Prostatitis includes infectious and noninfectious inflammatory phenotypes that can impair male reproductive potential and may influence couple-level reproduction via seminal inflammatory and microbial exposure. This review summarizes mechanisms linking prostatic inflammation and dysbiosis to semen dysfunction and sperm DNA damage and proposes an infertility-oriented diagnostic and management framework. This is a narrative review of clinical and translational evidence addressing semen inflammation, oxidative stress, sperm DNA fragmentation (SDF), microbiome signatures, and reproductive outcomes in prostatitis (National Institutes of Health (NIH) categories I-IV). Across prostatitis phenotypes, leukocytospermia and elevated seminal cytokines (especially interleukin-8) are associated with impaired motility, altered viscosity and liquefaction, oxidative stress, and higher SDF. Persistent infection or dysbiosis may sustain immune activation and redox injury, while ductal remodeling and pain-related sexual dysfunction can further reduce natural conception. Seminal cytokines and microbes may affect female reproductive tract biology, although clinical outcome data remain limited. Prostatitis-related infertility requires evaluation beyond routine semen analysis. A biomarker-guided workup integrating inflammatory markers, oxidative stress testing, targeted microbiology (culture plus nucleic acid amplification tests when indicated), SDF testing in selected men, and imaging when obstruction is suspected can identify treatable drivers and guide timing and selection of assisted reproduction strategies. Future studies should standardize fertility endpoints and validate biomarker-guided and microbiome-directed interventions.

Sickle cell disease (SCD) is an inherited hemoglobinopathy in which hemoglobin S polymerization drives hemolysis and vaso-occlusion with progressive organ morbidity. Male reproductive impairment is increasingly recognized but remains underreported. This narrative review summarizes mechanistic pathways, clinical manifestations, and fertility preservation options relevant to men with SCD. PubMed, the Cochrane Library, and Medscape were searched through 31 December 2025 for human studies addressing endocrine changes, semen quality, priapism and erectile dysfunction, oxidative stress, and treatment-related gonadotoxicity. Evidence supports converging mechanisms: recurrent vaso-occlusion and chronic hypoxia may injure the seminiferous epithelium and impair Leydig cell steroidogenesis; oxidative stress and inflammation contribute to sperm DNA and membrane damage; and disease-modifying or curative therapies such as hydroxyurea and hematopoietic stem cell transplantation can further compromise spermatogenesis. Clinically, men with SCD may present with oligozoospermia, azoospermia, hypogonadism, and sexual dysfunction, particularly after recurrent ischemic priapism. Fertility preservation should be discussed early, ideally before prolonged hydroxyurea exposure or transplantation, and may include semen cryopreservation and testicular sperm extraction (TESE) with assisted reproduction when needed. Prospective longitudinal studies are required to define reproductive trajectories and optimize counseling and management.