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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 3 808-811
Copyright © 1997 by The Endocrine Society

Endocrinological Oncology

MRI-Demonstrable Regression of a Pituitary Mass in a Case of Primary Hypothyroidism after a Week of Acute Thyroid Hormone Therapy

Nicholas J. Sarlis, Françoise Brucker-Davis, John L. Doppman and Monica C. Skarulis

Laboratory of Molecular and Cellular Biology (N.J.S.) and Molecular and Cellular Endocrinology Branch (F.B-D., M.C.S.), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and Department of Radiology (J.L.D.), Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892

Address correspondence and requests for reprints to: Nicholas J. Sarlis, MD, PhD, Steroid Hormones Section, Laboratory of Molecular and Cellular Biology (LMCB), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bldg 8/Rm B2 A11, 8 Center Drive, MSC 0805, Bethesda, Maryland 20892-0805; E-mail: njsarlis{at}box-n.nih.gov


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Discussion
 References
 
Although magnetic resonance imaging (MRI) characteristics of pituitary gland hyperplasia in primary hypothyroidism have been previously described, the time span necessary for the regression of the hyperplasia in response to acute thyroid hormone (TH) therapy has not been defined.

A 26-yr-old woman underwent 131I ablation 11 yr before admission. Intermittent poor compliance to levothyroxine (LT4) therapy led to inappropriately high serum thyroid-stimulating hormone (TSH) for her triiodothyronine (T3) and thyroxine (T4) levels. The patient was investigated to rule out TSH-secreting pituitary adenoma or resistance to TH. On admission, the patient’s clinical features and thyroid function tests, as well as thyrotropin-releasing hormone (TRH) and acute T3 suppression tests, were in favor of profound primary hypothyroidism. MRI revealed symmetrical enlargement of the pituitary gland with distinct morphological characteristics of a macroadenoma. The patient began high-dose TH therapy and was rescannned six days later. The follow-up scan revealed a dramatic shrinkage of the pituitary gland. Four weeks later, serum T4 and TSH were within the normal range, and repeat MRI scan of the pituitary at that time showed a normal gland.

This case is the first to document dramatic shrinkage of pituitary hyperplasia in long-standing primary hypothyroidism within one week of acute TH therapy. MRI alone is unable to reliably differentiate between a TSH-secreting pituitary adenoma and hypothyroidism-induced pituitary hyperplasia. Dynamic endocrine testing as well as repeat pituitary MRI after a brief TH trial may provide a firm diagnosis in similar cases.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Discussion
 References
 
PITUITARY and sella enlargement in patients with long-standing primary hypothyroidism is well established (1, 2). The volume of the sella turcica correlates with circulating TSH levels (3). Thyrotroph cell hyperplasia is believed to be caused by a decrease in the negative feedback exerted by circulating thyroid hormones (TH) (4). Moreover, although not firmly established in humans, the occurence of an autonomous TSH-producing pituitary adenoma in the context of pituitary hyperplasia remains theoretically possible (5). The computed tomography (CT) and magnetic resonance imaging (MRI) characteristics of pituitary hyperplasia and its regression after therapy with TH have been previously described (6, 7, 8, 9, 10); however, the time course of the regression of thyrotroph hyperplasia and its clinical significance have not been adequately studied.

We hereby report a patient with profound hypothyroidism and MRI findings of a pituitary macroadenoma, which regressed after six days of high dose TH therapy. To our knowledge, this is the first case in which MRI-demonstrable pituitary thyrotroph hyperplasia has responded in such an acute and dramatic way to short-term TH administration.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Discussion
 References
 
