PubMed Health⌕ Search

Biomedical subjects

M Hüfner

Publications and source records attributed to M Hüfner.

At least 91 records · Page 5Linked to original sources
PubMed1977

Induction of the thyroxine (T4) to triiodothyronine (T3) converting enzyme in rat liver by thyroid hormones and analogs.

In thyroidectomized, unsubstituted rats the T4 to T3 converting activity of liver homogenate is reduced to about 30% of that in unoperated control animals. The enzyme activity can be reinduced dose-dependently with T4. To achieve a normal activity, high, non-physiological plasma T4 concentrations are needed. Plasma T3 levels are much better correlated to the T4 to T3 converting activity. Pure T3 proved to be a more potent enzyme inducer than T4. No difference could be detected between L- and D-T3. Tyrosine, diiodotyrosine, 3,3'-diiodothyronine and 3,3',5'-T3 (reverse-T3) showed no inductive effect for the enzyme. These results demonstrate that the T4 to T3 converting enzyme is specific and shows regulatory properties.

Animals↗
PubMed1977

Properties of the thyroxine (T4) monodeiodinating system in rat liver homogenate.

The monodeiodination of T4 in rat liver homogenate was studied. The two possible products of this reaction show very different properties. The metabolically very active T3 is rather stable in this system whereas the biological inactive reverse T3 (rT3) disappears very rapidly. This explains the low apparent rT3 production in the incubation mixture even under optimal conditions and the peculiar pH profile. The T4 to T3 converting reaction can be increased by the addition of mercaptoethanol to the medium; no further activation is possible by several cofactors tested. The apparent KM of the reaction is 1.6 x 10(-6) M. Reverse T3 does inhibit the reaction non competitive; Ki = 2 x 10 (10-8) M. Alpha-methyl-para-tyrosine, a specific inhibitor of tyrosine hydroxylase, has no significant effect on the reaction.

Animals↗
PubMed1977

3,3',5'-Triiodothyronine (Reverse T3) in amniotic fluid and cord serum.

3,3',5'-triiodothyronine (reverse T3, rT3) was measured in 122 samples of amniotic fluid obtained between the 29th--40th weeks of gestation, and in the blood of 37 newborn and their mothers. The mean rT3 concentration in amniotic fluid was 0.769 +/- 0.47 ng/ml, with a slight decrease from the 29th--40th weeks of gestation which was not statistically significant. Because of the great scatter of rT3 concentrations in amniotic fluid, its estimation does not seem to be useful in prenatal diagnosis of hypothyroidism. The mean rT3 concentration in cord blood (2.62 ng/ml; range 1.4--4.9 ng/ml) was greatly elevated in comparison to the mean maternal level at delivery (0.34 ng/ml; range 0.08--0.69 ng/ml). The possible use of rT3 measurements in cord blood as a screening test for congenital hypothyroidism is discussed.

Amniotic Fluid↗
PubMed1977

Hyperparathyoidism: influence of glomerular filtration rate on urinary excretion of cyclic AMP.

Urinary cyclic AMP excretion per 24 h or per g creatinine in primary hyperparathyroidism (1 degrees HPT) has been evaluated by several authors with conflicting results. In 50 patients with 1 degrees HPT, 25 patients with secondary (2 degrees) HPT and 35 healthy control persons we determined urinary cyclic AMP per 24 h or per g creatinine. These parameters did not satisfactorily discriminate patients from controls, especially when glomerular filtration rate (GFR) as determined by creatinine clearance was reduced. Since urinary cyclic AMP is derived from plasma by glomerular filtration and from kidney by tubular production-the amount of tubules is reflected by GFR-the cyclic nucleotide was related to GFR. In controls urinary cyclic AMP correlated better with GFR than with creatinine excretion. Additionally, in 45 of 50 patients with 1 degrees HPT and in all with 2 degrees HPT, urinary cyclic AMP/GFR was raised. In 1 degrees HPT serum levels of parathyroid hormone correlated closer with urinary cyclic AMP/GFR than with urinary cyclic AMP/g creatinine. The ratio cyclic AMP/GFR decreased to normal or subnormal values after removal of adenomatous or hyperplastic glands in 1 degrees HPT and during infusion of calcium in 2 degrees HPT. In 50 patients with renal lithiasis caused by diseases other than 1 degrees HPT (anatomical variations, pyelonephritis, immobilization after tetraplegia) the ratio cyclic AMP/GFR was not raised. Urinary cyclic AMP/GFR, therefore, reflects parathyroid hormone excess more reliably than cyclic AMP/g creatinine.

