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Biomedical subjects

A Shibata

Publications and source records attributed to A Shibata.

At least 451 records · Page 25Linked to original sources
PubMed1988

[Clinical studies of natural interferon alpha (HLBI) in chronic myelogenous leukemia--a multi-institutional cooperative study in Japan].

Clinical trials of natural interferon-alpha (HLBI) in the treatment of Philadelphia chromosome (Ph1) positive chronic myelogenous leukemia (CML) were carried out in a cooperative study of 22 institutions in Japan. Patients with CML in chronic and accelerated phase were given intramuscular or subcutaneous injections of HLBI at the dose of 6 X 10(6) U/body on consecutive days. Of the 47 patients in this study, forty-one were evaluable for clinical effects, and 42 could be assessed for adverse effects. Among 30 evaluable patients in the chronic phase, 9 (30.0%) achieved complete remission (CR) and 20 (66.7%) partial remission (PR). Only one patient had no response (NR), and the response rate (CR + PR) in chronic phase was 96.7% (29/30). Among 11 patients in the accelerated phase, 3 (27.3%) achieved CR and 4 (36.4%) PR. The response rate in the accelerated phase was 63.6% (7/11). In all 41 evaluable patients, the response rate was 87.8% (36/41). In 5 of 13 responding patients treated for more than 6 months, cytogenetic investigation showed the decline of Ph1 positive bone marrow cells from 100% to 92-0% (mean 46%). Adverse effects such as fever (52.4%), general fatigue (35.7%), and liver dysfunction (21.4%), were observed, but they were usually mild and reversible. No patient was taken off this study because of these toxicities. The results confirm the clinical efficacy of HLBI in patients with CML in the chronic and accelerated phase.

Adolescent↗
PubMed1988

[Perspectives in familial hypercholesterolemia: with particular reference to associated ischemic heart disease].

Seventy heterozygous patients with familial hypercholesterolemia (FH), aged 3 to 91 years (37 men and 33 women), from 38 different families were studied to ascertain their clinical profiles including the pattern of distribution of total cholesterol (TC), Achilles tendon thickness (ATT), and a sex difference in age at the onset of ischemic heart disease (IHD). Eighteen family members who died of IHD were included in this study. The TC level was 332.2 +/- 95.0 mg/dl (mean +/- SD), and the ATT was 12.0 +/- 2.7 mm. IHD was observed in 20 men and 8 women, with an incidence in men 2.5 times higher than that in women. The mean age at the onset of IHD in men was in the sixth decade, one decade younger than in women. IHD was even observed in patients with TC levels of nearly 230 mg/dl. One of the 18 family members was considered a homozygote of the disease by autopsy findings. Twelve of the remaining members died suddenly, and another five had fatal myocardial infarction. We conclude that, (1) IHD is frequently associated with FH, even though TC levels are 230-300 mg/dl, (2) complications of IHD peak earlier in men (sixth decade) than in women (seventh decade) and (3) relatively large numbers of family members died suddenly, especially men.

Achilles Tendon↗
PubMed1988

[Evaluation of therapeutic interventions of sustained monomorphic ventricular tachycardia guided by an electrophysiologic study: a case report].

Therapeutic evaluation of sustained monomorphic ventricular tachycardia (VT) using electrophysiologic study (EPS) is presented in a case of refractory VT. A 54-year-old man with a history of recurring syncope underwent coronary angiography which revealed total occlusion of the posterior descending branch of the right coronary artery. Left ventriculography showed a left ventricular aneurysm at the cardiac apex. Ejection fraction of the left ventricle was 36%. He had four VTs of different QRS morphologies in 12 lead electrocardiograms. According to our programmed ventricular stimulations, single or double, and rarely triple, extra stimuli were administered after eight basic stimuli at two basic cycle lengths. Rapid ventricular pacing, up to 210 bpm, was then added. The stimuli were delivered to two different sites in the right ventricle and to at least one site in the left ventricle. When the entire protocol could not induce VT, isoproterenol was given intravenously, and the same protocol was repeated. No drug could prevent VT attacks, even after the surgical resection of two VT foci, VT was still inducible. Postoperative drug therapy could not prevent VT induction in EPS. However, changes in the mode required for VT induction were observed. Among 47 patients with sustained monomorphic VT treated in our hospital, 24 had EPS to evaluate the efficacies of therapeutic interventions, such as drugs and surgery. In 14 patients, no VT was induced by the entire VT induction protocol. Among the remaining 10 patients, four showed changes in the VT induction mode, but VT recurred in their clinical courses even after their treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1988

A notable change in mortality of aplastic anemia observed during the 1970s in Japan.

