ABSTRACT 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.

ABSTRACT BACKGROUND: The prevalence of Helico bacter pylori (H. pylori) infection is decreasing worldwide, but is still high in developing countries. We previously observed an H. pylori infection rate of 52% among children and adolescents with chronic non-ulcer dyspepsia. OBJECTIVE: To investigate the prevalence of H. pylori infection among asymptomatic children living in a single region and to evaluate the risk factors for this infection. DESIGN AND SETTING: Cross-sectional study in which 161 children aged 5-13 years (mean age 7.8 years), at a public school in Botucatu, state of São Paulo, southeastern Brazil, were assessed. METHOD: The children's H. pylori infection status was determined through the urea breath test and the risk factors for acquisition of the infection were determined based on a sociodemographic questionnaire. RESULTS: The overall prevalence of H. pylori infection was 20.5%: 18.7% among females and 22.2% among males. The results from the sociodemographic survey did not differ between children with and without H. pylori infection. 30.9% of the children had previous records of upper gastrointestinal symptoms, which consisted of H. pylori infection in only 26.5% of these cases. Family histories of gastritis and peptic ulcer disease were found in relation to 50% and 32.3% of the children with H. pylori infection respectively. CONCLUSION: The prevalence of H. pylori infection among asymptomatic children in southeastern Brazil is lower than that recorded among symptomatic children in the same region and similar to the prevalence of H. pylori infection observed in developed countries.

ABSTRACT 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 normal-appearing 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.

Abstract Purpose: To investigate the role of omeprazole and nitrites on the gastric mucosa of rats submitted to specific techniques to induce duodenogastric reflux. Methods: One hundred and twenty Wistar rats were divided into three groups: Group I (n=40) -gastrotomy; Group II (n=40) - duodenogastric reflux after gastrojejunoanastomosis latero-lateral (DGR); Group III (n=40) - retrograde duodenogastric reflux through the pylorus (DGR-P). The groups were divided into 4 subgroups of 10 animals, respectively treated for 16 weeks with water, omeprazole 1.6 mg / rat / day, nitrite 600 mg / kg / day and omeprazole plus nitrite simultaneously. Results: The proliferative lesions found were: squamous hyperplasia - 69.1%, adenomatous hyperplasia in the anastomosis - 29.1% and prepyloric adenomatous hyperplasia - 42.5%. Adenocarcinomas were registered in 7 animals (5.8%): one in Group I (omeprazole plus nitrite), two in Group II (omeprazole and nitrite plus omeprazole) and four in Group III (water, nitrite, omeprazole and omeprazole plus nitrite). Conclusions: The occurrence of squamous hyperplasia, adenomatous hyperplasia and adenocarcinoma increased after gastrojejunal anastomoses, which cause duodenogastric reflux. The association of omeprazole did not protect the development of proliferative lesions and cancer induced by duodenogastric reflux in rats.

PURPOSE: To evaluate the usefulness of the Glasgow Prognostic Score (GPS) in patients with esophageal carcinoma (EC).METHODS: A total of 50 patients with EC were analyzed for GPS, nutritional and clinicopathologic parameters. Patients with CRP ≤ 1.0mg/L and albumin ≥ 3.5mg/L were considered as GPS=0. Patients with only CRP increased or albumin decreased were classified as GPS=1 and patients with CRP > 1.0mg/L and albumin < 3.5mg/L were considered as GPS=2.RESULTS: GPS of 0, 1 and 2 were observed in seven, 23 and 20 patients, respectively. A significant inverse relationship was observed between GPS scores and the survival rate. The survival rate was greatest in patients with GPS= 0 and significantly higher than those from patients with GPS=1 and GPS=2. Minimum 12-month survival was observed in 71% patients with GPS=0 and in 30% patients with GPS=1. None of the patients with GPS=2 survived for 12 months. A significant relationship between CRP or albumin individually and the survival rate was observed. No significant relationship among nutritional, clinic pathological parameters and survival was found.CONCLUSION:Glasgow Prognostic Score is an useful tool to predict survival in patients with esophageal carcinoma.