Case report

A 26-yr-old woman was admitted for investigation of inappropriate secretion of TSH. The patient presented for the first time 11 yr before our evaluation with weight gain, dry skin, fatigue, left-sided periorbital enlargement, left eye proptosis, and a small nonnodular goiter. Thyroid function tests were borderline, in favor of mild hyperthyroidism, with a serum T3 level of 3.0 nmol/L (normal range: 1.1–2.9 nmol/L) and TSH of 0.5 mU/L (normal range: 0.5–4.9 mU/L), and with a 123I thyroid uptake that was normal. The patient was given the presumptive diagnosis of unilateral Graves’ ophthalmopathy. Tapazole (60 mg daily) and prednisone (60 mg daily) administration did not lead to significant changes in her thyroid function tests. The tapazole was discontinued, but generalized fatigue persisted. At that time, and because of an abnormally high 123I thyroid uptake of 74.6% at 24 h, the patient underwent ablation of the thyroid gland with 15.3 mCi (566 MBq) of 131I. Levothyroxine (LT4) replacement was started at a dose of 150 µg/day. The patient did well for the next 4–1/2 yr, with appropriate thyroid function tests on a LT4 dose between 150 and 200 µg/day (range of serum TSH of 0.1–1.7 with normal T4 and T3 levels). Subsequently, however, thyroid function tests fluctuated widely (TSH range between 3.5 and 563 mU/L for high or normal levels of T4 and T3), raising the question of inappropriate TSH secretion. The possibility of malabsorption of TH was entertained, as the patient was on oral iron supplementation (11), but the abnormal hormonal profile persisted even after discontinuation of this therapy.

The patient was studied at the Clinical Center at the National Institutes of Health, after having discontinued LT4 therapy for three months, for better assessment of her underlying pathophysiology. The patient did not complain of headaches, visual acuity changes, visual field changes, amenorrhea, galactorrhea, polydipsia, polyuria, or pretibial edema. She also repeatedly denied a history of noncompliance in LT4 therapy in the past. Physical examination revealed nongoitrous hypothyroidism. A left-sided periorbital tissue edema without chemosis or exophthalmos and normal visual fields by Goldmann perimetry were noted. Initial biochemical profile, repeated twice, was indicative of primary hypothyroidism, with extremely high levels of serum TSH: T4: 60.5 nmol/L (normal range: 62–140 nmol/L), T3: 1.4 nmol/L (normal range: 1.1–2.4 nmol/L), free T4: 5.15 pmol/L (normal range: 12.5–24 pmol/L), free T3: 1.89 pmol/L (normal range: 3.5–6.45 pmol/L) and TSH: 563.3 mU/L (normal range: 0.4–4.4 mU/L), while thyroxine binding globulin was 27.2 mg/L (normal range: 12–28 mU/L). Antithyroid peroxidase (anti-TPO) antibodies were present at a significant titer (3'900 U/L; normal range: 0–1'900 U/L).

Dynamic tests of thyroid function included a TRH stimulation test and an acute T3 suppression test (12). Administration of TRH led to strong stimulation of TSH from a baseline value of 573.5 mU/L to a peak response of 2536.5 mU/L at 30 mins post-TRH. Pituitary glycoprotein {alpha}-subunit plasma level was 155 ng/L at 0 mins and 418 ng/L at 30 mins post-TRH, while the {alpha}-subunit/TSH molar ratio was 4.58 at 0 mins and 6.28 at 30 mins post-TRH. Baseline serum prolactin was moderately elevated at 95.4 µg/L (normal range: 1–24 µg/L) and rose to 397.6 µg/L 30 mins post-TRH. The acute T3 suppression test showed a sharp decline in TSH levels from 352.7 mU/L at baseline to 35.1 mU/L, 48 h after T3 administration (suppression of TSH to levels <10% of those at baseline; normal range: 0.4–4.4 mU/L); concomitant serum T3 was 1.8 nmol/L at 0 h and 4.3 nmol/L at 48 h (normal range: 1.1–2.4 nmol/L), while serum free T4 was 8.24 pmol/L at 0 h and 9.88 pmol/L at 48 h (normal range: 12.5–24 pmol/L). Both the above dynamic tests were consistent with profound primary hypothyroidism and not with inappropriate secretion of TSH.

