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Biomedical subjects

J Matsui

Publications and source records attributed to J Matsui.

At least 73 records · Page 4Linked to original sources
PubMed1992

[Hypergastrinemia and type A gastritis in Basedow's disease].

Hypergastrinemia is a very important clinical condition for the reason that a growing body of evidence obtained from animal and human experiments has revealed gastric carcinoids induced by hypergastrinemia. We investigated 35 patients with Basedow's disease (BD) to elucidate the mechanism of hypergastrinemia associated with BD as well as the relationship between type A gastritis and BD. Fasting serum gastrin levels in BD (296.1 +/- 251.4 pg/ml; mean +/- S.D.) were significantly (p less than 0.001) higher than those in age-matched 27 healthy subjects (106.1 +/- 69.2), and in the BD group, significant positive correlation was detected between fasting serum gastrin levels and thyroid hormones (i.e. T3 and free T4). In the hyperchlorhydria group in BD with hypergastrinemia, the levels of fasting serum gastrin were normalized after euthyroidism was attained due to antithyroidal drugs. On the other hand, in the achlorhydria group in BD significant hypergastrinemia was persisted in spite of normalization of thyroid function. Twenty % of the BD patients had histologically proved type A gastritis with achlorhydria, and all patients with type A gastritis were older than 60 years old. Endoscopic examination revealed that one patient with type A gastritis had an early gastric cancer. However, no gastric carcinoids were demonstrated in this study. In conclusion, the results described as above suggested, 1) hypergastrinemia observed in patients with BD may be induced by gastrin hypersecretion due to hyperthyroidism as well as type A gastritis, 2) BD patients with type A gastritis were recommended to undertake regular endoscopic examination for detecting gastric cancers as well as gastric carcinoids.

Adult↗
PubMed1992

[Improved measurements of anti-L-asparaginase IgG antibody and its clinical applications].

To elucidate the usefulness in prediction of hypersensitive reactions of L-asparaginase (L-asp), anti-L-asp IgG antibody was measured by two kinds of enzyme-linked immunosolvent assay (ELISA) with improved microplate method and original immunobeads method. The correlation coefficient of both methods matched very well (R = 0.949). Nine out of the 10 patients who were treated with L-asp for the first time showed the elevation of the anti L-asp IgG antibody and returned to normal range within 9 months thereafter. Twenty-two out of 26 patients (84.6%) who had ever developed hypersensitive reactions showed the positive anti-L-asp antibody. There was no positive correlation between the anti-L-asp titer and the severity of the hypersensitive reactions. We concluded that the ELISA with microplate was simple and useful methods to determined the anti-L-asp IgG antibody.

Asparaginase↗
PubMed1990

[Electron microscopic cytochemistry of pseudo-Chediak-Higashi granules in 5 cases of AML].

Blasts from 5 cases of AML with pseudo-Chediak-Higashi granules were examined ultrastructurally and histocytochemically using peroxidase, acid phosphatase, high iron diamine (HID) and periodic acid-thiocarbohydrazide-silver proteinate (PA-TCH-SP) stainings. Pseudo-Chediak-Higashi granules, which appeared as vacuole-like inclusions by light microscopy, generally contained electron-lucent materials. All pseudo-Chediak-Higashi granules were, positive for peroxidase but some were negative for acid phosphatase. Pseudo-Chediak-Higashi granules were HID positive, indicating that they contained sulfated glycoconjugates. Glycogen-like particles were observed in the pseudo-Chediak-Higashi granules with the PA-TCH-SP method, as occasionally observed in granules in drug resistant ALL blasts. In conclusion, the contents of pseudo-Chediak-Higashi granules, which seems to be formed by fusion of small granules, differed from those of normal azurophillic granules.

Adult↗
PubMed1984

[Studies on the suppressor T cell function in patients with autoimmune thyroid diseases].

Suppressor T cell function induced by concanavalin A (con A) was evaluated in patients with Graves' disease and Hashimoto's thyroiditis. Patients with Graves' disease were divided into the following two groups: (1) untreated, and (2) euthyroid during antithyroid drug (methylmercaptoimidazole) therapy. T cells (2 X 10(5)), activated by con A for 48 hours, were added to preincubated responder cells (2 X 10(5)) and re-incubated for 7 days in the presence of pokeweed mitogen (PWM). IgG produced in the culture medium was measured by radioimmunoassay and then % suppressions (IgG) were calculated. Thyroid stimulating activity (TSA) in serum was measured by McKenzie's method by means of normal human thyroid slices, and % suppressions (c-AMP) were calculated. IgG produced in lymphocyte culture medium was suppressed by added con A-activated cells in untreated and euthyroid groups of Graves' disease, Hashimoto's thyroiditis and normal controls. The value of % suppression (IgG) was reduced in each group of Graves' disease compared to normal controls. No significant relation was observed between TSA in serum and % suppression (IgG), but three cases with high serum TSA showed low % suppressions (IgG). In 12 cases of Graves' disease, % suppression (IgG) had a positive relation with % suppression (c-AMP) in same medium. The amount of c-AMP produced in thyroid slices incubated in medium, in which responder cells (8 X 10(5)), was elevated in all 7 untreated cases of Graves' disease, while not elevated in 7 euthyroid cases. The value of % suppression (c-AMP) in euthyroid cases with Graves' disease was significantly higher than that in untreated cases. The value of % suppression (IgG) was reduced and had a significant negative relation with logarithm of serum antimicrosomal antibody titer in patients with Hashimoto's thyroiditis. These results indicate that low activity of suppressor T cell had a role on antibody production, including thyroid stimulating antibody, and pathogenesis of autoimmune thyroid diseases.