PURPOSE: To analyze the epidemiological features of patients with esophageal cancer according to the histopathological types: squamous cell carcinoma or adenocarcinoma. METHODS: A total of 100 patients with esophageal cancer, being 50 squamous cell carcinomas and 50 adenocarcinomas were analyzed for demographics, nutritional factors, lifestyle habits, benign pathological conditions associated, like Barrett's esophagus and megaesophagus, tumor stage and survival rates. The nutritional factors evaluated included body mass index, percent weight loss, hemoglobin and albumin serum levels. RESULTS: Esophageal cancer occurred more often in men over 50 years-old in both histological groups. No significant differences on age and gender were found between the histological groups. Squamous cell carcinoma was significantly more frequent in blacks than adenocarcinoma. Alcohol consumption and smoking were significantly associated with squamous cell carcinoma. Higher values of body mass index were seen in patients with adenocarcinoma. Barrett's esophagus was found in nine patients (18%) with adenocarcinoma, and megaesophagus in two patients (4%) with squamous cell carcinoma. The majority of patients were on stages III and IV in both histological groups. The mean survival rates were 7.7 ± 9.5 months for patients with squamous cell carcinoma and 8.0 ± 10.9 months for patients with adenocarcinoma. No significant differences on tumor stage and survival rates were detected between the histological groups. CONCLUSION: Epidemiological features are distinct for the histopathological types of esophageal cancer. Squamous cell carcinoma is associated with black race, alcohol and smoking, while adenocarcinoma is related to higher body mass index, white race and Barrett's esophagus.

PURPOSE:To assess whether late introduction of a specific COX-2 inhibitor (Meloxicam) can treat and/or prevent the progression of tumors in the stomach of rats submitted to duodenogastric reflux. METHODS: Seventy five male Wistar rats, weighing 150 grams, were submitted to the induction of duodenogastric reflux through the pylorus. At 36 weeks of follow-up were established three experimental groups: DGR36 sacrificed immediately, DGR54 and DGR54MLX both sacrificed at 54th week of follow-up . The animals of the latter group were fed with a rat chow premixed with Meloxicam (2.0 mg/ kg feed; 0.3 mg / kg bw / day) and the other two with standard rat chow. The lesions found in the pyloric mucosa and gastrojejunal anastomosis were analyzed macroscopically and histologically. For statistical analysis was adjusted a generalized linear model assuming a binomial distribution with LOGIT link function. RESULTS: No significant differences were found when comparing the incidences of benign tumor lesions (Adenomatous Hyperplasia), p=0.4915, or malignant (Mucinous Adenocarcinoma), p=0.2731, among groups. CONCLUSION: Late introduction of specific COX-2 inhibitor (Meloxicam) did not treat and was not able to prevent the progression of tumoral lesions induced by duodenogastric reflux in the rat stomachs.

PURPOSE: To analyze the clinicopathological features and outcome of patients with pathologically proven superficial squamous cell carcinoma of the esophagus. METHODS: A total of 234 consecutive cases of esophageal carcinoma in a 15-year period were reviewed. RESULTS: Superficial esophageal cancer was found in five patients (2.1%). They were four men and one woman and the mean age was 52.5 years. Smoking and alcohol were the main risk factors. Achalasia due to Chagas disease occurred in one patient and a second primary tumor developed in the larynx in another patient. Four patients underwent esophagectomy and one patient received chemoradiotherapy. The histopathologic diagnosis was of squamous cell carcinoma in all cases. Intramucosal tumor (Tis) was identified in three cases and superficially invasive carcinoma in two cases. Four patients are free of disease with survival times of two, four, six and nine years. The patient who developed laryngeal cancer died six years after esophagectomy. CONCLUSION: Long-term survival in patients with esophageal cancer is related to early diagnosis. Therefore, a less aggressive surgical approach, such as endoscopic resection, may be a good option for these patients, if depth of tumor invasion can be accurately predicted by the new imaging tools.

OBJETIVO: Avaliar as alterações histológicas e biomecânicas do diclofenaco de sódio na mucosa intestinal do rato e a associação com o uso de Imipenem. MÉTODOS: Foram estudados 240 ratos Wistar distribuídos aleatoriamente em quatro grupos experimentais: GI: 60 ratos tratados com injeção IM de soro fisiológico 0,9%; GII: 60 ratos tratados com injeção IM de diclofenaco de sódio na dose de 6mg/kg de peso por 4 dias; GIII: 60 ratos tratados com injeção IM de Imipenem na dose de 30 mg/kg de peso por 4 dias; GIV: 60 ratos tratados com injeção IM de soro fisiológico e diclofenaco de sódio nas doses acima. Em cada grupo os animais foram posteriormente divididos em 4 momentos de 15 animais em cada um para sacrifício, respectivamente, no 4º, 7º, 14º e 21º dias após o início do tratamento. As alterações da cavidade abdominal, assim como as características histológicas e de força de ruptura do intestino delgado foram analisadas em cada momento, em cada grupo. RESULTADOS: Não foram encontradas alterações histológicas e biomecânicas nos animais do Grupo I nesse estudo. Lesões ulceradas na mucosa do intestino delgado foram observadas nos animais tratados com diclofenaco de sódio, assim como diminuição da força de ruptura. As lesões ulceradas encontradas foram prevenidas pelo uso de Imipenem. CONCLUSÃO: O diclofenaco de sódio induz lesões ulceradas na mucosa intestinal do rato que podem ser prevenidas pelo uso de Imipenem.

