The relationship between iron deficiency in patients with Helicobacter pylori-infected nodular gastritis and the serum prohepcidin level.

BACKGROUND AND AIMS: Helicobacter pylori (H. pylori) is recognized as a causative agent for unexplained iron-deficiency anemia (IDA). We evaluated many background factors influencing an iron-deficiency state in adult patients with various H. pylori-infected upper gastrointestinal tract diseases. METHOD: Study 1: H. pylori-infected 121 patients (nodular gastritis (NG) (n = 19), duodenal ulcer (DU) (n = 30), or gastric ulcer (GU) (n = 47), or gastric hyperplastic polyp (GHP) (n = 25)) were enrolled. The RBC count and hemoglobin, iron, ferritin, pepsinogen (PG) I, PG II, gastrin, and anti-H. pylori antibody (Ab) levels in the serum were measured. Study 2: H. pylori-infected 105 patients (NG, n = 19; DU, n = 43; GU, n = 32; GHP, n = 11) and non-H. pylori-infected individuals (n = 35) were examined for the levels of prohepcidin, ferritin, and iron in the serum. In addition, we measured the data before and after the H. pylori eradication. RESULTS: In the patients with GHP and NG, hypoferritinemia was observed in comparison with the GU and DU patients. In the GHP patients, low levels of PG I, a decreased PG I/II ratio, and hypergastrinemia were observed. The levels of serum prohepcidin in the patients with H. pylori-associated disease were higher than those in the uninfected adults. In the patients with NG, the serum prohepcidin levels were higher than those in the other H. pylori-infected patient groups and decreased after the eradication. CONCLUSION: H. pylori-related iron-deficiency state might be associated with several factors, such as hypochlorhydria and hepcidin, in patients with GHP or NG.

Size-dependent expression of cyclooxygenase-2 in sporadic colorectal adenomas relative to adenomas in patients with familial adenomatous polyposis.

Several studies have indicated that administration of non-steroidal anti-inflammatory drugs (NSAID) to patients with familial adenomatous polyposis (FAP) results in a regression of colorectal adenomas through inhibition of cyclooxygenase-2 (COX-2). It is thought that sporadic colorectal adenomas might also be useful targets for the chemoprevention of colorectal cancer, but a marked effect of NSAID on the regression of sporadic adenomas has not been observed. We investigated the immunohistochemical expression of COX-2 in sporadic tubular adenomas (n = 100) from 63 patients and in tubular adenomas (n = 121) from 12 patients with FAP, in order to determine if chemoprevention might be more successful in sporadic adenomas once they have reached a certain size. COX-2 scores were significantly lower (P < 0.0001) in small (< 5 mm in diameter) adenomas than in large (> or = 5 mm) adenomas. This was observed in both sporadic cases and in cases involving patients with FAP. With regard to small (< 5 mm) adenomas, significantly higher (P = 0.02) COX-2 scores were obtained in adenomas resulting from FAP than sporadic adenomas. The variation in COX-2 expression observed among sporadic adenomas of different sizes should be taken into account when making decisions regarding attempts at chemoprevention using NSAID. Sporadic adenomas 5 mm or larger with upregulated COX-2 expression are potentially useful targets for the antiproliferative effects of NSAID.

Prophylactic clip application does not decrease delayed bleeding after colonoscopic polypectomy.

BACKGROUND: The most common major complication of colonoscopic polypectomy is postpolypectomy hemorrhage. Although several factors have been implicated in the occurrence of hemorrhage, accurate prediction of delayed bleeding remains difficult. This randomized controlled trial evaluated the efficacy of prophylactic clip application for prevention of delayed postpolypectomy bleeding. METHODS: Postpolypectomy ulcers created by colonoscopic removal of polyps (mean size 7.8 [4.0] mm) with the endoscopic mucosal resection technique were randomly assigned to prophylactic clip placement (n = 205) or no clip (n = 208). Baseline characteristics of the patients and polyps excised were comparable between the groups. Delayed bleeding was defined as the postprocedure passage of bloody stool or massive hematochezia. The site of delayed bleeding was identified at emergent colonoscopy. RESULTS: Delayed bleeding was identified from 2 ulcers in each group from 1 to 4 days after resection (mean 2.3 days). Delayed bleeding occurred from 0.98% of ulcers in the clip group and 0.96% in the non-clip group (p > 0.9999). No patient with delayed bleeding required transfusion or surgery. CONCLUSIONS: Prophylactic clip placement did not decrease the occurrence of delayed bleeding after colonoscopic polypectomy.

Comparison of cyclo-oxygenase 2 expression in colorectal serrated adenomas to expression in tubular adenomas and hyperplastic polyps.

BACKGROUND AND AIMS: Serrated adenoma (SA) is a newly defined category of colorectal neoplasia that contains features of both adenoma and hyperplastic polyp, and has two patterns, hyperplastic and cerebriform patterns. Since cyclooxygenase 2 (COX-2) has been found upregulated in colorectal cancers and adenomas, we examined whether either the hyperplastic or cerebriform pattern of SA has the potential for tumor progression and should be a target for clinical treatment. PATIENTS AND METHODS: An immunohistochemical scoring system was used to compare COX-2 expression in colorectal SAs (n=79), tubular adenomas (n=66), and hyperplastic polyps (n=21). RESULTS: COX-2 scores were significantly higher in SA of the cerebriform pattern (n=44) than in SA of the hyperplastic pattern (n=35). There was no difference in COX-2 scores between SA of the cerebriform pattern and tubular adenoma. In SA accompanied by hyperplastic polyp (n=26) the hyperplastic components expressed little COX-2, the same as traditional hyperplastic polyps. COX-2 expression in the SA component was similar to that in pure SA. CONCLUSION: SA of the cerebriform pattern should be treated similarly as traditional tubular adenomas. COX-2 induction may additionally be involved in progression from hyperplastic polyp to SA.