Summary:A prospective study was conducted in 71 evaluable patients who received myeloablative hematopoietic stem cell transplantation (HSCT) at our facility from 1995 to 2002, to find a sensitive marker for post-transplant heart failure, including echocardiographic systolic and diastolic markers and QTc interval. QTc was found to be an independent and significant risk factor for acute heart failure (AHF) on multivariate logistic regression analysis (OR 1.5, P ¼ 0.01, 95% confidence interval (CI) 1.1-2.0), while no significant differences between patients with AHF and those without AHF were found in age, sex, treatment history, type of conditioning regimen, and echocardiographic systolic and diastolic markers. On further analysis, post-transplant risk of AHF appeared to be increased as QTc was prolonged. The posttransplant risk of AHF in the group with longest QTc on multivariate logistic regression analysis was found to be 9.8 times that in the group with shortest QTc (P ¼ 0.04, 95% CI 1.0-100). These results suggest that echocardiographic markers are less valuable predictors of posttransplant AHF, but that prolongation of the QTc, an ECG marker, before HSCT is strongly associated with onset of AHF after HSCT.

The effect of a nucleoside-nucleotide mixture on liver injury of rats induced by D-galactosamine was studied by examining changes in function and histopathology of the liver. Animals with liver damage received total parenteral nutrition with glucose and amino acids supplemented with a nucleoside-nucleotide mixture containing inosine, cytidine, GMP, uridine and thymidine, or with uridine which inhibits galactosamine injury, or with liver cell extract containing flavin adenine dinucleotide and nucleic acid derivatives. As control, animals with liver damage received total parenteral nutrition with glucose and amino acids only. The serum GOT and GPT concentrations were significantly lower in the group supplemented with nucleoside-nucleotide mixture than those in other groups. A large dose (1.2 g/kg) of uridine inhibited liver injury, but a lower dose (0.14 g/kg) did not have any effect, whereas nucleoside-nucleotide mixture containing the same amount of uridine inhibited the injury. Liver cell extract also did not improve liver function. Thus infusion of a physiological and balanced mixture of nucleosides or nucleotides may improve liver function in rats with liver injury.

A 61-year-old Japanese woman was hospitalized because of general malaise. The patient demonstrated hypertension, hypokalemia and chronic renal failure (CRF). Plasma aldosterone concentration and urinary excretion of aldosterone were elevated. Abdominal computed tomographic scan revealed right adrenal tumor and multiple cysts in both kidneys. Adrenal scintigram using ¹³¹I-adosterol disclosed uptake of the isotope in the area corresponding to the adrenal tumor. Plasma aldosterone concentration and renin activity (PRA) in an upright posture and daily variations in adrenocorticotropic hormone, cortisol, aldosterone levels and PRA were compatible with aldosterone-producing adrenocortical adenoma. After administration of spironolactone and manidipine hydrochloride, a calcium antagonist, general malaise disappeared, and blood pressure and serum potassium level returned to the normal range without adrenalectomy. Although adrenalectomy is known to be effective for the treatment of aldosterone-producing adrenocortical adenoma, several papers reporting cases of aldosterone-producing adrenocortical adenoma with CRF indicated that surgical therapy was not always optimal in terms of postoperative conditions. Taken together, the conservative therapy may be one of the choices considering the prognoses of hypertension and renal dysfunction in patients with aldosterone-producing adrenocortical adenoma with CRF.

A 69-year-old male diabetic patient was hospitalized with pneumonia in February 1996.Abdominalultrasonography performed as a routine examination on admission revealed marked dilatation of gallbladder with a fasting maximal size of 25.7 cm2 compared with 8.8±2.9 cm2 evaluated in 30 male healthy controls aged 67±8 years old. Four months after recovery from pneumonia, abnormal gallbladder dilatation remained unchanged (25.0 cm2), while dilatation had not been observed on an examination performed 6 years earlier (9.8 cm2). Because of accompanying neurological defects, we suppose that cholecystoparesis may be caused by progression ofautonomic neuropathy in this patient with diabetes mellitus.

The specialized conduction system in the heart was electrophysiologically delineated under cardiotomy in 74 patients with congenital heart disease primarily to determine the topographic relationship of the conduction system to intracardiac structures. Histological study was also done to evaluate the electrophysiological data. Differences were found between the ordinary ventricular septal defect (VSD), inlet-type perimembranous defect, and the ordinary tetralogy of Fallot (TOF), outlet-type perimembranous defect. A superficial run of the His bundle along the lower rim summit of defect was often demonstrated electrophysiologically in large VSD of types II or III, whereas the bundle took marked leftward course in TOF. The right bundle branch (RBB) ran beneath or slightly posterior to the Lancisi equivalent structure (LES) in VSD, while it ran under or slightly anterior to LES in TOF. This papillary muscle could be a rough landmark of the RBB. The course of the RBB in TOF, however, had to be histologically confirmed, since its deep location made electrophysiological delineation difficult. All the sites with a high deflection were the areas where the conduction system was histologically demonstrated beneath the endocardium.