especially in Caroli's syndrome. Combined liver-kidney transplantation is indicated when both liver and renal issues are present.     

Management of portal hypertension after variceal hemorrhage

Each variceal bleed is associated with 20% to 30% risk of dying. Management of portal hypertension after a bleed consists of (1) control of bleeding and (2) prevention of rebleeding. Effective control of bleeding can be achieved either pharmacologically by administering somatostatin or octreotide or endoscopically via sclerotherapy or variceal band ligation. In practice, both pharmacologic and endoscopic therapy are used concomitantly. Rebleeding can be prevented by endoscopic obliteration of varices. In this setting, variceal ligation is the preferred endoscopic modality. B-blockade is as effective as endoscopic therapy and, in combination, the two modalities may be additive.     

B1 selective adrenoreceptor blockade for the long term management of variceal bleeding. A prospective randomised trial to compare oral metoprolol with injection sclerotherapy in cirrhosis

Oral metoprolol, in a dose sufficient to reduce resting pulse rate by 25%, was compared with repeated injection sclerotherapy for the long term management of variceal bleeding. The prospective, randomised study was undertaken in 32 patients with biopsy proven cirrhosis and variceal bleeding who were Grade A or B on a modified Child's classification. In the 15 patients receiving metoprolol, portal pressure showed a mean fall of 3.7 mmHg (17.3 +/- 1.2 to 13.6 +/- 1.2 mmHg, p less than 0.01) after four weeks of continuous therapy, as compared with pretreatment levels. Nine of the 15 patients taking metoprolol had further bleeding (total of 21 episodes) compared with six of 17 in the sclerotherapy group (nine episodes). The risk of bleeding per patient/month of follow up was three times higher in the metoprolol group compared with those treated by sclerotherapy (0.14 and 0.04 respectively, p less than 0.025). Rebleeding in the metoprolol group occurred in six of the patients who had a fall in portal pressure of 10% or more.     

The effects of chronic endoscopic variceal sclerotherapy on portal pressure in cirrhotics

The effect of obliterating esophageal varices by endoscopic sclerotherapy on portal pressure was prospectively studied in 11 cirrhotic patients with variceal hemorrhage. Portal venous pressure gradient, determined as the difference between transhepatic portal and hepatic vein pressure, increased by a mean of 31.1% +/- 14.5% in 8 (73%) and decreased by a mean of 30.1% +/- 11.7% in 3 (27%) patients, with no statistically significant change overall (P = 0.1). These changes in portal venous pressure gradient occurred despite an improvement in the laboratory and clinical parameters of hepatic function. Deep abdominal sonography with color flow imaging at variceal obliteration showed patent paraumbilical veins in 6 (55%) patients, 3 of whom had decreases in portal venous pressure gradient (29%, 19%, 42.5%) at variceal obliteration. In 5 (45%) patients without patent paraumbilical veins, a statistically significant increase in portal venous pressure gradient between initial endoscopic variceal sclerotherapy and variceal obliteration was noted (P = 0.008). Rebleeding (single episode in all 4 patients, before obliteration in 3 patients) occurred in those with an increase in portal venous pressure gradient; all patients with portal venous pressure gradient decreases were nonbleeders. No correlation between changes in portal venous pressure gradient and time to variceal obliteration, number of sclerotherapy treatments, or rebleeding episodes was observed. Thus, an increase in portal venous pressure gradient was noted in the majority of patients at variceal obliteration. Although the portal venous pressure gradient decrease may be explained by a patent paraumbilical vein, the mechanism of portal venous pressure gradient increase is not clear. It is speculated that this portal venous pressure gradient increase may be caused by an increase in collateral resistance or flow or a combination of both, resulting from obliteration of esophageal varices by endoscopic sclerotherapy.     

