Pulmonary alveolar proteinosis diagnosed during leuprorelin acetate therapy for ovarian endometrioma: a case report.
This case highlights a potential association between leuprorelin therapy and pulmonary alveolar proteinosis, but causality cannot be determined without baseline imaging.
Where it sits
this study against the rest of the gonadorelin (gnrh) corpusSummary and findings
This case report describes a 29-year-old woman diagnosed with pulmonary alveolar proteinosis (PAP) during leuprorelin acetate therapy for ovarian endometrioma. The patient underwent surgery in August 2025 and started therapy three days postoperatively, with imaging revealing ground-glass opacities one month later. The relationship between therapy and PAP is noted, but causality cannot be established due to the lack of baseline imaging.
Abstract
Background Pulmonary alveolar proteinosis (PAP) is a rare pulmonary disorder characterized by impaired surfactant clearance due to alveolar macrophage dysfunction. Leuprorelin acetate, a gonadotropin-releasing hormone agonist, is widely used in the treatment of ovarian endometriosis; however, pulmonary findings associated with this therapy have not been well characterized. We report a case of PAP diagnosed during leuprorelin acetate therapy for ovarian endometrioma and describe its temporal relationship with treatment. Case presentation A 29-year-old woman underwent laparoscopic surgery for an ovarian endometrioma in August 2025 and initiated leuprorelin acetate therapy three days postoperatively. A routine chest computed tomography (CT) performed one month later revealed scattered bilateral ground-glass opacities (GGOs), which persisted on repeat CT in November 2025. Although the patient remained asymptomatic, video-assisted thoracoscopic surgery (VATS) lung biopsy was performed to obtain a histopathological diagnosis and confirmed PAP. Serum anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antibody testing was negative (3.2 µg/mL; reference range, ≤ 5 µg/mL), not supporting autoimmune PAP. During treatment, the patient developed transient Common Terminology Criteria for Adverse Events (CTCAE) grade 2 leukopenia (white blood cell nadir, 2.94 × 10⁹/L), which resolved spontaneously after completion of leuprorelin acetate therapy without intervention. Hematological evaluation did not suggest an underlying clonal disorder, including myelodysplastic syndrome. Because baseline chest imaging was unavailable, pre-existing subclinical PAP could not be excluded. Follow-up CT performed three months after completion of therapy showed regression of GGOs. Conclusion This case shows a temporal relationship between leuprorelin acetate therapy and non-autoimmune PAP. However, causality cannot be inferred in the absence of baseline imaging. Only a temporal association can be observed. This observation is hypothesis-generating and highlights a potential rare pulmonary finding observed in the context of gonadotropin-releasing hormone agonist therapy.
Background
Pulmonary alveolar proteinosis (PAP) is a rare lung disease characterized by the accumulation of surfactant in the alveoli. Previous literature has indicated that certain medications, including leuprorelin acetate, may have adverse pulmonary effects. This case report is significant as it highlights a potential association between leuprorelin therapy and the development of PAP.
Methods
Not reported in abstract.
Results
Not reported in abstract.
Interpretation
The findings in this case report suggest a possible link between leuprorelin acetate therapy and the onset of PAP, although causality cannot be established. The lack of statistical data and the single-case nature of the report limit the ability to draw broader conclusions. Further studies are needed to explore this potential association and its clinical implications.
Key findings
- Not reported in abstract.
Limitations
- Case report with no control group
- No statistical analysis provided
- Single patient report limits generalizability
- Not applicable for broader clinical guidelines