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(Radiology. 1999;213:383-388.)
© RSNA, 1999

Neuroradiology

Rapid Progression of Pituitary Hyperplasia in Humans with Primary Hypothyroidism: Demonstration with MR Imaging1

Taro Shimono, MD, Hiroto Hatabu, MD, Kanji Kasagi, MD, Yukio Miki, MD, Sadahiko Nishizawa, MD, Takashi Misaki, MD, Akira Hiraga, RT and Junji Konishi, MD

1 From the Department of Nuclear Medicine and Radiology, Faculty of Medicine, Kyoto University, 54 Shogoinkawahara-cho Sakyo-ku Kyoto, 606-8507, Japan (T.S., H.H., K.K., Y.M., S.N., T.M., A.H., J.K.), and the Department of Radiology, Beth Israel Deaconess Medical Center, Boston, Mass (H.H.). Received November 20, 1998; revision requested January 18, 1999; revision received February 22; accepted April 15. Address reprint requests to T.S. (e-mail: shimono@kuhp .kyto-u.ac.jp).


   Abstract
TOP
 Abstract
Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
PURPOSE: To use magnetic resonance (MR) imaging to evaluate the morphologic changes of the pituitary gland during the development of hypothyroidism.

MATERIALS AND METHODS: Fourteen patients who had undergone thyroidectomy were evaluated before radioactive iodine 131 therapy. In each patient, MR imaging and measurement of serum hormone levels were performed twice: 5 weeks before 131I treatment as the "euthyroid state" with thyroid hormone supplementation and on the day of 131I treatment as the "hypothyroid state" after a 3-week depletion of thyroid hormone supplements. Nine healthy volunteers also underwent MR imaging twice at an interval of 5 weeks. Pituitary volume and the relative signal intensity ratio of the anterior pituitary to the pons were measured. The shape and signal intensity of the pituitary gland were also visually assessed. The paired Student t test was used to evaluate the significance of the data. A P value less than .05 indicated a statistically significant difference.

RESULTS: The patients had significantly larger pituitary volume in the hypothyroid state than in the euthyroid state both quantitatively (P < .001) and visually. No significant differences were found in the relative signal intensity ratios of the anterior pituitary to the pons. In healthy volunteers, no significant differences in pituitary volumes or signal intensity were found between the two MR images.

CONCLUSION: Rapid progression of hyperplasia of the anterior pituitary may occur with acute development of hypothyroidism.

Index terms: Pituitary, abnormalities, 145.144, 145.458, 145.521 • Thyroid, hypothyroidism, 273.458, 273.521 • Pituitary, MR, 145.12141


   Introduction
TOP
 Abstract
 Introduction
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Pituitary and sella turcica enlargement in patients with long-standing primary hypothyroidism has been established (1,2). The volume of the sella turcica has been reported to correlate with circulating thyrotropin levels (3). Computed tomographic (CT) and magnetic resonance (MR) imaging characteristics of pituitary hyperplasia in patients with primary hypothyroidism and subsequent regression after thyroid hormone therapy have been previously described (4–9).

However, the time course of the progression and regression and the clinical importance of hyperplasia of the thyrotroph have not been established. To our knowledge, there has been only one case of documented dramatic shrinkage of pituitary hyperplasia in a patient with long-standing primary hypothyroidism within 1 week of short-term thyroid hormone therapy (9). In this article, we present study findings that demonstrate the time course of the progression of pituitary hyperplasia in human beings with primary hypothyroidism.

We hypothesized that MR imaging can demonstrate in vivo the temporal change of pituitary hyperplasia in patients who develop hypothyroidism in a short time. One such group was composed of patients who underwent thyroidectomy and were prepared for radioactive iodine 131 treatment, which has been widely used to treat metastases of differentiated thyroid carcinoma. In these patients, the hypothyroid state was purposely induced as follows. These patients developed a euthyroid state with thyroid hormone replacement therapy after total thyroidectomy. To prepare for 131I therapy, however, the administration of thyroid hormones was discontinued for 2–3 weeks to stimulate the accumulation of 131I in metastatic tumor cells by increasing the serum thyrotropin concentrations (10). During this interval, primary hypothyroidism was induced iatrogenically.

The goal of our study was to evaluate prospectively the changes in shape, volume, and signal intensity of the pituitary gland at MR imaging 5 weeks following withdrawal of exogenous thyroid hormones in patients who had undergone thyroidectomy and were preparing for 131I therapy.


