Benign Prostate Hyperplasia


prostate_glandBPH – Causes, Epidemiology and Medication

Epidemiology of BPH:

The study of the distribution and the determinants of diseases in manlike beings is titled Epidemiology. hyperplasia or Benign Prostatic Hyperplasia is a term used to indicate the rousing or “hyperplasia” of the endocrine gland. There being no globally accepted medicine definition of BPH, the prevalence and incidence rates of this disease are commonly viewed in context of the definitions chosen by the physician reporting the data. Prevalence of hyperplasia is commonly not compared based on clinical criteria, because clinical definitions have been found to vary greatly. So physicians commonly choose autopsy or histological evidence to compare the prevalence of the disease.

Pathogenesis of BPH:

The development of hyperplasia in men is commonly attributed to testicular hormones and aging. Though the role of androgens as the anorectic factor for hyperplasia is debated, they definitely have at least some role as a anorectic agent. It has been seen that men castrated before puberty do not develop hyperplasia as compared to those in the same age assemble and belonging to the same strata of society. It has also been seen that men having diseases that inhibit the production of androgens are less likely to have BPH.

The principal prostatic ketosteroid responsible for hyperplasia is dihydrotestosterone or DHT. DHT is actually a figuring of testosterone – the male sex hormone. It has been seen that though the concentrations of DHT and testosterone in blood (plasma) modification with age, they rest in connatural concentration in the endocrine with aging. There are different theories as to the exact cause of BPH. Though none of them have been evidenced to be conclusive singularly, yet the theory of DHT is probably the most referred to by physicians. The other most common theories are:

· The theory of interaction between stroma and epithelium

· The theory of reduction of the cellular death rate

· The theory of estrogenic synergy

· The theory of genetic and familial factors.

Role of DHT in BPH:

Though the levels of Testosterone and Dihidrotestosterone in serum decline with age, the concentration of DHT remains unchanged in the prostate. The reason for this is probably the fact

that DHT has a very high affinity for ketosteroid receptors. For a better understanding of ketosteroid receptors, we can consider the receptors to be something like magnets and the DHT molecules like iron filings. When Testosterone gets converted into DHT cod to the participation of a endocrine specific enzyme titled 5α-reductase, the DHT molecules rush off and get settled on the ketosteroid receptors and then complex cellular reactions are initiated. Since this phenomenon is independent of the old process, ketosteroid dependent cell ontogeny is maintained finished out the old process. Careful examination has shown that hyperplasic tissues (inflamed areas of the prostate) commonly have higher concentrations of ketosteroid receptors as compared to connatural areas. These are supposed to be the major culprits for feat BPH.

Role of Stromal – Epithelial Interactions in BPH:

The endocrine gland is histologically divided into two parts – Stroma and Epithelium. Experiments suggest that both the compartments communicate with each other and the ontogeny of the endocrine is highly dependent on the behave or regulatory signaling between them.

DHT is believed to behave either in autocrine (secretes a chemical signal and binds to the same cell) fashion by protection with the stromal cells or by protection with neighboring epithelial cells in paracrine (opposite of autocrine) fashion. In both these instances DHT binds with ketosteroid receptors and triggers the transcription (synthesis of RNA or ribo nucleic acid) of ontogeny factors, which in turn cause prostatic tissue growth.

Medical treatment for BPH:

It has been seen that 5α-reductase inhibitor assemble of drugs like Finasteride, Dutasteride etc. are efficient in arresting hyperplasia progression. These drugs inhibit the formation of 5α-reductase enzyme and thereby hinder the transmutation of Testosterone into DHT. Though clinicians have reportable of other anorectic agents of BPH, the fact that arresting DHT formation arrests hyperplasia progression proves that DHT is one of the vital anorectic agents of BPH.

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