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Activation of ulcerative colitis with mesalamine has rarely been reported. In case 1, a 34-year-old man was treated with oral mesalamine, resulting in an exacerbation of colitis that rapidly improved with glucocorticoids and mesalamine withdrawal. Oral cromolyn sodium and occasional low-dose prednisone therapy has maintained long-term remission. In case 2, a 28-year-old man receiving prednisone treatment developed chest pain and myalgias 1 week after initiation of mesalamine that resolved on mesalamine withdrawal. A lower dose of mesalamine with continued glucocorticoids resulted in clinical improvement, and both drugs were tapered. Mesalamine sensitivity was documented endoscopically and histologically by evaluating mucosal changes after two mesalamine enemas during a 24-hour period. There was dramatic progression from quiescent disease to active colitis in 24 hours. Mesalamine sensitivity must be included in the differential diagnosis of ulcerative colitis exacerbations. Concurrent steroid therapy can suppress systemic side effects, making the diagnosis even more elusive.

A 17-year-old girl with a history of ulcerative colitis and a recent pilonidal cyst excision was admitted to the hospital with fever, severe abdominal pain, and frequent, bloody diarrhea. The diagnosis of idiopathic ulcerative colitis was made 4 years before admission and was based on colitis symptoms, endoscopic pancolitis, and unequivocal histological changes. The patient was started on sulfasalazine and prednisone therapy but failed to achieve a complete remission. One year before admission she was having three episodes of bloody diarrhea daily. Her medications were prednisone, 30 mg daily, and sulfasalazine, 1 g t.i.d. She complained of intolerable mood swings due to prednisone, but tapering resulted in continuous diarrhea. Her colonic mucosa was edematous, erythematous, granular, and friable from the mid-descending colon to the rectum. The patient responded well to the addition of one 4-g mesalamine enema per day, and steroid therapy was tapered off completely over the next 8 months. She experienced a brief relapse 3 months before admission manifest by abdominal cramping and two to three blood-streaked, loose stools per day. The patient attributed this relapse to a viral upper respiratory infection she had contracted several days earlier. She observed that her colitis flared “every time she had a cold.” This relapse resolved with an increase in oral sulfasalazine and mesalamine enemas. When the patient was seen 10 weeks before admission she was in clinical and sigmoidoscopic remission, with no complaints of pain, diarrhea, or bleeding on a regimen of sulfasalazine, 2 g daily, and mesalamine enemas, 2 g daily. The patient was scheduled to have a pilonidal cyst excised. The case was discussed with the surgeon, who agreed not to use antibiotics perioperatively unless treating a specific infection because of the concern about provoking antibiotic-induced diarrhea or Clostridium dijjkile colitis. Several days before surgery the patient developed recurrent fevers and pharyngitis. Her examination showed tonsilar hyertrophy, but there was no significant adenopathy or splenomegaly. Her white blood cell count was elevated to 1300 with 78% lymphocytes, most of which were atypical. Results of a mono spot test were positive, and infectious mononucleosis was presumed to be the cause of the patient’s fevers. Surgery was performed 7 weeks before admission. The patient’s ulcerative colitis remained in clinical remission throughout her febrile illness and during the immediate postoperative period. However, 2 weeks after surgery (5 weeks before admission) she developed abdominal cramping, tenesmus, and bloody stools. Her symptoms became worse despite an increase in her sulfasalazine to 4 g daily and mesalamine enemas to 4 g daily. A flexible sigmoidoscopy performed approximately 2 weeks before admission revealed mucosal edema, erythema, granularity, and friability from the rectum to the descending colon. The hematocrit was 29.5%, the white cell count was 8100, the platelets were 625,000, and the erythrocyte sedimentation rate was 58 mm/h. The differential white blood cell count showed 16% segmented neutrophils, 16% banded neutrophils, 39% lymphocytes, 9% monocytes, and 20% eosinophils. Because of the patient’s eosinophilia and worsening condition, the sulfasalazine dosage was reduced to 2 g daily. Abdominal pain, stool frequency, and bleeding all continued to increase. The patient, complaining of progressive weakness, was admitted to the hospital after a syncopal episode during a phlebotomy. Physical examination revealed a pale, thin, and mildly diaphoretic female patient. Her temperature was 37.8”C, her heart rate was 100 per minute, and her systolic blood pressure was 100 mm Hg supine but fell to 90 mm Hg in the sitting position. She had no ocular or oral lesions, and the chest examination results were normal except for tachycardia. The patient had active bowel sounds, and her abdomen was soft and nondistended with mild, diffuse tenderness. There was no rebound, guarding, or liver or spleen enlarge

