Alterações duodenais na hipertensão portal da esquistossomose mansônica / Duodenal changes in portal hypertension schistosomiasis

A Hipertensão Portal (HP) na Esquistossomose Mansônica (EM) tem, como repercussão, varizes esofagogástricas, gastropatia, colopatia, sendo pouco estudadas as repercussões duodenais já evidenciadas em cirróticos. As lesões duodenais observadas na esquistossomose podem ser secundárias à HP (Duodenopatia da Hipertensão Portal - DHP) ou à agressão parasitária, duodenite, sendo importante saber a causa das lesões duodenais em pacientes esquistossomóticos a fim de realizar uma abordagem terapêutica com maior segurança e especificidade nos pacientes. Objetivos: avaliar a ocorrência e as características de alterações duodenais em pacientes com esquistossomose mansônica na forma hepatoesplênica; a frequência da DHP endoscópica e histológica; verificar a associação da DHP endoscópica com DHP histológica; presença de GHP; presença e grau das VE; presença de HDA; presença de circulação colateral; diâmetro longitudinal do baço e padrão ultrassonográfico da Fibrose Periportal (FPP). Métodos: avaliados 65 pacientes portadores de EM, estudo tipo série de casos. Preencheram critérios de inclusão 50 pacientes, com a forma hepatoesplênica, com ou sem história de HDA, exames realizados (parasitológico de fezes, marcadores virais para VHB e VHC, bioquímica, função e testes hepáticos, hemograma, ultrassonografia e endoscopia digestiva alta - EDA com biopsia de estômago e duodeno). Resultados: a média de idade de 50, 58 anos, sendo 29 (58%) do sexo feminino: apenas 8/50 (16%) tinham história de HDA. Lesões duodenais foram observadas à EDA em 47/50 (94%) dos pacientes, sendo, as mais frequentes, o eritema em 16/50 (32%), a congestão em 9/50 (18%) e associados (eritema e congestão) em 16/50 (32%). DHP à EDA foi observada em 56% (28/50) dos pacientes, 53,6% (15/28) com intensidade acentuada. DHP à histologia foi evidenciada em 62% (31) dos pacientes. Houve associação do diagnóstico endoscópico e histológico da DHP em 23/28 (82,1%) pacientes (p=0,001). Houve associação entre DHP endoscópica com diâmetro longitudinal do baço (P=0,045) e com padrão da FPP (p=0,038). Não houve associação entre DHP endoscópica com a GHP (p=0,569), com presença e grau das VE (p=0,444; p=0,350), nem com história de HDA (p=0,116). Conclusão: na EM forma hepatoesplênica, as lesões duodenais são bastante frequentes, sendo as mais encontradas o eritema, eritema e congestão, a erosão e a congestão. A DHP foi evidenciada à EDA em 56%, histologia em 62% dos casos. Houve concordância do diagnóstico endoscópico com histológico em 82,1%. Não houve significância estatística entre DHP endoscópica com GHP, VE e HDA. Houve significância entre o padrão da FPP com a presença de DHP à endoscopia e relação inversa entre o diâmetro longitudinal do baço e a presença de DHP à endoscopia.

