Search PubMed⌕ Search

Biomedical subjects

S Matsuki

Publications and source records attributed to S Matsuki.

At least 73 records · Page 4Linked to original sources
PubMed1982

Erythrocyte aging changes evaluated by the deoxyuridine suppression test.

Many hematologic studies have shown that the erythrocyte count decreases while the size of the individual cell increases in the aged. This study was performed in order to (1) evaluate changes in the blood erythrocyte level and mean erythrocyte size in the elderly and (2) evaluate use of the deoxyuridine (dU) supression test to determine whether deficiency of vitamin B12 or folate plays any role in age-related changes of hematopoiesis. Selected for study were 102 healthy men whose ages ranged from 20 to 79 years. The erythrocyte count and hemoglobin level decreased significantly, whereas the mean corpuscular volume and mean corpuscular hemoglobin increased after 70 years of age. Fresh bone-marrow cells were obtained from 10 young (20-38 yr) and 10 aged (70-82 yr) men. Wickramasinghe's dU suppression test was modified by application of an automatic cell harvester. The results were normal in both groups. Thus, the route of dU to dTMP in a DNA synthetic pathway appeared intact, and there was no evidence of B12 or folate deficiency in the aged to explain the observed macrocytosis. However, 3H-thymidine uptake by nucleated bone-marrow cells was significantly decreased, and the ratio of 3H-uridine to 3H-thymidine uptake was greater in the old group than in the young group. These results could be explained by altered nucleic acid metabolism (unbalanced cell growth) or by a change in the proportion of the different fractions of nucleated cells.

Adult↗
PubMed1982

Transient thyrotoxicosis occurred after cessation of steroid therapy in a patient with autoimmune thyroiditis and rheumatoid arthritis.

A 51-year-old woman with chronic lymphocytic thyroiditis showed transient thyrotoxicosis at seven weeks after cessation of steroid therapy for treatment of rheumatoid arthritis. Radioactive iodine uptake was only 3% even in the thyrotoxic state. Aspiration biopsy, performed just before the development of hypothyroidism, revealed histological features compatible with chronic lymphocytic thyroiditis. At two months after the onset of thyrotoxicosis, hypothyroidism developed, and she was kept in a euthyroid state by 1-thyroxine replacement therapy. Irreversible hypothyroidism was confirmed by the recurrence of hypothyroidism after cessation of thyroid replacement therapy at one year after the onset of thyrotoxicosis. The causal relationship between the cessation of steroid therapy and the occurrence of transient thyrotoxicosis is discussed.

Arthritis, Rheumatoid↗
PubMed1980

[Studies on the mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome (author's transl)].

The mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome was studied in 10 patients with primary aldosteronism and in 3 patients with Cushing's syndrome in in vivo and in vitro experiments. In all of the 10 patients with primary aldosteronism, ACTH stimulated aldosterone secretion from the adenomas more significantly than did angiotensin II and III. DOC and cortisol which were contained in the adenomas were also stimulated more significantly by ACTH than by angiotensin II and III. Responses of the adenomas of Cushing's syndrome to various stimulations were less than those of primary aldosteronism. Secretion of cortisol and aldosterone from the adenomas of Cushing's syndrome was stimulated by ACTH and angiotensin II to a similar degree. From these studies, it seems that secretion of adrenal steroid hormones from adenomas of primary aldosteronism is more sensitive to extradrenal stimulations than that of Cushing's syndrome, and ACTH is the main factor in the control of the secretion of adrenal steroid hormones from the adenomas.

Adenoma↗
PubMed1980

Renin and aldosterone in hypothyroidism: relation to excretion of sodium and potassium.

Changes in plasma renin activity (PRA) and plasma aldosterone (PA) were studied together with the urinary excretion of sodium and potassium in patients with hypothyroidism. The basal levels of PRA and PA were significantly less than those in normal subjects. However, there was no significant relationship between PRA and PA. The response of PRA after administration of 40 mg of frusemide in patients with hypothyroidism was significantly less than that in normal subjects, although the excretion of sodium was slightly higher than that in normal subjects. On the other hand, the excretion of potassium in patients with hypothyroidism was significantly lower than that in normal subjects. The responses of PA to various stimulations, such as ACTH, angiotensin II, potassium and frusemide, were equally suppressed. These results suggest that PRA and PA may be suppressed independently in hypothyroidism ,probably due to dysfunction of juxtaglomerular cells and glomerulosa cells, respectively, and the possibility that suppression of PRA and PA in patients with hypothyroidism is related to exaggerated sodium excretion and a decrease in potassium excretion cannot be ruled out.

