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Although the incidence of postbulbar duodenal ulcers is low, many complications occur, such as hemorrhage, stenosis and perforation, and there are many points to be paid attention to with regard to its pathology. A high acid level has been pointed out as a cause, but this is not conclusive, and its association with Helicobacter pylori (Hp) infection is also unclear. We investigated chronic cases excluding acute cases such as acute duodenal mucosal lesion we encountered between 2001 and 2015. Five cases corresponded, accounting for 1.4% of all chronic duodenal ulcer cases, and there were more male patients (four patients were male), as previously reported. All cases were solitary punched-out ulcer on the medial side near the superior duodenal flexure, and many complications were observed such as melena in all patients, narrowing in 2, and penetration in 1. No specific pathology, such as Crohn’s disease, vasculitis, or Zollinger-Ellison syndrome, was noted, no patient was previously medicated with NSAIDs or low dose aspirin, and 3 patients were infected with Hp. All cases were healed by proton pump inhibitor administration or gastric acid secretion-suppressing treatment with selective proximal vagotomy. Recurrence after Hp eradication occurred in all of the 3 Hp-infected patients, suggesting that involvement of Hp in the cause of disease is unlikely.

Objectives: Recent reports on venous blood gas analysis have shown that venous bicarbonate concentration is useful in the evaluation of the body acid-base status. Most of these reports have been based on the Bland-Altman analysis comparing arterial and venous blood gas values. We intended to elucidate any factors that decrease the agreement between venous and arterial bicarbonate concentrations, which might impair the usefulness of venous blood gas analysis. Methods: Healthy volunteers and patients with various diseases (n = 141) were evaluated by simultaneous arterial and venous blood sampling and Bland-Altman analysis. The venous-arterial bicarbonate concentration difference was compared between healthy volunteers and untreated respiratory alkalosis patients. Intentional hyperventilation (30 or 60 breaths/min, for 3 min) was also performed on 6 healthy volunteers and the venous-arterial bicarbonate concentration difference was evaluated. Results: The relative average bias in bicarbonate concentration was 2.00 mEq/l with venous bicarbonate higher than arterial bicarbonate with 95% limits of agreement of ±4.15 mEq/l. Hyperventilation challenges increased the venous-arterial bicarbonate concentration difference in an intensity-dependent manner. The venous-arterial bicarbonate concentration difference was higher in untreated respiratory alkalosis patients than in healthy volunteers (P Conclusion: Although venous bicarbonate may be useful to evaluate the body acid-base status, hyperventilation increases the venous-arterial bicarbonate concentration difference. Physicians should keep this phenomenon in mind.

A middle-aged man with no symptom or history visited our hospital due to duodenal abnormality and fecal occult blood detected by health screening. Upper gastrointestinal endoscopy showed marked enlargement of the papilla of Vater surrounded by nodules, and biopsy disclosed non-caseating granuloma. Colonoscopy yielded findings suggestive of intestinal tuberculosis such as annular ulcers. Examination of the biopsy samples failed to make a diagnosis of tuberculosis, and no pulmonary lesion was found, but whole-blood interferon gamma release assay was positive. The duodenal lesion was also suspected to be tubercular, so antitubercular drugs were administered. As this resulted in the resolution of both lesions, a definite diagnosis of tubercular papillitis of Vater was made. Duodenal tuberculosis is rare, and a localized lesion of the major duodenal papilla is extremely rare. However, this case suggests that tuberculosis must be considered in the differential diagnosis of lesions of the papilla of Vater.