Jejunal varices after choledochojejunostomy treated with laparotomic transcatheter variceal embolization.

Portal hypertension induces collateral shunt formation between the portal and systemic circulation, decompressing the elevated portal pressure. Ectopic varices outside of the gastroesophageal region, such as jejunal varices, are rare conditions. This report describes the successful embolization of ruptured jejunal varices resulting from an extrahepatic portal obstruction. A 62-year-old man was admitted to our hospital with recurrent massive gastrointestinal bleeding. Fourteen months earlier, he had undergone a choledochojejunostomy and pancreatic cystojejunostomy for bile duct stenosis with an enlarged pancreatic pseudocyst due to severe chronic pancreatitis. Contrast-enhanced computed tomography showed jejunal intramural dilated vessels close to the choledochojejunal anastomosis, but extravasation was not observed. Due to the lack of a rapid definitive diagnosis, the patient required massive blood transfusions. Hemorrhagic scintigraphy using 99mTc-HSAD finally identified the site of the hemorrhage. Angiography and double-balloon endoscopy revealed the anastomotic jejunal varices to be the result of an extrahepatic portal obstruction. Laparotomic transcatheter variceal embolization with microcoils was successful in halting the refractory gastrointestinal bleeding. This surgery preserved hepatopetal portal venous flow by another route, and no complications were observed. At present, 4 years post-surgery, there has been no recurrence of gastrointestinal hemorrhage. The development of jejunal varices is often associated with postoperative adhesions. Some patients with a history of hepatico- or choledochojejunostomy may experience portal hypertension resulting from extrahepatic portal obstruction, leading to the formation of jejunal varices as hepatopetal portal collaterals. The choice of therapy in each patient should be based on the individual hemodynamics of the ectopic varices.

Simultaneous combined balloon-occluded retrograde transvenous obliteration and partial splenic embolization for gastric fundal varices.

BACKGROUND: We previously reported the techniques and usefulness of simultaneous combined balloon-occluded retrograde transvenous obliteration (B-RTO) and partial splenic embolization (PSE), based on the hypothesis that concomitant PSE can diminish the increase in portal venous pressure after B-RTO. OBJECTIVE: After experiencing more cases and performing longer-term follow-up, we re-evaluated the efficacy of simultaneous combined B-RTO and PSE for gastric fundal varices (GVs). METHODS: We performed B-RTO in 36 consecutive patients treated for GVs from 2005 to 2013. Twenty-three patients underwent simultaneous combined B-RTO and PSE (Group 1) and 13 underwent B-RTO monotherapy (Group 2). The outcomes were retrospectively evaluated. RESULTS: There were no significant differences in baseline characteristics between the two groups except that the splenic volumes were larger in Group 1 than 2. B-RTO was technically successful in 21 of 23 patients (91.3%) in Group 1 and in 12 of 13 patients (92.3%) in Group 2. In all patients with ruptured GVs (six in Group 1 and five in Group 2), complete hemostasis was obtained by B-RTO. Exacerbation of esophageal varices was significantly less frequent in Group 1 than 2 (p = 0.0017). CONCLUSION: Concomitant PSE with B-RTO may contribute to prevention of the exacerbation of esophageal varices after B-RTO.

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.

[A case of malignant peritoneal mesothelioma successfully treated with systemic chemothrapy].

A 64-year-old man with a 2-month history of abdominal distension was admitted for transient cerebral ischemic attack. A CT scan revealed massive ascites. Laparoscopy showed multiple whitish nodules on the visceral peritoneum and the omentum. Peritoneal biopsy revealed tumor cells consistent with malignant peritoneal mesothelioma (MPeM). Pemetrexed in combination with cisplatin was administered because it has been reported to be active in patients with MPeM. However his disease progressed. As second-line therapy paclitaxel was tried which yielded a complete response (CR). Eighteen months later he developed abdominal pain of the right upper region where a CT scan showed a mass with surrounding inflammation. As third-line therapy, gemcitabine was administered and again resulted in a CR. He is alive at 3 years from first presenting. Searches for case studies published in medical journals on MPeM were carried out, and 59 cases were analyzed in comparison with this case.

Simultaneous combined balloon-occluded retrograde transvenous obliteration and partial splenic embolization for portosystemic shunts.

