A case of successful endoscopic injection sclerotherapy with N-butyl-2-cyanoacrylate for ruptured duodenal varices]

Duodenal varix is a rare cause of hemorrhage in patients with portal hypertension, however their rupture is serious and often life threatening. Treatments for duodenal variceal bleeding include endoscopic procedures, surgery, or interventional radiologic procedures. We report a case of duodenal varices rupture in a 45-year-old man with alcoholic liver cirrhosis who presented with melena and dizziness. Emergent upper endoscopy revealed large nodular varices with a ruptured erosion on the top in the distal second portion of duodenum. Two consecutive injections with 1.0 mL of n-butyl-2-cyanoacrylate (Histoacryl; Braun-Melsungen, Germany) mixed with 1.0 mL of lipiodol (Laboratoire-Guerbet, France) were performed intravariceally and achieved successful hemostasis. This suggests that endoscopic injection sclerotherapy with histoacryl may be an effective therapeutic option for the control of ruptured duodenal variceal bleeding.     

Duodenal epithelial thymidine uptake in patients with duodenal ulcer or endoscopic duodenitis

To evaluate the relationship between duodenal ulcer disease and duodenitis, duodenal epithelial cell renewal was measured in mucosal biopsies by the incorporation of [³H]thymidine. When 14 patients with duodenal ulcer were compared to 13 control subjects or 7 with endoscopic duodenitis alone, the crypt size was the same in all groups. Similar to other inflammatory processes of the gastrointestinal tract, patients with endoscopic duodenitis showed increased proliferative indices including a greater number of cells incorporating [³H]thymidine. In contrast, the proliferative indices from the duodenal mucosa of patients with duodenal ulcers did not differ from a control group. In a group of 6 patients with both endoscopic duodenitis and duodenal ulcer, the [³H]thymidine incorporation was intermediate between control subjects or patients with duodenal ulcer alone and those with endoscopic duodenitis alone. When subjects were divided according to the histologic appearance of the duodenal mucosa, those having chronic duodenitis demonstrated enhanced [³H]thymidine incorporation in comparison to a control group or patients with chronic active duodenitis (polymorphonuclear leukocytes present). Although there are many possible explanations of these findings, one may speculate that duodenal ulceration does not stimulate duodenal epithelial proliferation. This project was supported by the Yale Digestive Cancer Research Fund. Dr. Gorelick was supported by a Research Fellowship Award from the National Foundation for Ileitis and Colitis during a portion of this study and is currently a recipient of a Clinical Investigator Award (KO8-AM-00659) from the National Institute of Arthritis, Metabolism and Digestive Diseases.     

Hallazgos endoscópicos no relacionados con hipertensión portal en pacientes con cirrosis hepática sometidos a un programa de cribado de varices

AimTo determine the prevalence of endoscopic lesions unrelated with portal hypertension in patients with cirrhosis.Patients and methodsCross-sectional study including a consecutive cohort of patients with liver cirrhosis enrolled in a screening program of oesophageal varices who underwent an upper gastrointestinal endoscopy from November, 2013, to November, 2018. Clinical predictors of endoscopic lesions unrelated to portal hypertension were analyzed by univariate and multivariate logistic regression.ResultsA total of 379 patients were included. The most frequent aetiology of liver disease was alcohol consumption (60.4%). The prevalence of endoscopic lesions unrelated with portal hypertension was 39.6% (n=150). Among 96 patients with peptic lesions, urease was obtained in 56.2% of patients (positive in 44.4% of them). The prevalence of endoscopic lesions unrelated to portal hypertension was not associated with age, gender, liver function or ultrasound findings of portal hypertension. The prevalence of endoscopic lesions unrelated to portal hypertension was not associated with age, gender, liver function or ultrasound findings of portal hypertension. Smokers had a trend to increased prevalence of endoscopic lesions unrelated to portal hypertension (43.2% vs. 34.6%; p=0.09), particularly peptic ulcer (6.4% vs. 0.6%; p=0.05) and peptic duodenitis (17.3% vs. 6.3%; p=0.002). Active smoking was the only independent predictor of peptic ulcer or duodenitis (OR=2.56; p=0.017).ConclusionActive smoking is a risk factor for endoscopic lesions unrelated to portal hypertension. This finding should be further investigated to reassess endoscopic screening programs in cirrhotic smokers.     

