Peutz-Jeghers syndrome: an unusual autopsy finding in pregnancy

Peutz-Jeghers syndrome (PJS) is a rare autosomal dominant polyposis entity that often remains undiagnosed. The major problems associated with PJS are acute complications due to (i) polyp-related intestinal obstruction, (ii) intussusception, and (iii) the risk of cancer in the long-term. We report the case of a 32-year-old female who presented at the emergency room with signs of acute abdomen and died during the clinical workup. She had a one-month history of nausea, vomiting, and diarrhea and was pregnant at about 30 weeks. There was no contributing past history except for undergoing small bowel resection in infancy. The postmortem examination revealed multiple arborizing polyps throughout the gastrointestinal tract, chiefly in the small bowel. Intestinal obstruction was found at the proximal jejunum with necrosis, perforation, and peritonitis. Histologically, the polyps were composed of tree branch-like bundles of smooth muscle covered by normalappearing glandular epithelium, confirming the diagnosis of hamartomatous polyps. No malignant or premalignant lesions were detected in the gastrointestinal tract or other organs. This case was an opportunity to analyze the natural history and the pathological features of the Peutz-Jeghers syndrome in an adult and to investigate the presence of neoplastic lesions associated with this condition

Necrotizing amebic colitis in an elder patient: an unexpected autopsy finding

Necrotizing amebic colitis is an uncommon amebiasis complication associated with high mortality. We present a case of necrotizing amebic colitis in an old patient whose diagnosis was revealed at postmortem examination. An 81-year-old man died at home without medical attention. The postmortem examination revealed ulcers involving the entire colon and intestinal perforation. The ulcers were large, geographic, and necrotizing, extending from the cecum to the rectum. The histological examination disclosed the infectious etiology by showing amebic trophozoites at the base of the ulcers. No extra-intestinal lesions were found. No information about previous episodes of dysentery or travel could be obtained. The potential role of aging or drug-causing immunosuppression and the evolution of chronic and latent intestinal infection to a severe and invasive form of amebiasis is discussed. This case reinforces the value of postmortem examination for diagnosing diseases not clinically identified

Lesões proliferativas gástricas induzidas pelo refluxo duodenogástrico em ratos

PURPOSE: To analyze mucosal proliferation and its characteristics, through specific models of duodenogastric reflux, in the stomach of Wistar rats. METHODS: Seventy-five healthy and adult male rats were divided into three groups: group I - control (n = 25 animals), submitted to gastrotomy of the posterior wall of the glandular stomach; group II - DGR (n = 25 animals), submitted to duodenogastric reflux through latero-lateral gastrojejunal anastomosis in the posterior wall of the glandular stomach and group III - DGR-P (n = 25 animals), submitted to duodenogastric reflux through the pylorus following the same procedure of group II, sectioning and closing the afferent loop. The animals were observed during 36 weeks and subsequently the mucosal lesions were analyzed, with macroscopic and microscopic examination of the prepyloric, the gastrojejunostomy and the squamous area of the stomach. RESULTS: Group I did not present any kind of lesion. Macroscopic lesions of the prepyloric area in groups II and III were 0% and 20%, respectively. Macroscopic lesions of the gastrojejunal stoma in groups II and III were 36% and 88%, respectively, and 12% and 28%, respectively, in the squamous area. Microscopically, adenomatous hyperplasia (AH), squamous hyperplasia (SH) and adenocarcinoma (AC) were diagnosed. The occurrence of AH at the prepyloric area in groups II and III was 0% and 40%, respectively, and in the gastrojejunal stoma, 40% and 72%, respectively. The occurrence of SH in the squamous area in groups II and III was 12% and 20%, respectively, without statistical differences between the groups. AC was found only in three animals of groups III (12%). CONCLUSIONS: The duodenogastric reflux in this experimental model caused high frequency of proliferative lesions of the gastrojejunal stoma and in the prepyloric area, while adenocarcinoma was a rare occurrence.OBJETIVO: Avaliar as lesões proliferativas que se desenvolvem na mucosa gástrica de ratos Wistar após modelo específico de refluxo duodeno-gástrico. MÉTODOS: Foram utilizados 75 ratos adultos machos divididos em três grupos experimentais: o grupo I (controle) submetido a gastrotomia na parede posterior do estômago glandular (25 animais); o grupo II (RDG), foi submetido a gastrojejunoanastomose látero-lateral na parede posterior do estômago glandular (25 animais) e o grupo III (RDG-P) submetido a gastrojejunoanastomose látero-lateral na parede posterior do estômago glandular, com secção e fechamento da alça (25 animais). Os animais foram observados durante 36 semanas, após o que foram realizados estudos macroscópicos e microscópicos da anastomose gastrojejunal, da região pré-pilórica e região escamosa do estômago. RESULTADOS: Os animais do Grupo I não apresentaram nenhum tipo de lesão. No grupo II observou-se 40% de lesões do tipo hiperplasia adenomatosa na anastomose e 12% de hiperplasia escamosa. No grupo III obteve-se 40% de hiperplasia adenomatosa na mucosa pré-pilórica, 72 % de hiperplasia adenomatosa na mucosa da anastomose, 20% de hiperplasia escamosa e 12 % de adenocarcinoma. CONCLUSÕES: O refluxo duodeno-gástrico induz a alta freqüência de lesões proliferativas na mucosa adjacente à anastomose gastrojejunal ou na mucosa pré-pilórica e o adenocarcinoma é um evento raro neste modelo experimental.20721

