MR Imaging-Based Evaluations of Olfactory Bulb Atrophy in Patients with Olfactory Dysfunction.

BACKGROUND AND PURPOSE: Although the olfactory bulb volume as assessed with MR imaging is known to reflect olfactory function, it is not always measured during olfactory pathway assessments in clinical settings. We aimed to evaluate the utility of visual olfactory bulb atrophy and neuropathy analyses using MR imaging in patients with olfactory dysfunction. MATERIALS AND METHODS: Thirty-four patients who presented with subjective olfactory loss between March 2016 and February 2017 were included. Patients underwent a nasal endoscopic examination, olfactory testing with the Korean Version of the Sniffin' Sticks test, and MR imaging. All patients completed the Sino-Nasal Outcome Test and Questionnaire of Olfactory Disorders. Olfactory bulb atrophy and neuropathy were evaluated on MR images by 2 head and neck radiologists. RESULTS: The etiology of olfactory loss was chronic rhinosinusitis with/without nasal polyps in 15 (44.1%) patients, respiratory viral infection in 7 (20.6%), trauma in 2 (5.9%), and idiopathic in 10 (29.4%) patients. Although 10 (29.4%) of the 34 patients were normosmic according to the Sniffin' Sticks test, their scores on the other tests were like those of patients who were hyposmic/anosmic according to the Sniffin' Sticks test. However, the detection rate of olfactory bulb atrophy was significantly higher in patients with hyposmia/anosmia than it was in patients with normosmia (P = .002). No difference in olfactory bulb neuropathy was identified among patients with normosmia and hyposmia/anosmia (P = .395). CONCLUSIONS: MR imaging evaluations of olfactory bulb atrophy can be used to objectively diagnose olfactory dysfunction in patients with subjective olfactory loss.

Difference in the distribution pattern of Helicobacter pylori and grade of gastritis in the antrum and in the body between duodenal ulcer and benign gastric ulcer patients.

OBJECTIVES: To investigate the relationship between the Helicobacter pylori (H. pylori) colonization and the grade of gastritis in the antrum and in the body of patients with duodenal ulcer (DU) or benign gastric ulcer (BGU). METHODS: This study was performed in H. pylori-positive 220 DU patients and 180 BGU patients. H. pylori density was evaluated by modified Giemsa staining and CLO test, and gastritis grade was graded by H&E staining in the antrum and in the body. RESULTS: H. pylori grade by Giemsa staining was 1.24 in the antrum and 0.82 in the body for DU group (p < 0.01), and those of BGU group were slightly reversed, 0.83 and 0.87, respectively, but without statistical significance. Similarly H. pylori grade by CLO test was 3.1 in the antrum and 2.8 in the body for DU group (p < 0.01), and those of BGU group 2.3 and 2.6 (p < 0.05), respectively. In contrast, gastritis grade was 1.7 in the antrum and 1.2 in the body for DU group (p < 0.01), and those of BGU group 1.6 and 1.3 (p < 0.01), respectively, similar to those of DU. However, there was a correlation between H. pylori grade and gastritis grade in the antrum and in the body, not only in DU but also in BGU group (p < 0.01). CONCLUSION: In spite of different distribution patterns of H. pylori between DU group and BGU group, gastritis grade of the antrum was significantly higher than that of the body in both DU and BGU. However, gastritis is correlated with H. pylori density not only in DU but also in BGU patients. It looks like the inflammatory reaction to H. pylori is stronger in the antrum than in the body.

Effect of eradication of Helicobacter pylori on the benign gastric ulcer recurrence--a 24 month follow-up study.

OBJECTIVES: To evaluate the effect of eradication of Helicobacter pylori (H. pylori) on the recurrence of benign gastric ulcer (BGU) in the patients with BGU. METHODS: This study was performed for 40 H. pylori-positive BGU patients cured of BGU and H. pylori eradicated, and for 25 H. pylori-positive patients (non-eradicated group) who were not treated with H. pylori eradication regimen or H. pylori was not eradicated. Four different methods--CLOtest, microscopy of Gram stained mucosal smear, culture and histology of modified Giemsa staining--were taken for identifying colonization of H. pylori before treatment, and 4 weeks after completion of triple therapy. For the control group in which triple therapy was not tried, follow-up gastroscopy was done to confirm the healing of the ulcer. To detect BGU recurrence, the gastroscopy was performed at 6, 12, 18, and 24 months after therapy. RESULTS: In the non-eradicated group, the BGU recurrence rate was 16% within 6 months, 40% within 1 year, 56% within 18 months and 60% within 2 years. The respective recurrence rates in the 40 patients in whom the bacteria had been eradicated were 0%, 7.5%, 10% and 10% (4 patients), respectively. Among the four BGU-recurred patients in whom H. pylori had been eradicated, one patient was found to have BGU recurring with H. pylori positive again in one year, and another two patients had NSAIDs ingestion history. CONCLUSION: The eradication of H. pylori in patients with BGU reduces the recurrence of BGU. In addition, the major causes of BGU recurrence look like NSAIDs ingestion and reinfection of H. pylori.