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Biomedical subjects

H Meinhold

Publications and source records attributed to H Meinhold.

At least 91 records · Page 5Linked to original sources
PubMed1978

A low T3 syndrome in diabetic ketoacidosis.

The pituitary-thyroid axis was investigated in nineteen euthyroid patients with severe diabetic ketoacidosis. A 'low T3 syndrome' was found, with the following characteristics: lowered serum concentrations of triiodothyronine (T3), increased reverse triiodothyronine (rT3), slightly low thyroxine (T4), normal thyrotrophin (TSH), slightly increased triiodothyronine uptake (RT3U) values, and a blunted TSH response to thyrotrophin-releasing hormone (TRH). These disturbances in thyroid-function tests required several days good control of the diabetes to be corrected, at least partially. The data suggest the presence of an abnormal extrathyroidal T4 metabolism as well as a pituitary defect. Caution is recommended in the interpretation of thyroid-function tests during and several days after the treatment of diabetic ketoacidosis.

Adult↗
PubMed1978

A radioimmunoassay for 3,5-diiodothyronine.

A radioimmunoassay for the measurement of 3,5-diiodothyronine (3,5-T2) using a 3H-labelled derivative of 3,5-T2 as tracer has been developed. The cross-reactivity of the antiserum was relatively high for T3 (3.1%) and low for T4 (less than 0.0015%). 3,5-T2 serum concentrations measured after fractional enrichment of 3,5-T2 were near or below the detection limit of 0.1 nmol/l in ten normal subjects and 0.38 nmol/l in five hyperthyroid patients. 3,5-T2 was also detected in thyroid tissue. The serum half-time of 3,5-T2 estimated after injection of 2 mg 3,5-T2 in three normal volunteers was 4.5 h.

Half-Life↗
PubMed1978

Relationship between thyroid status and Graves' disease-specific immunoglobulins.

The prevalence of TSI in Graves' disease was investigated with a radioligand receptor assay using human thyroid membranes and highly purified labeled porcine TSH or bovine TSH in 110 patients before treatment and in 39 patients after successful treatment with antithyroid drugs. In 11 patients, the assay was performed before, during, and after therapy. The results in the radioligand receptor assay were compared to thyroid function tests (TRH test, free T4 index, serum %3 level, and thyroid suppression test). Normal IgG inhibits nonspecifically, but dose dependently, the binding of [125I]TSH to thyroid membranes. IgG samples from patients were only considered to be positive if they reduced the binding of the labeled hormone below the mean value minus 2 SD of the controls. TSI activity was found in 50% of the patients with untreated diffuse toxic goiter, in 3 out of 27 cases who regained suppressible thyroid function, and in 5 out of 12 cases who were off therapy for more than 6 weeks and showed normal TRH tests and normal hormone levels but in whom the suppression test was not performed. Our data cannot prove the hypothesis that only humoral antibodies are responsible for the thyroid stimulation in Graves' disease, but of course they cannot exclude it; furthermore, they suggest the existence of antibodies which bind to the human thyroid cell membrane without necessarily stimulating thyroid cellular activity.

Antigen-Antibody Complex↗
PubMed1977

The thyroidal production of reverse triiodothyronine in autonomous adenoma.

The ratios of reverse triiodothyronine (rT3) to triiodothyronine (T3) concentrations were similar (0.89 +/- 0.09) in twenty-three autonomous thyroid nodules (fourteen decompensated, nine compensated) and paranodular tissues (0.82 +/- 0.08), whereas the serum ratio was significantly lower (0.098 +/- 0.014). This is compatible with the hypothesis that thyroidal rT3 and T3 production from mono- and diiodotyrosine may be a random process in contrast to non-random extrathyroidal rT3 and T3 formation.

Adenoma↗
PubMed1977

Radioimmunological measurement of 3,3'-diiodothyronine in serum and amniotic fluid.

