Yunju Jo

A Proton Pump Inhibitor's Effect on Bone Metabolism Mediated by Osteoclast Action in Old Age: A Prospective Randomized Study

Background/Aims Proton pump inhibitors (PPIs) act by irreversibly binding to the H+-K+-ATPase of the proton pump in parietal cells and may possibly affect the vacuolar H+-ATPase in osteoclasts. Methods We investigated the effect of 8 weeks of PPI treatment on the parameters of bone turnover and compared PPI with revaprazan, which acts by reversibly binding to H+-K+-ATPase in proton pumps. This study was a parallel randomized controlled trial. For 8 weeks, either a PPI or revaprazan was randomly assigned to patients with gastric ulcers. The parameters of bone turnover were measured at the beginning of and after the 8-week treatment period. Results Twenty-six patients (PPI, n=13; revaprazan, n=13) completed the intention-to-treat analysis. After the 8-week treatment period, serum calcium and urine deoxypyridinoline (DPD) were increased in the PPI group (serum calcium, p=0.046; urine DPD, p=0.046) but not in the revaprazan group. According to multivariate linear regression analysis, age ≥60 years was an independent predictor for the changes in serum calcium and urine DPD. Conclusions In elderly patients, administering a PPI for 8 weeks altered bone parameters. Our study suggested that PPIs might directly alter bone metabolism via the vacuolar H+-ATPase in osteoclasts.

Clinical significance of minimal change lesions of the esophagus in a healthy Korean population: A nationwide multi‐center prospective study

Background and Aim:  At least half of the patients with typical reflux symptoms have non‐erosive reflux disease (NERD). Minimal change lesions are commonly seen in the screening endoscopic examinations for individuals without clinically significant symptoms. We evaluated the correlation between minimal changes and symptoms in individuals visiting the hospital for routine health check‐up by a nationwide survey in 2006.

Clinicopathologic Analysis of Proton Pump Inhibitor-Responsive Esophageal Eosinophilia in Korean Patients

Background/Aims Proton pump inhibitor-responsive esophageal eosinophilia (PPI-REE) is a newly recognized form of eosinophilic esophagitis (EoE) that responds to PPI therapy. It remains unclear whether PPI-REE represents a subphenotype of gastroesophageal reflux disease, a subphenotype of EoE, or its own distinct entity. The aim was to evaluate the clinicopathologic features of PPI-REE. Methods Six patients were diagnosed with PPI-REE based on symptoms, endoscopic abnormalities, esophageal eosinophilia with ≥15 eosinophils/high-power field, and a response to PPI treatment. Symptoms and endoscopic and pathological findings were evaluated. Results The median follow-up duration was 12 months. Presenting symptoms included dysphagia, heartburn, chest pain, foreign body sensation, acid reflux, and sore throat. All patients had typical endoscopic findings of EoE such as esophageal rings, linear furrows, nodularity, and whitish plaques. Three patients had a concomitant allergic disorder, and one had reflux esophagitis. Four patients exhibited elevated serum IgE, and five had positive skin prick tests. All patients experienced symptomatic resolution within 4 weeks and histologic resolution within 8 weeks after starting PPI therapy. There was no symptomatic recurrence. Conclusions PPI therapy induced rapid resolution of symptoms and eosinophil counts in patients with PPI-REE. Large-scale studies with long-term follow-up are warranted.

A case of eosinophilic esophagitis with food hypersensitivity.

Eosinophilic esophagitis (EoE) is a disorder characterized by isolated eosinophilic infiltration of the esophagus with esophageal symptoms. Although some patients with EoE are related to food hypersensitivity, it is hard to identify causative foods. This report describes a case of EoE with dysphagia. A 28-year-old man presented with dysphagia and substernal discomfort for 15 days. He had taken a protein complex for 2 months. Endoscopy showed several linear furrows and multiple mucosal nodularities on the lower and mid esophagus, and the biopsies of esophagus revealed marked eosinophil infiltration in the mucosa. The skin testing for the protein complex was positive. The patient was successfully treated with withholding treatment.

Diaphragm disease compared with cryptogenic multifocal ulcerous stenosing enteritis.

