Molecular pathology of benign prostatic hyperplasia is multifactorial and involves endocrine, biochemical, immunological interactions. The mechanisms involved in the onset and progression of benign prostatic hyperplasia are: infections, 50 years of age, hormones and neurotransmitters imbalances, inflammation, oxidative stress. The potential role of glycosylation in the pathogenesis of prostate disease has been neglected. In this study we documented the profile of gangliosides in normal and pathological prostatic tissues together with the pathologic changes seen in the level of extracellular gangliosides in patients with prostate pathology. Analysis of the data in the literature suggests that gangliosides may represent immunologic markers useful in the differential diagnosis between prostate cancer and benign prostatic hyperplasia.
Oxidative stress parameters in patients with prostate cancer, benign prostatic hyperplasia and asymptomatic inflammatory prostatitis: A prospective controlled study
