Hajime Futami

Effect of cytochrome P4502C19 genotypic differences on cure rates for gastroesophageal reflux disease by lansoprazole

The acid‐inhibitory effect of lansoprazole depends on differences in cytochrome P450 (CYP) 2C19 genotypes. We assessed whether therapeutic effects of lansoprazole on gastroesophageal reflux disease (GERD) depended on the CYP2C19 genotype status in relation to the grade of GERD.

PYODERMA GANGRENOSUM COMPLICATING ULCERATIVE COLITIS : SUCCESSFUL TREATMENT WITH METHYLPREDNISOLONE PULSE THERAPY AND CYCLOSPORINE

Abstract: A 32-year-old woman with ulcerative colitis had a relapsed of pyoderma gangrenosum during puerperium. Both the pyoderma gangrenosum and ulcerative colitis had been well controlled with oral prednisolone, but ulcerative colitis relapsed in pregnancy, and pyoderma gangrenosum relapsed in the puerperium. The pyoderma gangrenosum responded to methylprednisolone pulse therapy initially, but relapsed when prednisolone was tapered. A second trial of pulse therapy combined with cyclosporine resulted in complete remission of the pyoderma gangrenosum, and no recurrence was recognized after prednisolone was tapered. This is a very rare case of successful treatment with methylprednisolone pulse therapy combined with cyclosporine for pyoderma gangrenosum complicating ulcerative colitis.

Effects of lansoprazole with or without amoxicillin on ulcer healing: relation to eradication of Helicobacter pylori.

We studied the effects of lansoprazole with or without amoxicillin on the quality of ulcer healing in relation to eradication of Helicobacter pylori. Ulcer healing rates for lansoprazole 30 mg q.d. alone (group A) were 100% for duodenal ulcers (DU; n = 20) and 92% for gastric ulcers (GU; n = 15). The healing rates for lansoprazole 30 mg plus amoxicillin 1–2 g q.d. (group B) were 100% for both DU (n = 20) and GU (n = 12). Endoscopic findings after treatment showed that the red scar/white scar ratio in group A was 16/4 for DU and 12/1 for GU. The red scar/white scar ratio in group B was 4/16 for DU and 6/6 for GU. The numbers of H. pylori in gastric mucus did not change throughout the course of treatment in group A but decreased significantly, without H. pylori relapse, in group B. Changes in ammonia concentration in gastric juice, as well as serum gastrin and pepsinogen I and II levels, differed between group A and group B. Concomitant treatment with lansoprazole and high-dose amoxicillin eradicated H. pylori and modified gastric secretory function, resulting in high-quality ulcer healing.

Further evidence that exacerbation of ulcerative colitis causes the onset of immune thrombocytopenia: a clinical case

ABSTRACTUlcerative colitis associated with immune-mediated thrombocytopenia is rare. It has been suggested that antigenic mimicry between platelet surface antigen and bacterial glycoprotein plays a role in this association. We present a case in which exacerbation of UC sequentially induced development of ITP associated with elevation of PAIgG. In the case, two episodes of ITP occurred, with each preceded by exacerbation of UC. After remission of UC, ITP remitted and PAIgG simultaneously decreased. In the first episode, the onset of ITP was about 1 month after the exacerbation of UC. However, in the second episode, the onset of ITP was much faster, 11 days after that of UC, and the magnitude of elevation of PAIgG was much higher in the second episode. This may provide further evidence that ITP is causally associated with UC, and is the result of immunostimulation from luminal antigens and altered immunoregulation.

Relationship between Helicobacter pylori infection and gastric metaplasia in the duodenal bulb in the pathogenesis of duodenal ulcer

Background: The aim of this study was to determine whether the amount of Helicobacter pylori and the extent of gastric metaplasia in the duodenal mucosa play critical roles in the pathogenesis of duodenal ulcer.

Adenoma of the common bile duct in Gardner's syndrome may cause relapsing acute pancreatitis

Familial adenomatous polyposis of the colon, or Gardners syndrome, is often accompanied by adenomas of the stomach and duodenum. We experienced a rare case of Gardners syndrome, with adenomas of the common bile duct, in a patient who presented with relapsing acute pancreatitis. Our findings indicate that adenoma in the common bile duct or pancreatic duct should be considered as a possible etiology when patients with familial polyposis or Gardners syndrome present with pancreatitis, particularly relapsing acute pancreatitis.

Amount of Helicobacter pylori in gastric mucus during anti-H. pylori treatment

Helicobacter pylori is present in infected patients not only on the gastric epithelial cell surface but also in gastric mucus. We developed a competitive polymerase chain reaction (cPCR) method for quantitative measurement of H. pylori in gastric mucus. The aim of this study was to determine the number of H. pylori in gastric mucus before and after anti‐H. pylori treatment. Patients with duodenal ulcer were treated with lansoprazole alone (n=11) or lansoprazole and amoxycillin (n=12). The amount of H, pylori in gastric mucus was measured over time by a cPCR assay. Helicobacter pylori infection was also tested for using histology, culture, and the rapid urease test (RUT). Although most patients treated with lansoprazole alone had become H. pylori‐negative by the end of treatment when tested by histology, RUT, and culture, a large number of H. pylori organisms were found in the gastric mucus at that time by cPCR. These patients returned to being H. pylori positive 1 to 12 months later on the basis of histology, RUT, and culture. However, cPCR results indicated eradication of H. pylori by the end of treatment in eight of the 12 patients treated with lansoprazole and amoxicillin, and these patients remained H. pylori negative on histology, RUT, culture, and cPCR 1 to 12 months later. Testing for H. pylori in gastric mucus is thus useful for precise determination of the success or failure of H. pylori eradication therapy.