结节型十二指肠炎的内镜表现及其临床病理学特征

目的 探讨结节型十二指肠炎内镜下表现与其组织学特征的关系及其发病机制。方法 观察内镜下136例结节型十二指肠炎的表现，对其活检标本均行H-E染色，观察病理改变，Giemsa染色及快速尿素酶试验诊断幽门螺杆菌感染，十二指肠黏膜兼作AB／PAS染色，观察十二指肠胃上皮化生。结果 136例结节型十二指肠炎内镜下表现为直径0．2～1．0cm大小不等的结节，伴有不同程度的充血、水肿，其中伴糜烂21例，出血点及（或）瘀斑30例。检出率占同期15820例内镜检查的0．9％，十二指肠炎的3．8％。病理诊断为十二指肠炎107例，其中慢性十二指肠炎53例，表现为间质内可见慢性炎性细胞浸润，肠绒毛缩短或萎缩、变平．肠腺不同程度减少；活动性十二指肠炎54例，除慢性炎性细胞外，黏膜层及固有层内还有不同程度的中性粒细胞浸润，伴Brunner腺增生51例，胃型上皮化生59例。136例中检出胃黏膜异位增生7例以及血吸虫虫卵所致的炎性病变4例，107例结节型十二指肠炎中，幽门螺杆阳性（Hp^＋）者为45．8％（49／107）。其中，53例慢性十二指肠炎患者中HP^＋者为32．1％（17／53），54例活动性十二指肠炎中Hp^＋检出率为59．3％（32／54），后者的Hp^＋检出率显著高于前者（P〈0．01）。结论 结节型十二指肠炎是一类特殊的非特异性十二指肠炎，内镜下表现与组织学改变存在不一致性。其发生可能与Hp感染及胃上皮化生、Brunner腺增生有关。     

Quantitative histological study of mucosal inflammatory cell densities in endoscopic duodenal biopsy specimens from dyspeptic patients using computer linked image analysis.

Inflammatory cell counting in endoscopic biopsy sections was carried out on duodenal mucosal samples from defined sites in patients with duodenal ulcer, duodenitis but no ulcer, non-ulcer dyspepsia, and asymptomatic controls using computer linked image analysis. The variables measured included polymorphonuclear and mononuclear cells per mm of superficial epithelium and per mm2 lamina propria. Duodenal ulcer crater margin and mucosal biopsy specimens from endoscopically inflamed mucosa in the group with duodenitis but no ulcer showed significantly higher inflammatory cell counts than endoscopically normal non-ulcer dyspepsia and control mucosa. Biopsy specimens from non-ulcer dyspepsia patients showed significantly higher lamina propria polymorphs than control group mucosa. Endoscopically normal duodenal ulcer and duodenitis but no ulcer mucosa also showed significantly higher acute and chronic inflammatory cell counts than controls. The prevalence of Helicobacter pylori in duodenal biopsy specimens was low (0-22%) and unrelated to local inflammatory response. Despite histological appearances, duodenal biopsy specimens from non-ulcer dyspepsia patients showed significantly higher inflammatory cell infiltration than control specimens, suggesting that at least some represent part of a spectrum of subclinical peptic disease.     

Peptic ulcers and abdominal aortic aneurysms

Upper gastrointestinal endoscopy was performed in 106 of 204 Chinese patients with intact abdominal aortic aneurysms, ninety-seven for screening and nine for gastrointestinal bleeding or pain. Peptic disease was discovered in 38 patients: 12 duodenal ulcers, 12 gastric ulcers, four duodenal and gastric ulcers, three duodenitis, three gastritis and four previously operated for ulcers. The eight patients who bled before aneurysmectomy all had gastric ulcers; four required emergency operation and two died. Only two patients bled from duodenal ulcers, both after aneurysmectomy and one died. Excluding gastritis and duodenitis, peptic ulcer was found in 26.4% of patients with abdominal aortic aneurysms. Half of these ulcers were gastric ulcers and 50% of them bled before aneurysmectomy. Duodenal ulcers tend to remain asymptomatic before operation and two of 12 (16.7%) bled postoperatively. The risk of bleeding for ulcers associated with aneurysms was 10 of 28 (35.7%) ulcers. The result of this uncontrolled study suggests that routine endoscopic screening should be used in all patients with aortic aneurysms and early surgery should be offered for gastric ulcers.     