PURPOSE: To study diclofenac sodium induced histological and mechanical alterations and their prevention with Imipenem in rat intestine. METHODS: Male Wistar rats (n=240) were randomly assigned to four experimental groups: GI: n=60 treated with 0.9% saline IM; GII: n=60 treated with 6mg/kg body weight diclofenac sodium IM for four days; GIII: n=60 treated with 30mg/kg body weight Imipenem IM for four days, and GIV n=60 treated with diclofenac sodium plus Imipenem at the above doses IM for 4 days. Each group was further divided into 4 subgroups of 15 rats each and sacrificed at 4, 7, 14, and 21 days of follow-up, respectively. Abdominal cavity macroscopy and histology, and small bowel breaking strength were analyzed at each sacrifice moment. RESULTS: There were no histological or mechanical alterations in normal control rats throughout the study. Ulcerated lesions in intestinal mucosa were observed and breaking strength decreased in all diclofenac sodium treated rats. Ulcerated lesions in intestinal mucosa were prevented by Imipenem in all rats. CONCLUSION: Diclofenac sodium induced ulcerated lesions in rat intestinal mucosa can be prevented by Imipenem treatment.

OBJETIVO: Investigar os efeitos do refluxo duodenogástrico e sua interação com o cancerígeno químico N-methil-N'-nitro-nitrosoguanidina (MNNG) no desenvolvimento de lesões no estômago glandular, anastomose gastrojejunal e no estômago escamoso do rato. MÉTODOS: Foram utilizados 80 ratos Wistar divididos em 4 grupos: G1: MNNG + Refluxo, G2: Refluxo, G3: MNNG e G 4: Gastrostomia. O MNNG foi oferecido na água de beber (100mg/ml) por 12 semanas. A seguir foi feita anastomose gastrojejunal na porção glandular do estômago nos grupos G1 e G2, com secção da alça aferente junto ao estômago e sutura de ambos os cotos para permitir o refluxo do conteúdo duodenal para o estômago pelo piloro. Os animais foram sacrificados 18 e 36 semanas após a cirurgia. As lesões identificadas foram submetidas à exame histopatológico. RESULTADOS: O refluxo duodenogástrico levou ao desenvolvimento de lesões proliferativas no estômago glandular e na porção escamosa. No antro, hiperplasia adenomatosa (HA) foi diagnosticada em 20 e 50% dos animais (G2) na 18ª e 36ª semanas, respectivamente. Na anastomose gastrojejunal 85% dos animais (G2) apresentaram HA e 60% apresentaram hiperplasia escamosa no estômago escamoso, na 36ª semana. No grupo MNNG+Refluxo foram identificados na 18ª semana, 30% adenocarcinomas no antro e 45% carcinomas escamosos. A freqüência destas lesões malignas aumentou, respectivamente, para 50% e 65% na 36ª semana. CONCLUSÃO: O refluxo duodenogástrico potencializou o desenvolvimento de lesões proliferativas benignas e malignas no estômago glandular e em sua porção escamosa, no rato.

