Intravenous and Peroral TRH Stimulation in Sporadic Atoxic Goitre

Abstract

Thyrotrophin releasing hormone (TRH) stimulation test with 200 \g=m\g iv was performed in 35 patients with atoxic sporadic goitre. In 23 patients with diffuse goitre 7 showed a lack of increase in serum thyrotrophin (TSH) at a significantly increased frequency compared to controls (P = 0.0028). In 4 patients with solitary nodules 2 showed no significant response to TRH (negative), while 3 of the 8 patients with multinodular goitres had negative TRH test. Only 6 of the 12 TRH negative patients also had non-suppressible 131I uptake following T3. No significant difference in age and thyroid parameters was found between the TRH negative and TRH positive patients. In 7 TRH negative patients the test was repeated with 400 \g=m\g TRH but all remained negative. Five of these patients were given TRH perorally 80 mg daily for 2 weeks resulting in a significant increase in serum T4 and T3. No detectable increase in TSH was found. The response to iv bovine TSH in 4 TRH negative patients was found to be normal, suggesting that there was normal thyroid sensitivity to TSH. Our findings suggest that patients with TRH negative atoxic goitre can release biological active TSH following prolonged TRH stimulation. The high frequency of a negative standard TRH test in atoxic goitre seems to diminish the diagnostic value of the standard TRH test.Several studies on the thyrotrophin (TSH) response to intravenous doses of thyrotrophin releasing hormone (TRH) in clinical euthyroid patients with sporadic atoxic goitre have demonstrated a lack of response in a varying percentage of the patients studied (Pickardt et al. 1973;Ridgway et al. 1973; Dige-Petersen 8c Hummer 1974).

Characteristics of Patients With Normal T3 and T4 and a Low TSH Response to TRH

“…The results of the present study help to define the thyroid status of patients with normal T3 and T4 but blunted TSH response to TRH. As was the case in some other studies (Kirkegaard et al, 1977;Smeulers et al, 1977;Elte et al, 1978;Morgans et al, 1978;Bianchi et al, 1979;Kallner & Ljunggren, 1979;Langer et al, 1979;Kirkegaard et a/., 1980;Gemsenjager & Girard, 1983), we detected no significant difference between the basal thyroid hormone levels (T3, T4. free T4) of these patients and ofcontrols.…”

“…These two characteristics, absence of TSAb and hypersensitivity to TSH, delineate a thyroid disorder clearly different from Graves' disease.Absent or blunted TSH response to TRH in patients with normal T4 and T3 remains a clinical problem of uncertain aetiology. It has been described mainly in patients with multinodular goitre (Hall et al, 1973; Dige-Peterson & Hummer, 1977;Kirkegaard et al, 1977; Smeulers etal., 1977;Morgans et al, 1978) but can also occur with diffuse goitre and…”

“…It has been suggested that this disorder represents a state of preclinical hyperthyroidism (Hall et al, 1973;Gemsenjager et al, 1976). Indeed, many studies have shown significantly higher T3 levels in patients presenting with this disorder when compared to controls (Kirkegaard et al, 1977;Smeulers el al., 1977;Elte el al.. 1978;Bianchi el al., 1979;Langer et a/., 1979).…”

Physiological aspects of the thyroid trapping function and its suppression in iodine deficiency using 99m Tc pertechnetate

“…Iodine-deficient goi¬ tres are frequently associated with functional thy¬ roid autonomy (Miller & Block 1970;Gemsen¬ jäger et al 1976;Dige-Petersen & Hummer 1977;Kirkegaard et al 1977;Emrich & Bahre 1978) which can cause thyrotoxicosis after iodine con¬ tamination (Fradkin & Wolff 1983). Iodine-deficient goi¬ tres are frequently associated with functional thy¬ roid autonomy (Miller & Block 1970;Gemsen¬ jäger et al 1976;Dige-Petersen & Hummer 1977;Kirkegaard et al 1977;Emrich & Bahre 1978) which can cause thyrotoxicosis after iodine con¬ tamination (Fradkin & Wolff 1983).…”

Responses to TRH, T3 suppression tests and histological findings by needle biopsy in patients with simple goitre in Japan

“…However, the possibility that the range of set points for serum T3 and T4 of the hypothalamohypophyseal axis ('thyrostat') is abnormal in these subjects cannot be excluded. Kirkegaard et al (1977) have reported that patients with TRH nega¬ tive atoxic goitre can release biologically active TSH following prolonged TRH stimulation. An¬ other explanation for the negative TRH test may be that a physiologically significant increase in serum TSH was undetectable in the assay used (Kohler et al 1973).…”