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Biomedical subjects

M Azukizawa

Publications and source records attributed to M Azukizawa.

At least 37 records · Page 2Linked to original sources
PubMed1979

Effect of a single dose of glucocorticoid on the diurnal variations of TSH, thyroxine, 3,5,3'-triiodothyronine, 3,3'5'-triiodothyronine and cortisol in normal men.

Plasma thyrotropin (TSH) and cortisol concentrations were suppressed immediately after an intravenous bolus dose of 8 mg betamethasone in 6 male subjects. The circadian variations of these hormones disappeared for 40 hr (TSH) and 44 hr (cortisol). Plasma thyroxine (T4), 3, 5, 3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3) levels did not show diurnal variations before betamethasone administration. Plasma T3 levels decreased to 66% of the basal levels 20 hr after batamethasone administration, whereas plasma reverse T3 levels increased to 163% of the basal levels at 24 hr. These changes were reversed by 3 to 5 days after betamethasone. The earlier recovery of the diurnal rhythm of TSH than that of cortisol suggests that the TSH rhythm is not under the direct control of circulating cortisol.

Adult↗
PubMed1978

Differentiation of thyrotoxicosis induced by thyroid destruction from Graves' disease.

Thyroid function was tested in untreated patients with Graves' disease or thyrotoxic subacute thyroiditis, and in patients with autoimmune thyroiditis who showed postpartum or spontaneous transient thyrotoxicosis. The serum triiodothyronine/thyroxine ratio (T3/T4) was greater than 20 ng/microgram in Graves' disease but less than 20 in all patients with subacute thyroiditis and 9 of 11 patients with autoimmune thyroiditis. Thus, like radioactive iodine uptake, the serum T3/T4 ratio is useful for differentiating destruction-induced thyrotoxicosis from the stimulation-induced hyperthyroidism of Graves' disease.

Adult↗
PubMed1978

Thyroid function in patients undergoing maintenance hemodialysis: unexplained low serum thyroxine concentration.

Thyroid function was studied in 55 patients undergoing maintenance hemodialysis who were all judged to be clinically euthyroid. The dialysis patients, in comparison to normal control subjects, had significantly lower mean values for serum T4 (4.0 +/- 1.4 [SD] microgram/dl versus 7.9 +/- 1.5 microgram/dl, p less than 0.001), T3 (118 +/- 31 ng/dl versus 147 +/- 28 ng/dl, p less than 0.001), free T4 measured by equilibrium dialysis (1.22 +/- 0.38 ng/dl versus 2.15 +/- 0.67 ng/dl, p less than 0.001), free T3, free T4 index, and free T3 index. Serum TBG, measured by radioimmunoassay, was similar to that of the controls and serum TSH, 2.2 +/- 1.3 micromicron/ml, was also similar to that of control values, 2.0 +/- 1.1 micromicron/ml. The serum PBI did not change during the dialysis procedure, but serum inorganic iodine fell slightly from 2.1 +/- 1.1 microgram/dl before dialysis to 1.2 +/- 0.6 microgram/dl after dialysis (p less than 0.05). The marked reduction in serum total T4 and free T4 concentrations and the moderate reduction in serum total T3 and free T3 levels in apparently euthyroid patients undergoing hemodialysis has not been explained. The normal serum TSH levels in the face of these low concentrations of thyroid hormone suggests an abnormality in the control of TSH secretion in these patients.

Adult↗
PubMed1978

A new method of paired thyrotropin assay as a screening test for neonatal hypothyroidism.

