Endoscopic Prediction for Acid Reflux in Patients without Hiatus Hernia / 대한소화기학회지

Background/Aims@#A diagnosis of gastroesophageal reflux disease is challenging in patients who have reflux symptoms but do not respond to proton pump inhibitors nor have reflux esophagitis and hiatal hernia (HH) on endoscopy. This study examined the predictive role of the endoscopic findings, including the flap valve grade for pathologic acid exposure (PAE) to establish an endoscopic prediction model in patients with neither reflux esophagitis nor HH. @*Methods@#Five hundred seventy-eight patients who underwent upper endoscopy and 24 hours pH monitoring for reflux esophageal symptoms without evidence of reflux esophagitis and HH were analyzed. The gastroesophageal flap valve (GEFV), esophageal metaplasia, and chronic atrophic gastritis were assessed. The association between the endoscopic parameters and PAE was evaluated. @*Results@#Four hundred ninety-four patients were enrolled. The most common complaint was chest discomfort (42.3%) followed by globus (31.8%), dysphagia (7.9%), and heartburn (7.7%). PAE was present in 43 patients (8.7%). Multivariable analysis revealed PAE to be associated with the GEFV grade (p<0.001) and inversely associated with the chronic atrophic gastritis grade (p=0.005). Using these features, a predictive model was established and showed an area under the receiver operating characteristic curve of 0.705 (95% CI 0.619-0.790). The cutoff value of 12.0 had a sensitivity and specificity of 44.0% and 84.0%, respectively. @*Conclusions@#A loosened GEFV is associated with a risk of PAE in patients with neither reflux esophagitis nor HH, while atrophic gastritis is preventive. On the other hand, the endoscopic predictive model revealed a low sensitivity for detecting PAE. Thus, reflux testing needs to be performed further when gastroesophageal reflux disease is suspected, even without endoscopic evidence.

Wernicke's encephalopathy after total parenteral nutrition in patients with Crohn's disease

Micronutrient deficiencies in Crohn's disease (CD) patients are not uncommon and usually result in a combination of reduced dietary intake, disease-related malabsorption, and a catabolic state. Decreased serum thiamine levels are often reported in patients with CD. Wernicke's encephalopathy (WE) is a severe form of thiamine deficiency that can cause serious neurologic complications. Although WE is known to occur frequently in alcoholics, a number of non-alcoholic causes have also been reported. Here, we report two cases of non-alcoholic WE that developed in two severely malnourished CD patients who were supported by prolonged total parenteral nutrition without thiamine supplementation. These patients complained of sudden-onset ophthalmopathy, cerebellar dysfunction, and confusion. Magnetic resonance imaging allowed definitive diagnosis for WE despite poor sensitivity. The intravenous administration of thiamine alleviated the symptoms of WE dramatically. We emphasize the importance of thiamine supplementation for malnourished patients even if they are not alcoholics, especially in those with CD.

Esophagogastric Junction Outflow Obstruction Transformed to Type II Achalasia

No abstract available.

Relapsing polychondritis presenting with inflammatory pseudotumor

No abstract available.

Bilateral Adrenocortical Masses Producing Aldosterone and Cortisol Independently

A 31-year-old woman was referred to our hospital with symptoms of hypertension and bilateral adrenocortical masses with no feature of Cushing syndrome. The serum aldosterone/renin ratio was elevated and the saline loading test showed no suppression of the plasma aldosterone level, consistent with a diagnosis of primary hyperaldosteronism. Overnight and low-dose dexamethasone suppression tests showed no suppression of serum cortisol, indicating a secondary diagnosis of subclinical Cushing syndrome. Adrenal vein sampling during the low-dose dexamethasone suppression test demonstrated excess secretion of cortisol from the left adrenal mass. A partial right adrenalectomy was performed, resulting in normalization of blood pressure, hypokalemia, and high aldosterone level, implying that the right adrenal mass was the main cause of the hyperaldosteronism. A total adrenalectomy for the left adrenal mass was later performed, resulting in a normalization of cortisol level. The final diagnosis was bilateral adrenocortical adenomas, which were secreting aldosterone and cortisol independently. This case is the first report of a concurrent cortisol-producing left adrenal adenoma and an aldosterone-producing right adrenal adenoma in Korea, as demonstrated by adrenal vein sampling and sequential removal of adrenal masses.

Idiopathic Splenic Vein Thrombosis Presenting as Splenic Infarction and Consequent Gastric Variceal Bleeding

Left-sided portal hypertension and consequent gastric varices can occur in patients with isolated splenic vein thrombosis. It is a rare but clinically significant and curable cause of gastrointestinal hemorrhage. Our patient, a 20-year-old woman, with left flank pain was diagnosed with having idiopathic splenic vein thrombosis with resultant splenic infarction. Thorough workups for the possible etiologies of splenic vein thrombosis were all negative. After six months of anticoagulation, follow-up computed tomography revealed formation of gastric varices; one month following the discovery, she developed gastrointestinal bleeding. Splenectomy was performed, resulting in the resolution of gastric varices.