   MATERIALS AND METHODS
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Subjects
Fourteen patients (eight women, six men; age range, 32–83 years; mean age, 61.8 years) who underwent 131I therapy for distant metastases of histopathologically proved differentiated thyroid carcinoma (nine had papillary carcinoma, and five had follicular carcinoma) were entered into a prospective study. An additional five patients had to be excluded during the research period: Two had an empty sella defined as a height of the pituitary gland less than 2 mm, two could not undergo MR imaging on the scheduled day, and one could not achieve the euthyroid state in spite of thyroid hormone replacement therapy. All 14 patients included in the study had previously undergone total thyroidectomy. None were pregnant or had pituitary gland disease. Seven of the eight women were postmenopausal. All patients provided informed consent for participation in the study, which was approved by our institutional review board. MR imaging and serum hormone level measurements were performed in all patients.

Replacement doses of levothyroxine sodium (Thyradin-S tablets; Teikoku Hormone, Tokyo, Japan) given to patients after surgery were replaced with liothyronine sodium (Thyronamin; Takeda Pharmaceuticals, Osaka, Japan) 5 weeks before 131I (sodium iodine 131 capsules; Daiichi Radioisotope Laboratories, Tokyo, Japan) treatment, and liothyronine sodium administration was stopped 3 weeks before 131I treatment. Ingestion of foods containing iodine was prohibited, and iodine-containing medications were withheld for 1 month before and 1 week after 131I treatment. All patients were hospitalized for 7–14 days in a single room for 131I therapy. A single therapeutic dose of 131I (2.5–5.5 GBq) was administered orally to each of the 14 patients. One week after 131I therapy, replacement doses of levothyroxine sodium were restarted.

In each patient, MR imaging examinations and serum hormone measurements were performed twice: 5 weeks before 131I treatment at the euthyroid state during the administration of levothyroxine sodium and several hours before the 131I treatment at the hypothyroid state, that is, when thyroid hormones were not being administered. In the interval between repeated MR imaging and serum hormone level measurements, replacement therapy with thyroid hormones was discontinued for only 3 weeks. The liothyronine sodium dose of 50 µg/d was sufficient to prevent an increase in serum thyrotropin concentrations.

Nine healthy volunteers (six men, three women; age range, 25–51 years; mean age, 39.8 years) without thyroid or pituitary disorders also underwent MR imaging twice with an interval of 5 weeks (without serum hormone tests) and constituted the control group. All the volunteers gave informed consent in accordance with approval by the institutional review board.

Serum Hormone Level Measurements
Serum hormone level measurements were performed to confirm that patients were maintained in the euthyroid state for the first MR study and to confirm the developing hypothyroidism on the day of the second MR study.

Blood was drawn for measurements of serum free levothyroxine sodium, free liothyronine sodium, thyrotropin, and prolactin levels. Serum free levothyroxine sodium and free liothyronine sodium levels were measured with radioassay by using commercially available kits for free levothyroxine sodium levels (normal range, 0.98–1.77 ng/dL [13–23 pmol/L]; Amerlex MABFT4; Ortho-Diagnostics, Amersham, UK) and for free liothyronine sodium levels (normal range, 2.8–4.6 pg/mL [4.3–7.1 pmol/L]; Amerlex MABFT3; Ortho-Diagnostics). Serum thyrotropin was determined with immunoradiometric assay by using a monoclonal antibody against the ß subunit (normal range, 0.3–3.9 mIU/L; Riagnost tTSH kit; CIS Bio International, Paris, France). The serum prolactin level was determined by immunoradiometric assay (normal range, 1.5–9.7 µg/L for male, 1.4–14.6 µg/L for female subjects; Daiichi Radioisotope Laboratories).

MR Images
MR examination of the pituitary gland was performed in all patients and volunteers with a 1.5-T system (Horizon; GE Medical Systems, Milwaukee, Wis).

T1-weighted images obtained without contrast material enhancement in the sagittal and coronal planes and T2- and intermediate-weighted images in the sagittal plane were acquired by using a multisection two-dimensional Fourier transform conventional spin-echo technique.

On sagittal and coronal T1-weighted images, imaging parameters included a repetition time of 400 msec and an echo time of 14 msec (400/14), two signals acquired, a 20-cm field of view, an image acquisition matrix of 256 x 256, and a 3-mm section thickness with a 1-mm intersection gap.

On sagittal T2- and intermediate-weighted images, imaging parameters included 3,000/30, 90, one signal acquired, a 20-cm field of view, an image acquisition matrix of 256 x 192, and a 3-mm section thickness with a 1-mm intersection gap.

