Acta Physiologica 85. (1997-1998)

3. szám - Syed Tabrez Ali: Measurement of the residual urine index in insulin-dependent and non-insulin dependent diabetic men with and without neuropathy

Syed Tabrez Ali Thickening of the capillary basement membrane, arteriosclerosis, and arteriolosclerosis account for many of the problems in diabetes. Neuropathy involving both parasympathetic and sympathetic supply to the lower genitourinary system produces significant problems of the bladder and sexual dysfunction. The neuropathic changes in the genitourinaiy system chiefly affect the bladder and the sexual function. In diabetes the common lesion produces damage to the afferent or sensory part of the reflex arc resulting in a bladder of diminished or absent tone. This tends to produce incomplete emptying of the bladder [1, 10]. With marked loss of sensation, and a minimal rise of pressure of 5 to 10 cm even up to a volume of 1000 ml associated with a strong urge to void. These symptoms are often associated with incontinence [15]. There is a close correlation with other neuropathic changes in these individuals; i.e. diminished anal sphincter tone, absence of bulbocavernosus reflex, absence or diminution of knee jerks and ankle jerks, and neuropathic changes in the bladder [3, 6]. Although disturbances of micturition have long been recognized as a feature of diabetes [5, 9, 14], but the pathologic changes responsible for bladder dysfunction have not been extensively studied. Only a few studies of the pathologic changes in the autonomic nervous system in diabetes have been reported in the literature [2, 11, 29]. Alterations in capillary permeability, impaired axonal flow, and abnormal myo­inositol metabolism have been suggested as possible étiologie factors in the development of diabetic neuropathy [8, 27]. Diagnosis of urinary bladder dysfunction in diabetes mellitus has been facilitated during the past decade by increasingly sophisticated techniques for bladder evaluation [10, 13, 14]. Diabetic autonomic neuropathy affecting the gastrointestinal tract and vascular reflexes have also been reported [20, 23]. A bladder capacity of 500 ml is regarded as the upper limit of normal [18]. The earliest neurological deficit in diabetic patients with neurogenic bladder is said to be the loss of bladder sensation due to involvement of the afferent sympathetic nerves [22], and the increased capacity probably arises from defective perception of bladder filling. Peripheral neuropathic changes are also often sub-clinical while motor as well as sensory nerves may be affected [21, 25]. Neurogenic bladder dysfunctions are now established as a frequent complication of diabetes mellitus [12, 14] and are considered as a manifestation of autonomic neuropathy [17]. Vesicle ultrasonography is a simple technique for the determination of residual urine [29]. In the present studies we have used the vesicle ultrasonographic technique to evaluate residual urine index in both IDDM and NIDDM diabetic men (with and without neuropathy). The main aim of this study is therefore to provide data on the prevalence of neurogenic bladder dysfunction, as appreciated by incomplete voiding in these patients, and to determine possible relationship with the type of diabetes and the presence of manifestations of autonomic neuropathy. A cm Physiologien Hungarian 85, 1997/98

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