Management of hydatidiform mole in women over 45 years old.
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Biomedical subjects
Publications and source records attributed to K Isaka.
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Serum concentrations of PP5 were measured by radioimmunoassay in 219 women with normal pregnancies and 163 women whose pregnancies were complicated. PP5 in serum disappeared rapidly after delivery, with a half-life of 5-10 min in the first 10 min. Serum PP5 levels were higher in uterine than in antecubital venous blood. In normal pregnancies, PP5 was detectable at 7-8 weeks of gestation; its mean concentration rose gradually to a maximum of 17.8 +/- 10.2 ng/ml at 34-35 weeks of gestation. Elevated serum PP5 concentrations were noted in patients whose pregnancies were complicated by toxemia of pregnancy with appropriate-for-date baby or by twin pregnancy. Low serum PP5 concentrations tended to be found in patients whose pregnancies were complicated by abortion, intrauterine fetal death, and hydatidiform mole. Marked abnormal PP5 levels were not found in patients with maternal diabetes and placenta previa. These findings suggest that the assay of serum PP5 concentrations can be a useful parameter in determining the prognosis of abnormal pregnancies.
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In order to investigate changes in endocrine function, various tests were performed on eleven patients with anorexia nervosa. In two of them, endocrine function before and after treatment was also studied. The responses of plasma LH and FSH to LH-RH were decreased in the patients as were plasma LH-RH, and LH and FSH responses to the oral administration of clomiphene citrate. In more than half of the cases, plasma TSH showed a delayed response to TRH. The basal levels of plasma GH were elevated, and plasma GH responses to hypoglycemia or 1-arginine were lowered in half of the patients. Plasma GH showed a paradoxical rise after glucose load in three out of six cases. Plasma IRI responses to 1-arginine load were decreased in some cases, but plasma IRG responses to 1-arginine were rather excessive. Plasma IRI after glucose load showed low or delayed responses in most of the cases. After the body weight was increased to normal levels by the treatment, pituitary and pancreatic endocrine functions were normalized. These findings indicate that hypothalamic function is primarily impaired in this disease and causes nutritional disorder followed by the dysfunction of some endocrine organs. Such a possibility could be supported by the improvement of endocrine function after body weight has been recovered.
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With the purpose of investigating the pathogenesis of obesity and hyperinsulinemia in rats with hypothalamic lesions (HTL), HTL were made in vagotomized rats, and the development of obesity was serially followed up to 15 weeks as well as the changes of plasma triglyceride and immunoreactive insulin (IRI) levels. Even in vagotomized rats, obesity developed after HTL and plasma triglyceride and IRI levels increased significantly. However, obesity was slightly less in grade and occurred later as compared with sham-vagotomy-HTL rats. Plasma IRI levels in vagotomized rats significantly correlated with the body weight, Lee's index, the weight of adipose tissue and plasma triglyceride level. Similar results were also obtained in rats with HTL which were pair-fed following vagotomy. These results suggest that the hyperinsulinemia in obese rats with HTL may be involved not only by hypersecretion of insulin mediated by hypothalamo-vagal nerve system but also by some insulin-antagonistic factors such as increases of adipose tissues and plasma lipids.
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Clinical and pathological studies have been conducted on two brothers with unusual encephalopathy of Binswanger's type. The disease started in the third decade with steady progressive course leading to death in eight or nine years. The clinical picture was summarized as a combination of organic dementia, extrapyramidal disorders associated with pseudobulbar symptoms and marked pyramidal tract signs. The blood pressure remained always normal during the course. Pathologically, there were diffuse and focal demyelination with sparing of U-fibers, multiple small foci of perivascular softening in the cerebral white matter and in the basal ganglia and severe arteriosclerotic changes of memingeal small arteries and long arteries with 100 to 400 micron caliber in the cerebral white matter. Vessel changes consisted of fibrous intimal proliferation, severe hyalinosis and splitting of intima and/or internal elastic membrane. The histopathological process belonged to the category of subcortical arteriosclerotic encephalopathy of Binswanger's type. There has been some discussion as to differential diagnosis among various forms of vasculitis such as cerebral endangiitis obliterans, periarteritis nodosa, systemic lupus erythematosus, rheumatic vascular disease and giant cell arteritis.
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