Pituitary Gland Evaluation and Measurements
Images were transferred to an Advantage Windows workstation (GE Yokogawa Medical Systems, Tokyo, Japan). An electronic cursor was used to measure the vertical (height), transverse (width), and anteroposterior (length) dimensions of the pituitary gland. The midsagittal T1-weighted image was used to measure the height and length, and the coronal T1-weighted image through the pituitary stalk was used to measure the width. The midsagittal cross-sectional area of the gland was also measured by tracing the outline of the gland with the cursor, and the mean signal intensities on the T1-weighted image of the anterior pituitary gland and of the pons were measured by using the region of interest program on the image display. The measurements were performed by an independent observer (A.H.) who had no knowledge of the subjects' clinical information.

Pituitary volume (in cubic millimeters) was estimated by using two formulas: (a) volume 1 = 1/2 x length x width x height, as reported by Di Chiro and Nelson (11) and Gonzalez et al (12), and (b) volume 2 = cross-sectional area x width, as reported by Lurie et al (13).

Signal intensity of the anterior pituitary gland was evaluated by using the relative signal intensity ratio of the anterior pituitary to the pons on the T1-weighted image (14).

In addition to the quantitative measurements, the shape and the signal intensity of the pituitary gland on T1-, T2-, and intermediate-weighted images were evaluated visually by two experienced radiologists (Y.M. and S.N.), who had no knowledge of the clinical information of the subjects. Each made his or her initial evaluations independently, and any disagreements over the final conclusions were resolved by consensus between the two radiologists. The pituitary shape was assessed by using the midsagittal projection on the T1-weighted images and was classified into three groups on the basis of the superior contour of the gland: concave, flat, or convex. The measurements and evaluation were performed in the same way for both patients and volunteers.

Statistical Analysis
All data, including serum hormone measurements, pituitary volumes, and relative signal intensities, were reported as means ± SDs. The paired Student t test was used to evaluate the difference in pituitary volumes and relative signal intensity ratios in each subject between the euthyroid state and the hypothyroid state. The paired Student t test was also used to evaluate the difference in pituitary volumes and relative signal intensity ratios in each healthy volunteer between the two MR images obtained with an interval of 5 weeks. In each analysis, a P value of .05 was considered to indicate a significant difference.


   RESULTS
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
The Table shows all data from serum hormone measurements, pituitary volumes, and relative signal intensity ratios in the patients.


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  		Serum Hormone Level and MR Imaging Measurements in 14 Patients
 
In all 14 patients, serum free liothyronine sodium and thyrotropin levels were within normal limits, which indicated the achievement of the euthyroid state before liothyronine sodium supplementation, whereas the serum free liothyronine sodium level was lower than 2.8 pg/mL (4.3 pmol/L) and the serum thyrotropin level was higher than 3.9 mIU/L, which indicated a hypothyroid state after stopping liothyronine sodium supplementation (Table). The thyrotropin level increased remarkably (P < .001), and the prolactin level also increased significantly (P = .004 for male patients and P = .048 for female patients) after discontinuing thyroid hormone supplementation.

The volume of the pituitary gland was shown to have increased significantly at 5 weeks following withdrawal of exogenous thyroid hormones: 331 mm3 ± 68 versus 453 mm3 ± 109 in volume 1 (P < .001) and 453 mm3 ± 107 versus 626 mm3 ± 173 in volume 2 (P < .001) (Table). Figure 1 shows the comparison of pituitary gland volumes between euthyroid and hypothyroid states.



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  		Figure 1a. Pituitary gland volumes in 14 patients. Graphs show (a) volume 1 and (b) volume 2 for the euthyroid and hypothyroid states. The hypothyroid state was associated with significantly larger pituitary gland volumes (volume 1 = 453 mm3 ± 109, volume 2 = 626 mm3 ± 173) than was the euthyroid state (volume 1 = 331 mm3 ± 68, volume 2 = 453 mm3 ± 107). Two (patients 2 and 7) of the 14 patients had the same volume 1 (385 mm3 for the euthyroid state and 539 mm3 for the hypothyroid state). In a and b, • indicates the calculated pituitary gland volume, {lozenge} indicates the mean, and the vertical bar indicates the SD.