PURPOSE: To investigate the combined effects of reflux of duodenal contents through the pylorus and treatment with N-methyl-N'-nitro-nitrosoguanidine (MNNG) on the development of lesions in the glandular stomach, at the gastrojejunal anastomosis and in the forestomach of rats. METHODS: Eighty Male Wistar rats were divided into 4 groups: G1: MNNG + Reflux, G2: Reflux, G3: MNNG and G4: Gastrostomy. MNNG was given in the drinking water (100 mg/ml) for 12 weeks and then two groups (G1 and G2) were submitted to a gastrojejunal anastomosis followed by section of the afferent loop and suture of both stumps to allow reflux of duodenal contents through the pylorus. The animals were sacrificed 18 and 36 weeks after surgery. The lesions obtained in the antral mucosa, at the gastrojejunal anastomosis and in the forestomach were analysed histologically. RESULTS: Duodenal reflux induced proliferative lesions at both glandular and squamous mucosa of the stomach. In the antrum, adenomatous hyperplasia (AH) was observed in 20% and 50% of the animals at the 18th and 36th weeks respectively. Aditionally 85% of the animals presented AH at the gastrojejunal anastomosis and 60% developed squamous hyperplasia at the squamous portion of the stomach. MNNG treatment plus duodenal reflux enhanced the development of malignant tumors at both glandular and squamous mucosa, since there were 30% of antral adenocarcinomas and 45% of squamous carcinomas at the 18th week and the frequency of these malignant tumors rose to 50% in the antrum and 65% in the squamous mucosa at the 36th week. CONCLUSION: The reflux of duodenal contents through the pylorus enhanced the development of proliferative lesions, benign and malignant, in the glandular stomach and in the forestomach of rats.

Investigou-se a prevalência de infecções parasitárias do apêndice cecal e suas relações com a apendicite. Dos 1.600 apêndices estudados 24 (1,5%) apresentaram infecção parasitária. Enterobius vermicularis foi encontrado em 23 casos (95,8%) e Taenia sp em apenas um (4,2%). Dezesseis pacientes (66,7%) eram menores de 10 anos; 15 eram masculinos e 9 femininos. A análise histopatológica demonstrou inflamação aguda supurativa em 12 casos (50%), eosinofilia em 13 (54,2%) e hiperplasia linfóide em 10 (41,7%). Complicações como peritonite ocorreram em 11 e gangrena em 3 casos. As infecções parasitárias do apêndice são causa pouco freqüente de apendicite aguda em crianças e adolescentes.

From 1,600 surgically removed appendices, 24 (1.5%) were found to have helminths. Enterobius vermicularis was observed in 23 of the 24 specimens (95.8%) and Taenia sp was detected in only 1 (4.2%) case. Sixteen patients (66.7%) were less than 10 year-old; 15 patients were male and 9 female. Pathologic analysis disclosed acute neutrophilic inflammation in 12 cases and lymphoid hyperplasia in 10 of the 24 appendices. Gangrenous appendicitis was diagnosed in 3 cases and peritonitis was found in 11 of the 24 infested appendices. Parasitic infection of the appendix is an uncommon cause of acute appendicitis in children and adolescents.

RACIONAL: O carcinoma de pequenas células primário do esôfago é tumor raro, agressivo, morfologicamente indistinguível de seu correspondente no pulmão. OBJETIVO: Apresentar os aspectos clínico-patológicos de dois pacientes com carcinoma de pequenas células do esôfago. RELATO DE CASOS: Paciente 1: masculino, 56 anos com disfagia progressiva há seis meses e emagrecimento, com antecedentes de tabagismo e etilismo. A endoscopia mostrou lesão vegetante dos 30 aos 40 cm da arcada dentária superior e o exame anatomopatológico, diagnosticou neoplasia maligna indiferenciada de pequenas células com marcadores imunoistoquímicos positivos para cromogranina e sinaptofisina, caracterizando a linhagem neuroendócrina da neoplasia. Após dois ciclos de quimioterapia (cisplatina e etoposide) associada à radioterapia ele apresentou remissão da disfagia. Paciente 2: masculino, 55 anos, com queixas de pirose, disfagia, rouquidão há seis meses, com emagrecimento de 10 kg no período. A endoscopia mostrou lesão vegetante à 30 cm da arcada dentária superior, obstrutiva. O exame anatomopatológico revelou carcinoma de pequenas células, com os mesmos marcadores imunoistoquímicos positivos para linhagem neuroendócrina. Tomografia computadorizada mostrou metástases hepáticas. Frente ao estadio avançado da doença optou-se pela indicação de gastrostomia. O paciente desenvolveu pneumonia e faleceu dois meses após o diagnóstico. CONCLUSÃO: A evolução dos portadores de carcinoma de pequenas células do esôfago depende do estadiamento da doença e apesar da alta agressividade biológica, este tumor apresenta boa resposta à quimioterapia associada à radioterapia.