Adolescent↗
PubMed1977

Influence of D-thyroxine on plasma thyroid hormone levels and TSH secretion.

Triiodothyronine (T3), thyroxine (T4), basal TSH and TSH after stimulation with TRH were determined in healthy subjects and patients treated with D-thyroxine (DT4). After a dosage of 6 mg DT4 the D/L T4 plasma concentration rose about 4-fold 4 hours after application and was only moderately elevated 14 hours later. To achieve constantly elevated T4 levels 3 mg DT4 were applied in the further experiment every 12 hours. The D/L T4 plasma concentration rose 2.5-4-fold and there was a small but significant increase of the D/L T3 plasma concentration. 74 hours after onset of treatment basal TSH was below detectable limits and the increase of TSH 30 min after injection of 200 mug TRH (TRH test) was only about 15% compared to zero time. The time course of TSH suppression was investigated after treatment with DT4 and LT4 (single dosage of 3 mg). TRH-tests were performed before, 10, 26, 50 and 74 hours after the first dosage of D or LT4. There was no difference in the time course of basal TSH and TSH stimulated by TRH. In 10 patients on DT4 long-term therapy, basal and stimulated TSH were found to be below the detectable limits of 0.4 mug/ml. Our results show that (1) plasma half-life of DT4 is less than 1 day, (2) TSH suppression after D and LT4 treatment is very similar, and (3) in patients on long-term DT4 treatment, TSH plasma concentration is below detectable limits even after stimulation with TRH.

Dextrothyroxine↗
PubMed1977

[Hormone concentrations in thyroid gland tissue and plasma in autonomous thyroid adenomas with and without thyrostatic pretreatment].

The thyroid hormone concentrations of T2, T3 (and the inactive R-T3) were determined in thyroid tissue of 20 patients with autonomous adenomas. High concentrations were found in scintigrafically decompensated adenomas without preoperative thyrostatic treatment. Decompensated adenomas after thyrostatic treatment, compersated adenomas and a group of 9 euthyroid goiters showed no difference in tissue-concentrations of T4 and T3. The amount of tissue-R-T3 seems to be lowered in autonomy. The plasma-concentration of T3, which was intraoperatively elevated in the venous effluent from decompensated adenomas without thyrostatic treatment, was significantly lower in the blood draining decompensated adenomas after thyrostatic treatment as well as compensated adenomas.

Adenoma↗
PubMed1977

Sensitive radioimmunoassay for thyrotropin by use of commercially available tracer and antibody.

The time course of the association and dissociation of radiolabeled thyrotropin with its antibody was studied. The binding is maximal after five days of incubation. The dissociation is much slower. Highest sensitivity is obtained by a total incubation time of five days with addition of the labeled ligand after three days of preincubation with the unlabeled thyrotropin. An improvement in the sensitivity from 0.4 mU/l to 0.08 mU/l is obtained by that method compared with equilibrium technique thus significantly diminishing the percentage of undetectable serum levels of euthyroid and hyperthyroid subjects. Average sensitivity is 0.14 mU/l, intraassay variance is 2%, interassay variance is about 13% in the normal range. Normal values for euthyroid subjects averaged 1.53 mU/l, for hyperthyroid subjects 0.19 mU/l.

Dose-Response Relationship, Immunologic↗
PubMed1976

Pharmacological influences on T4 to T3 conversion in rat liver.

Five groups of 8 rats were treated with normal diet, diphenylhydantoin, dexamethasone, thyroxine (T4) and phenobarbital respectively for 14 days. After this period plasma triiodothyronine (T3), T4 and reverse T3 (rT3) concentrations as well as the T4 to T3 converting activity in the liver homogenates were determined. Plasma T3 was low after dexamethasone, T4 and phenobarbital. Plasma T4 was low after dexamethasone and elevated after T4. rT3 plasma concentrations were at the lower limit of detection in all groups. The converting activity in the liver homogenate was significantly increased after diphenylhydantoin and very much depressed after dexamethasone. These results support the concept that different drugs may influence the peripheral thyroid hormone metabolism, especially the T4 to T3 conversion. However other pathways might be affected also because plasma T3 levels did not always reflect the converting activity in the liver.

Animals↗
PubMed1976

Radioimmunoassay for 3,3',5'-triiodothyronine (reverse T3, R-T3) in unextracted human serum.

