Hyperthyroidism in a patient with a pituitary adenoma

Nyhan, William L.; Green, Morris

doi:10.1016/s0022-3476(64)80292-4

Cited by 28 publications

(9 citation statements)

References 8 publications

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“…Until 1960 there appear to have been eight cases reported of hyperthyroidism associated with chromophobe adenoma (Nurnberger & Korey, 1953;Werner & Stewart, 1958;Kappeler, 1959;Nyhan & Green, 1964;Jackson, 1965;Maurer et al, 1966). It had been presumed that these tumours had secreted excess TSH.…”

Section: Discussionmentioning

confidence: 99%

Case of Hyperthyroidism Due to a Chromophobe Adenoma*

Baylis

1976

Clinical Endocrinology

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A A 23-year-old man with secondary hypogonadism was also found to be thyrotoxic. Results of thyroid function tests were in the hyperthyroid range but the serum TSH was inappropriately high. A pituitary tumour was demonstrated and following hypophysectomy he became biochemically hypothyroid. Evidence is presented and discussed that his hyperthyroidism was due to excessive TSH production by the pituitary tumour.

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Section: Discussionmentioning

confidence: 99%

Case of Hyperthyroidism Due to a Chromophobe Adenoma*

Baylis

1976

Clinical Endocrinology

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“…This rare combination has also been encountered in children. In 1964, Nyhan and Green [27] reported on an 11-year-old child with a pituitary chromophobe adenoma and hyperthyroidism. In reviewing the literature these authors found two additional cases in childhood and suggested that examination of visual fields and x-rays of the skull be obtained in order to uncover this association in children with thyrotoxicosis.…”

Section: Discussionmentioning

confidence: 99%

Thyrotropin Behavior in Thyroid Disorders of Childhood

1973

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Through the use of a double antibody radioimmunoassay method, the mean serum concentration of thyrotropin (TSH) in 51 normal children aged 1 month-18 years was 3.7 ng/ml. There was no change with age, sex, or time of the day at which the sample was obtained.In six of nine newly diagnosed hyperthyroid children concentrations of TSH fell below the limit of detection, whereas in the remaining three concentrations were in the low normal range. Knowledge of the TSH fluctuations during medical treatment (antithyroid drugs or radioactive iodine plus 127 I) were useful in insuring a smooth clinical course. Elevations in TSH above 10 ng/ml served to indicate a need for change in therapy. Radical subtotal thyroidectomy evoked an acute compensatory rise (> 20 ng/ml) in TSH levels which was sometimes sufficient to maintain the level of serum thyroxine above 4 ^ig/100 ml. Hemithyroidectomy did not influence TSH or other thyroid parameters in previously euthyroid subjects.There was a clear separation between normal subjects and patients with primary hypothyroidism with values for TSH always exceeding 20 ng/ml in the latter. The TSH levels were below 3.7 ng/ml in pituitary hypothyroidism. In hypothyroid patients receiving adequate replacement therapy, elevations of serum TSH of > 20 ng/ml were encountered 2 weeks after discontinuation of treatment.Investigation of the pituitary-thyroidal axis in two untreated cretinous infants showed preservation of the functional integrity of the pituitary-thyroidal feedback system despite prenatal thyroid insufficiency as evidenced by a fall of TSH from levels >80 to <5 ng/ml in the presence of free thyroxine (FT 4 ) levels >2 ng/100 ml.In three patients (two females and one male) with longstanding juvenile hypothyroidism and TSH levels >80 ng/ml, pituitary dysfunctions characterized by luteinizing hormone (LH) concentrations above 20 mlU/ml and blunted growth hormone (HGH) responses to hypoglycemia were documented prior to therapy. Only the male had evidence of sexual precocity on physical examination. All three showed an abnormal circadian rhythm of cortisol secretion manifested by 8 PM values greater than 10 jug/100 ml. Acute restoration of euthyroidism in the two girls by means of parenteral thyroxine (T 4 ) improved the HGH response and normalized the cortisol rhythms in 72 hr, coincident with a sharp decline in TSH levels toward normal. In contrast, the high levels of LH declined much more slowly, failing to reach normal for as long as 7 weeks posttreatment.TSH in company with T 4 measurements permitted segregation of patients with Hashimoto's thyroiditis into three groups: (a) euthyroid with normal TSH and T 4 , 28Thyrotropin behavior in childhood thyroid disorders 29 (b) compensated with TSH values ranging between 19 and 28 ng/ml and T 4 in the 6-8 /zg/100 ml range, and (c) hypothyroid with T 4 below 3 ^g/100 ml and TSH values greater than 40 ng/ml. Speculation

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“…TSH-omas are rare in adults and to our knowledge our patient is one of the youngest children with hyperthyroidism due to TSH-oma ever reported. Other 13 children or adolescents described were 8-yr. or older (8 to 16yr) and had macroadenoma except a 13 yr-old girl who had microadenoma and a 15 yr-old girl whose tumor size was not decribed [7][8][9][10][11][12][13][14][15][16][17][18][19].…”

Section: Journal Of Endocrinology and Thyroid Research Discussionmentioning

confidence: 99%

“…*Basal cortisol = 3.43 mg/dL(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19); urine density = 1005; ** Total testosterone = 106 ng/dL (<100); peak LH and FSH after GnRH = 1.1 and…”

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confidence: 99%

Long-Term Follow-Up in a Male Patient with Micro-TSH-Oma Diagnosed at 8-Yr-Old

Cardoso-Demartini¹

2019

JETR

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Triiodothyronine (T3) suppression test is generally reserved for patients with inconclusive results in above tests, because genetic tests for detection of mutations in thyroid receptor (TR)α and TRβ genes are expensive. Administering long-acting somatostatin analogs has been proposed for distinguishing between thyrotropinomas and RTH, since patients with thyrotropinomas would be likely to show a significant reduction in free thyroxine (fT 4 ) and T 3 levels. Approximately one third of patients with TSH-oma were misdiagnosed as having primary hyperthyroidism and mistakenly treated with thyroidectomy or radioiodine [2]. The majority of TSH-omas is monoclonal in origin, like other types of pituitary adenomas. Pituitary-specific transcription factor-1 (Pit-1) may play a role in adenomatous

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Hyperthyroidism in a patient with a pituitary adenoma

Cited by 28 publications

References 8 publications

Case of Hyperthyroidism Due to a Chromophobe Adenoma*

Case of Hyperthyroidism Due to a Chromophobe Adenoma*

Thyrotropin Behavior in Thyroid Disorders of Childhood

Long-Term Follow-Up in a Male Patient with Micro-TSH-Oma Diagnosed at 8-Yr-Old

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