Adult↗
PubMed1980

Control of aldosterone in 17 alpha-hydroxylase deficiency.

The control mechanism of aldosterone in 3 patients with 17 alpha-hydroxylase deficiency was compared to that in a patient with a deoxycorticosterone-producing tumor. The basal levels of plasma renin activity (PRA) and plasma aldosterone (PAC) were decreased in 2 of the 3 patients with 17 alpha-hydroxylase deficiency and in the patient with a tumor. However, in the third patient with accelerated hypertension, those levels were normal. In the 3 patients with low PRA and PAC, PAC was stimulated by various procedures, although the responses were lower than those in control subjects. In the patient with accelerated hypertension, the responses were similar to those of the control subjects. After 6 months' treatment with dexamethasone, the low levels of PRA and PAC gradually returned to the lower limit of normal in 2 of the patients with 17 alpha-hydroxylase deficiency. These results suggest that the suppression of PAC in patients with 17 alpha-hydroxylase deficiency is probably due to a suppression of the renin-angiotensin system.

Adolescent↗
PubMed1979

Responses of aldosterone-producing adenomas to ACTH and angiotensins.

To elucidate the control mechanism of aldosterone production in primary aldosteronism, in vivo and in vitro studies were done in 7 patients with aldosterone-producing adenomas. In the in vivo study, plasma aldosterone was stimulated more significantly by (Formula: see text), synthetic ACTH than by angiotensin II or furosemide. Diurnal variations of plasma aldosterone, which were studied in 4 patients, were similar to those seen in normal controls. In agreement with the results in the in vivo study, the in vitro study also revealed ACTH stimulated aldosterone and deoxycorticosterone (DOC) from the adenoma more markedly than angiotensin II or III. There was no adenoma which was more sensitivie to angiotenion II or III than to ACTH. From these results it is considered that changes in plasma aldosterone induced by the exogenous administration of angiotensin II or ACTH in patients with aldosterone-producing adenoma are mainly based on changes in aldosterone production in the adenoma. Furthermore, in patients with an aldosterone-producing adenoma in whom diurnal variations of plasma aldosterone similar to those in normal subjects are observed, responses of aldosterone to angiotensin II are supposed to be less than those to ACTH.

Adenoma↗
PubMed1978

Renin and the juxtaglomerular apparatus in diabetic nephropathy.

In order to study the role of the renin-angiotensin system in patients with diabetic nephropathy, renin release and the juxtaglomerular apparatus were studied in 17 diabetic patients with proteinuria and in 23 without proteinuria; 8 normal subjects were used for conctrls. Despite hypertension and marked arteriosclerosis, plasma renin activity (supine posture) was normal; however, the renin response to salt restriction and upright posture was less in the diabetic patients with proteinuria than in the controls. Renal renin content, determined at autopsy, was also normal. Examination of the juxtaglomerular apparatus in the diabetic patients with proteinuria revealed hyalinization of the afferent and efferent arterioles in most of the glomeruli and various degrees of destruction of the juxtaglomerular cells. The findings suggest that renin production is not increased in diabetic patients with proteinuria plus marked vascular damage, and that the renin-angiotensin system in patients with diabetic nephropathy apparently does not play an important role in the exacerbation of hypertension or the degree of vascular damage.

Adult↗
PubMed1978

Hypertension induced by adrenocortical dysfunction--hypertension in 17 alpha-hydroxylase deficiency and metopirone-induced hypertension.

Hypertension in 17 alpha-hydroxylase deficiency was studied by comparing it with hypertension in Cushing syndrome or that in primary aldosteronism. Furthermore, the role of endogenous increases of ACTH, deoxycorticosterone, and 18 alpha-hydroxy-deoxycorticosterone upon blood pressure was studied in rats by administerating metopirone. Hypertension in 17 alpha-hydroxylase deficiency was considered to be more similar to that in primary aldosteronism from the studies on renin components, pressor responses to angiotensin II and norepinephrine, and renin responses to stimulations. Plasma catecholamines were slightly decreased in 17 alpha-hydroxylase deficiency. The hypertension was alleviated by the administeration of dexamethasone in 2 of 3 patients with 17 alpha-hydroxylase deficiency. However, in the remaining one who had an accelerated hypertension and normal renin, the hypertension was not alleviated by dexamethasone. In the animal studies, hypertension induced by metopirone was accelerated by salt loading of uni-lateral nephrectomy plus salt loading. In those rats, plasma ACTH, and deoxycorticosterone were markedly increased.

Adrenal Hyperplasia, Congenital↗