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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 23  |  Issue : 1  |  Page : 20-22

Time bound regression of pituitary hyperplasia in primary pituitary hypothyroidism following treatment


1 Department of Radiology, Vikram Hospital, Bengaluru, Karnataka, India
2 Department of Endocrinology, BGS Global Hospital, Bengaluru, Karnataka, India

Date of Web Publication6-Jan-2016

Correspondence Address:
Ravindra Bhimrao Kamble
Department of Radiology, Vikram Hospital, Bengaluru - 560 052, Karnataka
India
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DOI: 10.4103/1115-3474.162145

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  Abstract 

Aim: The aim was to prospectively study radiological regression of pituitary hyperplasia following the treatment for primary hypothyroidism by serial magnetic resonance imaging (MRI). Subjects and Methods: Seven patients (1 male and 6 females) with profound hypothyroidism were included, age ranging from 13 to 42 years. MRI for pituitary was done at first visit and on follow-up. Pituitary size on imaging was matched with baseline T3, T4, thyroid-stimulating hormone (TSH), and thyroid peroxidase antibody antibodies and TSH on follow-up. Results: By 6 weeks all patients showed clinical improvement with near normalization of thyroid function tests in most patients. The TSH normalization was well correlated with regression of the pituitary enlargement on imaging at 6 weeks. The height of pituitary gland at baseline was 13.24 ± 3.61 mm, at first follow-up 9.68 ± 1.32 mm, and at second follow-up 7.80 ± 3.95 mm. The diameter of the pituitary gland at baseline was 14.47 ± 4.14 mm, at first follow-up 11.83 ± 3.99 mm, and at second follow-up 7.25 ± 4.59 mm. The height of the pituitary gland significantly reduced in first and second follow-up (P < 0.05) and reduction in diameter on second follow-up (P < 0.05). Conclusion: Pituitary hyperplasia secondary to primary hypothyroidism regresses with treatment within 6 weeks of initiation of treatment in its height however, it takes months for reduction in the diameter of the gland. We recommend repeat imaging in enlarged and homogenously enhancing pituitary gland in patients of primary hypothyroidism at 6 weeks of initiation of treatment to prove or disprove hyperplasia.

Keywords: Hypothyroidism; magnetic resonance imaging; pituitary hyperplasia


How to cite this article:
Kamble RB, Babu S, Nagaraj D, Mudakavi SJ. Time bound regression of pituitary hyperplasia in primary pituitary hypothyroidism following treatment. West Afr J Radiol 2016;23:20-2

How to cite this URL:
Kamble RB, Babu S, Nagaraj D, Mudakavi SJ. Time bound regression of pituitary hyperplasia in primary pituitary hypothyroidism following treatment. West Afr J Radiol [serial online] 2016 [cited 2019 Sep 22];23:20-2. Available from: http://www.wajradiology.org/text.asp?2016/23/1/20/162145


  Introduction Top


The occurrence of pituitary hyperplasia in primary or secondary hypothyroidism is well-documented.[1],[2],[3],[4] However, this enlargement of the pituitary gland in hypothyroidism can also mimic pituitary adenoma.[5] Thus, it is important to understand this entity for proper diagnosis.

Current imaging tools like magnetic resonance imaging (MRI) can detect time bound radiological response during treatment of primary hypothyroidism.

Establishing gland size regression will differentiate hyperplasia from adenoma, as well as help guide treatment follow-up.


  Subjects and Methods Top


Seven consecutive patients (1 male and 6 females), age ranging from 13 to 42 years (mean 21) were included in the study presenting to our hospital over 18 months with profound hypothyroidism for 1st time with thyroid-stimulating hormone (TSH) >75. Exclusion criteria were known cases of hypothyroidism already on treatment and previous history of hypothyroidism but now not on treatment. All patients underwent routine blood investigations along with T3, T4, TSH, and thyroid peroxidase antibody (TPO) at baseline and at follow-up, TSH was done. MRI was done in 1.5 T (Wipro GE, Milwaukee, WI, USA) machine at first visit and at follow-up shown in [Table 1]. Contrast MRI was done at baseline with subsequent plain MRI on follow-up. Ethical approval was not obtained for the study as every patient had to undergo follow-up imaging at regular intervals for confirmation; this study was formulated and combined with it. Following magnetic resonance parameters were used for calculating the height and width of the pituitary gland (T1-weighted FSE coronal and sagittal TR740 TE18, ETL-4, bandwidth 20.83, FOV 18 × 16.2, slice thickness 3 mm with 0.3 mm interslice gap, NEX 4, frequency 384, phase 224, matrix 320 × 224) (T2-weighted coronal and sagittal TR 2940 TE112, ETL-22, bandwidth 20.83, FOV 18 × 16.2, slice thickness 3 mm with 0.3 mm interslice gap, NE × 4, frequency 384, phase 256, matrix 320 × 224). Meglumine gadopentetate - Magnevist (Bayer Zydus Pharma) contrast was used with 0.1 mmol/kg dose. Height was calculated in sagittal (T1-weighted) and coronal (T2-weighted) sequence, width in coronal sequence and anteroposterior diameter in sagittal sequence. Pituitary height and width were matched with baseline T3, T4, TSH and TPO antibodies, and TSH on follow-up.
Table 1: Details of follow-up MRI

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Statistics

Paired Student's t-test was done for comparing the height and width of the gland at baseline and on follow-up and P < 0.05 was taken as significant.


