Relationship between serum cholinesterase level and urinary bladder activity in patients with or without overactive bladder and/or neurogenic bladder

Abstract

We compared the serum cholinesterase (ChE) level and various parameters between patients with or without overactive bladder (OAB) and/or neurogenic bladder (NB). A total of 258 patients who met the following criteria were enrolled: the presence/absence of OAB and/or NB was documented, laboratory data were available, and liver and renal functions were normal. Patients were divided into the 3 groups: 1) a NB /OAB + group, a higher serum albumin or ChE level was associated with a better therapeutic outcome. These results suggest that a decrease of serum ChE level is related to the occurrence of OAB and the poor response to treatment in OAB patients without NB.The symptom of urinary urgency (usually combined with frequency and nocturia) with or without urge incontinence is characteristic of the overactive bladder (OAB) syndrome (1). OAB occurs in patients with neurogenic bladder (NB) caused by damage to the brain, spinal cord, or peripheral nerves, or in patients without neurogenic bladder, among whom it usually arises due to bladder outlet obstruction (BOO) secondary to conditions such as benign prostatic hyperplasia (BPH) and urethral stricture (2). Bladder smooth muscle cells undergo contraction when exposed to acetylcholine secreted from the parasympathetic nerve terminals, and the efficacy of anticholinergic agents is usually assessed on the basis of blocking the micturition reflex in animal studies. However, recent studies reported that acetylcholine is produced by the bladder epithelium as well as by nerve terminals (7, 23), and its production by the bladder epithelium increases after the occurrence of BOO (5,22). It has also been suggested that the bladder epithelium express receptors for various neurotransmitters, including adrenergic, nicotinic and muscarinic receptors, and release not only acetylcholine but also nitric oxide, prostaglandin and adenosine triphosphate (ATP), and that muscarinic mechanisms may also have a role in urothelial sensory function (9). Clinically, anticholinergic agents are the main type of drug used for the treatment of OAB because these agents can usually

Spontaneous release of acetylcholine from autonomic nerves in the bladder

“…Whether this mechanism is present in the normal human bladder and whether it is enhanced in overactive bladder would be of great interest. Recently, it has been shown that a decrease of serum cholinesterase is related to occurrence of overactive bladder (Sugaya et al. , 2007).…”

Cholinergic Crisis Caused by Cholinesterase Inhibitors: a Retrospective Nationwide Database Study

“…Although reversible cholinesterase inhibitors are beneficial for the treatment of Alzheimer's disease [4][5][6], myasthenia gravis [7], and neurogenic bladder [8,9], they can still cause adverse cholinergic reactions. Excessive cholinesterase inhibition can cause cholinergic crisis, defined by symptoms including pupils ≤ 2 mm in diameter, fasciculations, heart rate ≤ 60 beats per minute, systolic blood pressure ≤ 80 mmHg, decreased consciousness (Glasgow Coma Scale < 15), excessive sweating, or poor air entry due to bronchorrhea and/or bronchospasm [10,11].…”

Diagnostic Potential of Low Serum Platelet, Albumin and Prolong PT-INR for Overactive Bladder and Nocturia in Chronic Hepatitis-Related Liver Cirrhosis

“…This condition has been reported to result in delayed removal of the large acetylcholine burst secreted by the parasympathetic nerve terminals in the bladder when the micturition reflex is activated [20]. Sugaya et al also reported a significant association between the serum levels of cholinesterase and albumin [21]. The presence of a cholinergic effect will cause a bladder spasm, resulting in frequency and urgency.…”