A pituitary MRI revealed symmetrical enlargement of the pituitary gland, measuring 12 mm in height, with a bright gadolinium-enhancing rim of tissue at the superior aspect of the gland, compatible with compressed normal pituitary tissue (Fig. 1Go-A1 and 1-B1). These morphological characteristics suggested a pituitary macroadenoma.



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  		Figure 1. MRI characteristics of the pituitary gland. Panels A, 1–3, show coronal views and panels B, 1–3, mid-sagittal ones. Baseline images on presentation are shown in panels A1/B1 (day 0), before the initiation of TH therapy. Images on days 6 and 31 following initiation of TH are shown in panels A2/B2 and A3/B3 respectively. The arrows in Panel A1 underline the rim of enhancing gland, which could be mistaken for compressed normal pituitary tissue, in the context of a macroadenoma.

 
Because the patient’s hormonal work-up was not compatible with a pituitary tumor, the possibility of pituitary hyperplasia was entertained. The patient was started on LT4 at a dose of 300 µg/day (3.9 µg/kg) immediately after the completion of the acute T3 suppression test. She underwent another MRI scan of the pituitary six days later, revealing a dramatic shrinkage of the pituitary gland to 7 mm in height. The most dramatic diminution in size was in the central portion of the pituitary gland at the site of the insertion of the stalk and mostly anteriorly (Fig. 1Go-A2 and 1-B2). Concomitantly, serum TSH decreased to a level of 13.8 mU/L from an initial level of 563.3 mU/L on admission.

Four weeks later, the patient was reassessed with the following findings: TSH: 4.89 mU/L, T4: 175.1 nmol/L, T3: 2.59 nmol/L, free T4: 20.6 pmol/L, free T3: 4.77 pmol/L, while PRL serum levels were normal (10.1 µg/L). Repeat MRI scan of the pituitary showed a further shrinkage of the pituitary gland now measuring 5.5 mm in height. The pituitary actually presented with a slightly concave superior margin and the insertion of the stalk was visualized quite adequately (Fig. 1Go-A3 and 1-B3). LT4 dose was decreased over the next four months to within the range of physiologic replacement (150 µg/day).


   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Discussion
References
 
The present case demonstrates the acute reversal of pituitary hyperplasia after TH therapy and highlights the limitations of MRI in differentiating pituitary hyperplasia caused by primary hypothyroidism from thyrotroph cell adenoma. Pituitary enlargement in the context of primary hypothyroidism has been recognized since the nineteenth century (13). Up to 81% of patients with primary hypothyroidism have been found to have increased volume of the sella turcica on skull x-ray (3). Pituitary enlargement in primary hypothyroidism is mainly asymptomatic (5); however, symptoms of a pituitary mass may be present (i.e. chiasmatic compression, galactorrhea, headache, etc.). It is believed that this enlargement represents hyperplasia of pituitary thyrotroph and, less consistently, lactotroph cells in response to low circulating levels of TH (4).

With the advent of CT, direct visualization of the pituitary gland provided nonsurgical confirmation of pituitary enlargement in hypothyroidism and regression thereof after replacement with TH (14, 15, 16). The traditional CT criteria for pituitary macroadenoma include homogeneous enlargement of the gland to a height of greater than 10 mm, with or without erosion of the floor of the sella and deviation of the stalk (17). The CT findings of macroadenoma overlap considerably with those of a diffusely enlarged pituitary gland. CT demonstration of a presumed macroadenoma has led to inadvertent transsphenoidal surgery and discovery of pituitary thyrotroph and lactotroph hyperplasia in an otherwise normal gland (5).

