Hyperthyroidism caused by a pituitary thyrotrophin-secreting tumour with excessive secretion of thyrotrophin-releasing hormone and subsequently followed by Graves' disease in a middle-aged woman

1985 ◽  
Vol 110 (3) ◽  
pp. 373-382 ◽  
Author(s):  
Kyuzi Kamoi ◽  
Terunori Mitsuma ◽  
Hiroshi Sato ◽  
Motoharu Yokoyama ◽  
Kazuo Washiyama ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Clinical Signs ◽  
Antithyroid Drug ◽  
Reciprocal Relationship ◽  
Serum Prolactin ◽  
Graves Disease ◽  
Α Subunit ◽  
Thyrotrophin Releasing Hormone ◽  
Aged Woman ◽  
Serum Tsh

Abstract. A 46-year-old woman had signs of thyrotoxicosis and galactorrhoea. Serum immunoreactive TSH and its α-subunit increased in the presence of high serum triiodothyronine (T3), thyroxine (T4), and free T4 concentrations, whereas β-subunit TSH was undetectable. Exogenous TRH failed to increase serum TSH. Serum TSH was markedly suppressed by glucocorticoid, but was increased by antithyroid drug. l-Dopa or bromocriptine partially suppressed, but nomifensine had no influence on serum TSH. Serum prolactin (Prl) was above normal and markedly increased by TRH, but depressed by bromocriptine and not suppressed by nomifensine. Plasma TRH was normal in the hyperthyroid state, but was increased by glucocorticoid and antithyroid drug. Excess thyroid hormone depressed plasma TRH concentrations. Basal serum GH levels were constantly low. Transsphenoidal removal of the tumour normalized serum hormones (T3, T4 free T4, TSH, α-subunit and Prl), and eradicated the clinical signs of hyperthyroidism and galactorrhoea. Histological study of the tumour tissue demonstrated both thyrotrophes and somatotrophes. A reciprocal relationship between serum TSH and T4 concentrations shifted to a higher level before but was normalized after removal of the tumour. Ten months later, the clinical signs of thyrotoxicosis and the increase in serum thyroid hormone recurred without a concomitant increase in serum TSH and its α-subunit. Thyroidal auto-antibodies were slightly positive, but thyrotrophin-binding inhibitor immunoglobulin (TBII) was negative. Administration of antithyroid drug produced a euthyroid state, but 3 years later, discontinuation of the treatment resulted in recurrent hyperthyroidism without suppressed plasma TRH and with no evidence of regrowth of the pituitary tumour. It is suggested that the patient initially had hyperthyroidism owing to excessive TSH secretion from the tumour caused by abnormal TRH secretion, and subsequently had hyperthyroidism owing to Graves' disease.

scholarly journals Correlation of Serum Prolactin and Thyroid Hormone in Female Infertility

2019 ◽  
Vol 17 (2) ◽  
pp. 32-34
Author(s):  
Fahat Banu
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Dysfunction ◽  
Female Infertility ◽  
Serum Prolactin ◽  
Psychological Consequences ◽  
Medical College ◽  
Hormone Profile ◽  
Hormonal Imbalance ◽  
High Incidence ◽  
Serum Tsh

Background: Infertility is a growing problem with adverse medical, social and psychological consequences globally. Apart from several causes of infertility, hormonal imbalance especially thyroid dysfunction and hyperprolactinemia can lead to female infertility. Both these conditions are treatable so Proper management of hormonal imbalance can result in restoration of normal fertility. Aims and objectives: Correlation of serum Prolactin and Thyroid hormone in female infertility. Materials and methods: Descriptive hospital based study was conducted at Nepalgunj medical college and teaching hospital, Nepalgunj, Banke, Nepal. The data was collected from September 2018 to August 2019. Total 30 cases of females of primary and secondary infertility attending outpatient department of gynecology department of Nepalgunj medical college were included in the study. A detailed history and clinical evaluation was done along with estimation of serum Prolactin and Thyroid hormone profile. Result: Hormonal status of subjects showed 15 i.e. 50% participants were thyroid whereas 11 (36.33%) were hypothyroid and 4 (13.33%) were hyperthyroid. Serum Prolactin was raised in 17 (57%) and normal in 13 (43%). Serum TSH and prolactin were found to be significantly positively correlated in female infertility (r=0.507, p =0.004). Conclusion: There is a high incidence of hyperprolactinaemia and thyroid dysfunction in female infertility.

