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Biomedical subjects

K W Wenzel

Publications and source records attributed to K W Wenzel.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1975

[Variation of the thyrotropin-releasing-hormone (TRH) stimulated thyrotropin (TSH) response in comparison with the tyhroid-gland-suppression test and the triiodothyronine (T3) and thyroxine (T4) blood levels in the so-called euthyroid endocrine ophthalmopathy].

21 patients with active signs of euthyroid Graves' disease were given 400 mug thyrotropin-releasing hormone (TRH) i.v. All subjects with unresponsiveness to TRH had a nonsuppressible thyroidal 131I-uptake. On the basis of serum total T3 14 patients were hyperthyroid, 2 more had an elevated value of free T3. 4 patients with normal total T3 and nonsuppressible 131I-uptake were unresponsive to TRH, in 2 of them the free T3 fraction was elevated, however. 4 subjects with nonsuppressible 131I-uptake had a TRH stimulated TSH response. 2 of these subjects had hyperthyroid values of free and total T3 in serum and responded to TRH with an exaggerate TSH increment. The variations of TRH responsiveness may demonstrate a different threshold of the pituitary and the peripheral T3 receptors.

Graves Disease↗