MRI alone has also proven unable to reliably differentiate between tumor and hyperplasia. Increased use of MRI in the evaluation of patients with amenorrhea, galactorrhea, and hyperprolactinemia, as well as inappropriate secretion of TSH, may increase the detection of pituitary hyperplasia, thus leading to the need to differentiate between pituitary adenoma and hyperplasia. Different pituitary enhancement patterns between tumor and hyperplasia by MRI have been described in some cases (18), while a midline prominence of a pituitary mass with smooth contours (the "nipple sign") has been proposed as suggestive of pituitary hyperplasia (19). Despite the above theoretical considerations, MRI findings suggestive of a TSH-secreting adenoma, i.e. central enhancing mass with a rim of normal compressed pituitary tissue, may also be seen in hypothyroidism-induced pituitary hyperplasia (10), as well as in the rare entity of hypophysitis (20). Indeed, the most frequent radiologic finding in primary hypothyroidism both by CT and MRI is a pituitary mass with suprasellar extension (21).

Therefore, the diagnosis must rely heavily on the patient’s past history (especially in regards to the level of serum TSH at initial presentation, co-existence of disorders or medications that could affect LT4 absorption, and the level of patient’s compliance) and on detailed endocrine work-up. The laboratory parameters classically used to distinguish cases of non-compliance to TH replacement from TSH-producing pituitary tumors and resistance to TH in patients with iatrogenic hypothyroidism have been: a) serum TSH levels before and after 123I therapy; b) the responses of serum TSH to TRH administration; and c) baseline serum {alpha}-subunit levels and the {alpha}-subunit/TSH molar ratio (22).

Nevertheless, the interpretation of a TRH stimulation test may be particularly problematic in patients with history of hyperthyroidism and subsequent iatrogenic hypothyroidism, especially when the initial TSH level on presentation was not measured. The correct interpretation of this test is also based on the assumption that the hypothalamo-pituitary-thyroid axis is in "steady state". Lapses in compliance of hypothyroid patients to TH therapy disrupt this "steady state" and make the results of a TRH stimulation test virtually uninterpretable (22). Indeed, similar interpretation problems often arise in cases of TSH-producing pituitary tumors or resistance to TH that are mistaken for primary hyperthyroidism and especially following erroneous treatment of these patients with 131I (23). An acute T3 suppression test has recently been proposed (12) and may be of considerable help in cases similar to the ones described above. This test has been shown to produce a highly predictable serum TSH suppression response pattern (suppression of TSH to levels <=10% of those at baseline) in normal individuals and patients with primary hypothyroidism. Acute administration of a high dose of T3 should be considered as safe in young, otherwise healthy adults; however, in the setting of advanced age and/or the presence of atherosclerotic cardiovascular disease, this acute test should be avoided, as the precipitation or exacerbation of angina, arrthythmias, and congestive heart failure may ensue (24). Finally, a therapeutic trial of TH may lead to normalization of pituitary MRI characteristics in patients with primary hypothyroidism, sparing them unnecessary surgery (21).

The kinetics of the regression of pituitary thyrotroph/lactotroph hyperplasia has not been studied in detail, although no cases of this phenomenon have been reported to occur sooner than 4 weeks following the initiation of TH therapy (6, 9, 10, 14, 25). The present case is the first one to document dramatic shrinkage of pituitary hyperplasia in long-standing primary hypothyroidism within six days of acute TH therapy. Thus, the combination of dynamic endocrine testing, including TRH stimulation and acute T3 suppression tests, and repeat pituitary MRI after an acute TH trial, confirmed the diagnosis within a week.

The rapidity of the TH-induced effect observed in our case may be partly caused by the initiation of LT4 therapy after the administration of a large single dose of T3, given as part of an acute T3 suppression test. The cellular mechanism of TH-induced acute regression of thyrotroph hyperplasia may be similar to that of bromocriptine-induced reduction in pituitary volume in macroprolactinomas (26). The molecular mechanism(s) underlying this effect of TH remains speculative.