Non-cirrhotic portal hypertension in HIV mono-infected patients

Background and Aim: Unexplained liver injury including fibrosis and portal hypertension has rarely been reported among patients with HIV in the absence of co‐infection with hepatitis B (HBV) or hepatitis C (HCV). We describe a series of HIV mono‐infected patients with evidence of non‐cirrhotic portal hypertension. Methods: HIV‐infected patients with evidence of portal hypertension who were anti‐HBV and anti‐HCV negative and HBV and HCV RNA polymerase chain reaction (PCR) negative were identified from patients managed by the Victorian statewide HIV referral service located at The Alfred Hospital, Melbourne. Portal hypertension was defined as either radiological or endoscopic evidence of varices, portal vein flow obstruction, or elevated hepatic venous pressure gradient (HPVG). Results: Five patients were found to have portal hypertension. These patients were male, aged 41 to 65 years, with known duration of HIV infection between 11 to 25 years. All had been treated with antiretroviral therapy, including didanosine. Tests for metabolic, autoimmune, and hereditary causes of liver disease failed to establish an etiology for the liver injury. All had radiological or endoscopic findings of varices, and four patients had radiological features of portal vein obstruction or flow reversal. Only one patient underwent HPVG measurement, which was elevated. Non‐invasive fibrosis assessment revealed increased liver stiffness in three (out of four) patients, and no cirrhotic features were found on those who underwent liver biopsy. Conclusions: To our knowledge, this is the largest published series of non‐cirrhotic portal hypertension in HIV mono‐infected patients in Australia. Further research is needed to understand what relationship, if any, HIV or its treatments might have on liver injury over time.     

病毒性肝炎患者的胃镜表现

目的：探讨病毒性肝炎患者的胃镜表现。方法：２６４例肝炎病人中肝硬变１７３例,慢性肝炎６１例,急性肝炎３０例,分别观察其胃镜下胃粘膜改变的特征及其与临床的关系。结果：门脉高压性胃病、消化道溃疡及糜烂性胃炎、浅表性胃炎、Ｈｐ阳性等均为病毒性肝炎患者的常见胃镜表现。门脉高压性胃病多发性在胃底、胃体;溃疡多发生于胃窦及球部。门脉高压性胃病及胃粘膜糜烂的范围和程度与食道静脉曲张程度相关。结论：病毒性肝炎患者     

Nodular duodenitis in chronic maintenance hemodialysis patients

A retrospective study of 138 cases of chronic hemodialysis between 1977 and 1982 were reviewed for endoscopic, radiographic, and histologic characteristics of duodenitis. Forty patients underwent upper gastrointestinal barium x-rays; 13 were found to have multiple duodenal bulb nodules and three of these patients had very prominent duodenal bulb folds. There were 42 patients on whom upper panendoscopy was performed, and multiple duodenal nodules were seen in 15 patients and thickened folds in three patients. There were five patients in whom nodules were seen only on endoscopy. The size of the nodules varied between 3 and 8 mm in diameter and mucosal folds between 4 and 8 mm. Duodenal mucosal hyperplasia with chronic inflammatory cell infiltrate was found on biopsy of the nodules in 12 cases, while three cases with nodules revealed blunted villous structure with chronic inflammatory cells.     

