CYP2C19 genotype status, as well as the grade of GERD before treatment, is one of the determinants for the success or failure of treatment of GERD with lansoprazole. The low cure rate in patients with the homozygous extensive metabolizer genotype appeared to be a result of these patients having the lowest plasma lansoprazole levels among the 3 genotype groups.

may not be effective; in such cases, total colectomy is mandatory.We present a patient with extensive PG complicating UC who responded once to methylprednisolone pulse therapy, but relapsed during the tapering of prednisolone. Eventually, with pulse therapy plus cyclosporine, prednisolone was tapered without recurrence of PG. Case reportA 32-year-old woman was admitted because of severe PG and bloody stool on April 13, 1994. Six years previously, she had been diagnosed with UC that involved the rectum and the sigmoid and descending colon. Although PG occurred 2 years later, it and the UC had been well controlled until 1 year before admission, with maintenance therapy of 5 mg/day oral prednisolone. At 10 weeks' gestation, she had abdominal discomfort and passed bloody loose stools once or twice per day. The dose of prednisolone was increased to 10 mg, and the hematochezia and loose stool gradually decreased in frequency but still occurred occasionally. She gave birth normally on December 20, 1993 (Fig. 1). Four weeks after the delivery, active skin lesions developed on her face, neck, upper arm, and thigh (Fig. 2). The dose of prednisolone was increased to 20 mg/day but this failed to ameliorate the skin lesions. She was then hospitalized.On admission, she was well-nourished (56 kg, 154 cm) with cushingoid features. Body temperature was 37.3°C. Hemoglobin was 14.2 g/dl, white blood cell count 10 400 per mm 3 , erythrocyte sedimentation rate 34 mm/h, serum protein, 7.0 g/dl; serum albumin, 3.8 g/dl; aspartate aminotransferase (AST), 30 IU/l (11-30); alanine aminotransferase (ALT), 32 IU/l (5-42); lactic dehydrogenase (LDH), 259 IU/l (101-193); alkaline phosphatase, 34 IU/l; total bilirubin, 0.4 mg/dl; and C-reactive protein (CRP), 2.9 mg/dl (Ͻ0.15). 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.

The seroprevalence of Helicobacter pylori in a group of 1,043 healthy Japanese people was compared with that of hepatitis A virus (HAV), which was used as a marker of fecal-oral exposure. No statistically significant relationship was observed between seropositivity for HAV and that for H. pylori. Therefore, the fecal-oral spread of H. pylori is of limited relevance in Japan.

Helicobacter pylori is closely related to upper gastrointestinal diseases, and the precise evaluation of H. pylori infection is necessary for the treatment of these diseases. The aim of the present study was to establish a method for the quantitative detection of H. pylori. We applied a competitive PCR method using various amounts of synthetic DNA fragments containing the same primer-binding and a subset of the same template sequences as the target competing for primer binding and amplification in order to quantify H. pylori in gastric mucus. The results obtained by this method were compared with the results of histological examination, the rapid urease test, bacterial culture, the [ 13 C]urea breath test, and urea and ammonia measurements in gastric juice. As the quantity of H. pylori in gastric mucus increased, the rates of positivity of histological examination, the rapid urease test, and bacterial culture increased. The quantity of H. pylori in gastric mucus was also significantly correlated with the results of the [ 13 C]urea breath test and was negatively correlated with the urea/ammonia ratio in gastric juice. The competitive PCR method provides an objective measure of the quantity of H. pylori and makes it possible to distinguish true negatives from false negatives due to incomplete PCR and true positives from false positives due to contamination. This method is very useful for the precise evaluation of gastric H. pylori infection.

The findings of this study indicate that H. pylori colonization in the duodenal bulb may play a critically important role in the pathogenesis of duodenal ulcer and that the amount of H. pylori in the duodenal bulb may be related to the amount of H. pylori in the gastric antrum and the extent of gastric metaplasia in the duodenal bulb.