Search PubMed⌕ Search

Biomedical subjects

T Kunieda

Publications and source records attributed to T Kunieda.

230 records · Page 13Linked to original sources

Hemosuccus pancreaticus: diagnosis with CT and MRI and treatment with transcatheter embolization.

We report the case of a 56-year-old woman with a presyncopal episode followed by melena. A sentinel clot sign in the pancreatic duct on precontrast computed tomography and the presence of a splenic artery aneurysm on postcontrast computed tomography strongly suggested a fistula between the aneurysm and the duct, as visualized by magnetic resonance imaging. The patient was treated successfully by complete embolization of the splenic artery aneurysm.

Aneurysm↗

CT appearance of hepatic parenchymal changes after percutaneous microwave coagulation therapy for hepatocellular carcinoma.

PURPOSE: The purpose of this study was to evaluate the changes in the CT appearance of the hepatic parenchyma surrounding the necrotic area in the early period after percutaneous microwave coagulation therapy (PMCT) for hepatocellular carcinoma (HCC). METHOD: We reviewed enhanced CT scans obtained before and within 2 weeks, at 1 month, and at 3 months after PMCT of 61 lesions in 47 patients with HCC. RESULTS: On dynamic CT, early enhancement of the hepatic parenchyma around the treated area was a frequent finding within 1 (87%) or 2 (68%) weeks after PMCT, but such enhancement disappeared on follow-up. Arterioportal shunts were also demonstrated by enhanced CT after treatment (21% at < or =2 weeks), and these shunts tended to persist for >1 month. CONCLUSION: We should evaluate the effect of PMCT by performing dynamic enhanced CT not only within 2 weeks to determine the end-point of treatment but also at 1 month or more after finishing treatment for definite assessment of tumor necrosis.

Adult↗

Percutaneous microwave coagulation therapy for unresectable hepatocellular carcinoma.

BACKGROUND/AIMS: Percutaneous microwave coagulation therapy (PMCT) has recently been introduced as a new treatment for hepatocellular carcinoma (HCC) in Japan. This study was performed to evaluate its efficacy and safety. METHODOLOGY: Thirteen patients with 17 nodules of unresectable HCC were subjected to PMCT under ultrasonic guidance. The tumors ranged from 1.2-4.4 cm in size. Assessment of the efficacy of PMCT was made by follow-up with dynamic computed tomography (CT). RESULTS: In the patients with small HCC (< or = 2.0 cm), 8 of 10 nodules (80%) showed complete remission after PMCT. In small nodules located on the liver surface, 3 out of 4 nodules (75%) showed complete remission. However, in the patients with larger HCC (> or = 2.1 cm), 5 out of 7 nodules developed local recurrence after PMCT. Regarding assessment of the necrotic area after PMCT, dynamic CT revealed enhancement that was possibly caused by congestion of the liver parenchyma surrounding the area of necrosis due to PMCT in the early phase of the treatment. Therefore, the necrotic area must be assessed carefully. Although a slight heat sensation and/or pain during microwave irradiation (a common effect of PMCT) occurred in all patients, there were no serious adverse effects. CONCLUSIONS: Complete remission of small HCC (< or = 2 cm in diameter) can be achieved with PMCT alone, but there seem to be limitations to its effectiveness with larger HCC (> or = 2.1 cm). There were no serious adverse effects from PMCT and the therapy can be safely carried out even in patients with poor liver function.

Aged↗

Development of a syngenic brain-tumor model resistant to chloroethyl-nitrosourea using a methylguanine DNA methyltransferase cDNA.

Chloroethyl-nitrosourea (CENU) is one of the most potent chemotherapeutic agents for brain tumors. However, acquired resistance to this drug has become a serious problem in the treatment of brain tumor patients. The main mechanism of the resistance is a recruitment of the O6-methylguanine-DNA- methyltransferase (MGMT) in tumor cells. Many approaches, including treatment with enzyme-depletions, antibodies, antisenses, and a ribozyme, have been reported to successfully overcome the resistance. In order to evaluate these approaches properly, we designed a syngenic rat brain-tumor model resistant to CENU. The 9L rat gliosarcoma cells were retrovirally transduced with MGMT cDNA and stereotactically implanted into the brain parenchyma. In this model, rats inoculated with resistant cells died significantly earlier than did rats with control cells after treatment with CENU. Because of the limited intracranial space, the animals presented a restricted survival. Since the survival was sensitive and reproducible, this system may have a role in the evaluation of approaches to drug-resistant brain-tumors.

