Inflammation‐associated pathologies in a case of prostate schistosomiasis: Implications for a causal role in prostate carcinogenesis

Abstract

Background Urogenital infection with Schistosoma haematobium is a risk factor for the development of squamous cell carcinoma of the urinary bladder. The pathophysiology is thought to be mediated in part by inflammation, cellular damage, and bladder regeneration induced by the parasitic infection. Herein, we report an unusual case of schistosomiasis of the prostate that was found concurrent with prostate adenocarcinoma in a radical prostatectomy specimen from a man in the United States. Methods The infecting Schistosoma species was characterized via histomorphology and acid‐fast stain. The concurrent Gleason score 6 prostate cancer was assessed for ETS transcription factor ERG (ERG), phosphatase and tensin homolog (PTEN), p27, and p53 status using immunohistochemistry (IHC). Cellular proliferation and the presence of intermediate cells in prostatic atrophy were assessed via immunostaining for Ki67 and CK903, respectively. Results Histomorphology and acid‐fast stain of the infecting species were consistent with S. haematobium. We classified the Gleason score 6 prostate adenocarcinoma via IHC as ERG positive, PTEN intact, p27 intact, and without p53 nuclear accumulation. The prostatic epithelium immediately adjacent to the schistosomiasis‐related granulomatous inflammation was atrophic and accompanied by increased cellular proliferation and the presence of intermediate cells. Upon literature review, we determined that prostate schistosomiasis is associated with a young age of prostate cancer diagnosis and highly aggressive prostate cancer. Conclusions This is a rare case of prostate schistosomiasis in the United States; however, prostate schistosomiasis occurs frequently in endemic areas. The patient had traveled to a Schistosoma‐endemic region, which was the likely location of exposure to the parasite. To our knowledge, this is the first report of the association of proliferative inflammatory atrophy and intermediate cells with schistosomiasis of the prostate. We propose that prostate schistosomiasis may be considered as a risk factor for the development of prostate cancer in geographic regions where Schistosoma species are endemic.

Association of schistosomiasis and risk of prostate cancer development in residents of Murehwa rural community, Zimbabwe

“…The elevated prostate-specific antigen levels we observed could have be attributed to old age, prostatitis, benign hyperplasia, urinary tract infections, ejaculation, prostate injury and medicine prolonged bicycles rides [ 43 ]. Prostatic inflammation due to S. haematobium or S. mansoni ova deposits can lead to elevated levels of systemic prostate-specific antigen levels [ 5 , 44 , 45 ]. Furthermore, other studies that reported prostatic schistosomiasis cases with high prostate-specific antigen levels were not associated with prostatic schistosomiasis cancer [ 44 , 45 ].…”

“…Prostate cancer is a common urogenital condition living in both schistosomiasis and non-schistosomiasis endemic areas. Despite geographical locations, coincidences of MGS infections and prostate cancer cases have also been reported in non-schistosome endemic areas [ 3 – 5 ]. The concurrent incidences of prostatic MGS and prostate cancer have prompted the suggestion of a causal association between the two diseases.…”

Oncogenic gene fusions in nonneoplastic precursors as evidence that bacterial infection can initiate prostate cancer

“…Prostate infections and inflammation are potential initiating factors in prostate cancer development (2)(3)(4)(5). Specifically, prostate infection or other inflammatory stimuli may drive the formation of proliferative inflammatory atrophy (PIA), a putative prostate cancer precursor lesion (6)(7)(8). The atrophic luminal epithelial cells in PIA are markedly proliferative compared to that of normal-appearing epithelium, are enriched with cells of an intermediate phenotype that have properties of both basal and luminal epithelial cells (9), and are sometimes observed in direct transition with prostatic intraepithelial neoplasia (PIN, the most accepted direct precursor to prostate cancer) and adenocarcinoma (10).…”