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Objective. Constipation in patients with mild spinal cord disease is not well investigated yet. We aimed to investigate anorectal function and the effect of biofeedback therapy in constipated patients with mild spinal cord diseases. Material and methods. A total of 14 constipated patients with myelopathy and 32 with radiculopathy were enrolled retrospectively. All patients were able to walk independently. The control group comprised of 100 constipated patients without any neurologic problem. Colonic transit time and the presence of dyssynergia were assessed before biofeedback therapy. All patients answered structured questionnaires on constipation, before and after biofeedback therapy. Results. The mean rectosigmoid colonic transit time of the myelopathy group was significantly delayed (myelopathy, 18.6 ± 14.6 h; radiculopathy, 12.8 ± 11.9 h; control, 9.6 ± 11.2 h; p = 0.032). Delay in total colonic transit time was more frequent in the myelopathy group (myelopathy, 57.1%; radiculopathy, 23.3%; control, 18.5%; p = 0.004). On anorectal manometry, the squeezing pressure of the anal sphincter was decreased in the myelopathy group (myelopathy, 132.3 ± 73.3 mmHg; radiculopathy, 179.9 ± 86.1 mmHg; control 200.4 ± 82.4 mmHg; p < 0.05). The success rate of biofeedback therapy was lower in the myelopathy group (28.6% for myelopathy vs. 62.0% for control group; p = 0.034). The response rate to biofeedback therapy was similar between radiculopathy and control group (62.5% for radiculopathy vs. 62.0% for control group; p = 1.000). Conclusions. In constipation associated with mild myelopathy, delayed colonic transit and dyssynergic defecation were major pathophysiologic abnormalities and biofeedback was less effective compared with control group. However, in the radiculopathy group, biofeedback was as effective as in the control group. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to evaluate the clinical characteristics and clinical course of Asian elderly-onset Crohn’s disease (EOCD) patients in a large well-defined cohort of South Korean IBD patients. Materials and methods: From the Asan inflammatory bowel disease registry, we identified 29 EOCD patients (diagnosed with CD in age of 60 years or over) out of 2989 CD patients (1.0%). After excluding two patients with unclear data, 27 EOCD were matched with 108 young-onset CD (YOCD) and 108 middle age-onset CD (MOCD) for the interval from symptom onset to diagnosis (±3 years) and follow-up duration (±3 years). Results: Females were predominant in the EOCD group (59.3%) compared to MOCD (31.5%) and YOCD (29.6%) groups (p = .012). In EOCD group, terminal ileal location was the most common (63.0%) at diagnosis, whereas ileocolonic location in other groups (57.4% in MOCD and 78.7% in YOCD, respectively) (p < .001). Patients with perianal fistula at CD diagnosis were less common (14.8% in EOCD vs. 28.7% in MOCD vs. 49.1% in YOCD, p < .001). During follow-up, thiopurines were used less frequently in the EOCD group (48.1% in EOCD vs. 87.0% in MOCD vs. 89.8% in YOCD, p < .001), but the risk for intestinal resection was comparable among three groups (p = .583). Conclusions: EOCD may have a better clinical course than MOCD and YOCD, as demonstrated by the similar risk for intestinal resection despite the less frequent use of thiopurines. [ABSTRACT FROM AUTHOR]

BackgroundThe impact of genetic variation in thethiopurine S-methyltransferase (TPMT)gene on thiopurine-induced leukopenia has been well demonstrated. Although xanthine dehydrogenase (XDH)is the second major contributor to azathioprine breakdown, polymorphisms inXDHhave rarely been studied in IBD patients. We aim to access association betweenXDHvariants and thiopurine-induced leukopenia by gene–gene interaction in a Crohn’s disease (CD) population.StudyA total of 964 CD patients treated with thiopurines were recruited from a tertiary referral center. The association between fourXDHvariants (p.Gly172Arg, p.Asn1109Thr, p.Arg149Cys, and p.Thr910Lys) and thiopurine-induced leukopenia was analyzed in cases with early leukopenia (n = 66), late leukopenia (n = 264), and in controls without leukopenia (n = 632). Three non-synonymous SNPs, which we previously reported association with thiopurine-induced leukopenia,NUDT15(p.Arg139Cys),SUCLA2(p.Ser199Thr), andTPMT *3Cwere selected for epistasis analysis with theXDHvariants.ResultsThere was no significant association for two variants ofXDHand thiopurine-induced leukopenia. In the epistasis analysis, onlyXDH(p.Asn1109Thr) *SUCLA2(p.Ser199Thr) showed a statistically significant association with early leukopenia [odds ratio (OR) = 0.16;p = 0.03]. After genotype stratification, a positive association on the background ofSUCLA2wild-type (199Ser) between theXDH(p.Asn1109Thr) and early leukopenia (OR = 4.39;p = 0.01) was detected.ConclusionGenes associated with thiopurine-induced leukopenia can act in a complex interactive manner. Further studies are warranted to explore the mechanisms underlying the effects of the combination ofXDH(p.Asn1109Thr) andSUCLA2(199Ser) on thiopurine-induced leukopenia. [ABSTRACT FROM PUBLISHER]

Objective. The long-term efficacy of azathioprine (AZA) in steroid-dependent ulcerative colitis (UC) is still unclear. We aimed to evaluate the efficacy of AZA in patients with steroid-dependent UC. Material and methods. We retrospectively reviewed die medical records of 106 patients with steroid-dependent UC who were administered AZA. Three-year outcomes of AZA therapy were evaluated. The outcome of the treatment was defined as (1) success, indicating induction and maintenance of remission throughout the study period (complete success) or remission followed by infrequent and short relapses (partial success); or (2) failure, indicating the absence of remission, frequent or prolonged relapses, infliximab administration, or colectomy. Results. Of the 106 patients, 73 (68.9%) continued on AZA for >6 months (AZA therapy group) and 33 (31.1%) discontinued AZA within 6 months due to intolerance (AZA intolerance group, n = 20), colectomy (n = 6), or follow-up loss (n = 7). Three-year outcomes for 106 patients were success in 54.7% (complete success, 35.8%; partial success, 18.9%), failure in 32.1% (frequent or prolonged relapses, 12.3%; infliximab administration, 5.6%; colectomy, 14.2%), and follow-up loss or death in 13.2%. The success rate increased to 71.2% (complete success, 46.6%; partial success, 24.7%) when the analysis was confined to the 73 patients who continued AZA for > 6 months. The 3-year success rate was higher in the AZA therapy group (71.2%) than the AZA intolerance group (25.0%) (p < 0.001). Conclusions. AZA is an effective treatment for steroid-dependent UC. The efficacy of AZA is well sustained over 3 years. [ABSTRACT FROM AUTHOR]