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Hyperthyroidism with an FSH- and TSH-Secreting Pituitary Adenoma

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Hyperthyroidism with an FSH- and TSH-Secreting Pituitary Adenoma • Hyperthyroidism with an FSH- and TSH-secreting pituitary adenoma JOHN BERMINGHAM, DO LOUIS C. HAENEL, DO A 34-year-old man was found noma is rare. The combined secretion of follicle- to have elevated thyroxine (T 4 ), triiodothy- stimulating hormone (FSH) and TSH by a pi- ronine (T3 ), calculated free T4 , thyroid- tuitary adenoma is rarer. But with current stimulating hormone (TSH), follicle-stimu- widespread use of TSH assays, plus the future lating hormone (FSH), and alpha subunits clinical availability of more sensitive TSH as- of TSH and FSH. A computed tomography says as well as TSH bioactivity testing, more scan of the head showed a 16-mm mac- patients will have pituitary-induced hyperthy- roadenoma of the pituitary gland. There roidism correctly diagnosed, and the disorder was no evidence of loss or excess secre- will be better understood. tion of other pituitary hormones. The large As illustrated in the following case study, chromophobe adenoma was removed via making the correct diagnosis of primary ver- a transphenoidal approach. The patient sus secondary hyperthyroidism is imperative has been taken off all medication. Thyroid because the treatment and potential conse- function has returned to normal and there quences of each of these diseases are totally has been no loss of pituitary secretory ca- different. pacity of other pituitary hormones. The oc- currence of a combined TSH- and FSH- Report of case secreting pituitary adenoma is rare; to the In August 1985, a 34-year-old man was seen with authors knowledge, only one case has complaints that were initially vague and nonspe- been documented in the literature. cific. On thorough questioning, however, he re- ported periods of excessive sweating, some degree of heat intolerance, mild insomnia, tremulousness, Hyperthyroidism caused by thyroid-stimu- dizziness, palpitations, emotional lability, anxiety, lating hormone (TSH )—secreting pituitary ade- and compulsive eating that had led to weight gain. The patient had no sexual dysfunction or loss of libido. From the department of endocrinology and metabolism, The patient, the father of two children, had a University of Medicine and Dentistry of New Jersey— benign medical history. He had had "infectious hepa- School of Osteopathic Medicine. titis" a few years previously. His father had "some kind of thyroid disorder 40 years ago," specifics of Dr Bermingham is chief pulmonary fellow; Dr Haenel which were unobtainable. is head, department of endocrinology and metabolism. Physical examination revealed an enlarged thy- Reprint requests to John Bermingham, DO, John F. roid gland, approximately 1.5 times normal size, Kennedy Memorial Hospital, University Medical Cen- slightly more full on the right side. No adventi- ter, Laurel Rd, Stratford, NJ 08084. tious sounds were heard over the gland or the chest 1560 • JAOA • Vol 89 • No 12 • December 1989 Case report • Bermingham and Haenel wall. The extraocular muscles were intact. Find- mal, 30%-40%); calculated free T4, 7.5 units (refer- ings of funduscopic examination were normal. An ence laboratory normal, 1.5-5.2 units); and TSH at eye examination revealed no detectable thyroid- 8.81.A.U/mL (reference laboratory normal, 0-7 RU/mL). related abnormalities. No dermopathy, tremors, A computed tomography (CT) scan of the head muscle weakness, or onycholysis could be found. showed a 16-mm pituitary macroadenoma. Arte- Penis and testes were of normal size. Male pattern rial digital subtraction angiography ruled out the hair distribution was normal. There was no gyne- possibility of a carotid artery aneurysm. Results comastia. of formal visual field testing were normal. Pitui- The patient underwent routine screening tests tary integrity of the secretory capacity for other including an electrocardiogram, a complete blood pituitary hormones was evaluated by use of a thy- cell count with differential, and a biochemistry pro- rotropin-releasing hormone (TRH )–stimulation file. All results were within normal limits. The se- testi-2 (Table 1); an insulin tolerance testa (Table rum thyroxine (T4) concentration by radioimmu- 2); and measurements of fasting TSH, FSH, leuti- noassay (RIA) was elevated to 16.3 Rg/dL (refer- nizing hormone (LH), and the alpha subunits of ence laboratory normal, 4.5-12.5 ti,g/dL). Thyroid TSH, LH, and FSH (Table 3). An elevation of FSH function tests performed again 14 days later at 23.6 mIU/mL (reference laboratory normal for showed elevated serum triiodothyronine (T3) by an adult male, 0-20 mIU/mL) and alpha subunit RIA at 316 ng/dL (reference laboratory normal, of FSH at 25p.U/mL (reference laboratory normal, 4.50-12.5 ng/dL). The TSH level was not measured. 