Erosive duodenitis after eradication therapy for Helicobacter pylori]

We studied the characteristics of erosive duodenitis after eradication therapy for Helicobacter pylori (Hp). Fifty-nine patients with Hp-positive peptic ulcer disease were treated with a combination of amoxicillin, clarithromycin, lansoprazol, and polaprezinc Subsequently, erosive duodenitis developed in 18 (43.2%) of 44 patients in whom Hp was eradicated successfully. There were no significant differences in demographic characteristics between the patients in whom duodenitis developed and those whom it did not, except that the incidence of duodenal ulcer before treatment was highte in the former group than in the latter. Erosions were located not only in the anterior wall of the first portion of the duodenum but also in the posterior wall or the second portion. Our results suggest that the development erosive duodenitis after Hp eradication therapy is a favorable, rather than an unfavorable, event, because erosive duodenitis appeared only in the patients with in whom Hp was successfully eradicated, moreover, the patients with duodenitis had no complaints and had a good prognosis without follow-up treatment.     

CLINICAL CHARACTERISTICS AND TREATMENT FOR PATIENTS PRESENTING WITH BLEEDING DUODENAL VARICES

Background and Aim: Bleeding from ectopic varices, including duodenal varices, is uncommon, but it can be difficult to manage. The clinical data of patients diagnosed and treated for duodenal varices were reviewed to investigate the strategy for treatment. Methods: The present study reviewed the clinical data of 10 patients with duodenal varices (mean age, 58.2 ± 15.6 years) at our associated institutes during the period between January 1996 and December 2008. Results: Nine patients had duodenal varices located in the second portion, whereas in one case they were located in the duodenal bulbus. The underlying diseases included liver cirrhosis in eight patients, and extrahepatic portal vein obstruction in two patients. The lesions were identified with bleeding from varices in eight of 10 patients. Initial hemostasis was achieved in all eight patients. However, among four patients treated endoscopically only, two patients died from rebleeding from varices and two died from hepatic failure resulting from variceal bleeding. Additional interventional radiology (IVR) was used in three patients and additional surgery was carried out in one case. One patient who was treated with balloon‐occluded retrograde transvenous obliteration rebled during IVR and died from bleeding. Two patients who underwent double balloon‐occluded embolotherapy and one case who had surgery achieved good clinical outcomes. Conclusions: Although endoscopic treatment is useful for initial hemostasis of hemorrhagic duodenal varices, the patients who underwent additional IVR after endoscopic treatment achieved good outcomes.     

Peripapillary duodenal varices as a rare cause of severe bleeding in a patient with no other signs of portal hypertension--successful endoscopic treatment with cyanoacrylate injection

Duodenal varices (DVs) are a rare cause of upper gastrointestinal bleeding and rather suspected in patients with portal hypertension. Bleeding DVs are difficult to manage and often fatal due to delayed diagnosis. We report on a 71-year-old patient with massive upper gastrointestinal haemorrhage, who did not show any clinical signs of portal hypertension; however, he had a history of duodenal segmental resection 8 years before. The source of bleeding could not be detected with different imaging methods such as angiography and computed tomography. Upper gastrointestinal endoscopy finally revealed DVs, which were located just adjacent to the papilla. After endoscopic injection therapy with n-butyl 2-cyanoacrylate the bleeding stopped immediately and the patient soon stabilised. Despite the peripapillar localisation no signs of pancreatitis or cholestasis occurred; during 10-month follow-up a marked regression of the varices without further signs of variceal bleeding was observed.     

Vascular liver diseases

This article reviews the primary circulatory liver diseases, which include Budd-Chiari syndrome, obstruction of the hepatic portion of the inferior vena cava, portal vein thrombosis, sinusoidal obstruction syndrome (veno-occlusive disease), nodular regenerative hyperplasia, and peliosis hepatis. In addition, two systemic cardiovascular diseases that impair hepatic circulation, ischemic hepatitis and congestive hepatopathy, are briefly discussed. A characteristic of the primary circulatory liver diseases is that portal hypertension usually precedes liver dysfunction; however, this is not the case with the primary parenchymal liver diseases, in which liver dysfunction always progresses before portal hypertension is manifested. Significant overlap exists among the diseases and risk factors that predispose patients to the primary circulatory liver diseases, though the pathogenesis of individual diseases varies.     

Duodenal varices as an unusual cause of gastrointestinal bleeding due to portal hypertension: a case report.

