[Stenotic ischemic enteritis secondary to intraperitoneal band infiltration: a case report].

A 55-year-old man presented with vomiting and upper abdominal pain. Two months later, computed tomography revealed jejunal wall thickening and contrast enhancement. Double-balloon endoscopy revealed severe jejunal stenosis and mucosal prolapse. The patient was diagnosed with stenotic ischemic small bowel inflammation and underwent partial small bowel resection. Clinicians should consider intraperitoneal band formation in the differential diagnosis of patients without a history of abdominal surgery or trauma. Surgical resection should be considered to prevent strangulation ileus.

A case of immunoglobulin G4-related sclerosing mesenteritis without other organ involvement.

A 64-year-old man presented to our hospital with abdominal pain and 4-5 episodes of watery diarrhea per day for 2 months. Abdominal ultrasound examination revealed a mass in the peritoneal cavity, and computed tomography showed a 13.4 cm mass in the mesentery and a 3 cm mass in the mesocolon. The patient underwent laparoscopic partial resection for diagnosis. Microscopically, abundant fibrosis and numerous immunoglobulin (Ig) G4-positive plasma cells were observed. The serum level of IgG4 was 665 mg/dl postoperatively. These findings suggested that the lesion was consistent with IgG4-related sclerosing mesenteritis. Oral steroids resulted in rapid disappearance of symptoms and a decrease in masses. Recently, sclerosing mesenteritis are reported as IgG4-related disease or mimicking IgG4-related disease but multiple lesions rarely occur in the same organ. We report a case of IgG4-related sclerosing mesenteritis with multiple lesions without involvement of other organs, such as the pancreas and salivary glands.

Two cases of liver cirrhosis with hyperammonemic encephalopathy caused by urease-producing bacteria in the urinary tract.

Hyperammonemia is often experienced as a complication of liver cirrhosis, but it is not well known that hyperammonemic encephalopathy is induced by urease-splitting bacteria in the urinary tract. We report two cases of hyperammonemia in two women in their 80s with liver cirrhosis. Both cases were treated as hepatic encephalopathy with usual treatment, but there was no improvement. Urinalysis showed marked alkalinuria and urine culture showed urease-splitting bacteria, which were thought to be related to the pathology. After drainage of urine and administration of antimicrobials, the blood ammonia level decreased and the urine pH level normalized. The mechanism of this is that ammonia is produced by the degradation of urinary urea by urease-producing bacteria in the bladder, and in the presence of dysuria, it is absorbed into the blood circulation from the bladder venous plexus, leading to hyperammonemia.Urine findings should be confirmed when a patient with liver disease develops hyperammonemia or is unresponsive to conventional hepatic encephalopathy treatment.