PITUITARY-THYROID FUNCTION IN THYROTOXIC PATIENTS IN RELATION TO LONG-ACTING THYROID STIMULATOR (LATS) LEVELS

1970 ◽  
Vol 65 (4) ◽  
pp. 577-582 ◽  
Author(s):  
Minoru Fukuchi ◽  
Tohru Matsuoka ◽  
Tadashi Inoue ◽  
Kiyoshi Miyai ◽  
Yuichi Kumahara
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Elevated Serum ◽  
Antithyroid Drug ◽  
Initial Values ◽  
Long Acting ◽  
Serum Tsh

ABSTRACT Serial changes in TSH, LATS, and thyroxine levels in the sera were studied following administration of an antithyroid drug or a thyroid hormone to thyrotoxic patients who became euthyroid after treatment. These changes were simultaneously determined by means of human TSH radioimmunoassay, McKenzie's bioassay. and the method of Murphy, respectively. Administration of 1-methyl-2-mercaptoimidazole (MMI) led to a decrease in thyroxine concentration and to a 6–10 times increase of the initial values in serum TSH concentration. Following administration of thyroxine at the end of the MMI treatment, the elevated serum TSH was rapidly decreased with an increase in thyroxine concentration. LATS activity, however, showed no significant changes throughout these experiments in which the reciprocal changes between TSH and thyroxine concentrations were observed.

Changes in thyroid volume during antithyroid drug therapy for Graves' disease and its relationship to TSH receptor antibodies, TSH and thyroglobulin

1990 ◽  
Vol 123 (4) ◽  
pp. 411-415 ◽  
Author(s):  
Yoshiyuki Yamaguchi ◽  
Toshihiko Inukai ◽  
Akira Iwashita ◽  
Michio Nishino ◽  
Takahiko Yamaguchi ◽  
...  
Keyword(s):  
Drug Therapy ◽  
Antithyroid Drug ◽  
Thyroid Volume ◽  
Graves Disease ◽  
Antithyroid Drug Therapy ◽  
Antithyroglobulin Antibodies ◽  
The Mean ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies ◽  
Serum Tsh

Abstract. Changes in thyroid volume during antithyroid drug therapy for Graves' disease compared with circulating thyroid parameters were evaluated. One hundred and forty-four patients with Graves' disease were treated with methimazole. Thyroid volume was measured by ultrasonography (thyroid volume = Π abc/6, where a is length, b width, and c depth). Serum TSH, TSH-binding inhibitory immunoglobulins, thyroid-stimulating antibodies, thyroglobulin, antimicrosomal antibodies, and antithyroglobulin antibodies were also measured. In the whole group of patients, thyroid volume correlated significantly with thyroglobulin (p<0.01) and TSH-binding inhibitory immunoglobulins (p<0.01), but not with TSH, antimicrosomal antibodies, and antithyroglobulin antibodies. Furthermore, a positive correlation was found between thyroglobulin and TSH-binding inhibitory immunoglobulins (p<0.01). In 11 patients the mean thyroid volume decreased significantly after one year of therapy (p<0.01), associated with decreasing levels of serum TSH-binding inhibitory immunoglobulins. Ten patients experienced transient hypothyroidism with an overdose of methimazole, and the mean thyroid volume increased significantly (p<0.01) with increasing serum TSH levels. In conclusion, it is suggested that TSH receptor antibodies may have a thyroid growth-stimulating effect. In addition, circulating thyroglobulin levels reflect thyroid volume in Graves' disease.

scholarly journals ThyrotropinomA: Diagnosing a Rare Cause of Hyperthyroidism

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A968-A968
Author(s):  
Monica Bhanot ◽  
Chase Dean Hendrickson
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Equilibrium Dialysis ◽  
Elevated Serum ◽  
Sex Hormone Binding Globulin ◽  
Molar Ratio ◽  
Graves Disease ◽  
Free Triiodothyronine ◽  
Α Subunit ◽  
Free Thyroid Hormones