The clinical evolution of the response of pituitary hyperplasia to TH should be monitored closely, because of the rare possibility of acute neurologic manifestations, such as the development of pseudotumor cerebri and "paradoxical" TH therapy-induced visual failure, or the possibility of an incidental nonthyrotropic pituitary tumor that will not regress on TH therapy (27, 28). In the case of marked regression of pituitary enlargement, without complete normalization in pituitary morphology, the clinical significance of a persistent minimal abnormality detectable by either CT or MRI remains unclear. Pituitary surgery in primary hypothyroidism should be indicated only for decompression of the optic chiasm or to obtain tissue diagnosis in the case of a pituitary mass not responding or worsening on TH therapy (10, 22).

In conclusion, in patients with iatrogenic hypothyroidism and noncompliance to TH therapy, baseline and post-TRH thyroid function tests and pituitary imaging may be unable to reliably differentiate between pituitary tumor and hyperplasia. In similar cases, as well as in other cases of primary hypothyroidism complicated by pituitary hyperplasia, an acute T3 suppression test and a repeat pituitary MRI after an acute trial of high-dose TH therapy (in the absence of advanced age or known cardiovascular disease) may provide a final diagnosis quickly, safely and reliably.

Received July 23, 1996.

Revised October 2, 1996.

Accepted November 12, 1996.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Discussion
 References
 