Animals↗

Intraperitoneal hemorrhage as a major complication of percutaneous ethanol injection therapy for hepatocellular carcinoma.

Two cases of intraperitoneal hemorrhage, which is one of the major complications of percutaneous ethanol injection therapy for hepatocellular carcinoma, are reported. A 70-year-old man was hospitalized for treatment of a small recurrent hepatocellular carcinoma located on the surface of the left lobe of the liver. Acute hemoperitoneum developed after percutaneous ethanol injection therapy, but he was treated conservatively with blood transfusion, and recovered. The other patient was a 72-year-old man who was admitted for treatment of a solitary superficial hepatocellular carcinoma on the dome of the liver. Immediately after percutaneous ethanol injection, he suffered the sudden onset of severe abdominal pain with shock and massive hemoperitoneum. His bleeding was successfully controlled by emergency transcatheter arterial embolization. Our experience suggests that care must be taken when using percutaneous ethanol injection to treat patients with superficial hepatocellular carcinomas located on the surface of the liver. Moreover, transcatheter arterial embolization should be considered the treatment of choice for the management of uncontrollable intraperitoneal hemorrhage after percutaneous ethanol injection therapy.

Aged↗

Asymmetric tonic seizures with bilateral parietal lesions resembling frontal lobe epilepsy.

We performed long-term video/ EEG monitoring and a single photon emission computed tomographic (SPECT) study to clarify generating mechanism of bilateral tonic motor seizures resembling seizures generated by the supplementary motor area (SMA), in patients with bilateral parietal lesions. We describe 2 patients (age 24 and 32 years), with bilateral parietal lesions. Clinically, seizures were preceded by lightning sensation in the body, followed by asymmetric tonic posturing of both hands and thrashing movements of the feet, lasting for less than 1 min. Ictal rhythmic (7-15 Hz) activity at the vertex was observed on the EEG in 1 patient. Interictal SPECT in 2 patients showed decreased blood flow in both parietal areas, consistent with bilateral parietal abnormalities on T2- and T1-weighted MRIs. Ictal SPECT in 1 patient showed increased blood flow in the right parietal and frontopolar areas. The present 2 patients had clinically asymmetric tonic seizures, most likely resulting from spreading of the ictal activity from the parietal lesions via the superior longitudinal fasciculus to the SMA. Bilateral, homologous lesions in the parietal area might cause disinhibition on the unilateral epileptogenic side.

Adult↗

Monocrotaline-induced pulmonary vascular disease after contralateral lung transplantation in the rat.

To test a hypothesis that reduction in pulmonary perfusion pressure and flow affect underlying vascular disease, pulmonary pathology was studied in monocrotaline-treated rats undergoing single lung transplantation. Inbred rats were treated with 40 mg/kg (group T1, n = 6) and 80 mg/kg of monocrotaline (group T2, n = 9), received a left lung isograft 2 and 4 weeks after medication, and were killed 4 and 6 weeks after single lung transplantation, respectively. For each group, rats receiving the same amount of monocrotaline (M1, M2) or vehicle (N1, N2) served as controls. Monocrotaline-treated rats developed pulmonary vascular disease and right heart failure, resulting in severe exercise intolerance in M1 or death in M2 unless single lung transplantation had been carried out. At death, pulmonary blood flow was directed toward the left lung isograft, and the retained right lung received a significantly reduced fraction of cardiac output. Right to left ventricular weight ratio was significantly reduced in both groups as compared to the respective control rats, suggesting reduced perfusion pressure. Although thickness of media in small pulmonary arteries (media/radius) was normal (34% +/- 4%) in the lung isografts, it was significantly increased in the contralateral lung (group T1, 45% +/- 5%; group T2, 48% +/- 3%), which was not significantly different from that of monocrotaline-treated control rats, respectively (group M1, 47% +/- 7%; group M2, 49% +/- 6%). Although single lung transplantation reduced perfusion pressure and flow toward the monocrotaline-treated native lung, it failed to affect vascular morphology significantly.

Animals↗