ArticleCureus2023
Sex Steroid Modulators and the Development of Buschke-Lowenstein Tumor: A Case Report of an Immunocompetent Patient.
Article in Cureus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Buschke-Lowenstein tumors (BLTs) are benign dermatologic manifestations of human papillomavirus (HPV). They originate from longstanding condylomata in individuals with compromised immune systems. In this case report, we present a 68-year-old immunocompetent female with HPV condylomata that had transitioned to a large, fungated BLT in her right groin. The patient's immunocompetency was determined by the absence of diabetes, corticosteroid therapy, organ transplant, cytotoxic therapy, or any known primary or other secondary immunodeficiencies. Notably, the patient had a history of breast cancer, managed through lumpectomy, local radiation, and two years of combined aromatase inhibitor and selective estrogen receptor modulator (SERM) therapy, followed by three years of further SERM therapy. We propose that the effect of her previously received SERM therapy shifted the T helper (Th)1 immune response to a Th2 response. This may have compromised the patient's HPV-specific cell-mediated immunity, favoring a non-protective Th2-dominant effect. Thus, it potentially enabled immune evasion, transitioning to a BLT phenotype. Additionally, the immune skewing of the SERM may have been initially opposed by the known ability of aromatase inhibitors to potentiate Th1 responses. Indeed, the patient first noticed the appearance of HPV condylomata progressing to the BLT phenotype with the cessation of the aromatase inhibitor therapy under the unopposed influence of the SERM. The resultant cytokine milieu may have contributed to the unusual progression to the BLT phenotype in this otherwise immunocompetent patient.
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