Not only diabetic polyneuropathy but also interstitial cells of Cajal dysfunction is a potential mechanism for diabetic cystopathy

Canda et al. [1] focused on the changes of interstitial cells of Cajal (ICCs) and neuronal tissue related to diabetes. The results of the current study showed that the number of ICCs in the lamina propria and detrusor muscle is decreased in diabetic patients. This may be an underlying pathomechanism of lower urinary tract symptoms in patients with diabetes. Long lasting diabetes results in different urological complications in over 50% of cases. The most common complications include diabetic bladder dysfunction (DBD), diabetic cystopathy, urinary tract infections and sexual dysfunction. Diabetic cystopathy (DC) was first described by Moller in 1976. DC features consist of an increased urinary bladder capacity, post voiding residual volumes and decreased urinary bladder sensation and motor activity as a result of diabetic polyneuropathy. DBD is referred to a wide range of lower urinary tract symptoms that encompass storage complaints (overactive bladder/ detrusor overactivity) and voiding complaints (poor urinary bladder emptying or overflow urine incontinence), as well as other less clinically defined phenotypes such as decreased sensation and increased capacity [2–5]. Past decades have shown an increasing appreciation for the important role of ICCs in gastrointestinal tract motility. Moreover, there is strong evidence of a correlation between some gastrointestinal diseases (e.g. achalasia, diabetic gastroenteropathy, gastro–esophageal reflux disease, gastroparesis, Hirschsprung’s disease, etc.) and morphological and Not only diabetic polyneuropathy but also interstitial cells of Cajal dysfunction is a potential mechanism for diabetic cystopathy