Abscesso gástrico após biópsia endoscópica: relato de caso e revisão da literatura / Gastric abscess after endoscopic biopsy: case report and literature review

Paciente apresenta dispepsia, vômitos e dor epigástrica uma semana após EDA com biópsia. Exames revelaram elevação de marcadores inflamatórios e tomografia contrastada do abdome, um espessamento parietal circunferencial do corpo gástrico e da região antropilórica. Nova EDA mostrou lesão na grande curvatura do antro, no local onde foi realizada a biópsia endoscópica, com drenagem de secreção purulenta e enantema, condizente com diagnóstico de abscesso gástrico. Realizados antibioticoterapia e drenagem endoscópica com sinais clínicos de melhora. Terceira EDA evidenciou resolução da lesão. Paciente recebeu alta hospitalar em uso de amoxicilina e clavulanato por 10 dias.O abscesso gástrico é uma rara infecção da submucosa e da muscular própria e sua patogênese envolve foco de injúria à mucosa gástrica por trauma penetrante, disseminação de infecções contíguas, fontes de infecção ou casos idiopáticos. Desconforto epigástrico é o sintoma predominante, associado ou não a náusea, vômitos, febre e calafrios. Alterações laboratoriais incluem leucocitose com desvio à esquerda e elevação de marcadores inflamatórios. A propedêutica é realizada por meio de EDA, TC de abdome e ecoendoscopia. A cultura da drenagem purulenta é útil no diagnóstico e no tratamento, sendo o Streptococcus o patógeno mais comum. Antibioticoterapia, associada à drenagem percutânea ou endoscópica é o pilar do tratamento. Cirurgia está reservada para dúvidas diagnóstica, falha de tratamentos menos invasivos ou peritonite.Devido à raridade dos abscessos gástricos e à ausência de marcadores específicos, o diagnóstico requer um alto grau de suspeição e deve ser confirmado por exames endoscópicos e de imagem. É importante também, incluir essa condição nos diagnósticos diferenciais dos tumores intramurais gástricos.

Patient presents dyspepsia, vomiting and epigastric pain one week after upper digestive endoscopy (UDE) with biopsy. Tests revealed elevation of inflammatory markers and contrasted tomography of the abdomen, a circumferential parietal thickening of the gastric body and the anthropiloric region. New UDE showed lesion in the great curvature of the antrum, where the endoscopic biopsy was performed, with purulent secretion and enanthema, consistent with the diagnosis of gastric abscess. Antibiotic therapy and endoscopic drainage evidenced clinical signs of improvement. Third UDE showed resolution of the lesion. Patient was discharged using amoxicillin and clavulanate for 10 days.Gastric abscess is a rare infection of the submucosa and the muscle layer. The pathogenesis involves a focus of injury to the gastric mucosa by penetrating trauma, dissemination of contiguous infections, sources of infection or idiopathic cases. Epigastric discomfort is the predominant symptom, associated with nausea, vomiting and fever. Laboratory changes include leukocytosis with left shift and elevation of inflammatory markers. Propaedeutics is performed by means of UDE, abdominal CT and echoendoscopy. The culture of purulent drainage is useful in diagnosis and treatment, Streptococcus is the most common pathogen. Antibiotic therapy and percutaneous or endoscopic drainage is the mainstay of treatment. Surgery is reserved for diagnostic doubts, failure of less invasive treatments or peritonitis.Due to the rarity of gastric abscesses and the absence of specific markers, the diagnosis requires a high degree of suspicion and must be confirmed by endoscopic and imaging testes. It is also important to include this condition in the differential diagnoses of gastric intramural tumors.

Isolation of Helicobacter pylori from the intestinal mucosa of patients with Crohn's disease.

BACKGROUND: Helicobacter species are associated with inflammatory bowel disease in rodents and in nonhuman primates. Therefore, we prospectively investigated the presence of Helicobacter species in the intestinal mucosa of patients with and without Crohn's disease by culture and polymerase chain reaction (PCR) assays. MATERIALS AND METHODS: Mucosal fragments were obtained from the ileum, different colon regions, and rectum of 43 patients with Crohn's disease and of 74 patients without inflammatory bowel disease. RESULTS: Helicobacter pylori strains, identified by 16S rRNA gene sequencing, were more frequently isolated and PCR-detected in the intestinal mucosa of patients with ulcerative colitis-like Crohn's disease than in intestinal mucosa of the control group. Otherwise, anti-H. pylori immunoglobulin G levels were significantly lower in fibrostenosing and fistulating Crohn's disease subgroups. No other Helicobacter species were found in the intestinal mucosa of the patients. CONCLUSIONS: Although our results suggest an association between the presence of H. pylori in the intestine and ulcerative colitis-like phenotype of Crohn's disease, H. pylori infection in the actual causality of Crohn's disease is still to be determined.