A simple and reliable method of paired TSH assay was developed and used in screening for neonatal primary hypothyroidism. In this method, a paired assay is first done. Equal parts of the extracts of dried blood spots on filter paper (9 mm diameter) from two infants 4-7 days old are combined and assayed for TSH by double antibody RIA. If the value obtained is over the cut-off point, the extracts are assayed separately for TSH in a second assay to identify the abnormal sample. Two systems, A and B, with different cut-off points were tested. On the basis of reference blood samples (serum levels of TSH, 80 microU/ml in system A and 40 microU/ml in system B), the cut-off point was selected as follows: upper 5 (A) or 4 (B) percentile in the paired assay and values of reference blood samples in the second individual assay. Four cases (2 in A and 2 in B) of neonatal primary hypothyroidism were found among 25 infants (23 in A and 2 in B) who were recalled from a general population 41,400 infants (24,200 in A and 17,200 in B) by 22,700 assays. This paired TSH neonatal hypothyroidism.

Congenital Hypothyroidism↗
PubMed1977

Transient postpartum hypothyroidism: fourteen cases with autoimmune thyroiditis.

Twenty-five episodes of postpartum primary hypothyroidism were observed in 23 patients without thyroid hormone treatment: three were cases of irreversible hypothyroidism and the others were of transient hypothyroidism. The characteristics of transient postpartum hypothyroidism deduced by serial observations on 14 patients were [1] a high incidence of previous goiter; [2] thyroid enlargement at 1/2 to 4 months postpartum; [3] hypothyroidism at 3 to 5 months postpartum; [4] spontaneous recovery at 5 to 10 months postpartum; [5] high titers of antithyroid microsomal antibodies; and [6] persistence of small goiter. Transient postpartum hyperthyroidism before the occurrence of hypothyroidism and the recurrence of transient postpartum hypothyroidism were observed during two consecutive postpartum periods in two patients. Transient hypothyroidism was also observed in two patients after abortion. Fourteen of the 23 patients first noticed thyroid abnormality after delivery. These changes seem to be induced during the course of autoimmune thyroiditis by the immunologic changes occurring after delivery.

Abortion, Therapeutic↗
PubMed1976

Pituitary-thyroid function in trophoblastic disease.

Pituitary-thyroid function was assessed in 12 patients with trophoblastic disease (4 hydatidiform mole, 3 invasive mole, and 5 choriocarcinoma). Thyroid-stimulating activity was detectable, by means of the McKenzie bioassay, in 6 patients (Group 1) but not in the other 6 patients (Group 2). In Group 1 serum thyrotropin (TSH) determined by radioimmunoassay was mostly undetectable and did not respond to the administration of thyrotropin-releasing hormone (TRH) determined by radioimmunoassay was mostly undetectable and did not respond to the administration of thyrotropin-releasing hormone (TRH), while in Group 2 basal TSH was detectable in half of the patients and responded to TRH in all cases. Serum concentrations of total thyroxine (T4) (18.7 +/- 2.0 mug/100 ml, mean +/- SE), free T4 (4.9 +/- 0.04 ng/100 ml), total triiodothyronine (T3) (352 +/- 72 ng/100 ml), and free T3 (0.57 +/- 0.11 ng/100 ml) in Group 1 were statistically greater than those in Group 2 (total T4, 9.2 +/- 1.0 mug/100 ml, free T4, 2.0 +/- 0.2 ng/100 ml; total T3 156 +/- 20 ng/100 ml, and free T3 0.23 +/- 0.03 ng/100 ml). Free T4 and T3 fractions were within normal limits in both groups. After treatment of 5 patients in Group 1, the thyroid stimulating activity determined by bioassay dropped to undetectable levels, the serum concentrations of thyroid hormones decreased to normal limits, and TSH response to TRH became positive. These findings indicate that an abnormal thyroid stimulator, derived from the trophoblastic tissue, stimulated the thyroid hormone secretion from the thyroid gland and in turn suppressed TSH response to TRH in some patients with trophoblastic disease.

Adult↗
PubMed1976

Plasma thyrotropin, thyroxine, and triiodothyronine relationships in man.