Abstract Case: The patient is a 40-year-old male who presented for evaluation of hyperthyroidism with symptoms including palpitations, increased bowel movements, anxiety, and worsening tremor. With a family history of Graves’ disease and an ultrasound showing a hyperemic thyroid, there was initial suspicion for Graves’ disease. Although a radioactive iodine thyroid scan showed diffuse uptake that was elevated, 21.4% at 4 hours and 33.1% at 24 hours, lab evaluation appeared inconsistent with Graves’ disease revealing: TSH 1.65 µU/mL (upper limit of normal [ULN] 4.5), free thyroxine (FT4) 1.99 ng/dL (ULN 1.17), free triiodothyronine 6.16 ng/dL (ULN 3.98), thyroid stimulating immunoglobulin 92% (ULN 122), and thyroid receptor antibodies less than 1.0 IU/L (ULN 1.75). Lab results were reproducible with elevated FT4 even by equilibrium dialysis at 3.9 ng/dL (ULN 2.4) and high-normal TSH with serial dilution that ruled out assay interreference. Given these findings, our focus turned to rare causes of hyperthyroidism including thyrotropinoma and thyroid hormone resistance (RTH). Unique to the diagnosis of thyrotropinoma is an elevated serum α subunit in 50-85% of cases (1). Therefore, we obtained an α subunit level which was 0.35 ng/mL (ULN 0.55) with a molar ratio of 2.2 (ULN 2.4). Since the α subunit level was normal, the patient obtained genetic testing for mutations in the thyroid hormone receptor β gene seen in 85% of RTH cases (1). However, no sequence variants were identified. Since initial lab and genetic analyses were undifferentiating, additional tests were obtained including an insulin-like growth-factor 1 level of 209 ng/mL (ULN 237) and prolactin level of 10.1 ng/mL (ULN 20) which can be elevated in 30% of mixed thyrotropinoma cases (1). The first evidence to suggest a thyrotropinoma was a mildly elevated sex-hormone binding globulin at 102 nmol/L (ULN 80). Further evaluation with pituitary magnetic resonance imaging showed a 6-milimeter lesion. Although the pituitary lesion is suggestive of a thyrotropinoma, it is not definitive, as they are present in 20% of RTH cases (1). Therefore, with increased suspicion of a thyrotropinoma, we pursued the more robust T3 suppression test which showed 56% suppression of TSH consistent with a thyrotropinoma. The patient had pituitary surgery with pathology confirming weak immunoreactivity for TSH. Post-operatively, his symptoms improved and free thyroid hormones normalized. Discussion: It is important to distinguish between thyrotropinoma and RTH as the treatment is different with 80% of thyrotropinoma cases achieving euthyroidism after surgery (1). In our case, the diagnosis was initially unclear thus it was important to broaden the lab and genetic evaluation considering the limitations of the studies. One such limitation is the α subunit may not be elevated in microadenomas as occurred in our case. 1. Beck-Peccoz et al. J Endocrinol Invest. 2019; 42:1401-6

THE THYROTROPHIN RESPONSE TO THYROTROPHIN RELEASING HORMONE DURING TREATMENT IN PATIENTS WITH GRAVES' DISEASE

1977 ◽  
Vol 85 (2) ◽  
pp. 335-344 ◽  
Author(s):  
E. Haug ◽  
H. M. M. Frey ◽  
T. Sand
Keyword(s):  
Serum Level ◽  
Thyroid Hormones ◽  
Pituitary Gland ◽  
Serum Levels ◽  
Graves Disease ◽  
Trh Test ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
First Time ◽  
Serum Tsh