 


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  		Figure 1b. Pituitary gland volumes in 14 patients. Graphs show (a) volume 1 and (b) volume 2 for the euthyroid and hypothyroid states. The hypothyroid state was associated with significantly larger pituitary gland volumes (volume 1 = 453 mm3 ± 109, volume 2 = 626 mm3 ± 173) than was the euthyroid state (volume 1 = 331 mm3 ± 68, volume 2 = 453 mm3 ± 107). Two (patients 2 and 7) of the 14 patients had the same volume 1 (385 mm3 for the euthyroid state and 539 mm3 for the hypothyroid state). In a and b, • indicates the calculated pituitary gland volume, {lozenge} indicates the mean, and the vertical bar indicates the SD.

 
There were no significant differences in the relative signal intensity ratios of the anterior lobe to the pons on T1-weighted images before versus after the depletion of supplemental thyroid hormones (0.95 ± 0.07 vs 0.99 ± 0.10; P = .17) (Table).

Healthy volunteers in the control group, on the other hand, showed no significant differences in pituitary volume and relative signal intensity ratios between the two MR images obtained with an interval of 5 weeks: 460 mm3 ± 240 vs 454 mm3 ± 219 (P = .77) in volume 1, 671 mm3 ± 305 vs 676 mm3 ± 283 (P = .84) in volume 2, and relative signal intensity ratios of 0.98 ± 0.10 versus 0.96 ± 0.05 (P = .55).

At visual evaluation of the gland shape, trends of enlargement were noted. In the euthyroid group, seven of the 14 patients (50%) had a concave gland, six of 14 (43%) had a flat gland, and one of 14 (7%) had a convex superior surface of the gland. In the hypothyroid group, one of 14 (7%) had a concave gland, six of 14 (43%) had a flat gland, and seven of 14 (50%) had a convex gland. Visual examination of the signal intensities of the glands revealed no differences on T1-, T2-, and intermediate-weighted images.

Figures 2 and 3 show examples of MR images obtained before and after the depletion of supplemental thyroid hormones.



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  		Figure 2a. Patient 7. Midsagittal T1-weighted images (400/14) of the pituitary gland in the (a) euthyroid and (b) hypothyroid states. The anterior gland (arrow in a and b) is remarkably enlarged in b compared with a.

 


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  		Figure 2b. Patient 7. Midsagittal T1-weighted images (400/14) of the pituitary gland in the (a) euthyroid and (b) hypothyroid states. The anterior gland (arrow in a and b) is remarkably enlarged in b compared with a.

 


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  		Figure 3a. Patient 12. Midsagittal T1-weighted images (400/14) of the pituitary gland in the (a) euthyroid and (b) hypothyroid states. The anterior gland (arrow in a and b) is remarkably enlarged in b compared with a.

 


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  		Figure 3b. Patient 12. Midsagittal T1-weighted images (400/14) of the pituitary gland in the (a) euthyroid and (b) hypothyroid states. The anterior gland (arrow in a and b) is remarkably enlarged in b compared with a.

 

   DISCUSSION
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
Circulating thyroid hormones normally act by means of negative feedback on the hypothalamic secretion of thyrotropin-releasing hormone. If the thyroid gland secretes an insufficient quantity of thyroid hormones, the serum level of thyrotropin-releasing hormone will increase. This eventually will result in hyperplasia of thyrotropin-producing cells (thyrotrophs) and in subsequent enlargement of the pituitary gland (15) (Fig 4). Thyrotrophs are commonly located in the anteromedial portion of the anterior lobe and make up about 15% of the adenohypophysial cells (16). Because thyrotropin-releasing hormone has a weak stimulatory effect on prolactin-producing cells (lactotrophs), prolactinemia may also occur (9,17). In our study, the serum prolactin level in each patient increased significantly. Histologic examination of the pituitary gland in some patients with primary hypothyroidism has shown hyperplasia of both thyrotrophs and lactotrophs in an otherwise normal gland (2,8,17).



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  		Figure 4. Diagram demonstrates that an insufficient quantity of thyroid hormones results in lack of inhibition of thyrotropin-releasing hormone (TRH) and thyrotropin (TSH). Increased thyrotropin-releasing hormone levels result mainly in increased thyrotropin release and weakly in prolactin (PRL) release. Then, increased thyrotropin levels result in increased release of thyroid hormones. - indicates negative feedback, and + indicates positive feedback.

 
With the advent of CT and MR imaging, direct visualization of the pituitary gland provided noninvasive volumetric confirmation of pituitary enlargement in patients with hypothyroidism and subsequent regression after replacement therapy with thyroid hormones (4–9).