Adult↗
PubMed1984

[Serum angiotensin I converting enzyme activity in patients with hyperthyroidism and hypothyroidism: relation to renin and aldosterone].

In order to ascertain whether angiotensin I converting enzyme (ACE) activity might be regulated by thyroid hormone, serum ACE activity was measured in a variety of thyroid states, including hyperthyroid and hypothyroid subjects. In addition, the correlation of serum ACE activity to plasma renin activity (PRA) and plasma aldosterone concentration (PAC) was evaluated in these patients. In hyperthyroid patients, the mean (+/- SD) serum ACE activity was 32.7 +/- 6.7 U/ml (n = 30), which was significantly higher than that in hypothyroid patients (20.4 +/- 4.3 U/ml, n = 7, p less than 0.001) and in normal subjects (22.5 +/- 3.4 U/ml, n = 51, p less than 0.001). No significant difference in serum ACE activity was found between the hypothyroid patients and normal subjects. There was a significant positive correlation between serum ACE activity and PRA (r = 0.524, n = 30, p less than 0.01) and also between serum ACE activity and PAC (r = 0.473, n = 30, p less than 0.01) in the patients with hyperthyroidism. By contrast, no significant relationship was observed between serum ACE activity and thyroid hormones (r = 0.115, for T3; r = 0.143, for T4) in hyperthyroid patients. Treatment with furosemide (1 mg/kg i.v.) and upright posture (2h) significantly increased PRA, PAC and serum ACE activity in both hyperthyroid patients and normal subjects, but not in hypothyroid patients. There was a significant positive correlation between changes in serum ACE activity and in PRA (r = 0.418, n = 23, p less than 0.05) in response to the treatment in hyperthyroid patients, while no significant relationship was observed between them in either hypothyroid patients (r = 0.216, n = 6, p less than 0.10) or normal subjects (r = 0.620, n = 10, 0.05 less than p less than 0.01). In one patient with hyperthyroidism, administration of propranolol decreased PRA from 3.4 to 2.3 ng/ml/h, corresponding to an apparent decrease in serum ACE activity from 38.7 to 29.6 U/ml. From these results, it is suggested that serum ACE activity in the hyperthyroid state is modulated by the renin-angiotensin system rather than by thyroid hormone.

Adult↗
PubMed1984

Evidence for the role of kinins in the acute antihypertensive effect of captopril in low-renin hypertension.

In low-renin hypertensive patients, the acute effect of the angiotensin I-converting enzyme inhibitor, captopril, was evaluated in relation to the response of plasma bradykinin (PBK) levels as a parameter of its inhibitory effect on kininase II. Captopril significantly lowered the blood pressure and increased PBK levels. While there was no significant relationship between the reduction of blood pressure and pretreatment plasma renin activity, a significant correlation was observed between the antihypertensive effect of captopril and changes in PBK (r = -0.834, p less than 0.01, n = 10). Furthermore, in a patient with primary aldosteronism and, also, in a patient with glucocorticoid responsive hyperaldosteronism, captopril increased plasma PBK with reduction of the blood pressure. It is likely, therefore, that in low-renin hypertension, the vasodepressor effect of acute converting enzyme inhibition is due mainly to kinin accumulation rather than inhibition of angiotensin II formation.

Adult↗
PubMed1983

[Acute antihypertensive effect of captopril in hypertensive patients: with special reference to kallikrein-kinin system].

In order to clarify the role of the kallikrein-kinin system in the hypotensive mechanisms of converting-enzyme inhibition, captopril was administered in a single oral dose of 50 mg to 17 hypertensive patients, of whom 14 had essential hypertension, one had chronic renal failure, one had primary aldosteronism, and one had glucocorticoid responsive hyperaldosteronism. Captopril lowered blood pressure remarkably in either low-renin or normal-, and high-renin hypertensives, however, there was no significant relationship between the fall in blood pressure and pretreatment levels of plasma renin activity (PRA) in any of the patients any time after the administration. PRA was significantly increased in normal- and high-renin hypertensives but not in low-renin patients. Plasma aldosterone concentration (PAC) was decreased significantly in normal- and high-renin patients, while no significant change in PAC was observed in patients with low-renin activity. Captopril elevated plasma bradykinin concentration (PBK) from a control value of 12.5 +/- 4.1 (mean +/- s.d.) to 20.3 +/- 7.7 pg/ml (p less than 0.001) at 30 min, and there was a significant correlation between changes in PBK and changes in mean blood pressure 120 min after the administration in all the patients (r = 0.741, p less than 0.01, n = 17). In one patient with primary aldosteronism, PBK increased from a baseline of 10.0 to a maximum value of 19.0 pg/ml, corresponding to the rapid fall in blood pressure. Also, in one patient with glucocorticoid responsive hyperaldosteronism, captopril increased PBK from a control of 14.1 to 27.9 pg/ml at 30 min, corresponding to the marked fall in blood pressure from 170/106 to 136/90 mmHg. From these findings, it is suggested that the accumulation of kinins following captopril administration plays a major role in the short-term reduction of blood pressure in hypertensive patients, especially in those with low renin-angiotensin activity.

Adult↗