PURPOSE: To evaluate the efficacy and safety of simultaneous combined balloon-occluded retrograde transvenous obliteration (B-RTO) and partial splenic embolization (PSE) for gastric varices and/or hepatic encephalopathy. MATERIALS AND METHODS: B-RTO was performed in 19 consecutive patients with gastric varices and/or hepatic encephalopathy, of whom 10 received simultaneous combined B-RTO and PSE (group 1) and nine received B-RTO monotherapy (group 2). To evaluate the safety of these techniques, we analyzed 20 patients who received PSE monotherapy during the same period as a control group (group 3). Outcomes were retrospectively assessed. RESULTS: No significant differences were observed in baseline characteristics among the three groups except for significantly lower platelet counts and larger spleen volumes in group 3. In all cases in groups 1 and 2, gastric varices disappeared and hepatic encephalopathy improved after treatment. Procedure times were not significantly different between groups 1 and 2 (P = .7435). In group 1, the volume of sclerosing agent required for B-RTO was significantly lower (P = .0355) and exacerbation of esophageal varices was significantly less frequent (P = .0146) than in group 2. Few serious complications occurred in patients who received combined therapy. CONCLUSIONS: This study indicates that concomitant PSE may help diminish the increase in portal venous pressure after B-RTO for portosystemic shunts, and may allow a reduction in the volume of hazardous sclerosing agent used. It is worth evaluating the efficacy of simultaneous B-RTO and PSE in a prospective study.

Early upsurge in anti-HBs titer possibly caused by the immunomodulative, not by the mutagenetic effect of interferon and ribavirin.

A patient with chronic hepatitis B and C undergoing treatment with interferon and ribavirin showed an upsurge in hepatitis B virus surface antibody (anti-HBs) titer, accompanied by a decrease in hepatitis B virus surface antigen (HBsAg) during the early treatment phase. Simultaneously, elevation of alanine aminotransferase (ALT) was observed. Subsequently, the hepatitis B virus (HBV) DNA titer decreased and HBV e antigen (HBeAg) to anti-HBe seroconversion occurred. The anti-HBs titer gradually returned to the pretreatment level after cessation of ribavirin treatment and HBV-DNA became undetectable. We found no nucleotide mutations in HBV-DNA that could explain the sudden elevation in anti-HBs titer. The appearance of anti-HBs was considered to be a break in immune tolerance against some epitopes in HBsAg, possibly the r epitope, stimulated by interferon/ribavirin treatment. The immunomodulatory effect of ribavirin might have caused this unexpected early immune response to HBsAg that preceded seroconversion to anti-HBe.

A primary follicular lymphoma of the duodenum treated successfully with radiation therapy.

A 48-year-old man was admitted to our hospital because of repeated episodes of epigastralgia. Endoscopy showed multiple whitish granules extending from the 2nd to 3rd portion of the duodenum. Biopsy specimens showed well circumscribed follicles with a monotonous population of predominantly small cleaved cells that were positive for CD20, CD10 and BCL2, but negative for CD5. A full staging study showed no abnormalities. The tumor was finally diagnosed according to the WHO classification as a stage I follicular lymphoma (FL), grade 1, of the duodenum and subsequently received irradiation to the involved area. After 3 years of followup, he is still in complete remission. Because FL arising in the duodenum has recently reported with increasing frequency, patients with multiple granules in the duodenum should be examined carefully.

Leukocytapheresis is effective in inducing but not in maintaining remission in ulcerative colitis.

GOALS AND BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by dense infiltration of lymphocytes, plasma cells, neutrophils, and monocyte-macrophages into the colonic mucosa. Leukocytapheresis is a procedure for selectively removing white blood cells from withdrawn blood. It is used for the treatment of several autoimmune diseases. This study was performed to evaluate the effectiveness of leukocytapheresis for inducing and maintaining remission in corticosteroid-resistant UC, as compared with corticosteroid-responsive UC. STUDY: Forty-five patients with active UC who were treated with a dose of 1 mg/kg per day or more of prednisolone given systemically for at least 2 weeks were evaluated. Twenty patients (6 males, 14 females) in whom improvement was induced only by high doses of prednisolone were allocated as the corticosteroid-responsive group. The other 25 patients (11 males, 14 females) who did not respond to the above-mentioned dose of prednisolone therapy were allocated as the corticosteroid-resistant group and received leukocytapheresis therapy once a week for 5 weeks. Of patients who had a remission, the corticosteroid-responsive group continued to have the conventional therapy and the corticosteroid-resistant group were given leukocytapheresis once every 4 weeks for at least 2 years as maintenance therapy. RESULTS: Remission was induced by 5 weeks of leukocytapheresis in 23 of the 25 (92%) patients with corticosteroid-resistant active UC. The number of days required to achieve remission of UC was fewer in patients who received leukocytapheresis than in those who did not. Follow-up study of the patients who had remission showed similar relapse rates at 2 years in the patients who received leukocytapheresis and those given high doses of prednisolone alone. CONCLUSIONS: Leukocytapheresis is an effective treatment of acute corticosteroid-resistant UC but does not prevent the recurrence of UC.

A novel NOD2/CARD15 haplotype conferring risk for Crohn disease in Ashkenazi Jews.