Although pituitary hyperplasia with primary hypothyroidism is well established, the kinetics of the progression and regression of pituitary thyrotropic or lactotropic hyperplasia have not been studied in detail in humans. To our knowledge, only one case of long-standing primary hypothyroidism has had documented dramatic shrinkage of pituitary hyperplasia within 6 days of short-term thyroid hormone therapy (9). To our knowledge, there were no reports on the time course in the progression of pituitary hyperplasia in humans with primary hypothyroidism, and pituitary enlargement has been reported to be associated with only long-standing primary hypothyroidism.

Our study findings demonstrated that the pituitary gland volumes increased significantly within only 3 weeks of developing hypothyroidism. The enlarging trends at visual evaluation of gland shape likewise reflect this result, and our study findings also show that physiologic changes of the pituitary gland in healthy volunteers do not occur in as short a period as 5 weeks. In our study, the patients (mean age, 61.8 years) at the euthyroid state had significantly smaller pituitary volumes than did healthy volunteers (mean age, 39.8 years). We believe that this difference in size is due to a difference in age. Lurie et al (13) reported that the pituitary volume of subjects older than 50 years was significantly smaller than that in subjects younger than 50 years, and the mean pituitary volume in the group older than 50 years in their study was similar to that in the patients in the euthyroid state in our study.

Supporting our data in humans are results of animal experiments performed by DeFesi et al (18) to assess the kinetics of changes in thyrotrophs in the anterior pituitary in rats after thyroidectomy and during liothyronine sodium treatment. The mean maximal increase in pituitary wet weight was 70%, which was reached 15 days after thyroidectomy during the development of hypothyroidism, and the pituitary weight remained relatively constant thereafter. Both pituitary DNA content and total pituitary cell number increased 30%–40% above euthyroid values after 15 days.

The anterior pituitary gland may be hyperintense on T1-weighted images due to the hyperfunction associated with pregnant or postpartum women and infants (14,19–21). Wolpert et al (19) and Cox and Elster (20) suggest that the mechanism of T1 shortening in the anterior pituitary gland in the newborn may be related to an increase in the amount of endoplasmic reticulum and high protein-synthesis activity. Tien et al (21) suggest that the mechanism may be related to an increase in the bound fraction of water molecules due to hormone secretion. Miki et al (14) believe that the mechanism of T1 shortening in pregnancy is the same as that in infancy and also suggest that the increase in the number of secretory granules may be one of the possible mechanisms responsible for the T1 shortening.

In our study, the relative signal intensity ratio of the anterior pituitary showed no significant difference between the euthyroid state and the hypothyroid state. It is uncertain why there is no significant T1 shortening of the anterior pituitary in the hypothyroid state in spite of hyperfunction of thyrotrophs and lactotrophs in our study. There are three possible explanations: (a) the amount of endoplasmic reticulum, protein-synthesis activity, or bound fraction of water molecules may be less than that in a pregnant woman or newborn; (b) the number of secretary granules may be less than that in a pregnant woman or newborn; and (c) the T1 shortening effect due to thyrotropin may be less than that due to prolactin.

In conclusion, the rapid progression of hyperplasia of the pituitary gland following hypothyroidism in humans is demonstrated by using an MR volumetric technique, while to our knowledge pituitary hyperplasia in patients with hypothyroidism has been reported in only those with chronic conditions. The finding of rapid progression of pituitary hyperplasia following hypothyroidism may provide new information about the mechanism and flexibility of thyroid hormone homeostasis.


   Acknowledgments
 
We thank Donna H. Wolfe, who assisted with the editing of the manuscript.


   Footnotes
 
Author contributions: Guarantor of integrity of entire study, T.S.; study concepts and design, T.S., H.H.; definition of intellectual content, T.S.; literature research, Y.M.; clinical studies, T.S., T.M., K.K.; data acquisition, A.H.; data analysis, Y.M., S.N.; statistical analysis, H.H., S.N.; manuscript preparation, T.S.; manuscript editing, T.S., H.H.; manuscript review, H.H., K.K., Y.M., J.K.