Background: Functional Gastrointestinal Disorders (FGIDs) are identified by the dominant presenting symptoms: functional heartburn (FH), irritable bowel syndrome (IBS), dyspepsia, etc. This nomenclature assumes an organ-specific origin of symptoms rather than symptoms associated with a common pathophysiology such as visceral hypersensitivity. The symptoms reported in most FGIDs overlap more than one gastrointestinal (GI) organ. FH patients report abdominal cramping, bloating and nausea with their FH symptoms. This study tested the primary hypothesis that there is a correlation of MPT in the esophagus and rectum in FH patients. Secondary aims evaluated correlations with IPT and PT. Methods:. This study explored objective sensory endpoints of initial perception threshold (IPT), pain threshold (PT), and maximum pain threshold (MPT) in the esophagus and rectum of FH subjects to determine whether visceral hypersensitivity is a generalized or organ specific observation Fourteen women with FH participated in this study. Each subject underwent a training sensory study protocol session including step volume and pressure ramp balloon barostat distention of the esophagus and rectum. A data collection visit occurred within 7-14 days to collect data on balloon volume and pressure measurements at IPT, PT, and MPT with esophageal and rectal barostat distention. The relationship of sensation and pain to volume, pressure, and compliance was analyzed. Results: The correlation between esophageal and rectal IPT balloon volume scores was highly and significantly correlated (r = 0.61, p = 0.02). The correlation between esophageal and rectal PT balloon volume scores was highly and significantly correlated (r = 0.6, p = 0.02). The correlation between esophageal and rectal MPT balloon volume scores was not correlated (r = 0.35, p = 0.26). In contrast to volume, the pressure endpoints were not significantly correlated. Conclusions: 1. In this study, there was weak correlation for the relationship of rectal and esophageal volume scores at MPT (Primary Aim). Findings revealed a strong positive correlation for the relationship of rectal and esophageal volume and pressure scores to IPT and PT (Secondary Aims). The lack of MPT correlation may provide insight into the organ specific stratification of FGIDs through identification of the most sensitive organ. 2. In this study, volume was superior to pressure in assessing changes in visceral sensitivity in FGID patients. 3. The correlation of visceral sensitivity in the esophagus and rectum in patients with FH supports the hypothesis that visceral sensory changes in FGIDs are not organ specific. 4. Visceral hypersensitivity throughout the GI tract may explain the overlapping symptoms in FGID patients suggesting visceral sensitivity may occur in two separate areas of the GI tract simultaneously.

Background & Aims: Recombinant human interleukin 11 (rhIL-11) is a cytokine with thrombocytopoietic activity and anti-inflammatory and mucosal protective effects. The objectives of this study were to investigate the safety and tolerability of rhIL-11 in patients with Crohn's disease and to explore the effects of dose and schedule on platelet count and Crohn's disease activity. Methods: A multicenter, double-masked, placebo-controlled, dose-escalation study of 76 patients with active Crohn's disease was performed. Patients were randomized to receive subcutaneous placebo or rhIL-11 at doses of 5, 16, or 40 μg · kg −1 · wk −1 given 2 or 5 times weekly for 3 weeks. Clinical and laboratory safety data were recorded, and disease activity was measured at each visit. Results: Subcutaneous injection of rhIL-11 generally was well tolerated. Significantly greater increases in platelet counts were found among patients receiving rhIL-11 40 μg · kg −1 · wk −1 as 2 or 5 weekly doses and 16 μg · kg −1 · week −1 as 5 weekly doses compared with patients receiving placebo ( P −1 · wk −1 had the highest clinical response rates, with a response seen in 42% of patients (5/12) receiving 5 weekly doses and 33% of patients (4/12) receiving 2 weekly doses, compared with 7% of patients (1/15) receiving placebo. Conclusions: Short-term treatment with rhIL-11 is well tolerated in patients with active Crohn's disease. The thrombocytopoietic effect of rhIL-11 seems to be both dose and schedule dependent and may be minimized with retained clinical benefit in Crohn's disease at 16 μg · kg −1 · wk −1 given in 2 equal doses. GASTROENTEROLOGY 1999;117:58-64

while changes in the CLP were subtle. Enhancer of zeste homolog2 (EZH2) protein increased significantly in the crypt at days–6 and 12 and coincided with expression of EZH2 target protein H3K27me3 that marks the repressive chromatin signature. Knockdown of EZH2 decreased TOP-Flash reporter activity due to loss of β-catenin concomitant with increases in Wnt-inhibitory factor–1 (WIF–1) protein expression. Intriguingly, simultaneous increases in both H3K4me3 and H3K27me3 in the crypt at days–6 and 12 coincided with dramatic increases in β-catenin, Jagged–1, and SMYD3 while expression of E-cadherin decreased significantly due to upregulation of Slug and Snail, respectively. In the CLP, an almost complete loss of H3K27me3 at days–6 and 12 compared to uninfected control correlated with trans-differentiation of cultured crypt epithelial cells into messenchymal cells that stained positive for vimentin and αSMA indicating an EMT-like behavior. Chromatin immunoprecipitation assay in the crypt showed accumulation of EZH2 around E-cadherin promoter while that of H3K4m3 around β-catenin, Jagged–1, SMYD3 and Snail promoter respectively further supporting EMT-like phenomenon. Conclusion: Epigenetic mechanism seems to play an important role in the regulation of crypt cell hyperplasia and may be EMT.