Evaluation of endoscopic variceal sclerotherapy in various grades of liver disease

Forty four patients with portal hypertension of varying etiology, including 25 patients with an acute episode of variceal bleeding and 19 with past history of hematemesis, were followed up for eighteen months following endoscopic variceal sclerotherapy (EVS). Of 11 patients in Child's A group, two died of acute bleed, three were subjected to shunt surgery and the remaining six survived the follow-up period. Ten of 11 cases in Child's C did not survive more than six months in spite of sclerotherapy. We conclude that rebleed and death due to rebleed following EVS occur more commonly in patients with poor hepatic reserve (Child's C) as compared to patients in Child's A and B.     

内镜下聚桂醇治疗食管静脉曲张对门脉高压性胃病的影响

[目的]探讨内镜下聚桂醇治疗食管静脉曲张对门脉高压性胃病(PHG)的影响.[方法]对连续100例门脉高压食管静脉曲张出血后接受内镜下硬化剂聚桂醇治疗的患者开展临床随访研究,评估聚桂醇治疗后对PHG的影响.[结果]注射聚桂醇前33例患者存有PHG(33％);初次注射聚桂醇治疗后PHG患者为74例,其中新增轻度PHG患者41例;2次及以上注射聚桂醇治疗后PHG患者达88例,经注射聚桂醇后PHG发生率明显增高(P＜0.01).注射聚桂醇的次数与PHG的发生相关(P＜0.01).[结论]内镜下硬化剂聚桂醇治疗术(EIS)治疗食管静脉曲张,在控制出血和消退曲张静脉的同时,具有产生和加重PHG的可能,但大多为轻度PHG.患者经硬化剂治疗后控制出血,全身状况好转后应择期手术治疗或长期应用降门脉压药物,控制和改善PHG,预防食管静脉曲张和PHG出血.     

Endoscopic sclerotherapy in children

Thirty-eight children, aged 1-15 years, with portal hypertension and recent variceal bleeding, were treated with repeated endoscopic sclerotherapy. Thirty-six of them had extrahepatic portal venous obstruction. Obliteration of varices was achieved in 35 (92%) patients requiring an average of 5.3 sessions per patient. Major complications occurred in seven patients, three of whom had oesophageal perforations and four had oesophageal stricture. Sclerotherapy significantly reduced the rate of rebleeding after the start of sclerotherapy and more so after variceal obliteration.     

Frequency and factors influencing portal hypertensive gastropathy and duodenopathy in cirrhotic portal hypertension

Portal hypertensive gastropathy and duodenopathy are distinct clinical and endoscopic entities. Data on factors influencing the development of these lesions are still emerging. Data on portal hypertensive duodenopathy are scarce. We prospectively studied 230 patients with liver cirrhosis and oesophageal varices attending the liver clinic of the Sanjay Gandhi Post Graduate Institute of Medical Sciences. One hundred and forty-two patients had no history of upper gastrointestinal bleeding, while the remainder had bled in the past. Endoscopic appearances were recorded before starting patients on a sclerotherapy programme. Forty-four patients were re-evaluated after variceal eradication. The frequency of portal hypertensive gastropathy (PHG) and duodenopathy (PHD) was 61 and 14%, respectively. Mild PHG was present in 85% and was severe in the rest. Portal hypertensive duodenopathy was mild in 50%, while in the other half it was severe. There was no relationship of PHG and PHD to: (i) a history of upper gastrointestinal bleed; (ii) size of oesophageal varices; (iii) aetiology of liver cirrhosis; or (iv) liver function status as assessed by Child Pugh's scores (P=NS for all). The prevalence of PHG was higher in those patients with oesophagogastric varices (74 of 107; 69%) compared with patients with oesophageal varices alone (68 of 123; 55%; P<0.05). However, no such increase in frequency of PHD was noted in patients with oesophagogastric varices. Sclerotherapy increased the frequency of PHG. Twenty-four patients had PHG before starting sclerotherapy, while it was noted in 33 patients 1–3 months after variceal eradication (P< 0.05). In contrast, there was no increase in the prevalence of portal hypertensive duodenopathy after sclerotherapy (P=NS). There was no correlation between endoscopic and histological changes of PHG and PHD. In conclusion, PHG is quite frequent in patients with cirrhosis and its frequency increases with the presence of oesophagogastric varices and after sclerotherapy. However, the frequency of PHD is low and is not affected by the factors studied.