Paradoxical modulation of thyrotrope responsiveness to TRH during the treatment of thyrotoxic patients: apparent absence of feed-back regulation
- 1. Brussels Univ. (Belgium). Inst. de Recherche Interdisciplinaire en Biologie Humaine et Nucleaire
- 2. Brussels Univ. (Belgium). Lab. of Experimental Medicine
- 3. Hopital Universitaire Saint-Pierre, Brussels (Belgium). Dept. des Radioisotopes
Description
Eight patients with active thyrotoxicosis have been followed up to one year after the onset of antithyroid treatment. At different time intervals during the investigation period, TRH tests were performed and total T4 and T3 basal levels were measured. The TRH-induced TSH release was delayed in all patients in spite of a normalization of the circulating levels of thyroid hormones. The delay varied according to the patients and lasted, in some cases, for as long as 24 weeks after the normalization of the thyroid hormone levels. Administration of thyroid hormones, together with methimazole, did not seem to prevent the pituitary thyrotropes responsiveness; moreover, it did not provoke an inhibition of the TRH-induced TSH release once the thyrotropes reactivity was fully restored. The feed-back mechanism does not seem to be the main modulator of the pituitary responsiveness to TRH in these circumstances. (orig.)
Abstract (German)
Acht Patienten mit aktiver Thyreotoxikose wurden bis zu einem Jahr nach Beginn der Antithyroidbehandlung ueberwacht. In bestimmten Zeitabstaenden wurden waehrend der Untersuchung TRH-Tests durchgefuehrt und die totalen T4- und T3-Grundwert gemessen. Die durch TRH-induzierte TSH-Freisetzung war bei allen Patienten trotz normaler Zirkulation der Schilddruesenhormone verzoegert. Die Verzoegerung war individuell verschieden und hielt in einigen Faellen bis zu 24 Wochen nach der Normalisierung des Schilddruesenhormonspiegels an. Die Verabreichung von Schilddruesenhormonen in Verbindung mit Methimazol hatte keinen Einfluss auf das Ansprechen des Hypophysen-Thyreotrophormons und bewirkte darueber hinaus auch keine Hemmung der TRH-induzierten TSH-Freisetzung mehr, sobald die Thyreotrop-Reaktivitaet voellig wiederhergestellt war. Der Feedback-Mechanismus scheint unter diesen Umstaenden nicht der Hauptmodulator des Ansprechens der Hypophyse auf TRH zu sein. (orig.)Additional details
Identifiers
Publishing Information
- Journal Title
- Hormone and Metabolic Research
- Journal Volume
- 8
- Journal Issue
- 02
- Series
- Horm. Metab. Res.
- Journal Page Range
- 128-131
- ISSN
- 0018-5043
INIS
- Country of Publication
- Germany
- Country of Input or Organization
- Germany
- INIS RN
- 7270745
- Subject category
- S60: APPLIED LIFE SCIENCES;
- Descriptors DEI
- ANTITHYROID DRUGS; DIAGNOSIS; DIAGNOSTIC TECHNIQUES; HYPERTHYROIDISM; IODINE 131; NUCLEAR MEDICINE; PATIENTS; PITUITARY GLAND; RADIOPHARMACEUTICALS; THYROID; THYROXINE; TRIIODOTHYRONINE; TSH
- Descriptors DEC
- AMINO ACIDS; BETA DECAY RADIOISOTOPES; BETA-MINUS DECAY RADIOISOTOPES; BODY; CARBOXYLIC ACIDS; DAYS LIVING RADIOISOTOPES; DISEASES; DRUGS; ENDOCRINE DISEASES; ENDOCRINE GLANDS; GLANDS; HORMONES; INTERMEDIATE MASS NUCLEI; IODINE ISOTOPES; ISOTOPES; LABELLED COMPOUNDS; MEDICINE; NUCLEI; ODD-EVEN NUCLEI; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANIC HALOGEN COMPOUNDS; ORGANIC IODINE COMPOUNDS; ORGANS; PEPTIDE HORMONES; PITUITARY HORMONES; RADIOACTIVE MATERIALS; RADIOISOTOPES; THYROID HORMONES
Optional Information
- Notes
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