ABSTRACT Thyrotrophin releasing hormone (TRH) tests were performed at 4 or 8 weeks intervals, after the initiation of anti-thyroid treatment in 15 patients with Graves' disease. All TRH tests were negative as long as the serum levels of thyroxine (T4) and triiodothyronine (T3) were elevated, and normalization of the serum levels of these hormones always occurred before the response to iv TRH was restored. In 13 patients the time from the patients for the first time were registered as biochemically euthyroid varied from 0–9 months (mean 3.1 months), before normal TRH response was restored. Two patients were still TRH non-responsive at the end of the study, even though they had been biochemically euthyroid for as long as 17 and 18.5 months. The TRH test, therefore, is not helpful in the evaluation of the effect of anti-thyroid treatment in patients with Graves' disease. There was an increase in the serum level of thyrotrophin (TSH) from 3.4 ± 0.3 (sem) to 4.3 ± 0.5 (sem) ng/ml (P <0.05), and a decrease in the serum level of total T4 from 19.4 ± 1.1 (sem) to 5.8 ± 0.8 (sem) μg/100 ml in 13 patients from the first examination until the last time they were examined before restored TRH response. This finding shows that the pituitary gland has retained its ability to synthesize and secrete TSH even though no TSH could be released by iv TRH. In 6 TRH non-responsive patients with Graves' disease, serum TSH levels were suppressed from 2.5 ±1.2 (sem) ng/ml before the administration of a single dose of 3 mg T4 orallly, to 0.9 ± 0.2 (sem) ng/ml, 7 days after the T4 administration. Thus, the negative feed-back effect on the pituitary gland of the thyroid hormones is operating in these patients. This finding indicates that the TRH non-responsiveness in euthyroid patients with Graves' disease is not due to pituitary depletion of TSH, since the negative feed-back effect of the thyroid hormones is operating normally.

Serum prolactin and thyrotrophin responses to thyrotrophin-releasing hormone at different times of the day in normal women

1981 ◽  
Vol 97 (1) ◽  
pp. 7-11 ◽  
Author(s):  
F. R. Pérez-López ◽  
G. Gómez ◽  
M. D. Abós
Keyword(s):  
Serum Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Before And After ◽  
The Mean ◽  
The Difference ◽  
Normal Women ◽  
Hormonal Release ◽  
Test Serum ◽  
Serum Tsh

Abstract. In order to determine whether or not the pituitary responsiveness to thyrotrophin-releasing hormone (TRH) changes during the nyctohemeral cycle, 10 healthy regularly cycling women were given 200 μg of TRH at 02.00 h, 10.00 h and 18.00 h with at least a 32 h interval between each test. Serum prolactin (Prl) and thyrotrophin (TSH) in 7 of the 10 women were measured serially before and after TRH administration. The mean basal Prl levels were significantly higher (P < 0.01) at 02.00 h than at 10.00 h and 18.00 h. The mean basal TSH levels were higher, although not significantly, at 02.00 h than at 10.00 h and 18.00 h. Although a higher TSH release occurred at 02.00 h than at 10.00 h and 18.00 h, the mean serum TSH and Prl peak responses to TRH were statistically similar in the three groups of tests. The integrated changes scores, calculated as the difference between the average post-TRH hormonal release and the average baseline levels, although higher in the 18.00 h test for Prl and the 02.00 h test for TSH, were not statistically different among the three tests.

SERUM THYROTROPHIN AND THE RESPONSE TO THYROTROPHIN RELEASING HORMONE IN SYMPTOMLESS AUTOIMMUNE THYROIDITIS AND IN BORDERLINE AND OVERT HYPOTHYROIDISM

1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg
Keyword(s):  
Autoimmune Thyroiditis ◽  
Elevated Serum ◽  
Mean Value ◽  
Primary Hypothyroidism ◽  
Overt Hypothyroidism ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Mean ◽  
The Individual ◽  
Serum Tsh

ABSTRACT Serum thyrotrophin (TSH) was determined by the double-antibody radioimmunoassay in 58 patients with primary hypothyroidism and was found to be elevated in all but 2 patients, one of whom had overt and one clinically borderline hypothyroidism. Six (29%) out of 21 subjects with symptomless autoimmune thyroiditis (SAT) had an elevated serum TSH level. There was little correlation between the severity of the disease and the serum TSH values in individual cases. However, the mean serum TSH value in overt hypothyroidism (93.4 μU/ml) was significantly higher than the mean value both in clinically borderline hypothyroidism (34.4 μU/ml) and in SAT (8.8 μU/ml). The response to the thyrotrophin-releasing hormone (TRH) was increased in all 39 patients with overt or borderline hypothyroidism and in 9 (43 %) of the 21 subjects with SAT. The individual TRH response in these two groups showed a marked overlap, but the mean response was significantly higher in overt (149.5 μU/ml) or clinically borderline hypothyroidism (99.9 μU/ml) than in SAT (35.3 μU/ml). Thus a normal basal TSH level in connection with a normal response to TRH excludes primary hypothyroidism, but nevertheless not all patients with elevated TSH values or increased responses to TRH are clinically hypothyroid.

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