Duodenal varices that develop in patients with portal hypertension rarely cause hemorrhage, but varix rupture is a serious and often fatal event. We report the case of a 38-year-old man with hepatic vein occlusion who was referred to our hospital for gastrointestinal hemorrhage of unknown origin. Upper gastrointestinal endoscopy revealed varices in the distal third of the duodenum. These varices were identified as the source of the bleeding. The patient was treated with endoscopic band ligation, and with coil embolization of a shunt between the superior mesenteric vein and the left renal vein.     

Bleeding duodenal varices after gastroesophageal varices ligation: a case report

Duodenal varices are rarely occurring sites of hemorrhage in patients with portal hypertension, and such hemorrhaging can be a life-threatening event. We report the case of a 58-year-old woman with cirrhosis who presented with melena after successful ligation of gastroesophageal varices 1 week earlier. Upper gastrointestinal endoscopy revealed bleeding duodenal varices in the second portion of the duodenum, which was considered to be the source of the bleeding. Endoscopic injection sclerotherapy with histoacryl and lipiodol achieved successful hemostasis. Nonetheless, the sclerosant spread to the lungs via a portosystemic shunt, causing a pulmonary embolism. This is a rare complication seldom reported in the world literature.     

Duodenitis.

Many questions regarding duodenitis remain unanswered. However, the evidence suggests that duodenitis is a clinical entity which can give rise to dyspepsia and, on rare occasions, gastrointestinal haemorrhage. Conventional and double contrast radiology has only a small part to play in the diagnosis of duodenitis but is important in helping to exclude other lesions such as duodenal ulcer. Provided care is taken during the fibre-optic visualization of the duodenal bulb, the endoscopic appearances of moderately severe duodenitis correlate well with the histological changes seen. A diagnosis of apparent duodenitis should be confirmed by the histological criteria described. Treatment at present is similar to that of peptic ulcer, with the withdrawal of any predisposing and precipitating factors such as aspirin, alcohol and smoking. Antacids may relieve the symptoms. It is not yet known what effect these measures may have on the duodenitis as opposed to the symptoms of dyspepsia. The H2-receptor antagonist, cimetidine, should be effective in treating duodenitis but double blind clinical and endoscopic studies are required to confirm this. The place of surgery is as yet undefined. With the data at present available, it appears that duodenitis is part of the pathophysiological spectrum of the duodenal ulcer diathesis rather than a separate disease. It may represent both the production and healing phases of duodenal ulceration. In some patients the duodenal mucosa may proceed from normal to duodenitis and then to normal again without the development of frank duodenal ulceration (Figure 4). Prospective studies are required which should include a long-term clinical follow-up of a large number of patients with duodenitis accurately and specifically diagnosed by endoscopy and histopathology.     

Observation of thoracic duct morphology in portal hypertension by endoscopic ultrasound

Background:Thoracic duct dilation has been demonstrated in portal hypertension and hepatic cirrhosis by lymphangiography and laparotomy and at autopsy. It is thought to be secondary to increased hepatic lymph flow and has been described in the absence of ascites or esophageal varices. The aim of the present study was to observe thoracic duct morphology by endoscopic ultrasound in various subsets of patients with portal hypertension and hepatic cirrhosis and also to validate existing radiologic/surgical data. Methods:The thoracic duct of 33 patients with cirrhosis and portal hypertension was studied by endoscopic ultrasound. Patients were divided into four groups: 1, patients with ascites and esophageal varices; 2, esophageal varices without ascites; 3, without esophageal varices or ascites; 4, extrahepatic portal hypertension due to pancreatic malignancy. The thoracic duct diameter was also measured in 14 control subjects (group 5). Results:When the thoracic duct diameter for the five groups was compared with analysis of variance, significance was p < 0.0001; by pairwise comparison, group 1 differed from the other four groups (p < 0.05). Thoracic duct dilation (5.61 mm) was seen in group 1 patients, whereas no dilation was present in groups 2 through 4. Additionally, thoracic duct diameter in 33 portal hypertensive and/or cirrhotic patients was significantly different from that in the 14 control subjects (p = 0.003). Conclusion:The thoracic duct can be reliably identified by EUS in patients with hepatic cirrhosis and portal hypertension. Dilation of the duct is seen only in patients with hepatic cirrhosis, ascites, and esophageal varices. No thoracic duct dilation is present in extrahepatic portal hypertension. Contrary to existing radiologic/surgical data, thoracic duct dilation is not seen in all patients with hepatic cirrhosis and portal hypertension signifying advanced disease. A dilated thoracic duct by endoscopic ultrasound should be considered yet another sign of portal hypertension. (Gastrointest Endosc 1998;48:588-92.)     

