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.