The physiologic relationships of plasma TSH, T4 and T3 levels measured every 20 min in seven healthy young men and one healthy young woman have been investigated. A nocturnal TSH surge was observed in all subjects on both nights of the 36-48 h baseline observation period. In males the maximum plasma TSH value occurred at 2300 h. The mean peak TSH level was 2.0 +/- 0.3 (se) muU/ml compared with a mean of 1.3 +/- 0.9 muU/ml for the entire baseline records of the 8 subjects. The effect of iv infusion of 32-1000 mug of somatostatin (SRIF) for 1 1/2-3 h was investigated in four of the male subjects during 2 or 4 consecutive nights following the control period. Temporal relationships between the hormonal fluctuations observed throughout the control period and during the nights of SRIF infusion were investigated using time series analysis and Student's t test. Rapid fluctuations of plasma T4 and T3 concentration were noted, even when corrected for changes in total protein concentration, with an average coefficient of variation of 10% for T3 and 12% for T4. No increment of plasma T4 or T3 followed the nocturnal TSH surge nor were the rapid fluctuations of the thyroid hormones altered by the TSH surge. SRIF infusion commencing at 2300 h suppressed the elevated TSH levels (P is less than 0.01) while similar infusions begun at 2100 h blocked the expected nocturnal TSH rise observed during control periods in male subjects. Plasma T4 and T3 levels were not significantly affected by the administration of SRIF. The relationship of the rapid plasma T4 and T3 variations to postural changes was investigated in four euthyroid male subjects. Serum levels of TSH, T4 and T3 and total protein were determined at 15 min intervals while postural changes were carefully monitored. The ratios of T4 and T3 to total protein were relatively stable (3-4% coefficient of variation) when the subjects were kept in a supine and motionless position. A 50 mug bolus infusion of T4 raised the basal T4 level by only 1-2 mug/dl. The data suggest that short-term fluctuation of plasma T4 and T3 result from changes in protein concentration due to hemodynamic responses to alteration of posture and physical activity and not to pulsatile secretion of T4 and T3.

Adult↗
PubMed1976

Effect of thyrotropin-releasing hormone on secretion of thyrotropin, prolactin, thyroxine, and triiodothyronine in pregnant and fetal rhesus monkeys.

The effect of thyrotropin-releasing hormone (TRH) on the pituitary-thyroid axis and on prolactin secretion was studied in pregnant Rhesus monkeys during the latter period of gestation and in non-pregnant female controls. The baseline plasma concentrations of TSH, T3, T4, and prolactin (PRL) of pregnant monkeys did not differ from those of non-pregnant monkeys. After administration of TRH, plasma prolactin rose to higher levels in pregnant monkeys than in non-pregnant monkeys whereas there was a similar response of plasma TSH, T4 and T3 in both groups. The baseline plasma TSH was elevated and plasma T3 was decreased in the fetus compared with the mother. Administration of TRH iv to the maternal monkey caused a larger response in the fetal plasma TSH than in that of the mother and was followed by larger increments in plasma T4 and T3 concentrations in the fetuses than in the mothers. The larger increments of plasma TSH and thyroid hormones in the fetus compared with the mother also occurred when TRH was given iv to the fetus. There was a significant rise of plasma prolactin in both mother and fetus after administration of TRH to mother or fetus; the increase of plasma PRL was much higher in the mother than in the fetus. The data show that TRH can cross the primate placenta in either the maternal to fetal or fetal to maternal direction. The fetal thyroid of the Rhesus monkey during the latter period of gestation can release both T4 and T3 in response to TSH.

Amniotic Fluid↗
PubMed1976

Failure of triiodothyronine to prevent propylthiouracil-induced hypothyroidism and goiter in fetal sheep.

Administration of propylthiouracil (PTU) to pregnant, third trimester sheep led to decreasing serum thyroxine and increasing serum thyroid-stimulating hormone in both mothers and fetuses. Hypothyroidism appeared more pronounced in the fetuses than in the ewes, and goiter formation was observed in all fetuses exposed to PTU. Concomitant administration of triiodothyronine failed to protect the fetuses from the effects of PTU.

Animals↗