Drugs & Meds Blog

Impotence in male diabetics is common. In a meta-analysis 1619 patients Neubauer (1971) noted impotence in 39% to 75 % (mean 55 %), a prevalence confirmed by others (Ellenberg 1971, Kolodny et al 1974, Faiburn et al 1982). Jensen (1981) found impotence in 34% of diabetics but in none of a control group of non-diabetics. When the internal urinary sphincter is weak retrograde ejaculation occurs (Greene et al 1963, Ellenberg & Weber 1966, Schirren et al 1973), as noted in about 14% of diabetics. In diabetic males morning erections are absent or rare. Karacan et al (1977, 1978) and Hirshkowitz et al (1990) found that men with diabetic polyneuropathy had fewer sleep-related erections, shorter tumescence time, diminished penile circumference increase and weaker penile rigidity than non-diabetic men.

A correlation between impotence and bladder dysfunction has been noted in diabetic men (Ellenberg 1971, Buvat et al 1985, Ertekin et al 1989), and ikmpotence is also correlated with clinically evident peripheral neuropathy (Ellenberg 1971, Kolodny et al 1974, Jensen 1981, Lehman & Jacobs, 1983). There is little correlation, nonetheless, with neurophysiological abnormalities in peripheral nerve function (Zgur et al 1993), although bulbocavernosus and urethro-anal reflex latencies, and penile (pudendal) evoked potentials are more often abnormal in impotent diabetic males than in potent diabetic males (Bemelmans et al 1994). Neurophysiological testing of pudendal nerve function, however, is not more sensitive in diagnosing neuropathy in impotent diabetics than limb nerve conduction tests (Vodusek et al 1993).

Histological and histochemical studies of the autonomic nervous system have shown reduced norepinephrine content in the corpora cavernosa in insulin-dependent and diet-controlled diabetic men compared with non-diabetic men. Choline acetyltransferase activity and morphological studies of nerve fibers in erectile tissue were normal (Melman et al 1980a, 1980b), although choline accumulation and acetylcholine synthesis and release were significantly reduced in penile tissue from impotent diabetic patients compared to that from impotent non-diabetic patients. Impairment in acetylcholine synthesis correlated with duration of diabetes (Blanco et al 1990). Morphological alterations have been identified in unmyelinated nerve fibres in the penis (Faerman et al 1974). Hyperglycemia, and some glycosylation products, promote inactivation of NO (Brodsky et al 2001) and there seems to be a selective nitrergic neurodegeneration in diabetes (Cellek et al 1999).

Studies of sexual function in women with diabetes mellitus have given conflicting results. In one study 35 % of the diabetic women were reported to have had orgasmic dysfunction in the preceding year as compared to 6 % of controls (Kolodny 1971), but Jensen (1981) found the frequency of sexual dysfunction was 25 % both in insulin-treated diabetic women and in age-matched controls. An important negative impact on sexual life was found in women with type II diabetes (Schreiner-Engel et al 1987); but not in type 1 diabetes (Newman & Bertelsen 1986, Campbell et al 1989). In a structured interview Hulter et al (1998) found that 26 % of 42 women with insulin dependent diabetes had a decreased sexual desire, 22 % had decreased vaginal lubrication (Tyrer et al, 1983) and 10 % had decreased capacity to achieve orgasm. Several women reported more than one dysfunction. Taken together the figure for sexual dysfunction was 40 %. Among age-matched controls without diabetes or any neurological disease only 7 % of women reported any sexual dysfunction. A number of autonomic and sensory symptoms, including higher vibration perception thresholds in the hands and in clitoris, reduced foot perspiration, increased gustatory perspiration, constipation and incontinence correlated with sexual dysfunction (Hulter et al 1998). Women with more diabetic complications have more sexual dysfunction (Enzlin et al 2002). Psychophysiological studies in women with diabetes mellitus revealed less physiological arousal to erotic stimuli (Wincze et al 1993), or no difference compared to controls (Slob et al 1990). Microvascular damage leading to decreased decreased blood flow to the cavernous tissues in both sexes is another possible factor (Ertekin 1998, Enzlin et al 1998).

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