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        Efficacy of conservative treatment of perianal abscesses in children and predictors for therapeutic failure

        Boenicke, Lars,Doerner, Johannes,Wirth, Stefan,Zirngibl, Hubert,Langenbach, Mike Ralf The Korean Pediatric Society 2020 Clinical and Experimental Pediatrics (CEP) Vol.63 No.7

        Background: The optimal management of perianal abscess in children is controversial. Purpose: To evaluate the efficiency of conservative treatment of perianal abscess in children and identify parameters that predict therapy failure. Methods: All cases of children younger than 14 years of age with perianal abscesses between 2001-2016 were evaluated. Results: Of the 113 enrolled patients, 64 underwent subsequent surgery for advanced disease (primary surgery group). Conservative treatment was initiated in 49 patients (primary conservative group) but was stopped because of inefficiency in 25 patients, who were referred for surgery after a median 7.03 days (range, 2 to 16 days). The other 24 patients (48%) initially achieved complete remission after conservative treatment, but 10 were readmitted after a median 34 months (range, 3 to 145 months) with recurrent disease. There were no significant differences in permanent success after conservative treatment between infants (10 of 29, 34%) and older children (4 of 20 [20%], P=0.122). Overall, conservative treatment alone was effective in only 14 of 113 patients. Recurrence after surgery occurred in 16 patients (25%) in the primary surgery group and 11 patients (22%) in the primary conservative group (P=0.75). Univariate analysis of predictors for conservative treatment failure revealed inflammatory values (C-reactive protein and white blood count, P=0.017) and abscess size (P=0.001) as significant parameters, whereas multivariate analysis demonstrated that only abscess size (odds ratio, 3.37; P=0.023) was significant. Conclusion: Conservative treatment of perianal abscess is permanently efficient in only a minority of children but is not associated with a higher recurrence rate after subsequent surgery. Abscess size is a predictor for therapy failure.

      • Free Paper Session : Lower Gastrointestinal Tract 2 ; Attenuation Of Colitis-Associated Carcinogenesis By Pharmacologic Or Genetic Inhibition Of Cyclooxygenase-2

        ( Jeong Sang Lee ),( Hyun Soo Lee ),( Hee Geum Lee ),( Young Joon Surh ),( Hyun Wook Baik ),( Robert Langenbach ),( Young Kee Shin ),( Ki Baik Hahm ) 대한소화기학회 2007 SIDDS Vol.9 No.-

        Background/Aims: COX-2 inhibition might be much more efficient way of preventing colitis associated cancer than sporadic or familial colon cancer because COX-2 is either an inflammatory or carcinogenic mediator. To prove this hypothesis, we generated colitic cancer with the administration of 2.5% dextran sulfate sodium (DSS) in drinking water for 7 days after a single i.p dose of 10mg/kg azoxy-methane (AOM) in male ICR mice. Results: 83.33% mice developed colorectal carcinoma after AOM plus DSS treated mice, whereas only 22% in the AOM-treated and none in the DSS-treated mice developed colon tumors at the 16 weeks. The expressions of COX-2, iNOS, mutated p53, matrix metalloproteinase (MMP)-2, -9, -13 were markedly elevated in the colon tumors of mice challenged with both AOM plus DSS. The finding that colitis promoted colon carcinogenesis through COX-2 stimulated us to confirm that COX-2 inhibition using celecoxib or genetic ablation of COX-2 using COX-2-/- mice could play role as cancer prevention. Oral administration of calecoxib for 14 weeks significantly lowered the AOM plus DSS-induced tumor incidence (44.8% vs 83.3%), tumor multiplicity (1.75 tumors/mice vs 6.00 tumors/mice), attenuated expressions of COX-2 and iNOS, and transcriptional repression of NF-κ B or AP-1 than control group. Tumor incidence and multiplicity after AOM plus DSS-treatment were significantly decreased in COX-2-/- mice than control mice. Conclusions: Colitis promoted colon carcinogenesis, supporting the causative association between inflammation and carcinogenesis and COX-2 could be a right target for chemoprevention of colitic cancer.

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