Highly specific antibodies against 3,3',5'-triiodothyronine (reverse T3, R-T3) have been produced in rabbits. The crossreaction with T4 is about 0.05%. A radioimmunoassay for R-T3 in unextracted serum was developed. ANS is used for blocking the binding of tracer and endogenous R-T3 to TBG. The sensitivity to the assay is 0.06 ng/ml plasma. The mean normal R-T3 concentration is 0.20 ng/ml. Thyrotoxic patients show elevated levels; in most hypothyroid patients R-T3 concentrations are below the detection limit.

Antibodies↗
PubMed1976

[Restitution of the thyrotropic function in goiter patients after discontinuing a long-term suppression therapy with thyroid hormones].

27 subjects with a negative TRH test were selected among patients with euthyroid goiter treated by thyroid hormones. The hormone therapy was stopped and T3 and T4 concentrations, basal and TRH stimulated TSH levels were determined after one, two and four weeks. A gradual increase of the mean basal and TRH stimulated TSH plasms concentration could be observed. However, after four weeks the TRH test was still negative in two patients and weak positive in another case. T3 plasma levels were lowest after one week which might indicate the presence of an intermittent thyrotropic insufficiency. It is concluded that the hormone-free interval should last four weeks at least before a reliable TRH test can be obtained.

Goiter↗
PubMed1976

On the time course of thyrotropin suppression by high doses of thyroid hormones.

Basal and stimulated TSH decreased progressively. Basal TSH was suppressed below the detection limit of 0.4 muU/ml after 74 h in 2 of the T3 and all of the T4 treated individuals. At this time in both groups 3 individuals could be significantly stimulated by TRH (abour 5% of the pretreatment stimulation). There was no significant difference in the time course of suppression obtained by T3 or T4 through plasma T3 levels in the T4 treated group were considerably lower.

Female↗
PubMed1976

[Secretion of TSH and stimulation-ability of the hypophysis after long-term suppression therapy in euthyroid nodular goiter and residual thyroid gland after subtotal resection of goiter].

In 51 patients, 33 with euthyroid goiter and 18 after subtotal thyroidectomy, plasma concentrations of T4, T3, and TSH before and after stimulation with TRF were determined under long term suppression with thyroid hormone and 1,2, and 4 weeks after stopping it. Even after complete suppression (delta TSH less than 0, 5 muU/ml) resumption of TSH secretion occurred within 4 weeks in all but two. A significantly higher increase of TSH and somewhat lower thyroid-hormone concentrations turned out in operated patients. An excessive decrease of T3 (and T4) concentrations within the 1st (and 2nd) week after therapy, dependent on the degree of previous TSH suppression, could be due to transitory thyrotropic insufficiency.

Goiter, Nodular↗
PubMed1975

[The euthyreotic hypotriiodothyroninemia].

In 33 patients with various, mainly severe diseases a subnormal triiodothyronine concentration (T3) and a normal thyroxin concentration (T4) were found. In addition to T3 and T4, the plasma TSH levels and T3 binding capacity were determined. In no case did the patient's history or clinical findings afford evidence of hypothyroidism. Diminished conversion of T4 to T3 is discussed as a possible cause of the inappropriately depressed T3 levels.

Disease↗
PubMed1975

[Evaluation of reliable pituitary suppression therapy through varying thyroid hormone dosage following total thyroidectomy due to a differentiated thyroid carcinoma].

The reliability of pituitary suppression by administration of 1-thyroxin (t4) or a combination of thyroxin and triiodothyronin (t3) of variable dosage following radical surgery for thyroid cancer in 13 patients was investigated by means of TRH-test and measurement of serum hormone levels. In contrary to generally applied higher doses the results were able to demonstrate that 0.2 to 0.3 mg 1-thyroxin is a sufficient dosage for a complete suppression of TSH-stimulation. In the presence of obviously more side effects the treatment with a combination of t4 and t3 is not of any advantage.

Carcinoma↗
PubMed1975

[Principals of hormone substitution in thyrectomized patients with carcinoma of the thyroid gland (author's transl)].

The substitution of thyrectomized patients with carcinoma of the thyroid with L-thyroxin has advantages compared to a substitution with triiodothyronine, 200 mug T4/d are sufficient to obtain a negative TRH test in most patients. For security it is suggested to performe a general substitution of these patients with 300 mug T4/d. This dose is very well tolerated. To high doses of substitution cause a "damage" of the thyreotrop in a part of the patients. This is demonstrated by a transient thyreotropic insufficiency after withdrawal of the substitution. The results demonstrated here suggest that the central suppression of TSH secretion is better correlated with plasma T4 than plasma T3 levels.

Humans↗