  1. Bigos ST, Ridgway EC, Kourides IA, Maloof F. 1978 Spectrum of pituitary alterations with mild and severe thyroid impairment. J Clin Endocrinol Metab. 46:317–325.[Abstract/Free Full Text]
  2. Scheithauer BW, Kovacs K, Randall RV, Ryan N. 1985 Pituitary gland in hypothyroidism. Histologic and immunocytologic study. Arch Pathol Lab Med. 109:499–504.[Medline]
  3. Yamada T, Tsukui T, Ikejeri K, Yukimura Y, Kotani M. 1976 Volume of sella turcica in normal subjects and in patients with primary hypothyroidism and hyperthyroidism. J Clin Endocrinol Metab. 42:817–822.[Abstract/Free Full Text]
  4. Koller K, Renee W, Marjorie W, et al. 1987 Thyroid hormones regulate the level of thyrotropin-releasing hormone mRNA in the paraventricular nucleus. Proc Natl Acad Sci USA. 84:7329–7334.[Abstract/Free Full Text]
  5. Katz MS, Gregerman RI, Horvath E, Kovacs E, Kovacs K, Ezrin C. 1980 Thyrotroph cell hyperplasia of the human pituitary gland associated with primary hypothyroidism: clinical and morphological features. Acta Endocrinol (Copenh). 95:41–48.[Abstract/Free Full Text]
  6. Silver BJ, Kyner JL, Dick AR, Chang CHJ. 1981 Primary hypothyroidism: suprasellar pituitary enlargement and regression on computed tomographic scanning. JAMA. 246:364–365.[Abstract/Free Full Text]
  7. Katevuo K, Välimäki M, Ketonen L, Lamberg B-A, Pelkonen R. 1985 Computed tomography of the pituitary fossa in primary hypothyroidism. Effect of thyroxine treatment. Clin Endocrinol (Oxf). 22:617–621.[Medline]
  8. Atchison JA, Lee PA, Albright AL. 1989 Reversible suprasellar pituitary mass secondary to hypothyroidism. JAMA. 262:3175–3177.[Abstract/Free Full Text]
  9. Hutchins WW, Crues JV, IIIrd, Miya P, Pojunas KW. 1990 MR demonstration of pituitary hyperplasia and regression after therapy for hypothyroidism. Am J Neuroradiol. 11:410.[Medline]
  10. Wolanski LJ, Leavitt GD, Elias BJ, Lee HJ, Dasmahapatra A, Byrne W. 1996 MRI of pituitary hyperplasia in hypothyroidism. Neuroradiology. 38:50–52.[CrossRef][Medline]
  11. Kaplan MM. 1981 Interactions between drugs and thyroid hormones. Thyroid Today. 4:1–6.
  12. Saad B, Liu A, Brucker-Davis F, Spencer C, LoPresti J, Nikoloff J. Simplified screening test for resistance to thyroid hormone (RTH): the T3 challenge test (T3CT). Proceedings of the 77th Annual Meeting of the Endocrine Society, Washington DC, 1995, p. 211, P1–396 (Abstract).
  13. Niepce B. 1851 Traité du goitre et du crétinisme. Paris, Baillière Ed.
  14. Jawadi MH, Ballonoff LB, Stears JC, Katz FH. 1978 Primary hypothyroidism and pituitary enlargement. Radiological evidence of pituitary regression. Arch Intern Med. 138:1555–1557.[Abstract/Free Full Text]
  15. Pita Jr J, Shafey S, Pina R. 1979 Diminution of large pituitary tumor after replacement therapy for primary hypothyroidism. Neurology. 29:1169–1172.[Abstract/Free Full Text]
  16. Okuno T, Sudo M, Momoi T, et al. 1980 Pituitary hyperplasia due to hypothyroidism. J Comp Assist Tomogr. 4:600–602.[Medline]
  17. Elster AD. 1993 Modern imaging of the pituitary. Radiology. 187:1–7.[Free Full Text]
  18. Kuroiwa T, Okabe Y, Hasuo K, Yasumori K, Mizushima A, Masuda K. 1991 MR imaging of pituitary hypertrophy due to juvenile primary hypothyroidism: a case report. Clin Imaging. 15:202–205.[CrossRef][Medline]
  19. Ahmed M, Banna M, Sakati N, Woodhouse N. 1989 Pituitary gland enlargement in primary hypothyroidism: a report of 5 cases with follow-up data. Horm Res. 32:188–192.[Medline]
  20. Beressi N, Cohen R, Beressi J-P, Legrand M, Iba-Zizen M-T. Modigliani E. 1994 Pseudotumoral lymphocytic hypophysistis successfully treated by corticosteroid alone: First case report. Neurosurgery. 35:505–508.[Medline]
  21. Chan AW, MacFarlane IA, Foy PM, Miles J B. 1990 Pituitary enlargement and hyperprolactinemia due to primary hypothyroidism: errors and delays in diagnosis. Br J Neurosurg. 4:107–112.[Medline]
  22. Beck-Peccoz P, Brucker-Davis F, Persani L, Smallridge RC, Weintraub BD. 1996 Thyrotropin-secreting pituitary tumors. Endocr Rev. In press.
  23. Gesundheit N, Petrick PA, Nissim M, et al. 1989 Thyrotropin-secreting pituitary adenomas: clinical and biochemical heterogeneity. Ann Intern Med. 111:827–835.
  24. Klein I. 1990 Thyroid hormone and the cardiovascular system. Am J Med. 88:631–638.[CrossRef][Medline]
  25. Valenta LJ, Tamkin JRS, Elias AN, Eisenberg H. 1983 Regression of a pituitary adenoma following levothyroxine therapy of primary hypothyroidism. Fertil Steril. 40:389–392.[Medline]
  26. Tindall GT, Kovacs K, Horvath E, Thorner MO. 1982 Human prolactin-producing adenomas and bromocriptine: a histological, immunocytochemical, ultrastructural, and morphometric study. J Clin Endocrinol Metab. 55:1178–1183.[Abstract/Free Full Text]
  27. Yamamoto K, Saito K, Takai T, Naito M, Yoshida S. 1983 Visual field defects and pituitary enlargement in primary hypothyroidism. J Clin Endocrinol Metab. 57:283–287.[Abstract/Free Full Text]
  28. McVie R. 1984 Abnormal TSH regulation, pseudotumor cerebri, and empty sella after replacement therapy in juvenile hypothyroidism. J Pediatr. 105:768–770.[CrossRef][Medline]



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