[A case of small intestinal endometriosis with bowel obstruction and perforation].

A 47-year-old woman was referred to our hospital with recurring lower abdominal pain persisting for more than 2 weeks. Imaging modalities showed small bowel obstruction caused by a mass lesion in the terminal ileum. Despite undergoing fasting, rehydration, and decompression through an ileus tube, her symptoms persisted. Furthermore, the condition deteriorated on day 4, with the onset of her menstrual period. An emergency surgery was conducted on the 7th day after hospitalization. Surgical observations indicated severe stenosis around the ileocecal valve and ileal perforation approximately 40cm from the oral stricture. As a result, ileocecal resection was performed. Pathological examination revealed endometrial tissue infiltration through the mucosal lamina propria to the ileal subserosa. Thus, the patient was identified with intestinal endometriosis of the ileocecum. Endometriosis of the small bowel is an uncommon condition that eventually causes intractable bowel obstruction. Although preoperative diagnosis is considered challenging, intestinal endometriosis should be included in the differential diagnosis in cases of bowel obstruction in women of childbearing age.

[A case of Lemmel syndrome caused by food residue in giant juxtapapillary diverticulum].

A woman in her 70s was admitted to our hospital because of epigastric pain and anorexia. Laboratory evaluations revealed elevated levels of liver transaminases, biliary enzymes, and amylase. CT and MRCP showed dilatation of the bile and pancreatic ducts and a large juxtapapillary diverticulum filled with contents. There were no gallstones or tumors present. Our differential diagnosis included obstruction of the papilla of Vater, so we performed an urgent ERCP. Endoscopic examination showed the juxtapapillary diverticulum filled with food residue;however, we were unable to locate the papilla of Vater. We rinsed out and removed food residue from the diverticulum using a retrieval balloon catheter used for gallstones. After the endoscopic removal of the food residue, the patient's epigastric pain immediately subsided and her cholangitis and pancreatitis improved gradually.

Glossopharyngeal Neuralgia with Syncope Caused by Recurrence of Esophageal Squamous Cell Carcinoma.

We herein report a case of glossopharyngeal neuralgia with repeated syncope caused by the recurrence of esophageal carcinoma. The typical symptoms of glossopharyngeal neuralgia are paroxysmal, stabbing, electric shock-like pain in the pharynx and/or base of the tongue on swallowing and talking. In addition, syncope can also be caused by glossopharyngeal neuralgia. The diagnosis of glossopharyngeal neuralgia is not always easy because of its rarity. In the present case, we suspected that repeated syncope was caused by glossopharyngeal neuralgia due to the recurrence of esophageal carcinoma. Concurrent chemoradiation therapy was effective in reducing the tumor size, which resulted in the complete resolution of the symptoms.

A case of adult-onset type II citrullinemia induced by hospital diet.

A 47-year-old Japanese man was first admitted to our hospital for 8 days because of an asthma attack. After discharge he changed his diet. On the 12th day after his discharge, he was re-admitted to our hospital because he exhibited transient loss of consciousness with flapping tremor. His plasma ammonia level was extremely high (245 µg/dL; normal, <90 µg/dL), suggesting hepatic encephalopathy. He underwent intravenous administration of branched-chain amino acids (Aminoleban(®)) and oral administration of lactulose and kanamycin sulfate; however, the hyperammonemia did not improve. Analysis of the amino acids and citrin gene led to the diagnosis of adult-onset type II citrullinemia (CTLN2). Following this diagnosis, the carbohydrate content of his diet was mildly restricted. As a result, his plasma ammonia level markedly improved (ammonia, 40-60 µg/dL) and he became symptom-free without any medication. CTLN2 is a metabolic disorder characterized by increased plasma concentrations of citrulline and ammonia, which occurs by the failure of compensatory mechanisms associated with diet. Here, we report a case of a patient for whom a change in eating habits during his hospitalization disturbed his compensatory mechanism resulting in clinical CTLN2, which was reversed with an appropriate diet.