BACKGOUND: Small-cell Carcinoma of the Esophagus is a rare tumor, aggressive, and morphologically indistinguishable from its correspondent well-known tumor in the lung. AIM: To present the clinical-pathological aspects of two patients presenting small-cell carcinoma of the esophagus. CASES REPORT: Patient 1- a 55-year-old man presenting progressive dysphagia for 6 months, weight loss, and previous smoking and alcohol abuse history. Endoscopy showed a polypoid lesion, located 30 to 40 cm from the superior arcade. Anatomopathological analysis revealed undifferentiated small-cell carcinoma and positive immunohistochemical staining for neuroendocrine markers, including chromogranin and synaptophysin. The patient presented dysphagia remission after two cycles of chemotherapy (cisplatin and etoposide) and radiotherapy. Patient 2 - a 55-year-old man complaining pirosis, dysphagia, and hoarseness for 6 months, associated to a 10 kg weight loss. Endoscopy showed an obstructive polypoid lesion located 30 cm from the superior dental arcade. Anatomopathological study revealed small-cell carcinoma and positive immunohistochemical staining for neuroendocrine tumor. Computed tomography showed liver metastases. Considering the advanced stage of the tumor, gastrostomy was performed. The patient developed pneumonia and died within two months. CONCLUSION: The evolution of patients presenting small-cell carcinoma of the esophagus depends on the tumor staging. Despite of its aggressiveness, the respective tumor responds positively to combined chemo-radiotherapy.

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.

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.

RACIONAL: O carcinoma basalóide escamoso ocorre com maior freqüência no trato aerodigestivo superior e raramente acomete o esôfago. OBJETIVO: Apresentar os aspectos clínico-patológicos e os atributos imunoistoquímicos de um paciente com carcinoma basalóide escamoso do esôfago. RELATO DO CASO: Dos 134 pacientes com câncer do esôfago atendidos no Hospital Universitário de Botucatu-Unesp, São Paulo, de 1990 a 1999, somente um paciente (0,74%) apresentou carcinoma basalóide escamoso do esôfago. Tratava-se de paciente masculino, 41 anos, branco, lavrador com disfagia, regurgitação e emagrecimento há três meses. Referia tabagismo e etilismo há muitos anos. O esofagograma e o exame endoscópico revelaram lesão vegetante no terço distal do esôfago. A biópsia demonstrou neoplasia intraepitelial de alto grau associada a blocos de células basalóides que infiltravam o cório da mucosa, caracterizando o carcinoma basalóide escamoso. Os marcadores imunoistoquímicos foram positivos para o antígeno carcinoembriônico e para citoceratinas de alto peso molecular. A tomografia computadorizada revelou múltiplas metástases nos pulmões, fígado, e nódulos linfáticos regionais, documentando a fase avançada de evolução da doença. O tratamento consistiu apenas na realização de gastrostomia. O paciente apresentou queda acentuada do estado geral e evoluiu para óbito com quadro de melena quatro meses após o diagnóstico. CONCLUSÃO: O carcinoma basalóide escamoso é uma forma rara e agressiva de câncer do esôfago e o prognóstico depende do estadiamento da lesão e das condições clínicas do paciente no momento do diagnóstico.

BACKGROUND: Basaloid squamous carcinoma is more frequently found in the upper aerodigestive tract, being rarely found in the esophagus. AIM: To present the pathological and clinical aspects, as well as immunhistochemical attributes of a basaloid squamous carcinoma of the esophagus patient. CASE REPORT: Of a total of 134 esophagus cancer patients in the Hospital Universitário de Botucatu-Unesp, in São Paulo, from 1990 through 1999, only one patient (0,74%), presented the basaloid squamous carcinoma of the esophagus. This patient, a 41 year-old Caucasian male farmer, presented dysfagia, regurgitation and weight loss for the last three months, being a smoker and alcoholic for many years. Endoscopy and esophagram revealed a vegetative lesion in the distal region of the esophagus. Biopsy showed a high-grade intra-epithelial neoplasm associated with basaloid cells infiltrating the corian mucosa, characteristic of the squamous basaloid carcinoma. Immunohistochemical markers were positive for carcinoembrionary antigen and high molecular weight citokeratins. Computerized tomography revealed multiple metastasis in the lungs, liver and regional lymphatic nodules, all evidence of an advanced evolution of the disease. Treatment consisted of gastrostomy. The patient presented an accentuated fall pertaining it's general state and died with a state of melena four months after diagnosis. CONCLUSION: The basaloid squamous carcinoma is a rare and aggressive form of esophagus cancer and the prognosis depends in the state at which the lesion is and in the clinical conditions of the patient at the time of diagnosis.