[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 steatohepatitis that developed after pancreaticoduodenectomy and progressed rapidly to liver cirrhosis and hepatocellular carcinoma.

Steatohepatitis has been reported to occur after pancreaticoduodenectomy (PD). We report a case of steatohepatitis that arose after PD and led to decompensated liver cirrhosis and hepatocellular carcinoma (HCC). A 65-year-old man underwent PD for suspected intraductal papillary mucinous neoplasm. Eight years after PD, he was diagnosed with liver cirrhosis by laboratory tests and computed tomography. Histological examination of liver biopsy revealed hepatic steatosis, inflammation with ballooning of hepatocytes, and fibrosis, indicating nonalcoholic steatohepatitis as the cause of liver cirrhosis. Ten years after PD, he developed HCC and radiotherapy was performed because of impaired liver function. Intrahepatic metastasis appeared subsequently, but no further treatment could be performed due to decompensated liver cirrhosis. Survival time after PD is being prolonged by improvements in imaging studies and therapeutic strategies. Accordingly, we consider that progression to liver cirrhosis and HCC will occur increasingly in cases such as the present patient, which will become a severe problem in long-term post-PD survival. Therefore, it is necessary to clarify the precise mechanism of steatohepatitis after PD and establish appropriate therapeutic strategies.

Hepatocellular Carcinoma Pseudoprogression Involving the Main Portal Vein, Right Ventricular Invasion, and Exacerbation of Lung Metastases in a Patient on Atezolizumab Plus Bevacizumab.

A 70-year-old man was diagnosed with hepatocellular carcinoma (HCC) with portal vein invasion and lung metastases, for which atezolizumab plus bevacizumab (ATZ/BEV) was initiated. After two months, computed tomography revealed tumor growth accompanied by ascites, right ventricular invasion, exacerbation of the lung metastases, and main portal vein invasion. However, continuation of ATZ/BEV caused remarkable size reductions in all lesions, finally resulting in the disappearance of the vascular invasion and lung metastases after nine cycles of treatment. The tumor growth was considered to reflect pseudoprogression, which is difficult to distinguish from hyperprogression. We herein report a remarkable HCC case of pseudoprogression on ATZ/BEV.