In 18 of 547 patients who had received nucleoside analogue preparations for 1 year or more, multi-drug resistance was detected, after a median follow-up of 53 months. No patient showed liver failure related to multi-drug resistance acquisition. Multi-drug resistance was associated with entecavir (ETV) therapy in 7 lamivudine (LAM) -resistant patients, combination therapy with adefovir dipivoxil (ADV) in 8 LAM-resistant patients, LAM switching to ETV in 2 patients, and initial ETV administration in 1. For treatment, combination therapy with LAM and ADV was performed. In non-responders, combination therapy with ADV and ETV was employed. In all LAM- and ADV-resistant patients, and the HBV DNA level decreased to 3.0LC/ml or less. However, a similar decrease was noted in 7 (58.3%) of 12 LAM- and ETV-resistant patients. Of the 18 patients, 1 did not respond to combination therapy with ADV and ETV. Therapy with tenofovir disoproxil fumarate (TDF) was required.
A 66-year-old man presented with anemia. Endoscopy revealed an elevated lesion with ulceration in the posterior wall of the lesser curvature of the lower gastric body. Endoscopic biopsy demonstrated pathological diagnosis, neuroendocrine carcinoma. A computed tomography scan showed liver metastasis and portal vein invasion. We started chemotherapy with S-1 and cisplatin. After six courses of treatment over seven months, partial response was assessed. We are continuing this chemotherapy now.
A 47-year-old man was found to have abnormal findings on chest radiography. Chest computed tomography (CT) and magnetic resonance imaging (MRI) showed that he had a pulmonary arteriovenous malformation. He had experienced epistaxis when he was a junior high school student, and since then, the symptom had frequently recurred. Further, he had telangiectasia on the lips. Thus, he was given a diagnosis of hereditary hemorrhagic telangiectasia (HHT). Endoscopy revealed gastric telangiectasia, and in addition, his colon had many juvenile polyps. When he was 49 years of age, he underwent genetic analysis for HHT. A diagnosis of juvenile polyposis-HHT combined syndrome (JP-HHT) was made since a heterozygous germline 4-base deletion in exon 9 of SMAD4 was detected. To the best of our knowledge, this is the first case of JP-HHT associated with SMAD4 mutation in Japan.
A 69-year-old man was admitted with difficulty in defecation and urination. CT showed a giant tumor connected with the rectum in the lower pelvic cavity, and also the presence of 4 smooth surfaced tumors, 3 of which were in the abdominal cavity, while the other one was in the left inguinal region. A core needle biopsy was performed in the left inguinal region indicated the presence of gastrointestinal stromal tumor (GIST), and we clinically diagnosed this case as having multiple metastatic rectal GISTs. The patient was treated with imatinib mesylate, and CT showed the size of the rectal GIST to have dramatically decreased, with only one metastatic tumor remaining in the abdominal cavity. Therefore, an abdominoperineal resection and metastasectomy were performed, and the tumors were completely excised. The patient is alive without recurrence at 18 months after surgery, while continuing to receive imatinib mesylate.
An 81-year-old woman presented with left hypochondrial pain and vomiting. CT showed incarceration of the entire stomach in the left pleural cavity with esophageal hiatus hernia with mesenteroaxial gastric volvulus. We diagnosed upside down stomach. Upper gastrointestinal endoscopy showed no impairment of blood supply to the gastric mucosa and she had cardiac complications, so nasogastric tube insertion and conservative management were performed. Two weeks later, her upside down stomach had resolved and only hiatus hernia was seen. We then performed a Nissen operation.
We describe a 69-year-old man with a history of multiple gastroduodenal ulcers, presenting with the onset of obstructive jaundice. Abdominal CT, MRI and EUS demonstrated a sheet-like mass in the pancreaticoduodenal groove. EUS-FNA did not reveal malignancy. Conservative treatment did not improve his clinical condition and repeated acute pancreatitis occurred during his treatment. Thus, pancreaticoduodenectomy was performed. Histopathological findings showed a duodenal ulcer penetrating the pancreas and infiltration of inflammatory cells and fibrosis in the pancreaticoduodenal groove. The spread of inflammation associated with the duodenal ulcer may have been one of the causes of groove pancreatitis.
A 71-year-old woman was admitted to our hospital for evaluation of a right upper abdominal tumor. A contrast-CT scan demonstrated a huge tumor extending from the hepatic hilum to the pelvic space. The rim of tumor was enhanced. The center of the tumor was not enhanced and thus considered to consist of mucus or necrotic tissues. Preoperative diagnosis as gallbladder carcinoma without infiltrating to peripheral organ was made and subsequent cholecystectomy with full-thickness dissection has been performed. The tumor itself was in a swollen gallbladder, 18cm in diameter, consisting of necrotic tissues in the lumen. Pathologic diagnosis was papillary adenocarcinoma, classified as pHinf1a, revealing fStage II. In many cases with undifferentiated carcinoma of the gallbladder, the neoplasms grow expansively to become large tumors with marked necrosis. We report a rare case of papillary adenocarcinoma of the gallbladder presenting both a clinical course and radiologic findings indistinguishable from undifferentiated carcinoma of the gallbladder.
A 50-year-old woman was admitted to our hospital with complaints of loss of vision, diarrhea and arthralgia. She was given a diagnosis of Behçet disease and given infliximab (IFX) to halt the progression of acute vision loss. Liver damage was detected after the fourth IFX dose. We assumed that this was a drug-induced condition caused by salazosulfapyridine (SASP). However, the liver damage worsened, and the condition did not improve even after discontinuing SASP. Thus, therapy to enhance hepatic function was initiated. Histological analysis of liver biopsy specimens showed centrilobular spotty necrosis and periportal hepatitis. We diagnosed autoimmune hepatitis rather than drug-induced liver damage. Because of liver function deterioration, we initiated steroid treatment and rapid improvement was observed. Therefore, liver function should be carefully monitored during IFX administration for patients with genetic predispositions to autoimmune hepatitis, such as human leukocyte antigen-DR4.