Pituitary macroadenoma revealing Hashimoto's thyroiditis: When peripheral biology rectifies central imaging!

 Corresponding author: O. El Gharnati Copyright © 2025 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution License 4.0. Pituitary macroadenoma revealing Hashimoto’s thyroiditis: When peripheral biology rectifies central imaging! O. El Gharnati 1, 2, *, M. Maouelainin 2, 3 and Pr. H. El Jadi 1, 4 1 Department of Endocrinology, Oued Eddahab Military Hospital, Agadir, Morocco. 2 Faculty of Medicine and Pharmacy, Ibn Zohr University, Agadir, Morocco. 3 Radiology Department, Oued Eddahab Military Hospital, Agadir, Morocco. 4 Faculty of Medicine and Pharmacy, Cadi Ayyad University, Marrakech, Morocco. World Journal of Advanced Research and Reviews, 2025, 28(02), 922-924 Publication history: Received on 17 September 2025; revised on 08 November 2025; accepted on 10 November 2025 Article DOI: https://doi.org/10.30574/wjarr.2025.28.2.3791 Abstract Background: Pituitary macroadenoma is often confused with pituitary hyperplasia, a benign proliferation of thyrotropic cells due to prolonged peripheral hypothyroidism. Case Presentation: We report the case of a 17-year-old female initially diagnosed with a pituitary macroadenoma, in whom we concluded that pituitary hyperplasia was secondary to Hashimoto’s thyroiditis. Conclusion: Differential diagnosis is essential to avoid unnecessary surgery, as hormone replacement therapy can lead to complete regression of the mass. Keywords: Pituitary Hyperplasia; Hashimoto’s Thyroiditis; Hypothyroidism; MRI; Endocrinology 1. Introduction Pituitary macroadenomas and pituitary hyperplasia secondary to hypothyroidism can share clinical and radiological similarities. Pituitary hyperplasia often arises in response to prolonged primary hypothyroidism, particularly of autoimmune origin such as Hashimoto's thyroiditis, resulting in compensatory hypertrophy of thyrotropic cells. Several studies report that pituitary hyperplasia can regress under L-thyroxine replacement therapy, thus avoiding unnecessary surgery [1]. We report the case of a patient whose initial diagnosis suggested a macroadenoma, before considering another diagnostic possibility: pituitary hyperplasia secondary to autoimmune hypothyroidism. This case highlights the importance of a thorough endocrine work-up and rigorous follow-up before considering any surgical intervention. 2. Case presentation A 17-year-old female with no significant past medical history presented with morning headaches, oligomenorrhea, and a 12-kg weight gain over eight months. Clinical and radiological assessments (MRI) revealed a pituitary mass initially suggestive of a macroadenoma. Hormonal evaluation showed profound primary hypothyroidism with TSH > 100 mIU/mL and moderate hyperprolactinemia. A reassessment of the MRI, in light of the biochemical findings, suggested pituitary hyperplasia rather than a true adenoma. Following progressive levothyroxine replacement therapy, marked clinical and radiological improvement was observed. World Journal of Advanced Research and Reviews, 2025, 28(02), 922-924 923 Figure 1 Sagittal T1-weighted MRI showing pituitary hyperplasia Figure 2 Sagittal T1-weighted MRI after three months of levothyroxine therapy showing complete resolution of pituitary hyperplasia 3. Discussion The differential diagnosis between pituitary adenoma and secondary pituitary hyperplasia is challenging due to overlapping clinical and radiological features. Pituitary hyperplasia results from increased thyrotropin-releasing hormone (TRH) secretion in response to prolonged primary hypothyroidism, particularly of autoimmune origin such as Hashimoto’s thyroiditis. On MRI, it typically presents with homogeneous gadolinium enhancement but may occasionally mimic a pituitary adenoma [2]. Several studies emphasize the importance of a comprehensive endocrine assessment before any surgical intervention [1]. The response of pituitary hyperplasia to L-thyroxine therapy is well documented, with multiple case series reporting a reduction in gland size within the first three months of treatment. In some instances, complete regression is observed between three and six months [3]. Regression may occur more slowly in autoimmune hypothyroidism, requiring extended imaging follow-up to confirm full resolution. This slower process is attributed to the persistent stimulation of the hypothalamic–pituitary axis caused by the chronic nature of Hashimoto’s thyroiditis [4]. Pituitary hyperplasia may also be associated with moderate hyperprolactinemia, resulting from TRH-induced stimulation of lactotroph cells, loss of dopaminergic inhibition due to pituitary stalk compression, World Journal of Advanced Research and Reviews, 2025, 28(02), 922-924 924 and reduced prolactin clearance [5]. Long-term follow-up is essential, as an empty sella may develop after regression of the hyperplasia, warranting regular MRI monitoring [6]. 4. Conclusion Secondary pituitary hyperplasia due to primary hypothyroidism should be considered in the differential diagnosis of pituitary masses to avoid unnecessary surgical procedures. L-thyroxine therapy remains the first-line treatment, leading to regression of the mass in most cases. Compliance with ethical standards Disclosure of conflict of interest The authors declare that they have no conflict of interest related to the publication of this case report. Statement of informed consent Informed consent was obtained from the patient for inclusion in the study and for publication of relevant data and images. References [1] Franceschi R, et al. Pituitary hyperplasia secondary to acquired hypothyroidism: case report. Ital J Pediatr. 2011;37(1):5. [2] Moumen A, et al. An unusual pituitary mass revealing a primary hypothyroidism! Radiol Case Rep. 2015;10(4):1072–1075. [3] Shimono T, et al. Rapid progression of pituitary hyperplasia in humans with primary hypothyroidism. Radiology. 1999;213(2):383–388. [4] Esdaile H, et al. Pituitary hyperplasia due to untreated hypothyroidism. Endocrine Abstracts. 2021;77:P39. [5] Dutta D, et al. Empty sella after pituitary hyperplasia due to chronic primary hypothyroidism. Indian J Endocrinol Metab. 2012;16(Suppl 2):S318–S320. 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