Search PubMed⌕ Search

Biomedical subjects

J Faber

Publications and source records attributed to J Faber.

At least 199 records · Page 11Linked to original sources
PubMed1979

Serum T4, T3 and reverse T3 during treatment with propranolol in hyperthyroidism, L-T4 treated myxedema and in normal man.

Serum concentrations of T4, T3 and reverse T3 were studied in two hyperthyroid groups (n = 13 and 11), in a group of normals (n = 9) and in a group of L-T4 substituted patients (n = 7) with severe pretreatment hypothyroidism. Serum T4 did not change except in one of the hyperthyroid groups change to in which a slight decrease was found. In all groups a significant fall in serum T3 and a significant rise in serum reverse T3 were found. An expected increase in serum TSH in the normal and in the L-T4 substituted groups could not be demonstrated.

Adult↗
PubMed1979

The influence of propranolol on the extrathyroidal metabolism of 3,3',5'-triiodothyronine (reverse T3).

The effect of propranolol 80 mg daily on the metabolism of 3,3',5'-triiodothyronine (reverse T3, rT3), 3,3',5'-triiodothyronine (T3) and thyroxine (T4) was studied by means of a non compartmental kinetic method in seven females with severe pretreatment hypothyroidism. The patients were maintained euthyroid on a constant L-T4 replacement therapy. Serum rT3 levels increased significantly during propranolol (p less than 0.02). This increase was explained by a decrease in metabolic clearance rate (MCR) (p less than 0.02), since the conversion rate from T4 and the distribution volume of rT3 were unchanged. By contrast the decreased serum levels of T3 were due to a significant decreased conversion from T4 (p less than 0.02) in spite of a decreased MCR. The results are compatible with the assumption of two different monodeiodinating enzymes, a 5-deiodinase responsible for the diodination of T4 to rT3 and a 5'-deiodinase responsible for the deiodination of T4 to T3.

Female↗
PubMed1979

Subclinical hypothyroidism in Addison's disease.

Fourteen patients with Idiopathic Addison's disease (IAD) were studied in order to detect a possible subclinical hypothyroid state. All were clinically euthyroid with normal serum thyroxine (T4) and serum 3,5',5'-triiodothyronine (T3). Eleven had circulating thyroid microsomal antibodies in blood. The mean basal serum TSH was significantly higher than that of the control group but only three patients had values above the upper normal range. The mean value of serum T4 was decreased as compared to that of the normal persons, while serum 3,3',5'-triiodothyronine was elevated. 7.5 mU bovine thyrotrophin per kilogram body weight injected intravenously caused a rise in serum T3 not different from the response in normals. However, as well increasing serum TSH as increasing microsomal antibody titer correlated significantly to decreasing thyroidal release of T3. Our results suggest that clinically euthyroid patients suffering from IAD might have a beginning thyroidal insufficiency because of a progressive immunological damage of the thyroid.

Addison Disease↗
PubMed1978

Shape: its development and regulation capacity during embryogenesis.

Although several theoretical approaches consider general methods for dealing with shape, recent observations and experimental data show that embryos exhibit marked changes in the properties of the biological material involved in shape development and shape regulation capacity. In vivo experiments have shown that the amphibian embryo gradually develops from a situation in which it is not able to maintain its shape to one in which it can not only maintain its shape but also possesses a maximal tolerance towards deformation together with a maximal shape regulation capacity. So far two especially clear conclusions have emerged: (i) the form of the embryo appears to be determined by cell activities intrinsic to each stage, and (ii) the morphogenetic programme can be executed normally within wide limits notwithstanding dramatic deformations of the embryo during quite a long period. Thus the hypothesis may be advanced that shape and morphogenesis to some extent become independent phenomena during embryonic development.

Animals↗
PubMed1978

Urinary excretion of 3,3',5'-triiodothyronine (reverse T3).

A simple and sensitive radioimmunoassay for reverse T3 in urine using small Sephadex G25 fine columns is described. The recovery of rT3 added to urine was on average 101.0 +/- 4.2% (mean +/- SEM). Detection limit was 4 pg/column. Urine excretion of rT3 (mean +/- SD) was 72.0 +/- 32.1 ng/24 h in 61 healthy euthyroid subjects with a slight increase with age (P less than 0.05), 28.8 +/- 18.2 ng/24 h in 12 hypothyroid patients and 183.6 +/- 79.7 ng/24 in 25 hyperthyroid patients.