Despite of the fact that Portal Hypertension (PH) in Mansoni Schistosomiasis can cause esophagogastric varices, gastropathy and colopathy, its duodenal repercussions, already evidenced in cirrhotic patients, have been little studied. The duodenal lesions seen in schistomiasis may be secondary to PH (Portal Hypertensive Duodenopathy -PHD) or parasitic aggression, duodenitis. It is particularly important to understand the cause of duodenal lesions in schistosomotic patients in order to approach their treatment with greater security and specificity. Aims: The present study has the following aims: to evaluate the occurrence of alterations and the type of duodenal lesions in patients suffering from the hepatosplenic form of mansoni schistosomiasis; to determine the frequency of PHD by histological and endoscopic means; and to associate the presence of PHD on endoscopy with the following: PHD on histology; the presence of portal hypertensive gastropathy (PHG); the presence and degree of esophageal varices, the presence of upper gastrointestinal bleeding; the longitudinal diameter of the spleen, and the pattern of periportal fibrosis. Patients and methods: Sixty- -five patients with mansoni schistomiasis were studied in a case series study. Fifty patients met the inclusion criteria; all of them had the hepatosplenic form, with or without a history of upper gastrointestinal bleeding, and underwent a series of investigations, namely parasitological feces examination, viral markers for HVB and HCV, ultrasound and endoscopy of the upper gastrointestinal tract with biopsy of the stomach and duodenum. Results: The mean age was 50.58 yr (range, 26-70 yr), 29 (58%) being females, and only eight of the 50 (16%) had a history of bleeding of the digestive tract. Duodenal lesions were observed on endoscopy of the upper gastrointestinal tract in 47 (94%) patients, the most frequent ones being erythema in 16 (32%), congestion in 9 (18%) and both erythema and congestion in 16 (32%). Portal hypertensive duodenopathy on endoscopy was observed in 28 (56%), and in 15 of these (53.6%) it was particularly intense. Portal hypertensive duodenopathy was evidenced on histology in 31 (62%) patients. In 23 of 28 (82.1%) patients the histological diagnosis of PHD was associated with the endoscopic diagnosis (p=0.001). Portal hypertensive duodenopathy was associated with the longitudinal diameter of the spleen (p=0.045) and with the pattern of the periportal fibrosis (p=0.038). There was no association between PHD on endoscopy with PHG (p=0.569), the presence and degree of esophageal varices (p=0.444; p=0.350) or a history of upper gastrointestinal bleeding (p=0.116). Conclusion: on the basis of the results of the present study, it is concluded that in the hepatosplenic form of mansoni schistosomiasis duodenal lesions are extremely frequent, the most common ones being erythema, erythema and congestion, erosion and congestion. Portal hypertensive duodenopathy was evidenced endoscopically in 56% and histologically in 62% of the cases, with an 82.1% agreement between the endoscopic and histological diagnoses. There was no statistically significant association between PHD on endoscopy and PHG, esophageal varices or upper gastrointestinal bleeding. There was a significant association between the pattern of periportal fibrosis in the presence of PHD on endoscopy and the inverse relationship between the longitudinal diameter of the spleen and the presence of PHD on endoscopy.

Duodenopatia hipertensiva portal: reporte de caso de complicacion poco investigada / Portal hypertensive duodenopathy: case report of a little known complication

Entre las complicaciones que puede ocasionar la hipertensión portal en el tracto gastrointestinal, también ha sido descrito el compromiso duodenal, aunque con menor frecuencia en comparación con las várices esofagogástricas o la gastropatía portal, existiendo muy pocos estudios que lo hayan investigado, siendo escaso lo que se conoce en cuanto a su diagnóstico, repercusión clínica y manejo. Presentamos el caso de un paciente con hipertensión portal por cirrosis hepática que presentó un episodio de encefalopatía hepática y hemorragia digestiva alta con hallazgos endoscópicos en duodeno compatibles con duodenopatía hipertensiva portal.

Between complications caused by portal hypertension in gastrointestinal tract, duodenal affectation has also been reported less frequently that esophagogastric varices or the portal gastropathy. However, only a few reports have investigated the duodenal lesions in patients with portal hypertension in detail. We describe a patient with cirrhotic hypertension portal and endoscopic findings in duodenum consistent with portal hypertensive duodenopathy.

Clinical Features of Duodenopathy Associated with Liver Cirrhosis / 대한소화기내시경학회지

BACKGROUND/AIMS: Congestive duodenopathy could be associated with liver cirrhosis with portal hypertension. The aims of this study were to assess the incidence of duodenopathy and to evaluate the relationship between duodenopathy and the presence of esophageal varices and portal hypertensive gastropathy in cirrhotic patients. MEHTODS: A total of 56 patients with liver cirrhosis and 481 controls were taken upper endoscopic examination. RESULTS: Prevalence of duodenopathy was significantly higher in the liver cirrhosis group (26.8%) compared to the control group (6.9%), although positive rate of Helicobacter pylori was significantly lower in the liver cirrhosis group. Duodenal erosions in cirrhotic patients were predominately located in 2nd portion of duodenum compared to contol group and tended to be circular or linear along the Kerck's ring. Vascular congestion was evident in 5 of the 10 cases. Presence of duodenal lesions had no relationship with the size and extent of esophageal varices and congestive gastropathy. CONCLUSIONS: Although histology of duodenopathy tends to show vascular congestion in patients with liver cirrhosis, few clinical markers of portal hypertension support them. Therefore, further studies including endoscopic ultrasonogram are needed to demonstrate the pathogenesis of the duodenal lesions in patients with liver cirrhosis.