Crohn disease (CD) exhibits a 2-4-fold increased frequency in Jews as compared with other ethnic/racial groups. Three coding variants of the NOD2/CARD15 have been reported as independent disease-predisposing mutations (DPMs), but these were found in only 30%-40% of patients with CD and could not account for all the linkage between CD and the IBD1 locus. The aim of the present study was to explore whether additional DPMs at the IBD1 locus exist in the high-risk Jewish group. Sixty-four Ashkenazi Jewish and 147 non-Jewish white families were studied. Six microsatellite markers spanning IBD1 were genotyped for linkage analysis in subgroups stratified on NOD2/CARD15 DPM status. SNPs in NOD2/CARD15 (R702W, G908R, 1007fs, and S268P) were then genotyped in family and independent case-control samples. On the basis of initial results, sequencing was done on NOD2/CARD15-translated regions in 12 Jewish individuals. Subsequently, a new NOD2/CARD15 variant was genotyped and analyzed. After excluding the influence of the three DPMs, significant linkage of IBD1 to CD in Jews remained with two peaks at D16S403 (mean allele sharing [MAS] = 0.70] and D16S411 (MAS = 0.59). Further, we observed an increased frequency of a haplotype carrying only the 268S variant in Jewish patients (OR = 3.13, P=.0023) but not in non-Jews, suggesting the existence of a Jewish-specific additional disease-predisposing factor on this haplotype. Sequencing of this haplotype revealed a new variant (IVS8+158; JW1). The 268S-JW1 combination exhibited a further increased risk (OR = 5.75, P=.0005) and the highest population-attributable risk (15.1%) for CD among reported DPMs in Jews. In Ashkenazi Jews, unrecognized population-specific predisposing factor(s) exist on the 268S-JW1 haplotype at the IBD1 locus. This factor may contribute to the higher risk for CD in Ashkenazi Jews as compared with non-Jews.

Immunomodulatory effects of granulocyte and monocyte adsorption apheresis as a treatment for patients with ulcerative colitis.

Our aim was to understand the mechanism of immunological changes associated with the use of an adsorptive-type extracorporeal device (Adacolumn) that has been developed for selective adsorption of granulocytes and monocytes/macrophages from peripheral blood of patients with active ulcerative colitis. The column is filled with carriers (G-1 beads) that have a diameter of 2 mm and are made of cellulose diacetate. In peripheral blood treated with the G-1 beads or peripheral blood from patients with active ulcerative colitis following granulocyte and monocyte adsorption apheresis, a significant suppression of proinflammatory cytokines (tissue necrosis factor-alpha, interleukin-1beta, interleukin-6, and interleukin-8) production by leukocytes, neutrophil chemotaxis, down-regulation of leukocyte adhesion molecule (L-selectin) and neutrophil adhesion to interleukin-1beta-activated endothelial cells were observed. Furthermore, after granulocyte adsorption therapy, the number of CD10-negative premature granulocytes increased, indicating increased turnover of these cells in the circulation. Our observations suggest that selective granulocyte and monocyte adsorption is associated with modified peripheral blood leukocyte function favorable to patients with ulcerative colitis and possibly other autoimmune disorders which reflect leukocyte hyperactivity.

Gastric carcinoid tumors without autoimmune gastritis in Japan: a relationship with Helicobacter pylori infection.

In Japan, most cases of gastric carcinoid tumor (GCT) are unassociated with either autoimmune gastritis (AIG) showing type-A chronic atrophic gastritis (CAG-A) or Zollinger-Ellison syndrome (ZES). However, the pathogenesis of this tumor remains unknown. Recent studies have determined that Helicobacter pylori infection induces gastric carcinoid in Mongolian gerbils and that H. pylori lipopolysaccharide exerts a mitogenic effect on ECL cells. We examined five patients with histologically diagnosed GCT, 40 patients with H. pylori-positive gastric ulcer (Hp+GU), 24 patients with H. pylori-positive duodenal ulcer (Hp+DU), and 12 patients with AIG showing CAG-A topographically. We compared the prevalence of H. pylori infection, and the levels of gastrin and pepsinogen (PG) in the serum of patients with GCT with those of patients with Hp+GU, or Hp+DU, and AIG. We also investigated the histological characteristics of the tumor and the gastric corpus mucosa in the GCT patients. The levels of serum gastrin and PG I and II were measured using an RIA kit. In all five (100%) patients with GCT, H. pylori infection was present, without any evidence of AIG or ZES. The serum levels of gastrin in the GCT patients were higher than those in either Hp+GU or Hp+DU patients and lower than those in the AIG patients. In contrast, serum PG I levels and the PG I/II ratio were lower in the GCT group than in the Hp+GU or Hp+DU groups. Histologically, all GCTs were ECL cell tumors and peritumoral corporal mucosal atrophy was observed in four of the five patients with GCT. In conclusions, H. pylori infection and hypergastrinemia were found in the patients with GCT without AIG. This finding suggests that H. pylori infection may induce corporal mucosal atrophy and hypergastrinemia that can produce a GCT with time.