LUTS treatment: Future treatment options

Abstract

Lower urinary tract symptoms (LUTS) are commonly divided into storage, voiding, and postmicturition symptoms, and may occur in both men and women. Male LUTS have historically been linked to benign prostatic hyperplasia (BPH), but are not necessarily prostate related. The focus of treatment for LUTS has thus shifted from the prostate to the bladder and other extraprostatic sites. LUTS include symptoms of the overactive bladder (OAB), which are often associated with detrusor overactivity. Treatment for LUTS suggestive of BPH has traditionally involved the use of alpha(1)-adrenoceptor (AR) antagonists; 5alpha-reductase inhibitors; and phytotherapy-however, several new therapeutic principles have shown promise. Selective beta(3)-adrenoceptor agonists and antimuscarinics are potentially useful agents for treating LUTS, particularly for storage symptoms secondary to outflow obstruction. Other agents of potential or actual importance are antagonists of P2X(3) receptors, botulinum toxin type A, endothelin (ET)-converting enzyme inhibitors, and drugs acting at vanilloid, angiotensin, and vitamin D(3) receptor sites. Drugs interfering with the nitric oxide/cGMP-cAMP pathway, Rho-kinase and COX inhibitors, as well as drugs targeting receptors and mechanisms within the CNS, are also of interest and deserving of further study for the treatment of LUTS.

The Effect of Combined Therapy with Tamsulosin Hydrochloride and Meloxicam in Patients with Benign Prostatic Hyperplasia Symptoms and Impact on Nocturia and Sleep Quality

“…COX is a key enzyme in inflammation and found in 2 isoforms, COX-1 and COX-2, the latter especially activated during inflammation in the bladder (20). Chronic inflammation continuously produces cyclooxygenase-2 (COX-2) (21).…”

Characteristics of Autonomic Nervous System Activity in Men With Lower Urinary Tract Symptoms (LUTS): Analysis of Heart Rate Variability in Men With LUTS

“…Current interest in LUTS has focused on additional mechanisms and sites of origin, particularly with respect to the pathogenesis of storage symptoms. 7 The lower urinary tract is generally under the control of the ANS, is innervated by 3 sets of peripheral nerves (parasympathetic, sympathetic, and somatic nervous systems), and contains afferent and efferent motor axons. 8,9 Therefore, we believe that the other condition rather than bladder outlet obstruction, such as disorder of ANS, may contribute to the development of storage symptoms.…”

The involvement of urothelial α1A adrenergic receptor in controlling the micturition reflex

“…Overactive bladder (OAB) is a new entity defined as a symptomatic syndrome of urinary frequency and urgency with or without incontinence (1), whose prevalence also increases during aging (26). In most cases, the cause of OAB is unclear, although a significant proportion of male OAB patients also have BPH (2,9). Since all three subtypes of α 1 adrenergic receptors are expressed in the hu- discrepancy of the effect on ICI is that there might be a facilitatory mechanism that normally and constitutively functions by intrinsic NA stimulation of α 1 receptors, and the fact that the mechanism was affected only by naftopidil and not by the other two agents, may have been due to the different drug delivery systems used for the three drugs or to some unknown reasons.…”