   References
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

  1. Bigos ST, Ridgway EC, Kourides IA, Maloof F. Spectrum of pituitary alterations with mild and severe thyroid impairment. J Clin Endocrinol Metab 1978; 46:317-325.[Medline]
  2. Scheithauer BW, Kovacs K, Randall RV, Ryan N. Pituitary gland in hypothyroidism: histologic and immunocytologic study. Arch Pathol Lab Med 1985; 109:499-504.[Medline]
  3. Yamada T, Tsukui T, Ikejiri K, Yukimura Y, Kotani M. Volume of sella turcica in normal subjects and in patients with primary hypothyroidism and hyperthyroidism. J Clin Endocrinol Metab 1976; 42:817-822.[Abstract]
  4. Okuno T, Sudo M, Momoi T, et al. Pituitary hyperplasia due to hypothyroidism. J Comput Assist Tomogr 1980; 4:600-602.[Medline]
  5. Pita JC, Jr, Shafey S, Pina R. Diminution of large pituitary tumor after replacement therapy for primary hypothyroidism. Neurology 1979; 29:1169-1172.[Abstract/Free Full Text]
  6. Hutchins WW, Crues JV, III, Miya P, Pojunas KW. MR demonstration of pituitary hyperplasia and regression after therapy for hypothyroidism. AJNR 1990; 11:410.[Medline]
  7. Wolansky LJ, Leavitt GD, Elias BJ, Lee HJ, Dasmahapatra A, Byrne W. MRI of pituitary hyperplasia in hypothyroidism. Neuroradiology 1996; 38:50-52.[Medline]
  8. Koyama T, Shinoda S, Tani S, Kamikubo T, Nakamura N, Okuda M. A case of pseudo-TSH.PRL-producing pituitary adenoma with secondary hypothyroidism. No To Shinkei 1991; 43:187-191[Japanese].[Medline]
  9. Sarlis NJ, Brucker-Davis F, Doppman JL, Skarulis MC. MRI-demonstrable regression of a pituitary mass in a case of primary hypothyroidism after a week of acute thyroid hormone therapy. J Clin Endocrinol Metab 1997; 82:808-811.[Abstract/Free Full Text]
  10. Harbert JC. Radioiodine therapy of differentiated thyroid carcinoma. In: Harbert JC, eds. Nuclear medicine therapy. New York, NY: Thieme, 1987; 37-90.
  11. Di Chiro G, Nelson KB. The volume of the sella turcica. AJR 1962; 87:989-1008.
  12. Gonzalez JG, Elizondo G, Saldivar D, Nanez H, Todd LE, Villarreal JZ. Pituitary gland growth during normal pregnancy: an in vivo study using magnetic resonance imaging. Am J Med 1988; 85:217-220.[Medline]
  13. Lurie SN, Doraiswamy PM, Husain MM, et al. In vivo assessment of pituitary gland volume with magnetic resonance imaging: the effect of age. J Clin Endocrinol Metab 1990; 71:505-508.[Abstract]
  14. Miki Y, Asato R, Okumura R, et al. Anterior pituitary gland in pregnancy: hyperintensity at MR. Radiology 1993; 187:229-231.[Abstract/Free Full Text]
  15. Koller KJ, Wolff RS, Warden MK, Zoeller RT. Thyroid hormones regulate levels of thyrotropin-releasing-hormone mRNA in the paraventricular nucleus. Proc Natl Acad Sci USA 1987; 84:7329-7334.[Abstract/Free Full Text]
  16. Phifer RF, Spicer SS. Immunohistochemical and histologic demonstration of thyrotropic cells of the human adenohypophysis. J Clin Endocrinol Metab 1973; 36:1210-1221.[Medline]
  17. Pioro EP, Scheithauer BW, Laws ER, Jr, Randall RV, Kovacs KT, Horvath E. Combined thyrotroph and lactotroph cell hyperplasia simulating prolactin-secreting pituitary adenoma in long-standing primary hypothyroidism. Surg Neurol 1988; 29:218-226.[Medline]
  18. DeFesi CR, Astier HS, Surks MI. Kinetics of thyrotrophs and somatotrophs during development of hypothyroidism and L-triiodothyronine treatment of hypothyroid rats. Endocrinology 1979; 104:1172-1180.[Medline]
  19. Wolpert SM, Osborne M, Anderson M, Runge VM. The bright pituitary gland: a normal MR appearance in infancy. AJNR 1988; 9:1-3.[Abstract]
  20. Cox TD, Elster AD. Normal pituitary gland: changes in shape, size, and signal intensity during the 1st year of life at MR imaging. Radiology 1991; 179:721-724.[Abstract/Free Full Text]
  21. Tien RD, Kucharczyk J, Bessette J, Middleton M. MR imaging of the pituitary gland in infants and children: changes in size, shape, and MR signal with growth and development. AJR 1992; 158:1151-1154.[Abstract/Free Full Text]



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