As the demographic structure of societies changes, benign prostatic hyperplasia (BPH) is
one of the most important health problems for older men, especially in developed
countries. Histologically, BPH is a benign proliferative process involving both
epithelial and stromal elements and is characterised by progressive enlargement of the
prostate. BPH is a lifelong chronic disease with an incidence of approximately 8% in men
aged 31-40 years, which increases rapidly with age and reaches 90% in the 9th decade.
Symptom complex including increased frequency of urination, sudden feeling of urge to
urinate, nocturia, difficulty in urinating, feeling of incomplete emptying of the
bladder, decreased flow rate and intermittent urination are called lower urinary tract
symptoms (LUTS). The most important cause of LUTS in men is BPH. Many structural and
physiological changes occur in the lower urinary system with bladder outlet obstruction.
Detrusor hypertrophy and bladder hyperactivity may occur due to bladder outlet
obstruction. Although the density of afferent and efferent nerves in the bladder
decreases after urethral obstruction, enlargement of their trunks indicates that changes
occur in these nerves.
In addition, changes also occur in the neural pathways of the central nervous system
following lower urinary tract obstruction. Nerve growth factor (NGF) and brain derived
neurotropin factor (BDNF) are trophic proteins that act as retrograde messengers between
peripheral effector tissue and the nerves that innervate it. In peripheral tissues, the
source of NGF and BDNF is presumed to be the target tissues innervated by nerves. Smooth
muscle cells, fibroblasts, astrocytes and other cells synthesise NGF and BDNF in culture
medium. NGF is required for survival, development and neurotransmitter synthesis
regulation of dorsal root ganglion and sympathetic cells in embryonic and postnatal life
. NGF receptor contains two subunits; the low affinity subunit is called p75 and the high
affinity tyrosine kinase subunit is called tyrosine kinase A which is responsible for the
growth and survival effects of NGF. Many potential stimuli that increase NGF in the lower
urinary system have been identified. These are denervation, inflammation and mechanical
tension. This information has led to the idea that autonomic innervation changes in the
bladder may be related with changing NGF levels. Altered afferent and adrenergic
innervation in the obstructed bladder increases the possibility that NGF plays an
important role in this neural growth because this type of nerves are highly sensitive to
this neurotrophin. Clinical and experimental data have shown a relationship between
urinary NGF and overactive bladder. Overactive bladder (OAB) is a complex of
uncomfortable symptoms accompanied by a feeling of urgency, frequent urination and
nocturia, with or without urge incontinence. Overactive bladder is thought to occur as a
result of an inflammatory process occurring in the bladder. The reason for this is shown
as high levels of inflammation mediators in bladder biopsies and urine of OAB patients.
NGF, which is one of the inflammation mediators, was found to be high in OAB patients in
studies and it was observed that NGF level decreased after antimuscarinic treatment or
botulinum neurotoxin injection.
In this study, we investigated NGF ve BDNF levels in urine samples obtained before
surgery (Transurethral Prostate Resection, Prostate Enucleation with Holmium Laser and
Prostate Enucleation with Thulium Fibre Laser) and after removal of obstruction in
patients with bladder outlet obstruction secondary to benign prostatic enlargement using
ELISA method, We aimed to determine the role of NGF and BDNF in bladder outlet
obstruction and bladder changes secondary to obstruction by comparing with control
patients without obstruction.
