Association of hormone therapy with spheno-orbital meningiomas: bridging evidence and unknowns

TL;DR

This paper reviews evidence linking hormone therapy, especially progestins, to the development and progression of spheno-orbital meningiomas and highlights gaps in clinical understanding.

Contribution

The study systematically reviews current literature to clarify the role of hormone therapy in spheno-orbital meningiomas and identifies areas needing further research.

Findings

Long-term progestin use is associated with SOM development and progression.

Stopping hormone therapy can lead to partial tumor regression, particularly in soft tissue components.

Surgical resection is the primary treatment, with total resection reducing recurrence risk.

Abstract

To evaluate the association between hormone therapy and the development, progression, and treatment response of spheno-orbital meningiomas (SOMs) and to identify current evidence gaps in clinical management.

A systematic literature review was conducted using an advanced search of PubMed, Embase, Scopus, and Cochrane databases for articles published in English. The selection process adhered to the PRISMA guidelines. Inclusion criteria targeted original research published from inception to May 2025, which discussed hormone therapy exposure and SOMs. Study quality was assessed with Joanna Briggs Institute critical appraisal tools appropriate to each study design.

Twenty articles were retrieved. After screening, 10 studies met the inclusion criteria and were analyzed. The studies comprised 2 case reports, 1 prospective cohort, and 7 retrospective cohorts, totaling 315 patients with SOMs. The gender distribution was predominantly female (166 women, 4 men) in the 7 studies that reported mean age data for patients with SOM. The patients had a mean (SD) history of 12.6 (3.67) years of hormone therapy exposure, with 90% of the therapies being progestins. Six studies reported a decrease in the SOM volume after hormone therapy cessation, and 4 studies documented a decrease in the soft tissue component with progression or stabilization of the intraosseous component. The therapeutic goal was surgical resection. Subtotal resection was associated with higher recurrence than total resection, especially when the residual tumor included soft tissue. Conservative management, involving hormone therapy cessation, was reported in 3 cases. Data were limited regarding progesterone receptor status and the use of radiation therapy.

Current evidence suggests that hormone therapy, particularly long-term exposure to progestins, may contribute to the development and progression of SOMs. Although cessation of hormone therapy can result in partial tumor regression, especially in soft tissue components, surgical resection remains the primary treatment. Hybrid strategies that combine hormone therapy cessation with surgery may be beneficial in selected cases, although prospective data are lacking. Standardized clinical guidelines and further studies are needed to clarify the role of hormone therapy in the management of SOM.

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