Helicobacter species in the intestinal mucosa of patients with ulcerative colitis.

In a search for Helicobacter species in the intestinal mucosae of 42 patients with ulcerative colitis (UC) and 74 without UC, only H. pylori was found. Although the bacterium was detected in UC patients by culture (7.1%) and nested PCR (19.0%), its presence was not associated with the disease (P = 0.13).

Factors associated with treatment failure of Helicobacter pylori infection in a developing country.

BACKGROUND: Although no regimen can eradicate in 100% of patients, factors that may affect the eradication rates have been poorly studied. GOAL: To evaluate factors associated with treatment failure. STUDY: One hundred patients were treated with pantoprazole plus clarithromycin and furazolidone for eradication. Clarithromycin and furazolidone resistance was evaluated by the agar dilution method. Point mutations in 23S rRNA genes related to clarithromycin resistance were investigated by polymerase chain reaction and restriction length fragment polymorphism and A by polymerase chain reaction. The data were analyzed by logistic regression. RESULTS: eradication occurred in 85 of 97 patients who completed the treatment (87.6%; 95% CI = 79.0-93.1). All strains were susceptible to furazolidone, and nine were resistant to clarithromycin (A2142G or A2143G mutation was detected in all of them). The treatment failure was significant and independently associated with clarithromycin resistance (OR = 7.79; 95% CI = 1.73-35.01), A-negative status (OR = 4.81; 95% CI = 1.14-20.14), and male gender (OR = 4.20; 95% CI = 1.01-17.78), but not with the type of disease, mean age, smoking, alcohol consumption, and the degree of the antral and oxyntic gastritis. CONCLUSION: Resistance to clarithromycin, A-negative status, and gender were predictive factors of eradication failure.

Changes of the proximal digestive tract in portal hypertension and their relationship with "Helicobacter pylori", histology and patient's hepatic function

Este trabalho analisa as alteraçöes observadas à endoscopia em pacientes portadores de hipertensäo portal por cirrose e esquistossomose e as correlaciona com os achados histológicos, presença ou näo de H. pylori e funçäo hepática do paciente. Os pacientes cirróticos apresentaram prevalência significativamente mais alta de úlcera péptica, correlaçäo positiva entre presença de gastrite crônica e de H. pylori, assim como relaçäo direta entre o grau das varizes e a presença de gastropatia hipertensiva (GH). Näo houve correlaçäo estatisticamente significativa entre presença de H. pylori e o grupo do paciente, entre a presença de GH e o índice de Child Pagh, nem entre a prevalência de H. pylori e de GH. Finalmente, näo houve diferença significativa na prevalência de gastrite crônica entre os grupos de pacientes

Alcoolizaçäo dos tumores inoperáveis do esôfago para paliar a disfagia: relato de 10 casos / Alcohol for unoperable esophageal tumors to lessen dysphagia: report of ten cases

Dez pacientes com disfagia causada por tumores esofágicos e da cárdia (nove com carcinomas de células escamosas e um com adenocarcinoma) foram submetidos a tratamento paliativo da disfagia pela injeçäo de álcool absoluto (95(GL), misturado ao azul de metileno a 0,5 por cento, intratumoral. O volume total injetado por via endoscópica variou de 4 a 41ml, em sessöes intervaladas de cinco dias. Avaliamos os resultados por estudo radiológico do esófago, observaçäo endoscópica e segundo os critérios de Bown, modificados. Anteriormente ao início do tratamento, o valor médio da disfagia era de 3,5 na escala de Bown. Ao fim das sessöes, essa média foi de 1,3. Todos os pacientes passaram a deglutir dieta pastosa, semi-sólida ou sólida. O tratamento era repetido quando havia recidiva da disfagia, com intervalo médio de 32,4 dias. Nao houve complicaçöes ou mortalidade em nossa casuística.