7-20 RU/rnL) was noted. The 24-hour thyroid uptake, using 105 of io- No water deprivation test was done to evaluate dine 123, was elevated at 63%. A thyroid scan re- vasopressin release, and no tests were done to meas- vealed a diffusely enlarged, symmetrically involved ure serum testosterone or LH-releasing hormone thyroid gland with no evidence of space-occupying stimulation, or sperm count. disease within the thyroid and no evidence of sub- Surgery was scheduled and the patient was sternal extension of functional tissue. A long-act- treated preoperatively with a 6-week course of pro- ing thyroid stimulator test (LATS) was not done. pranolol hydrochloride (20 mg orally tid) for high The data obtained to this point could be consis- blood pressure and PTU (100 mg orally tid). In Sep- tent with Graves disease. Because the patient was tember 1986, a transphenoidal hypophysectomy a young man with a relatively small thyroid gland was performed and a large macroadonoma was re- and the thyrotoxicity appeared to be relatively moved. Routine microscopic examination revealed mild, we decided to start him on propylthiouracil the mass to be a chromophobe adenoma. The ade- (PTU) therapy (100 mg orally three times a day). noma was not examined by electron microscopy or After 3 months of therapy, the patient appeared immunohistochemical staining of tissue. to be significantly improved. His weight was sta- Forty-eight hours following surgery, central dia- ble, and the thyroid gland was barely palpable. Re- betes insipidus developed and the patient was peat thyroid function tests had fallen to normal treated with desmopressin acetate (DDAVP). The levels: 13 resin uptake (T3RU), 33% (reference labo- desmopressin therapy led to iatrogenic syndrome ratory normal, 23%-34%); T4 (RIA), 11.5 il.g/dL (ref- of inappropriate secretion of antidiuretic hormone, erence laboratory normal, 4.5-12.5 lig/dL), and cal- and it was discontinued without further sequelae. culated free T4, 3.84 units (reference laboratory nor- Initially, the patient was placed on hydrocortisone mal, 1.1-4.4 units). supplementation. One week after surgery, the pa- The PTU therapy was discontinued after 6 tient was taken off all medication. Laboratory stud- months, at which time thyroid function tests ies at that time indicated normal levels of serum showed T3RU at 40% (reference laboratory normal, electrolytes; urine specific gravity, 1.013; TSH 23%-34%); calculated free T4 at 5.58 units (refer- (RIA), 3.3 mIU/mL (reference laboratory normal, ence laboratory normal, 1.0-4.3 units); T 4 (RIA) at 0-4.9 mIU/mL), and T4 (RIA) 9.7 p.,g/dL (reference 13.8 1.1.g/dL (reference laboratory normal, 4.5-12.5 laboratory normal, 4.5-12.5 Rg/dL). lig/dL); and elevated TSH, 11.1 mIU/mL (reference Currently, the patient has no complaints, and laboratory normal, 0-4.9 mIU/mL). A week later, blood pressure has returned to normal levels. The the same tests were done at an independent labo- patient will be followed up at 6-month intervals ratory indicating and confirming increased values: with thyroid function testing and measurement of T4 (RIA), 18.7 I.Lg/dL (reference laboratory normal, fasting FSH levels. The patient has been advised 5-13 ii,g/dL); T3RU, 40% (reference laboratory nor- that the macroadenoma could recur4 and that an- Case report • Bermingham and Haenel JAOA • Vol 89 • No 12 • December 1989 • 1561 Table 1 Table 2 Patients Thyroid-Releasing Hormone Patients Insulin Tolerance Test Results (TRH) – Stimulation Test Results Cortisol, Human growth Prolactin, Internal p.g/dL hormone, ng/mLt Internal TSH, mIU/L mIU/Lt Fasting (7 Am) 18.5 1.3 Fasting (7 AM) 6.6 19 Humulin R insulin TRHI: administered intravenously, 0.02 U/kg (more if 500 lig (9:30 Am) needed) administered At 30 minutes (10 Am) 8.2 36 intravenously 36 At 60 minutes (10:30 Am) 8.5 Postinsulin serum glucose nadir 32mg/dL TSH = thyroid-stimulating hormone; reference laboratory normal, 0.00 to 4.90 mIU/L. Results§ Reference laboratory normal range for an adult male, up to 25 mIU/ At 15 minutes (9:45 Am) 27.1 6.6 L. At 30 minutes (10 Am) 27.7 5.9 TRH stimulates TSH and prolactin secretion from the pituitary At 45 minutes (10:15 AM) 29.1 5.1 gland. At 60 minutes (10:30 AM) 28.5 5.3 At 75 minutes (10:45 Am) 24.0 5.2 At 90 minutes (11 Am) 22.0 5.2 *Laboratory reference normal, 7 to 25 pg/c1L at 8 Am; 2 to 9 ug/dL at 4 PM. tLaboratory reference normal, 5 ng/mL. Hypothalamic regulation of other course of therapy or alternate therapy will human growth hormone l hGH I secretion can be altered by drugs that affect catecholamine neurotransmitters. For example, 13-adrenergic blockade be discussed at that time. (propranolol) can facilitate hGH secretion in response to hypoglycemia. /Patient's blood glucose nadir was 32 mg/dL, obtained 25 minutes after injection of insulin. Nadir results should be < 40 mg/dL or 50'a of baseline Discussion level.
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