A rare case of peliosis hepatis in a patient with chronic renal failure and renal cell carcinoma.

Peliosis hepatis (PH) is a rare disease characterized by the presence of sinusoidal dilation and blood-filled cysts throughout the hepatic parenchyma. We report a case of PH in a 49-year-old woman with chronic renal failure (CRF) on hemodialysis and with renal cell carcinoma (RCC). Dynamic contrast-enhanced computed tomography (CT) showed a 35-mm-diameter, hypervascular tumor in the liver and RCC in the right renal cyst. Ultrasound and superparamagnetic iron oxide-enhanced magnetic resonance imaging were also performed; however, the liver tumor could not be distinguished from the metastasis of RCC. Therefore, echo-guided biopsy of the liver tumor using an 18-G Majima needle was performed. Histological evaluation of the specimen showed irregular sinusoidal dilatation and blood-filled cavities without malignant cells. She was ultimately diagnosed with PH. Subsequently, she underwent total right nephrectomy for RCC and was diagnosed with RCC stage 1 (pT1N0M0). A follow-up CT performed 4 months after nephrectomy showed no growth of PH. Although the development of PH in patients with CRF or RCC who do not undergo renal transplantation is extremely rare, it should be considered in the differential diagnosis to distinguish PH from the metastasis of RCC.

A case of pancreatic pseudocysts accompanied by infection, pseudoaneurysm ruptures, and pseudocystocolonic fistulae.

Pancreatic pseudocysts (PPs) can be accompanied by infection, pseudoaneurysm ruptures, and fistulae to other organs, which can be fatal without appropriate treatment. Herein, we present the case of an 82-year-old man with PPs accompanied by infection, pseudoaneurysm rupture, and pseudocystocolonic fistula that were managed via multidisciplinary treatment. Computed tomography (CT) revealed two inflamed PPs, one each in the pancreatic head and tail. He was, therefore, diagnosed with infectious PPs. The pancreatic head PP shrunk on endoscopic nasopancreatic drainage (ENPD), but the pancreatic tail PP did not. Endoscopic ultrasound (EUS)-guided transluminal drainage was performed to treat the pancreatic tail PP; his symptoms improved. However, he vomited blood at 14 day post-drainage. Angiography revealed pseudoaneurysm rupture in a left gastric artery branch. After successful angioembolization, he developed hematochezia 2 days later. We suspected re-bleeding of the pseudoaneurysm. The bleeding stopped spontaneously, but CT and radiography revealed the presence of a pseudocystocolonic fistula. Careful follow-up was performed, and he has not had any symptoms at 9 month post-discharge. We managed PP-related complications via ENPD, EUS-guided transluminal drainage, angioembolization, and careful follow-up. Infection, pseudoaneurysm rupture, and pseudocystocolonic fistula are rare, but can occur simultaneously. Therefore, clinicians should consider these complications when treating patients with PPs.

[Use of dexmedetomidine hydrochloride as a sedative during local therapy for hepatocellular carcinoma].

Sedation using dexmedetomidine hydrochloride (DEX) was administered to patients with hepatocellular carcinoma (HCC) prior to local therapy. Case 1 was a 58-year-old man undergoing radiofrequency ablation in combination with transcatheter arterial chemoembolization for HCC in S3. In accordance with the package insert, the initial loading dose was set at 6 µg/kg/hour. Although a favorable sedative effect was achieved, his blood pressure and pulse rate decreased. Case 2 was a 79-year-old woman undergoing percutaneous ethanol injection therapy for HCC in S6. Half the initial loading dose indicated in the package insert (3 µg/kg/hour) was administered, but the sedative effect was appreciable. No marked blood pressure or pulse rate decreases were observed. We believe that the use of DEX as a sedative agent in local therapy for HCC can be expected to increase. However, the optimal dose setting for DEX requires further examination.

The study of dynamic chemical magnifying endoscopy in gastric neoplasia.

BACKGROUND: We assessed the usefulness of acetic acid-enhanced magnifying endoscopy in the diagnosis of gastric neoplasia. METHODS: Forty-five patients (27 men, 18 women; median age 61.6 years) with gastric carcinoma or adenoma were enrolled in a prospective trial of enhanced magnifying endoscopy after instillation of 1.5% acetic acid. Acetic acid-enhanced magnified views of carcinoma or adenoma and the surrounding non-neoplastic mucosa were observed, and the duration of whitening time of each lesion was recorded. OBSERVATIONS: Magnified views of carcinoma showed a minute, grain-like pattern that differed from the surrounding noncancerous mucosa. The histopathologic diagnostic criteria were based on the Vienna classification of GI epithelial neoplasia. The mean duration of whitening differed with each histologic type: low-grade adenoma, 94 seconds; high-grade adenoma, 24.3 seconds; noninvasive carcinoma, 20.1 seconds; invasive intramucosal carcinoma, 3.5 seconds; and submucosal carcinoma or beyond, 2.5 seconds. The duration in the non-neoplastic surrounding mucosa was 90 seconds. After the disappearance of whitening in the carcinoma, the irregular pattern of the carcinoma reappeared, and the contrast between carcinomatous microvessels and the whitened non-neoplastic tissue became very clear on magnifying endoscopy. In accordance with the duration of whitening, more than 1 minute was termed "continuous whitening," from 31 to 60 seconds was "delayed disappearance of whitening," from 30 to 6 seconds was "early disappearance of whitening," and 0 to 5 seconds was "no response." CONCLUSIONS: Acetic acid-enhanced magnifying endoscopy was useful for the diagnosis of gastric adenocarcinoma. The duration of whitening differed among grades of neoplasia, and it was possible to observe changes in the whitening with time. Acetic acid-enhanced magnifying endoscopy, therefore, can be termed "dynamic chemical magnifying endoscopy."