Diffuse heterotopic submucosal cystic malformation of the stomach: ultrasonographic diagnosis.

The preoperative diagnosis of diffuse heterotopic submucosal cystic malformation of the stomach is very difficult to make with upper gastrointestinal (GI) series or endoscopy. We report a case of submucosal cysts associated with an early gastric carcinoma in which ultrasonography (US) and endoscopic ultrasonography (EUS) were very useful in the preoperative diagnosis.     

Intra-operative Total Enteroscopy for the Management of Peutz-Jegher's Syndrome

We present a case of Peutz-Jegher's syndrome in an 18 year old female who was followed for gastrointestinal polyps for 13 years from the age of 5 years. The patient was treated four times with surgical or endoscopic polypectomy for gastrointestinal polyps. At the age of 14 years, a combined surgical and endoscopic approach for the management of Peutz-Jegher's syndrome was carried out. A large polyp of the ileum required enterotomy for its removal, and another smaller polyp of the upper jejunum was identified and removed by intra-operative total enteroscopy via the anus. Intra-operative enteroscopy allows one to identify polyps that would previously have been missed. A more complete polypectomy can be performed using this technique, allowing the patient with Peutz-Jegher's syndrome a longer interval between laparotomies and a reduction in symptoms attributed to polyps.     

A case of salicylazosulfapyridine (Salazopyrin)-induced acute pancreatitis with positive lymphocyte stimulation test (LST)

A case of acute pancreatitis induced by salicylazosulfapyridine (Salazopyrin, SASP) was reported. A 33-year-old man with ulcerative colitis was given SASP. Five weeks later, P-type serum amylase was found to be elevated. The amylase/creatinine clearance ratio (ACCR) and serum lipase were also elevated. There were neither subjective symptoms nor abnormal ultrasound findings in the pancrease. Lymphocyte stimulation test (LST) to SASP was positive. Asymptomatic pancreatitis by SASP was suspected and SASP administration was halted. Afterwards the abnormal data became normal. Readministration of SASP because of relapse caused an episode of pancreatitis similar to the first occasion. LST was negative before SASP intake and became positive after intake. Desensitization to SASP was unsuccessful. LST was negative before attempting desensitization and became positive when the dosage of SASP increased to 100 mg daily. This is the second case of acute pancreatitis reported to be induced by SASP and this is the first case in which LST to SASP was described. To our knowledge, this is also the first case in which a positive LST was described in drug-induced pancreatitis. This case provides evidence for the role of delayed type hypersensitivity in the etiopathogenesis of SASP allergy and of dose-independent drug-induced pancreatitis.     

Role of prostaglandin E receptor subtypes in gastroduodenal HCO3- secretion

Gastroduodenal HCO3- secretion is a key process that aids in preventing acid-peptic injury. Endogenous prostaglandins (PGs) play a particularly important role in the local control of this secretion. The secretion of HCO3- in both the stomach and duodenum was increased in response to PGE2 as well as mucosal acidification, the latter occurring with concomitant enhancement of mucosal PG generation. These HCO3- responses in the duodenum were markedly reduced by prior administration of the EP4 antagonist in rats, and profoundly decreased in the animals lacking EP3 receptors but not EP1 receptors. In contrast, gastric HCO3- responses induced by PGE2 and mucosal acidification were prevented by the EP1 antagonist and disappeared in EP1, but not EP3-knockout mice. Consistent with these findings, duodenal HCO3- secretion was stimulated by both EP3 and EP4 agonists but not EP1 or EP2 agonists, while gastric HCO3- secretion was increased by the EP1 agonist but not EP2, EP3 or EP4 agonists. In addition, the HCO3- stimulatory action of sulprostone (EP1/EP3 agonist) in the stomach was inhibited by the Ca2+ antagonist verapamil but not affected by IBMX, the inhibitor of phosphodiesterase, while that in the duodenum was inhibited by verapamil and enhanced by IBMX. Forskolin, the stimulator of adenylate cyclase, increased HCO3- secretion in the duodenum but not the stomach. Thus, the HCO3- stimulatory action of PGE2 in the duodenum is mediated by both EP3 and EP4 receptors being coupled intracellularly with both Ca2+ and cAMP, while that in the stomach is mediated by EP1 receptors, coupled with Ca2+.     

A new manometry device for evaluating the sphincter of Oddi using a fiber-optic pressure sensor

Introduction: Although measuring the pressure of the sphincter of Oddi and the bile duct is considered to be an important examination, called Sphincter of Oddi manometry (SOM), some complications related to the SOM device remain unsolved.

Material and methods: To decrease adverse complications, we developed a 0.46?mm manometry and we performed some in vitro studies.

Results: We successfully developed a 0.46?mm SOM. The diameter is the thinnest size used in endoscopic examinations. The results of in vitro studies show the suitability as SOM.

Conclusion: This device will decrease the risks related to SOM examination. To confirm the safety and feasibility, further studies including in vivo studies will be needed.     

The Development of Foveolar-type Gastric Adenocarcinoma during Maintenance Therapy of Vonoprazan for Reflux Esophagitis

We herein report the first case of foveolar-type gastric adenocarcinoma that developed after the initiation of vonoprazan (VPZ). A 51-year-old man had heartburn at the first visit and reflux esophagitis endoscopically, so he started taking VPZ. An approximately 5-mm-sized reddish polyp with a raspberry-like morphology was detected at the anterior wall of the upper body of the stomach 156 weeks after starting maintenance therapy with VPZ 10 mg/day. It was diagnosed as foveolar-type gastric adenocarcinoma based on a biopsy. Another approximately 4-mm-sized foveolar-type gastric adenocarcinoma was also detected at the posterior wall of the middle body of the stomach.     

Ultra-Early Induction of General Anesthesia for Reducing Rebleeding Rates in Patients with Aneurysmal Subarachnoid Hemorrhage

ObjectiveRebleeding of aneurysmal subarachnoid hemorrhage (aSAH) is one of the significant risk factors for poor clinical outcome. The rebleeding risk is the highest during the acute phase with an approximate rebleeding rate of 9-17% within the first 24 h. Theoretically, general anesthesia can stabilize a patient's vital signs; however, its effectiveness as initial management for preventing post-aSAH rebleeding remains unclear. The purpose of this study was to determine the feasibility and safety of ultra-early general anesthesia induction for reducing the rebleeding rates among patients with aSAH.Materials and methodsWe retrospectively evaluated patients with aSAH who were admitted to our department between January 2013 and December 2019. All the patients underwent ultra-early general anesthesia induction as initial management regardless of their severity. We evaluated the rebleeding rate before definitive treatment, factors influencing rebleeding, and general anesthesia complications.ResultsWe included 191 patients with two-third of them having a poor clinical grade (World Federation of Neurological Society [WFNS] grade IV or V). The median duration from admission to general anesthesia induction was 22 min. Rebleeding before definitive treatment occurred in nine patients (4.7%). There were significant differences in the Glasgow Coma Scale score (p = 0.047), WFNS grade (p = 0.02), and dissecting aneurysm (p <0.001) between the rebleeding and non-rebleeding patients. There were no cases of unsuccessful tracheal intubation or rebleeding during general anesthesia induction.ConclusionUltra-early general anesthesia induction could be performed safely in patients with aSAH, regardless of the WFNS grade; moreover, it resulted in lower rebleeding rate than that reported in previous epidemiological reports.