  Results Top


By 6 weeks, all patients showed clinical improvement with near normalization of thyroid function tests (TFTs) in most patients. The TSH normalization was well correlated with regression of the pituitary enlargement on imaging at <6 weeks as shown in [Figure 1]. The height of pituitary gland at baseline and at follow-up is given in [Table 2]. [Table 3] shows baseline TFT. The height of the pituitary gland significantly reduced in first and second follow-up (P < 0.05) and reduction in diameter on second follow-up shown in [Table 2]. On follow-up, TSH returned to normal (not shown).
Figure 1: (a) Coronal T2-weighted and (b) sagittal T1-weighted images both pretreatment (left side images) and posttreatment (right side images) showing regression of the pituitary gland

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Table 2: Pituitary gland measurements at baseline and follow up

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Table 3: Baseline thyroid functions tests

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  Discussion Top


Reactive enlargement of the pituitary gland due to hypothyroidism is a well-established entity and its regression following the treatment of thyroxine is also well-documented.[1],[3],[4] It is important to differentiate this entity from pituitary adenoma as both appear similar, but management differs.[5],[6] This enlargement of the gland is due to decreased negative feedback causing increased release of thyrotrophin releasing and stimulating hormone leading to hyperplasia of thyrotroph cells in the pituitary gland, which regresses after replacement therapy.[3] There is also the correlation of volume of pituitary fossa and TSH.[7]

In our current study, we intended to find time bound decrease in size of the pituitary gland after initiation of the treatment. We followed up the patients who had high TSH values at presentation with primary hypothyroidism and did baseline MRI and TFTs. All the patients had features suggestive of pituitary hyperplasia at presentation. Patients were followed up with MRI after initiation of treatment. Of all the 7 patients, 4 patients were imaged <6 weeks (2 patients at 1-week, 1 patient at 2 week, 2 patients at 4 weeks, and 1 patient at 6 weeks including follow-up) and 3 patients had imaging done after 6 weeks (16, 22, and 44 weeks) of initiation of treatment as shown in [Table 1]. The height of the pituitary gland was seen reduced in all the patients. The regression of the pituitary height was seen as early as 1-week and all the patients who were imaged before 6 weeks.

Sarlis et al. have shown regression of the pituitary hyperplasia at 1-week following treatment and other case report demonstrate regression at 12 weeks.[8],[9] Thus, there is evidence of regression of pituitary hyperplasia as early as 1-week (including our 2 cases) but there are no studies, which demonstrate the exact time frame of regression. In our study, we have seen that the regression starts within 1-week of initiation of treatment and the gland normalizes by 6 weeks.

In the study done by Shimono et al., the volume of pituitary gland shows a significant increase by 5 weeks after the patient becomes hypothyroid. This probably suggests that hyperplasia of thyrotroph cells in pituitary gland starts immediately after hypothyroid state and reaches its maximum by 5 weeks.[3]

Thus interestingly, pituitary gland increases in size by 5 weeks (after development of hypothyroid state) and decreases in size within 6 weeks after initiation of treatment in patients of primary hypothyroidism as shown in our study supported by previous case reports.[8],[9]

Our study has important clinical implication. It shows that any patient with primary hypothyroidism can have enlarged pituitary gland, which suggests hyperplasia and this enlarged gland will decrease in size following treatment. However, if it does not decrease in size, then the possibility of adenoma should be considered requiring surgical treatment. Thus, in conclusion repeat imaging for enlarged pituitary gland should be done at 6 weeks after initiation of treatment in patients of primary hypothyroidism to prove or disprove hyperplasia and rule out adenoma.

The irregular follow-up is the only limiting factor for our study.


  Acknowledgment Top


Department of Pathology and Staff of Radiology in BGS Global Hospital, Bengaluru.

 
  References Top

1.
Babu S, Venkataramana NK, Kamble RB, Rao SA, Naik A, Shetty RV. Primary hypothyroidism presenting as a sellar mass which regressed with thyroid hormone therapy. A case report. Neuroradiol J 2010;23:433-6.  Back to cited text no. 1
    
2.
Xu AJ, Li T. Pituitary hyperplasia secondary to primary hypothyroidism in children: Report of 8 cases. Zhongguo Dang Dai Er Ke Za Zhi 2010;12:17-20.  Back to cited text no. 2
    
3.
Shimono T, Hatabu H, Kasagi K, Miki Y, Nishizawa S, Misaki T, et al. Rapid progression of pituitary hyperplasia in humans with primary hypothyroidism: Demonstration with MR imaging. Radiology 1999;213:383-8.  Back to cited text no. 3
    
4.
Franceschi R, Rozzanigo U, Failo R, Bellizzi M, Di Palma A. Pituitary hyperplasia secondary to acquired hypothyroidism: Case report. Ital J Pediatr 2011;37:15.  Back to cited text no. 4
    
5.
Simsek E, Simsek T, Savas-Erdeve S, Erdogmus B, Dösoglu M. Pituitary hyperplasia mimicking pituitary macroadenoma in two adolescent patients with long-standing primary hypothyroidism: Case reports and review of literature. Turk J Pediatr 2009;51:624-30.  Back to cited text no. 5
    
6.
Young M, Kattner K, Gupta K. Pituitary hyperplasia resulting from primary hypothyroidism mimicking macroadenomas. Br J Neurosurg 1999;13:138-42.  Back to cited text no. 6
    
7.
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;42:817-22.  Back to cited text no. 7
[PUBMED]    
8.
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;82:808-11.  Back to cited text no. 8
    
9.
Hutchins WW, Crues JV 3rd, Miya P, Pojunas KW. MR demonstration of pituitary hyperplasia and regression after therapy for hypothyroidism. AJNR Am J Neuroradiol 1990;11:410.  Back to cited text no. 9
    


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    Tables

  [Table 1], [Table 2], [Table 3]



 

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Abstract
Introduction
Subjects and Methods
Results
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