Esôfago de Barrett e displasia: critérios diagnósticos Barret's esophagus and dysplasia: diagnostic criteria

A presente revisão focaliza aspectos conceituais e os principais problemas diagnósticos referentes ao esôfago de Barrett e à displasia. O esôfago de Barrett resulta de complicação da doença do refluxo gastroesofágico de longa duração. É identificado endoscopicamente pela presença de mucosa glandular no esôfago tubular acima da junção esofagogástrica. Histologicamente, é caracterizado pela substituição do epitélio estratificado pavimentoso por epitélio colunar especializado com células caliciformes, expresso como metaplasia intestinal. A importância biológica do esôfago de Barrett é o risco de progressão para câncer. A displasia é o principal marcador biológico preditivo de evolução para adenocarcinoma. Identificar e graduar a displasia constitui importante questão na prática diagnóstica. O diagnóstico patológico do esôfago de Barrett deve conter informações sobre a investigação de displasia. O principal diagnóstico diferencial da displasia é feito em relação a reatividade e regeneração epitelial no contexto de inflamação da mucosa. Como a variabilidade de interpretação é um dos principais problemas no diagnóstico da displasia, os casos de esôfago de Barrett devem ser enviados à consulta para segunda opinião diagnóstica. O exame anatomopatológico é fundamental para definir o diagnóstico de esôfago de Barrett e para rastrear a displasia, que é o principal marcador de risco para câncer nesta entidade.<br>This review focuses on conceptual aspects of Barrett's esophagus and Barrett's related dysplasia and highlights current diagnostic problems on the interpretation of these lesions. Barrett's esophagus results from longstanding gastroesophageal reflux. Endoscopically it is recognized by the presence of glandular mucosa in the tubular esophagus above the esophagogastric junction at variable lenghts. Histologically it is characterized by the presence of specialized columnar epithelium with globet cells expressed as intestinal metaplasia. The importance of Barret's esophagus is the risk for developing adenocarcinoma. Dysplasia is the main biomarker for the progression to adenocarcinoma. The pathologic diagnosis of Barrett's esophagus should contain information on the presence and grade of dysplasia. Distinguishing betweeen dysplasia and regenerative changes in the face of active inflammation may be difficult. Correct interpretation and grading of dysplasia is an important goal for pathologists, since it is a major factor on follow-up and treatment of the patients

Does troncular vagotomy modify the proliferative gastric lesions induced in rats by duodenogastric reflux<A HREF="#back2"></A>?<A HREF="#back2"></A> A vagotomia troncular modifica as lesões proliferativas gástricas induzidas em ratos pelo refluxo duodenogástrico?

