We hypothesize that MCP-1 urinary levels correlate with OAB patients’ symptom severity. Our aim is to correlate normalized MCP-1 urinary levels to OAB symptoms before and after treatment. We conducted prospective study on patients with OAB symptoms and age-matched controlled.

Urinary MCP-1 levels were measured in 36 patients with OAB and 13 controls. Patients were treated after the first visit by different OAB treatments (anticholinergic, Beta-3 agonist and or, onabotulinum toxin A, neuromodulations). Urinary MCP-1 levels were measured using enzyme-linked immunosorbent assay (ELISA) and normalized by urinary creatinine levels. The urinary MCP-1 levels and OAB symptoms were compared at baseline, 1 month, and 3 months after treatments. Different validated OAB questionnaires were used.

The baseline urinary MCP-1 levels of patients with untreated OAB were significantly higher than that of controls with mean. Patients with OAB had significantly higher baseline urinary MCP-1 levels than that of controls. Urinary MCP-1 levels were significantly reduced at 3 months in 28 OAB-responders (77.8%). On other hand, 8 OAB− non−responders, showed unchanged in urinary MCP−1(Table 1).The severity of OAB symptoms and QoL had significantly decreased with urinary MCP−1 levels OAB− responders at 1 and 3 months of OAB treatments.

The OAB symptoms and the quality of life (QoL) of patients significantly changed with the changes in urinary MCP-1 levels of responders at different time points. The severity of OAB symptoms also correlates with the level of MCP-1.

The changes in urinary MCP-1 levels were associated with changes in OAB symptoms after treatment. Urinary MCP−1 levels were significantly higher in patients with OAB than in the controls. Patients with OAB who responded to treatments had significantly reduced urinary MCP−1 levels in association with a decreased severity of OAB symptoms at 3 months. 
These promising findings could help understanding the pathophysiology of OAB and neurophysiological signaling in the bladder function, identification of a potential marker, and/or developing new drug targets for treatment of patients suffering from OAB.