Confirming partial small bowel obstruction is often a diagnostic challenge. In this case report, 4-mm solid radiopaque markers were used in 4 patients to show partial small bowel obstruction. Results of enteroclysis were normal in 2 of the 4 patients, and the markers were used to challenge suspected partial obstruction. The markers coalesced in the region of the partial obstruction, which was confirmed at surgery. Enteroclysis is the examination of choice in the diagnosis of partial small bowel obstruction. However, examinations with false-negative results can occur, particularly with adhesive and/or intermittent obstructions. The use of radiopaque markers in these cases proved an effective and useful method of establishing the diagnosis of partial small bowel obstruction, particularly in the 2 cases in which enteroclysis results were normal. Prospective studies are needed to establish the feasibility of this novel technique.

Background:It has been proved thatH. pylori eradication prevents the incidence of metachronous gastric cancer after endoscopic resection (ER) of primary early gastric cancer during short-term follow-up. However, it has not been clarified whether preventive effect of H. pylori eradication for gastric cancer continues in the long term. To determine the long-term effect of H. pylori eradication on the development of gastric cancer, a follow-up study of a JGSG trial (Lancet 2008; 372: 392-7) was conducted. Methods: In this multi-center, openlabel, randomized controlled trial, 544 patients who received ER of early gastric cancer were randomly assigned to the H pylori eradication group (n=272) or to the control group (n= 272). Endoscopy was performed every year after randomization to evaluate metachronous cancer. Diagnosis of a new gastric cancer at another site of the stomach was defined as primary endpoint. Metachronous cancers were confirmed through histological examination. The frequency of metachronous cancer in the eradication group was compared to that in the control group. Results: There were no significant differences between eradication and control groups in baseline characteristics. The follow-up period was 10 years at maximum. After three years of follow-up, metachronous gastric cancer was detected in 32 participants. In the end, metachronous gastric carcinoma had developed in 22 patients in the eradication group and 43 in the control group. In the modified intention-to-treat population, including patients with at least one post-randomization assessment of tumor status and adjusting for loss to follow-up (255 patients in the eradication group, 250 in the control group), the hazard ratio for metachronous gastric carcinoma was 0.497 (95% CI 0.2970.831; p=0.008). The eradication group and the control group showed no difference in characteristics of metachronous cancer. Conclusions: This study showed that H. pylori eradication prevented the development of metachronous gastric cancers after ER during long-term follow-up.

G A A b st ra ct s the symptom response). Methods. In two randomized controlled trials of AZD0865 (a potassium-competitive acid blocker) 25-75 mg/day vs esomeprazole 20-40 mg/day, patients were recruited who had ‘burning feeling behind the breastbone’≥ 4 days/week at≥moderate intensity as their main symptom (1460 had non-erosive reflux disease [NERD] and 1514 had reflux esophagitis [RE]).1,2 No differences were found in either study between drugs or doses in terms of the response of heartburn to treatment. Pooled data from all treatment arms (N = 2875) were retrospectively reviewed to determine the impact of other RDQ items recorded in an e-diary on the response of heartburn. Results. The mean number of positive RDQ items at baseline was four. Heartburn was most responsive to therapy in the 3% of patients whose only baseline symptom was ‘burning feeling behind the breastbone’. The report of any other RDQ item at high severity of ≥ 4 days/week at ≥ moderate intensity (except for acid taste) was associated with a reduction in the responsiveness of heartburn both in patients with NERD and those with RE (Table). Low-severity concomitant symptoms (≥ 1 day/week at ≥ mild intensity, not including those with high severity symptoms) had similar, though less extreme, effects. Conclusions. Acid-suppressive therapy has the greatest effect in patients with GERD who have a symptom profile limited to ‘burning feeling behind the breastbone’ alone or in association with ‘acid taste in the mouth’. If other RDQ items, particularly pain (behind the breastbone or in the upper stomach), were present, the treatment effect was substantially reduced. References. 1. Dent et al. Am J Gastroenterol 2008;103:206 2. Kahrilas et al. Clin Gastroenterol Hepatol 2007;5:1385-91

female ratio was 1 : 1.02. The preoperative diagnosis was gallbladder cancer(67%), cholecystitis(24%), gallbladder polyp(7%), stone and cholecystitis(6%), stone(3%), gallbladder cancer and stone(2%), adenomyomatosis(1%). 15 patients of stage IA, 22 of stage IB, 9 of stage IIA, 23 of stage IIB, 3 of stage III and 6 of stage IV were confirmed by postoperative analysis. Age, sex, white blood cell count, hemoglobin, AST, ALT, total bilirubin, alkaline phosphatase, CEA, symptoms, and TNM stage were not statistically different from two groups (preoperative GBC Vs. non GBC). Conclusions : A third of the GBC patients who had a LC got a diagnosis as Cholecystitis, gallbladder polyp, gallstone or adenomyomatosis. Therefore, a careful diagnosis is required in the first workup. However, there turn out to be no difference in the illness stage not matter whether the patient has got an earlier diagnosis as the GBC. We think that LC does not deteriorate the prognosis of patients with incidentally detected GBC if appropriate re-operation is carried out according to the cancer staging.