Hyperplasia of Brunner glands: the spectrum of its radiographic manifestations

Radiographic features of the duodenal mucosa were analyzed in a series of 26 patients in whom the diagnosis of Brunner gland hyperplasis (BGH) had been established by endoscopic biopsies. The observed mucosal patterns could be classified into five categories: (1) focal BGH causing a solitary submucosal adenoma or a cluster of sessile polyps in the otherwise smooth duodenal bulb surface (five cases); (2) diffuse BGH manifested by a myriad of small and uniform mucosal elevations (six cases); (3) multifocal BGH producing large and well-demarcated polygonal masses (six cases); (4) BGH with concomitant acute and/or chronic duodenitis showing marked thickening and nodularity of duodenal folds (four cases); or (5) BGH with predominant erosive duodenitis, leading to ulcerations (five cases). These radiographic findings showed a good correlation with the endoscopic and histopathologic manifestations of BGH and the frequently coexistent duodenitis.     

Portal hypertension and portal hypertensive gastropathy in patients with liver cirrhosis: a haemodynamic study

BACKGROUND/AIM: The relationships between the levels of portal hypertension and the morphologic alterations of gastric mucosa in patients with liver cirrhosis--generally described as portal hypertensive gastropathy--are poorly defined. PATIENTS: In total, 62 patients with cirrhosis of different aetiologies, were examined by endoscopy and measurement of portal hypertension by hepatic venous pressure gradient. RESULTS: Portal hypertensive gastropathy was observed in 49 cases; six patients showed gastric antral vascular ectasia always associated with gastric lesions described as severe portal hypertensive gastropathy with different localizations. Hepatic venous pressure gradient showed severe portal hypertension in 37 cases, and averaged 17.7 +/- 4.3 mmHg. It was much higher in patients with severe lesions (p=0.0004). Hepatic venous pressure gradient in patients with endoscopic signs of isolated antral gastropathy was lower (p=0.04) than in those with isolated lesions in body-fundus. No relationship was found between hepatic function, as assessed by the Child-Pugh score, and portal hypertensive gastropathy. CONCLUSIONS: The present data suggest that the severity of portal hypertensive gastropathy is related to portal hypertension, but portal hypertension is not the sole determinant of the occurrence of endoscopic abnormalities of gastric mucosa. The derangement of liver function does not appear to play any role in the occurrence of portal hypertensive gastropathy.     

Prevalence of portal hypertensive duodenopathy in cirrhosis: clinical and haemodynamic features

OBJECTIVES: To estimate the prevalence of portal hypertensive duodenopathy (PHD) in patients with cirrhosis and portal hypertension, and to evaluate its relationship with clinical and haemodynamic parameters. PATIENTS AND METHODS: Endoscopy reports and clinical history of 549 consecutive patients with cirrhosis and portal hypertension were evaluated retrospectively. A diagnosis of PHD was obtained in those patients with a congestive vascular pattern of the duodenum. RESULTS: PHD was found in 46 patients (8.4%). Previous endoscopic band ligation and coexistence of severe gastropathy were significantly more frequent in PHD group. Systemic and hepatic haemodynamic evaluations were performed in 20 patients with PHD and 160 without PHD: the mean hepatic venous pressure gradient was higher in those cases with PHD (22.5 (5.4) vs. 19.8 (5.5) mmHg, P=0.045). Hypertensive colopathy was found in seven out of the 10 patients with PHD and a colonoscopic evaluation. In five of six patients PHD disappeared after liver transplant. CONCLUSIONS: PHD is an uncommon finding of portal hypertension in cirrhotic patients. It is associated with previous endoscopic band ligation, to manifestations of portal hypertension in other sites of the gastrointestinal tract and to greater values of hepatic venous pressure gradient. The clinical relevance of this syndrome remains to be determined.