A case of ulcerative colitis with a variety of autoimmune diseases including ankylosing spondylitis, type 2 autoimmune pancreatitis, and primary sclerosing cholangitis.

Ankylosing spondylitis (AS), primary sclerosing cholangitis (PSC), and autoimmune pancreatitis (AIP) are known as extraintestinal manifestations (EIMs) of ulcerative colitis (UC). A 74-year-old Japanese man visited our hospital because of white stool. He had been diagnosed with AS when he was 30 years old, and he was HLA-B27-positive. Based on various examination results, it was suspected that AIP had caused bile duct stricture. During the clinical course, he was diagnosed with UC and PSC. Then, AIP was diagnosed because he had localized pancreatic enlargement, irregular stenosis of the main pancreatic duct, PSC, and no tumor cells of pancreas. A patient with all four of these diseases, AS, AIP, PSC, and UC, is very rare. Therefore, we report a quite rare case with three EIMs (AS, PSC, and AIP) of UC.

[A case of aortic thrombus during chemotherapy for esophageal cancer].

A 59-year-old man presented to our hospital with a chief complaint of epigastric pain. Pertinent history included a distal gastrectomy for gastric cancer and alcohol dependence. He underwent contrast-enhanced computed tomography (CT) and esophagogastroduodenoscopy, which led to a diagnosis of esophageal cancer (cT2N2M1, stage IVb). Subsequently, he underwent chemotherapy using 5-fluorouracil and cis-diamminedichloroplatinum and radiotherapy. A total of 44 days after treatment initiation, the patient experienced nausea and hepatobiliary enzyme elevation. CT and abdominal ultrasonography were performed, and he was diagnosed with an abdominal aortic thrombus. Intravenous heparin was administered as an anticoagulant therapy. Twenty-two days after treatment initiation, the thrombus was no longer visible on abdominal ultrasonography. The patient was then treated with warfarin. It cannot be ruled out that the patient's hepatobiliary enzyme elevation was induced by the anticancer drugs. However, enzyme elevation improved with the disappearance of the abdominal aortic thrombus, suggesting that the aortic thrombus may have contributed to the hepatobiliary enzyme elevation. No thrombus recurrence was observed until the patient's death after an initial treatment with antithrombotic agents. This case indicates that malignant tumors and chemotherapy can cause aortic thrombi, and thus, care should be exercised in monitoring this potential complication.

[A case of ischemic proctitis caused by impaired venous blood flow 11 months after surgery for sigmoid colon cancer].

A Japanese male in his 50s was presented to our hospital with the chief complaint of positive fecal immunochemical test. He had a history of hypertension. He underwent colonoscopy and was diagnosed with sigmoid colon cancer. He also underwent laparoscopic sigmoid colectomy with D3 lymph node dissection for sigmoid colon cancer. The inferior mesenteric artery and inferior mesenteric vein were amputated at the root of the vessels. The patient received adjuvant chemotherapy and was recurrence-free. Eleven months after the surgery, lower abdominal pain during defecation appeared. Contrast-enhanced computed tomography (CT) and colonoscopy showed marked rectal mucosal edema and increased fatty tissue density (dirty fat sign) around the anorectal side of the anastomosis. Intestinal blood flow was maintained. There were many fine blood vessels around the rectal wall, and the amputated distal part of the superior rectal artery was retrogradely contrasted. Amputated superior rectal artery and superior rectal vein were dilated than before. Colonoscopy revealed mucosal redness, edema, and easy bleeding on the anorectal side of the anastomosis. Abdominal contrast-enhanced 3D-CT showed increased arterial blood flow and increased fine blood vessels around the rectal wall. It suggested the presence of an arteriovenous fistula and venous congestion. Conservative treatment with total parenteral nutrition and prednisolone infusion did not improve the patient's condition, and a colostomy was performed. After colostomy, the pain improved, and the CT scan of the abdomen showed improvement in arterial blood flow and venous congestion. Colostomy was closed after 10 months. There has been no relapse since the closure of the colostomy. There are few reports on ischemic proctitis on the anorectal side of the anastomosis after colon cancer resection due to impaired venous blood flow.

[A case of corrosive gastritis caused by accidental ingestion of calcium chloride that resulted in gastric stenosis and penetration].

A Japanese woman in her 40s came to our emergency room with vomiting and upper abdominal pain after drinking a bottle of milk tea at home. She had a history of bipolar disorder. Blood tests revealed hypercalcemia (calcium level of 18.6mg/dl). Abdominal computed tomography depicted thickening of the gastric wall and hyperabsorbed material in the stomach. Upper gastroduodenal endoscopy showed extreme mucosal redness from the gastric body to the pylorus. The hypercalcemia improved with intravenous infusion of zoledronic acid. The patient had not been taking any medication that could have caused hypercalcemia. Later, her father drank the same bottle of milk tea at home and developed upper abdominal pain. He was admitted to the hospital because of vomiting, and computed tomography showed hyperabsorbed material in the stomach, as in his daughter's case. Computed tomography of the bottle of milk tea revealed a highly absorbent substance. The bottle was sent to the forensics laboratory for testing, and it was found to contain calcium chloride. Thus both patients had consumed a beverage containing calcium chloride, and corrosive gastritis was diagnosed. Despite fasting and intravenous drip therapy, the first patient underwent a total gastrectomy because of severe stenosis and perforation of the gastric lumen.

[A case of leptomeningeal carcinomatosis involving loss of eyesight after total gastrectomy for gastric cancer].

A 78-year-old woman had undergone total gastrectomy and chemotherapy for gastric cancer (pT4N3bM0 Stage IIIC, poorly differentiated adenocarcinoma). She received S-1 monotherapy 3 times weekly (S-1 at 80mg twice daily for 14 days, every 3 weeks). She underwent routine examinations, including tumor markers and computed tomography. She had no signs of recurrent disease, but she suffered from a loss of eyesight 2 years and 8 months after the operation. A choked disc was found, but she had no headaches, nausea, or unconsciousness, which indicated high intraventricular pressure. Enhanced T2-weighted magnetic resonance imaging showed high intensity around the optic nerve. We performed cerebrospinal fluid cytological analysis, which showed poorly differentiated adenocarcinoma. She was diagnosed as having leptomeningeal carcinomatosis of gastric cancer. The patient chose best supportive care and died 2 months after symptoms appearance. Histological analysis during the autopsy showed moderately to poorly differentiated adenocarcinoma. The carcinoma had also infiltrated the spinal cord, peritoneum, and adrenal glands. Histologically, the carcinoma had infiltrated the optic nerve, which caused loss of eyesight. We have not yet established effective therapies for leptomeningeal carcinomatosis, and the prognosis is poor. Leptomeningeal carcinomatosis of gastric cancer that appears by loss of eyesight is very rare. This case illustrates that the possibility of leptomeningeal carcinomatosis should be considered when we treat patients with loss of eyesight of an unknown cause after surgery.