A radioimmunoassay for the measurement of 3,3'-diiodo-L-thyronine (rT2) in serum and amniotic fluid is described. Specific antisera to rT2 were produced by immunization of rabbits with rT2 conjugated to bovine serum albumin. The molar cross-reactivity tested for various iodothyronines and iodotyrosines was 0.3% for triiodothyronine and 0.001% for thyroxine. The sensitivity of the assay with a detection limit of 1.8 fmol/tube (0.94 pg/tube) was due to the high avidity of the antiserum and the use of 125I-labelled rT2 of maximum specific radioactivity. In most of 45 normal subjects, serum rT2 levels measured in evaporated ethanol extracts were below the detection limit of 0.018 nmol/1. Mean rT2 concentrations were 0.21 nmol/1 in newborn cord serum and 0.10 nmol/1 in amniotic fluid at 12 to 30 weeks of pregnancy. The molar concentration ratio of 3,3',5'-triiodothyronine (rT3) to rT2 was estimated to be 15.7 in cord serum of newborn. A similar rT3/T2 ratio was found in adults after intravenous application of 500 microgram rT3. Using these data and the known rT3 values, a hypothetical mean serum rT2 concentration in adult normal subjects of 0.015 nmol/1 was calculated. The radioimmunoassay described may be a useful analytical tool in studies of the synthesis as well as the metabolism of thyroid hormones.

Amniotic Fluid↗
PubMed1976

Effect of a single dose of dexamethasone on serum concentrations of thyroid hormones.

In ten euthyroid subjects, in whom endogenous thyroid-stimulating hormone (T.S.H.) production was suppressed by oral thyroxine (T4), a single dose of dexamethasone resulted in reduced serum-3,3'5-triidothyronine (T3) concentration and raised serum-3,3',5'-triiodothyronine (reverse T3 or rT3) concentration after 24 h. These changes were not related to changes in free hormones or binding proteins. Adrenal glucocorticoids may have a pathophysiological role in modulating the peripheral metabolism of thyroid hormones in stress.

Adult↗
PubMed1975

Radioimmunoassay of 3,3',-'-triiodo-L-thyronine (reverse T3) in human serum and its application in different thyroid states.

A radioimmunoassay for the measurement of 3.3',5'-triiodo-L-thyromine (reverse T3, rT3) has been developed. The known limitations of this technique have been overcome by the use of the biologically relevant L-compound for the production of highly specific antisera and for preparing the standard curve. The high sensitivity of the assay (lower limit of detection 20 ng/l serum) was obtained by using 125I-labelled rT3 of maximum specific radioactivity. Mean serum rT3 concentrations for various thyroid states were as follows: Normal subjects: 0.182 mug/l (0,280 nmol/l), hypothyroidism: 0.038 mug/l (0.058 nmol/l), hyperthyroidism: 0.522 mug/l (0.802 nmol/l), pregnants: 0.200 mug/l (0.307 nmol/l), newborn (cord serum): 2.11 mug/l (3.24 nmol/l). The method described should provide additional information with regard to the clarification of thyroxine metabolism.

Cross Reactions↗
PubMed1975

Different effects of oral doses of triiodothyronine or thyroxine on the inhibition of thyrotrophin releasing hormone (TRH) mediated thyrotrophin (TSH) response in man.

Since contradicting results about the existence of T3 or T3 and T4 receptors in pituitary tissue have been reported, the influence of L-triiodothyronine (L-T3) or L-thyroxine (L-T4) on TRH stimulated TSH release was investigated. Oral administration of 50 mug L-T3 caused an increasing inhibition of TSH response to 400 mug TRH from 64% 2 h after L-T3 intake to 29% after 24 h, while serum T3 peaks up to 5.45 ng/ml occurred between 2 to 4 h after L-T3 ingestion and became normal after 8 to 10 h. This delay in the T3 action on TRH inhibition agrees with the postulate that T3 induces the synthesis of an inhibiting protein which is blocking TSH liberation. Oral administration of 1000 mug L-T4 induced increments of serum T4 up to 221 ng/ml between 6 to 24 h after intake; however, a TRH inhibition of 62% did not become evident before 48 h. At this time T3 levels had risen to the upper normal range. These results support the theory that T3 is responsible for the regulation of TSH secretion. An intra-pituitary conversion from T4 to T3 seems more likely the cause of the TRH inhibition rather than the peripheral T4-T3 conversion or a direct action by T4 binding sites in the pituitary.

Administration, Oral↗