Hiroyuki Wakabayashi

Measurement of the expiratory ammonia concentration and its clinical significance

Alghough gaseous ammonia (NH3) can freely enter cells through the plasma membrane where NH3 is cyto(neuro)toxic, NH3 and ionic ammonia (NH4+) contents have not been studied in biological materials. We developed a new method for measurement of expiratory NH3 concentration, which may reflect blood NH3 concentrations. The method is a sensor tube type-gas assay system. Expiratory NH3 concentrations in patients with chronic liver diseases increased when their blood ammonia (NH4++NH3) concentrations increased above 90 μg/dl (normal range; 12–66 μg/dl). However, cirrhotic patients, who had relatively higher expiratory NH3 concentration compared to blood NH3 concentrations (calculated from Henderson-Hasselbalch formula), were found to have subclinical encephalopathy. Measurement of experatory NH3 concentration may be of clinical significance for the diagnosis of encephalopathy associated with hyperammonemia.

Effect of Helicobacter pylori infection on gastric mucosal phospholipid contents and their fatty acid composition

To investigate the effect of Helicobacter pylori infection on the ‘gastric mucosal barrier’, phospholipid contents and the fatty acid composition of endoscopic biopsy specimens of the gastric mucosa were analysed in healthy volunteers with and without H. pylori infection. The gastric corporeal phos‐phatidylcholine (PC) content of H. pylori‐positive healthy volunteers was less than that of H. pylori‐negative healthy volunteers (P < 0.05). Moreover, H. pylori‐positive healthy volunteers had a decrease in linoleic acid composition (P < 0.0001) and an increase in arachidonic acid composition (P < 0.0001) and in the arachidonic acid/linoleic acid ratio (P < 0.0001) of antral and corporeal PC compared with H. pylori‐negative healthy volunteers. These findings suggest that H. pylori infection enhances production of various eicosanoids, resulting in changes in the gastric mucosal phospholipid contents and their fatty acid composition, that may consequently cause the gastric mucosal barrier to be weakened.

Effect of Helicobacter pylori eradication on gastric mucosal phospholipid content and its fatty acid composition.

Background and Aims: Whether Helicobacter pylori eradication alters gastric mucosal phospholipid contents and their fatty acid composition remains unclear. The aim of the present study was to clarify the effect of H. pylori eradication on gastric mucosal phosphatidylcholine (PC) content and its fatty acid composition.

Helicobacter pylori alters n‐6 fatty acid metabolism and prostaglandin E2 synthesis in rat gastric mucosal cells

Little is known about whether Helicobacter pylori infection alters fatty acid metabolism in gastric mucosal cells. By using cultured rat gastric mucosal cells (RGM‐1), we investigated the effect of H. pylori broth culture filtrates on this point. Furthermore, our study aimed to find out whether n‐6 long chain polyunsaturated fatty acids from linoleic acid are formed in RGM‐1 cells.

Clinical relevance of cagE gene from Helicobacter pylori strains in Japan

It has been reported that H. pylori-containing cagE was associated with duodenal ulcer. The aims of the present study were to clarify the association between the cagE gene and clinical outcome and to analyze the relationship between the cagE gene and two other virulence factors—cagA and vacA—in two areas in Japan (Fukui and Okinawa) where the prevalence of duodenal ulcer and gastric cancer risk are quite different. Eighty of 81 isolates possessed the cagE gene, and all isolates possessed the cagA gene. The vacA genotype s1c/m1 was a major genotype in both areas in Japan. There was no significant association between cagE, cagA status, or vacA genotype and clinical outcome. Phylogenetic analysis of the cagE gene indicated that most Japanese isolates formed a different cluster from strains isolated in the West with an association with the vacA genotype. In conclusion, the strains with cagE, cagA, and the s1c/m1 genotype of vacA are predominant in Japan regardless of clinical outcome and construct a different phylogenetic cluster from those in the West.

Abnormality in fatty acid composition of gastric mucosal phospholipids in patients with liver cirrhosis and its correction with a polyunsaturated fatty acid‐enriched soft oil capsule

The abnormal composition of the fatty acids in gastric mucosal phospholipids was examined in 11 patients with non‐alcoholic liver cirrhosis accompanied by gastritis and in 10 healthy subjects without liver disease and gastritis. The cases positive for serum anti‐Helicobacter pylori immunoglobulin G antibody were excluded. The arachidonic acid (AA, C20:4n‐6) contents of the two main components of phospholipid, the phosphatidylcholine (PC) and phosphatidylethanolamine (PE) fractions, in gastric biopsy specimens were significantly lower in the cirrhosis group, although PC and PE contents in gastric biopsy specimens were not altered. In the cirrhosis group, AA contents of the PC fractions in gastric biopsy specimens were significantly correlated with AA contents of plasma PC fractions and serum albumin levels. Soft oil capsules containing polyunsaturated fatty acid (PUFA) such as AA, eicosapentanoic acid (EPA, C20:5n‐3) and docosahexanoic acid (DHA, C20:6n‐3) were administered after each meal daily for 4 weeks to six cirrhotic patients and four control subjects, who were randomly selected from the patients and control subjects. After administration of PUFA‐enriched oil capsules, gastric mucosal AA contents of PC and PE fractions were significantly improved almost to the control levels. In three cirrhotic patients with severe or mild gastritis whose gastric mucosal lesions were endoscopically shown to have responded to PUFA‐enriched oil capsules, AA contents of plasma PC and PE fractions before administration were much lower than in the remaining three cirrhotics that did not respond to the PUFA‐enriched oil capsules, but significantly improved to the control levels after administration of oil capsules. The results demonstrate that administration of PUFA‐enriched soft oil capsules increased AA contents of the phospholipids in gastric mucosa and thus improved gastric mucosal lesions endoscopically in cirrhotic patients with gastritis.

A Case of Cytomegalovirus‐Induced Gastric Lesions

Abstract: A 26‐year‐old woman was admitted to our hospital with epigastric pain, a husky voice, high‐grade fever, hepatosplenomegaly and enlargement of the kidneys. An upper gastrointestinal endoscopy revealed scattered non‐circular erythematous erosions, up to 5mm in diameter, in the gastric body and fornix. A histological examination of the biopsied specimens stained with hematoxylin and eosin showed the presence of intranuclear inclusion bodies in the glandular epithelial cells. Cytomegalovirus (CMV) antigen was found in the inclusion bodies using the enzyme‐labeled antibody method. Subsequently, a needle biopsy taken from the kidney revealed a non‐Hodgkins lymphoma. Our review of the literature indicates that CMV‐induced gastric lesions are endoscopically characteristic and can be diagnosed from their multiple, erythematous, non‐circular depressed lesions.