Takuya Tamai

FIVE CASES OF DIPHYLLOBOTHRIUM NIHONKAIENSE INFECTION WITH DISCOVERY OF PLEROCERCOIDS FROM AN INFECTIVE SOURCE, ONCORHYNCHUS MASOU ISHIKAWAE

Five persons from 2 families residing at Miyama Town, Mie Prefecture, Japan, ingested fresh raw fish Oncorhynchus sp. on 9 May 1999 that was caught at Owase district in Mie. They all expelled diphyllobothriid cestodes 11–37 days after ingesting the fish. The parasites were morphologically identical to Diphyllobothrium nihonkaiense Yamane et al., 1986. Five plerocercoids were detected from a portion of the fish. Nucleotide sequence of a region of the cytochrome c oxidase subunit I gene of mitochondrial DNA from an adult worm was identical with that from the plerocercoid. The fish was identified as Oncorhynchus masou ishikawae according to the nucleotide sequence of the nuclear ribosomal second internal transcribed spacer region II gene. This is the first record of D. nihonkaiense plerocercoids from O. m. ishikawae.

A case of primary cardiac lymphoma located in the pericardial effusion

Primary cardiac lymphoma is a rare disorder with a poor prognosis. We present here a case of 77-year-old woman who was diagnosed as having cardiac lymphoma antemortem according to a cytologic examination of the pericardial effusion. Determination of the levels of serum-soluble interleukin-2 receptor and serum deoxythymidine kinase was useful for the diagnosis. Echocardiography, computed tomography, magnetic resonance imaging, and gallium scan revealed neither lymphadenopathy nor tumor in the heart, so she was diagnosed as having malignant lymphoma that probably originated from the pericardium. Systemic chemotherapy with CHOP (cyclophosphamide, farmorubicin, oncovin, and prednisolone) resulted in a complete resolution of the pericardial effusion. She has been in remission 48 months after discontinuation of the chemotherapy.

An autopsy case of gallbladder cancer developing in a Japanese man with cerebrotendinous xanthomatosis: genetic analysis of the sterol 27-hydroxylase and p53 genes.

Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive lipid-storage disorder characterised by xanthomas, neurological dysfunctions and premature atherosclerosis. A case of a well differentiated adenocarcinoma of the gallbladder occurring in a 57-year-old Japanese man with CTX, confirmed clinically, biochemically and at autopsy is reported together with analyses of the sterol 27-hydroxylase (CYP27) and p53 genes. A missense mutation of the p53 (G for C) was detected in the gallbladder adenocarcinoma. Direct sequence analysis also showed a silent mutational substitution of unknown significance, C for A, in CYP27 at codon 89. In the past, CTX patients have only demonstrated this infrequently, indicating no direct relationship between CYP27 dysfunction and tumour development. Thus, the present case of gallbladder cancer appears to be a chance occurrence.

An autopsy case of gallbladder cancer developing in a Japanese man with cerebrotendinous xanthomatosis

&NA; Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive lipid‐storage disorder characterised by xanthomas, neurological dysfunctions and premature atherosclerosis. A case of a well differentiated adenocarcinoma of the gallbladder occurring in a 57‐year‐old Japanese man with CTX, confirmed clinically, biochemically and at autopsy is reported together with analyses of the sterol 27‐hydroxylase (CYP27) and p53 genes. A missense mutation of the p53 (G for C) was detected in the gallbladder adenocarcinoma. Direct sequence analysis also showed a silent mutational substitution of unknown significance, C for A, in CYP27 at codon 89. In the past, CTX patients have only demonstrated this infrequently, indicating no direct relationship between CYP27 dysfunction and tumour development. Thus, the present case of gallbladder cancer appears to be a chance occurrence.

Assessment by radionuclide ventriculography of postischemic regional left ventricular dysfunction in patients with healed myocardial infarction or angina pectoris

Postischemic left ventricular (LV) dysfunction has been observed in experimental animal models after brief, complete coronary artery occlusion followed by reperfusion, but less relevant information is available for humans. The incidence and duration of postischemic LV dysfunction was examined by exercise radionuclide ventriculography in 50 patients with coronary artery disease. Cardiac imaging was performed at rest and was repeated during exercise and then immediately after and 5, 10, and 20 minutes after exercise. LV regional wall motion abnormalities were noted in 50 segments during exercise; they persisted in 30 of 50 segments after exercise, and remained apparent for 20 minutes in 11 segments. In contrast, in 33 segments, wall motion abnormalities were noted only after exercise and continued for 20 minutes in 13 of 33 segments. Exercise-related wall motion abnormalities were observed in 63 segments (76%) after exercise, and in 24 of 63 segments abnormalities continued for 20 minutes after exercise, although parameters of LV hemodynamic functions approached normal values after exercise. The mechanism of postexercise dysfunction is considered to involve acute myocardial stunning after a brief episode of myocardial ischemia, whereas regional wall motion abnormalities observed only after exercise seem to be related to increased levels of catecholamines or sympathetic overdrive, which mask less significant myocardial ischemia during exercise.