As the use of drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs) increases, so too do gastrointestinal ulcers, bleeding, perforation and obstruction. Diaphragm disease of the small intestine is formed by submucosal fibrosis and destruction of lamina muscularis due to chronic ulceration, which corresponds to the most severe stage of NSAID enteropathy. It may lead to stricture of the small intestine. If such ulcerations and strictures in the small intestine are multiple, differential diagnosis is between diaphragm disease and cryptogenic multifocal ulcerous stenosing enteritis (CMUSE), because the gross findings of diaphragm disease are similar to those of CMUSE. We report a rare case of diaphragm disease caused by NSAID. It has been finally confirmed by capsule endoscopy and the origin of chronic obscure gastrointestinal bleeding was found to be multiple ulcers and strictures in the small intestine. After operation, we diagnosed the patient with diaphragm disease rather than CMUSE.

A Case of Oral-contraceptive Related Ischemic Colitis in Young Woman

Ischemic colitis is generally considered a disease of the elderly. The causes of ischemic colitis include low-flow states due to cardiac dysfunction or hypovolemia and certain medications including estrogen. Here we report a case of ischemic colitis in a 26-year-old woman. She had no specific medical history except taking oral-contraceptives for a long time. The mechanism of estrogen-induced ischemic colitis is not clearly understood. But we recommend that oral-contraceptives should be considered as a cause of ischemic colitis in young women.

Proton Pump Inhibitors Reduce the Size and Acidity of the Gastric Acid Pocket

Gastric acid pocket is a portion of unbuffered acid accumulations in the proximal stomach during postprandial period. It could be a reservoir of acid reflux in patients with gastroesophageal reflux disease (GERD). How proton pump inhibitors (PPIs) control the acid pocket is rarely known. Recently, Rohof et al1 reported PPIs might change the size, acidity, or position of the acid pocket, which contribute to the therapeutic effect in patients with GERD. Concurrent high resolution manometry and pH-impedance monitoring were performed in 36 patients with GERD (18 on PPIs and 18 off PPIs) after a standardized meal. The acid pocket was visualized using scintigraphy, and its size and position were measured using radionuclide markers. The pH of acid pocket was measured in its aspirates. In patients on PPIs, the number of acid reflux episodes was reduced, and the acid pocket was smaller and more frequently located below the diaphragm, and the mean pH of acid pocket was significantly higher. The number of reflux events was not altered by PPIs. It is interesting to show the acid pocket itself with and reflux episodes through a large hiatal hernia using scintigraphic images by the 99mTc-pertechnetate-labeling.

Gastric Emptying in Patients With Functional Dyspepsia and Patients With Migrain: Author's Reply.

TO THE EDITOR: Thank you for your comments, Dr. Lee. Gastric scintigraphy is a noninvasive, simple to perform, and quantitative method. This study tried to increase the objectivity and reproducibility by examination and interpretation according to the guidelines. We also tried to obtain our own data on gastric emptying (GE) times in our hospital, because we thought it was important to collect unique data in an individual institute. As Dr. Lee pointed out, functional dyspepsia (FD) and control group of this study showed delayed GE compared to previous studies. We already mentioned about that in the discussion. This might be because there was relatively large proportions of young female subjects enrolled in the FD and control group to match gender and age with the migraine group. Actually, females and premenopausal status showed more delayed GE than males and postmenopausal status, and a previous study found that female sex is the independent factor related to delayed GE in the patients with FD. Secondly, there was no significant correlation between GE and symptoms in our study as pointed out by Dr Lee. A tendency of delayed GE was shown in FD patients complaining postprandial fullness and early satiety. Regarding the association between GE parameters and dyspeptic symptoms in patients with FD, larger studies have shown the association of postprandial fullness and nausea with delayed GE. Our study had the limitation of a single-center study targeting a small number of patients, because we had selected the age and gender matched groups from the FD population who had undergone GE scintigraphy. However, the migraine and normal control groups were enrolled prospectively to perform gastric scintigraphy during the interictal period. Lastly, the relationship between migraine and GE is still controversial, and inaccurate evaluation of gastric symptoms during interictal period was the limitation in previous studies. Therefore, we enrolled the migraine patients without gastric symptoms during interictal period in order to minimize overlaps with FD. As pointed out by Dr. Lee, it could be better to perform scintigraphy in the ictal period to find the correlation with nausea and vomiting that occurs in the ictal period, but it should not allowed because of an ethical reason. Gastric symptoms, including nausea and vomiting, found in the ictal period might be caused by the central and peripheral nervous mechanisms. Nausea and vomiting in migraine patients during ictal period may be known to be not related to delayed GE, but other mechanisms.