The age adjusted mortality rate of aplastic anemia in Japan decreased sharply in the mid-1970s; before this time, it had increased only slightly. A report on the survival rate among a substantial number of patients with aplastic anemia showed that patients who sought medical care at the hospital after 1973 had a better survival rate than those who sought care before 1973; the extent of improvement in the survival rate was almost equal to the extent of decrease in the mortality rate. The supply of platelet concentrates was found to increase with the decrease in the age adjusted mortality rate. Although there were several factors that affected the mortality rate from aplastic anemia, the major recognizable factor seemed to be therapeutic improvement, mainly due to the platelet concentrates. Probably neither a decrease in the incidence nor factors related to the data processing of vital statistics played a major role.

Adolescent↗
PubMed1987

Platelet-type von Willebrand disease platelet aggregating factor: a novel functional assay of von Willebrand factor.

Blood platelets from patients with platelet-type von Willebrand disease (vWD) aggregate upon the addition of human von Willebrand factor (vWf) in the absence of ristocetin or other stimulating factors. We measured quantitatively the ability of vWf to induce directly aggregation of platelet-type vWD platelets (platelet-type vWD platelet aggregating factor [PT-PAF]). Cryoprecipitate and factor VIII concentrates were used as a source of vWf of various multimeric composition. The PT-PAF activity was dependent on the multimer size of vWf, like in the case of ristocetin cofactor (RCof) activity. However, PT-PAF activity was not equivalent to RCof activity and the relative PT-PAF/RCof ratio ranged from 1.00 to 0.18 in the materials studied. The preparations containing the higher-molecular-weight multimers had higher PT-PAF/RCof ratio. These findings suggest that PT-PAF activity is a functional expression of more highly polymerized multimers of vWf as compared with RCof activity. Measurement of PT-PAF would serve as a novel functional assay of vWf.

Factor VIII↗
PubMed1987

Platelet aggregation induced by cryoprecipitate infusion in platelet-type von Willebrand's disease.

Platelet-type von Willebrand's disease (VWD) is a recently described bleeding disorder characterized by a heightened interaction between platelets and von Willebrand factor (vWF) as the result of an intrinsic platelet-membrane abnormality. Administration of cryoprecipitate into a patient with this disorder was followed by thrombocytopenia in vivo and "spontaneous" platelet aggregation in vitro. However, a prolonged bleeding time was shortened and sufficient haemostasis was achieved without thromboembolic complications. These results provide evidence that human vWF infused with cryoprecipitate directly interacts with platelet-type vWD platelets, causing thrombocytopenia in vivo, and suggest that impaired primary haemostasis is related to the depletion of the high-molecular-weight vWF multimers in the circulating plasma.

Hemostasis↗
PubMed1987

Control of supraventricular tachycardia by VVI pacing in a patient with drug-induced enhanced atrioventricular conduction.

A 56-year-old male with atrial fibrillation developed rapid ventricular response up to 200 beats/min or more in the postoperative stage of emergency aortocoronary bypass surgery. Resuscitation for cardiac arrest triggered this rapid ventricular rate. The idea that retrograde conduction into atrioventricular node may prevent ventricular capture of atrial fibrillation was tested. The ventricle was then paced at rapid rate followed by a gradual decrease in the pacing rate to 120 beats/min. By this method, ventricular rate was controlled and hemodynamics stabilized, with more efficiency of intra-aortic balloon counterpulsation. VVI pacing may be used in this manner to control irregular and rapid ventricular response of atrial fibrillation.

Atrioventricular Node↗