Adolescent↗
PubMed1978

Effect of propranolol on extrathyroidal metabolism of thyroxine and 3,3',5-triiodothyronine evaluated by noncompartmental kinetics.

Kinetic studies of T4 and T3 using a noncompartmental approach were performed in seven patients with pretreatment severe hypothyroidism maintained on L-T4 replacement. Each subject received a combined tracer dose of labeled T4 and T3 as an iv bolus before and during peroral treatment with propranolol. Serum T4 was unchanged, while a significant decrease of 13% was found in serum T3. The disposal rates (DR) of T4 and T3 decreased significantly, and the ratio between the DR off T3 and the DR of T4, the conversion rate, was significantly reduced during propranolol treatment. The decrease in the DR of T4 suggests a reduction in the bioavailability of L-T4 during propranolol, possibly due to a decrease in intestinal absorption. The decrease in the conversion rate indicates a reduced extrathyroidal conversion of T4 to T3 during propranolol treatment.

Adult↗
PubMed1978

Extrathyroidal effects of propylthiouracil and carbimazole on serum T4, T3, reverse T3 and TRH-induced TSH-release in man.

A possible extrathyroidal effect of propylthiouracil (PTU) and carbimazole on serum levels of thyroxine (T4), triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3) and on thyrotrophin-releasing hormone (TRH) induced thyrotrophin (TSH) release was estimated in 19 patients with severe hypothyroidism treated with T4. During PTU medication a significant decrease in serum T3 from 90 +/- 16 (SD) to 79 +/- 23 ng/100 ml (P less than 0.01) and a reciprocal increase in serum reverse T3 from 51 +/- 14 (SD) to 58 +/- 20 ng/100 ml (P less than 0.025) were found. No significant changes in serum T4, basal serum TSH or response to TRH could be demonstrated. Carbimazole did not change any of the parameters studied.

Adult↗
PubMed1978

Radioimmunoassay of 3,3',5'-triiodothyronine (reverse T3) on small reusable sephadex columns.

A simple radioimmunoassay for serum reverse triiodothyronine on small reusable Sephadex G 25 fine columns has been developed. The assay was unaffected by serum volumes of up to 100 microliter. The recovery of reverse T3 added to serum was in the mean 98.3 +/- SEM 3.2% and the coefficient of variation within and between assay determinations 5.4% and 7.5%, respectively. The detection limit was 2.2 pg reverse T3/column. Serum reverse T3 in 58 euthyroid controls was in mean 48 +/- SD 9 ng/100 ml, and was positively correlated to age (P less than 0.001). No overlap was found between the control group, and the hypo- and hyperthyroid group respectively. Three patients with T3-toxicosis had a normal serum rT3.

Adsorption↗
PubMed1978

Urinary excretion of thyroxine, triiodothyronine, 3,3',5'-triiodothyronine (reverse T3) and renal function in human newborns.

The urinary excretion and serum levels of thyroxine (T4), triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3) was estimated in a longitudinal study of human newborns. The maternal and cord blood was also studied. Neonatal renal function was evaluated using endogenous creatinine clearance. In cord blood serum T3 was found to be lower than in maternal blood, but reverse T3 highly elevated. During the first 5 days of life serum T4 and T3 increased with maximum at 48 and 24 h in contrast to reverse T3 which remained high and then declined rapidly after 4 days. Creatinine clearance during the first 3 days of life increased from 5.3 to 21.9 ml/min/1.73 m2. In the same period the urinary T4 excretion increased from 79 to 281 ng/24 h, urinary T3 excretion from 16 to 44 ng/24 h and urinary reverse T3 from 4 to 15 ng/24 h. The renal excretion of thyroid hormones, corrected for body surface, was decreased compared to adult controls, corresponding to an immature renal function. The lack of ability to excrete thyroid hormones involved primary T3 and reverse T3 suggesting particular immaturity of tubular secretion of these hormones during the neonatal period.

Adult↗