The incidence of pouchitis after ileal J-pouch anal anastomosis is approximately 50% with two thirds of these patients having multiple episodes. Chronic pouchitis occurs in a minority of patients. In chronic pouchitis, the risk of pouch loss is substantial.
Carcinoid and neuroendocrine tumors of the colon and rectum arise from the amine precursor uptake and decarboxylation (APUD) cells of the intestine. Carcinoid tumors are most commonly found in the gastrointestinal tract and are located in decreasing order of frequency in appendix, ileum, rectum, stomach, and colon. The vast majority of lesions are asymptomatic and are found incidentally during endoscopy. The management of these lesions depends upon the size of the lesion, involvement of the muscularis, location, and presence of metastatic disease. Small lesions (1 cm) can often be treated locally, either endoscopically or transanally. However, larger lesions (> 2 cm) require a formal oncologic resection. Adjuvant therapy is indicated only for metastatic disease, and admirable advances have been made in the realm of chemotherapy for reduction of disease and palliation of the symptoms of carcinoid syndrome. In this article, we discuss the nature of these interesting and uncommon tumors, clinical presentation, treatment options, and prognosis.
A prospective study was conducted to determine the implications of acute pouchitis on the long-term functional results of restorative proctocolectomy with J-pouch ileoanal anastomosis (IPAA). Between July 1988 and June 1996, 137 consecutive patients underwent IPAA for treatment of ulcerative colitis. 127 patients (93%) have been available for follow-up. All patients completed diaries detailing bowel habits over a 7-day period at 3, 6, 9, 12, 18, 24 months, and yearly after reestablishment of intestinal continuity. Diaries were completed only during time periods in which patients were not suffering from acute symptomatic pouchitis. Patients with chronic pouchitis (n = 7) were excluded from this study leaving 120 patients for analysis. Fifty patients suffered at least one episode of pouchitis (Pouchitis Group). Seventy patients never had pouchitis (No Pouchitis Group). Patients with a history of pouchitis having significantly more bowel movements per day were more likely to ever have minor incontinence (75% vs. 45%, p < 0.005) or major incontinence (37% vs. 17%, p < 0.02). The stools of Pouchitis Group were less likely to be formed (24% vs. 31%, p < 0.001). Pouchitis Group patients also were more likely to wear a protective pad during the day (21% vs. 7% p < 0.04) or during the night (40% vs. 13%, p < 0.001). Even in the absence of clinically active pouchitis, patients who have suffered at least one episode of pouchitis have a poorer long-term functional result after IPAA. The results of this study suggest that ileal pouchitis may represent a chronic condition that displays episodic symptomatic exacerbations.
Primary EBV+ nodal T/NK-cell lymphoma (PTCL-EBV) is a poorly understood disease which shows features resembling extranodal NK/T-cell lymphoma (ENKTL) and is currently not recognized as a distinct entity but categorized as a variant of PTCL-NOS. Herein, we analyzed copy-number aberrations (n=77) with focus on global measures of genomic instability (GI) and homologous recombination deficiency (HRD) and performed gene expression (n=84) and EBV miRNA expression profiling (n=24) and targeted mutational analysis (n=16) to further characterize PTCL-EBV in relation to ENKTL and PTCL-NOS. Multivariate analysis revealed a significantly worse outcome of PTCL-EBV compared to PTCL-NOS (P=0.002) but not ENKTL. Remarkably, PTCL-EBV exhibited significantly lower GI and HRD scores compared to ENKTL and PTCL-NOS. Gene Set Enrichment Analysis revealed many immune-related pathways, interferon alpha/gamma response, and IL6_JAK_STAT3 signaling to be significantly upregulated in PTCL-EBV and correlated with lower GI-scores. We also identified NFκB-associated genes, BIRC3, NFκB1 (p50) and CD27, and their proteins to be upregulated in PTCLEBV. PTCL-EBV demonstrated mostly type 2 EBV latency pattern and, strikingly, exhibited downregulated expression of most EBV miRNAs compared to ENKTL and their target genes were also enriched in immune-related pathways. PTCL-EBV also showed frequent mutations of TET2, PIK3CD and STAT3, and are microsatellite stable. Overall, the poor outcome, low genomic instability, upregulation of immune pathways and downregulation of EBV miRNAs are distinctive features of PTCL-EBV. Our data support the consideration of PTCL-EBV as a distinct entity, provide novel insights into the disease pathogenesis and offer potential new therapeutic targets for this tumor.
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