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1.
J Surg Case Rep ; 2013(6)2013 Jun 26.
Article in English | MEDLINE | ID: mdl-24964449

ABSTRACT

Supralevator abscesses are the rarest manifestation of anorectal suppurative disease. We report a supralevator abscess in a 60-year-old male whose earliest presentation included poorly localized abdominal and pelvic pain, tenesmus, urinary retention and weight loss, initially treated as diverticular disease based upon imaging and presentation. Progressive symptoms led to the discovery of a pelvic abscess with subsequent percutaneous drainage, later followed by emergent laparotomy, where a single perforated diverticulum was revealed to be the source fistulization. He underwent a Hartmann procedure with concomitant drainage of supralevator and ischiorectal collections. Perirectal pain with neurological involvement is part of a constellation of signs and symptoms that should invoke a high index of clinical suspicion for supralevator abscess formation. Percutaneous attempts at drainage are often inadequate; definitive surgical therapy is the best approach to prevent recurrence and associated morbidity.

2.
Inflamm Bowel Dis ; 14(10): 1341-7, 2008 Oct.
Article in English | MEDLINE | ID: mdl-18452197

ABSTRACT

BACKGROUND: The impact of the antiinflammatory agent 5-aminosalicylic acid (5-ASA) on the risk for colitis-associated colorectal cancer remains controversial. The chemopreventive activity of 5-ASA was evaluated in the Swiss Webster model of azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colitis-associated neoplasia. METHODS: Mice were injected with AOM (7.4 mg/kg i.p.) and randomized to receive either vehicle or 5-ASA (75, 150, and 225 mg/kg) for the remainder of the study. DSS treatment began at 9 weeks of age and continued for 3 cycles. At the time of sacrifice (18 weeks of age), the entire colon and rectum were processed for histopathologic examination. RESULTS: An inverse trend was observed between dose and multiplicity of colonic dysplasias in all drug-treated groups (P = 0.03), with animals receiving 75 mg/kg 5-ASA exhibiting 56% of the number of dysplasias of the AOM/DSS controls (mean +/- SEM: 7.6 +/- 1.4 and 13.6 +/- 2.7, respectively). Administration of 75 mg/kg 5-ASA decreased both the mean multiplicity of flat dysplasias (1.8 +/- 0.4 for drug-treated versus 5.6 +/- 1.2 for AOM/DSS control) and the burden of polypoid dysplasias (tumor burden: 6.7 +/- 2.7 for drug-treated versus 14.9 +/- 3.9 units for AOM/DSS controls) significantly (P = 0.002 and 0.04, respectively). Inflammation was least severe in the 75 mg/kg group, which exhibited the fewest number of colorectal tumors. CONCLUSIONS: These data suggest that low-dose 5-ASA may be efficacious in preventing colitis-associated dysplasias and provide strong support for optimizing this therapy for the prevention of colonic neoplasms in patients with ulcerative colitis.


Subject(s)
Colitis/chemically induced , Colitis/prevention & control , Colorectal Neoplasms/prevention & control , Mesalamine/pharmacology , Animals , Azoxymethane/toxicity , Colitis/pathology , Colorectal Neoplasms/pathology , Cyclooxygenase 2/isolation & purification , Dextran Sulfate/toxicity , Disease Models, Animal , Dose-Response Relationship, Drug , Female , Humans , Immunohistochemistry , Mice , Random Allocation
3.
Mol Carcinog ; 44(1): 31-41, 2005 Sep.
Article in English | MEDLINE | ID: mdl-15937958

ABSTRACT

The relevance of the Apc(+/Min) mouse model in the study of human colorectal cancer remains uncertain due to the predominance of small intestinal adenomas and few, if any, colorectal adenomas. A new strain of Apc(+/Min) mice (Apc(+/Min-FCCC)) with significantly greater numbers of colorectal adenomas has been generated and characterized. Male C57BL/6J-Apc(+/Min) mice (the Jackson Laboratory, Bar Harbor, ME) were crossed with wild-type (Apc(+/+)) C57BL/6J females from an independent colony at this institution (offspring=Apc(+/Min-FCCC)) and 233 animals were evaluated over 20 generations. In order to determine the contribution of genetics to the enhanced colorectal adenoma phenotype, breeding pairs (Apc(+/Min) male x wild type female C57BL/6J) were purchased from the Jackson Laboratory and offspring (Apc(+/Min-JAX)) were maintained in our facility under identical conditions (n=98). Animals were fed Purina Rodent chow (#5013) diet containing 5% fat. The entire intestinal tract was examined histopathologically in both strains. Both the Apc and Pla2g2a (candidate for Mom1) genes were sequenced and found to be identical for both the Apc(+/Min-FCCC) and Apc(+/Min-JAX) mouse strains. The multiplicity of colorectal adenomas in the Apc(+/Min-FCCC) mice was much higher than reported in the literature and significantly greater than the multiplicity of colorectal adenomas in Apc(+/Min-JAX) mice maintained in our facility (P=0.01). Apc(+/Min-FCCC) had a significantly greater incidence of rectal prolapse (P = 0.02) and small intestinal adenocarcinomes (P=0.001), and multiplicity of small intestinal adenocarcinomas (P=0.001) compared to Apc(+/Min-JAX) mice. Male Apc(+/Min-FCCC) mice had significantly greater numbers of colorectal adenomas compared to female Apc(+/Min-FCCC) mice (P=0.0002), as did male Apc(+/Min-JAX) mice vs. female Apc(+/Min-JAX) mice (P< 0.0001). These results allow us to conclude: (1) Apc(+/Min-FCCC) mice are unique in that they develop significantly greater numbers of colorectal adenomas and small intestinal cancers, and a significantly greater incidence of small intestinal cancers and rectal prolapse than Apc(+/Min-JAX) mice. (2) This study represents the first report of a significant gender difference in multiplicity of colorectal adenomas. (3) Differences between Apc(+/Min-FCCC) and Apc(+/Min-JAX) mice in currently undefined genetic modifiers may contribute to the enhanced colorectal phenotype. (4) The Apc(+/Min-FCCC) strain is highly suited for the investigation of colorectal neoplastic disease and chemoprevention studies.


Subject(s)
Adenoma/genetics , Adenoma/pathology , Colorectal Neoplasms/genetics , Colorectal Neoplasms/pathology , Genes, APC , Animals , Breast Neoplasms/genetics , Breast Neoplasms/pathology , Cecal Neoplasms/genetics , Cecal Neoplasms/pathology , Female , Incidence , Male , Mice , Rectal Prolapse/genetics , Rectal Prolapse/pathology
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