PURPOSE: to investigate if combining VT to DGR through the pylorus can modulate the biological behavior of PL induced by DGR and to verify if TV alone can induce morphologic lesions in the gastric mucosa. METHODS: 62 male Wistar rats were assigned to four groups: 1 - Control (CT) gastrotomy; 2 - Troncular Vagotomy (TV) plus gastrotomy; 3 - Duodenogastric reflux through the pylorus (R) and 4 - Troncular vagotomy plus DGR (RTV). The animals were killed at the 54 week of the experiment. DGR was obtained by anastomosing a proximal jejunal loop to the anterior gastric wall. TV was performed through isolation and division of the vagal trunks. Gastrotomy consisted of 1 cm incision at the anterior gastric wall. PL were analyzed gross and histologically in the antral mucosa, at the gastrojejunal stoma and at the squamous portion of the gastric mucosa. RESULTS: Groups R and RTV developed exophytic lesions in the antral mucosa (R=90.9%; RTV=100%) and at the gastrojejunal stoma (R=54.54%; RTV=63.63%). Histologically they consisted of proliferative benign lesions, without cellular atypias, diagnosed as adenomatous hyperplasia. Both groups exposed to DGR presented squamous hyperplasia at the squamous portion of the gastric mucosa (R= 54.5%; RTV= 45.4%). TV, alone, did not induce gross or histological alterations in the gastric mucosa. TV did note change the morphologic pattern of the proliferative lesions induced by DGR. CONCLUSIONS: DGR induces the development of PL in the pyloric mucosa and at the gastrojejunal stoma. TV does not change the morphologic pattern of the proliferative lesions induced by DGR. TV alone is not able to induce morphologic lesions in the gastric mucosa.<br>OBJETIVO: investigar se a adição da VT ao RDG através do piloro, interfere no comportamento biológico das LP induzidas pelo RDG e observar se a VT isoladamente leva ao desenvolvimento de lesões morfológicas na mucosa gástrica. MÉTODOS: Foram utilizados 62 ratos Wistar machos, distribuídos em quatro grupos experimentais: 1- Controle (CT) Gastrotomia; 2- Vagotomia Troncular + gastrotomia (VT); 3-Refluxo duodeno-gástrico (R) e 4- RDG através do piloro e VT (RTV). Os animais foram sacrificados na 54ª semana do experimento. O RDG foi obtido através de anastomose do jejuno proximal com a parede gástrica anterior. A vagotomia troncular foi realizada através da dissecção e divisão dos troncos vagais. A gastrotomia consistiu de secção e síntese de um cm na parede gástrica anterior. As LP foram analisadas macroscopicamente e histologicamente na mucosa gástrica, na anastomose gastrojejunal e no estômago escamoso. RESULTADOS: Os grupos R e RVT desenvolveram lesões exofíticas na mucosa do antro gástrico (R=90,9% e RVT=100%) e na anastomose gastrojejunal (R=54,5% e RVT=63,6%) que se caracterizaram no exame histológico por lesões proliferativas epiteliais benignas, sem atipias celulares, diagnosticadas como hiperplasia adenomatosa. Na região do estômago escamoso, ambos os grupos expostos ao RDG apresentaram hiperplasia escamosa (R= 54,5% e RVT= 45,4%). A VT não modificou o padrão histopatológico das LP induzidas pelo RDG. Os grupos VT e CT não apresentaram alterações macroscópicas ou histológicas significativas. CONCLUSÕES: o RDG induz o desenvolvimento de lesões proliferativas (LP) benignas na mucosa do antro gástrico e na anastomose gastrojejunal. A VT isoladamente não induz alterações proliferativas na mucosa gástrica e não modifica as características morfológicas das LP induzidas pelo RDG através do piloro