could be one possible link between CAN and the observed deterioration in glomerular filtration rate [78].
There are no population-based studies reporting the prevalence or incidence of gastrointestinal symptoms or motor abnormalities in diabetic patients. A number of clinic-based studies reported relatively high rates of delayed gastric emptying in diabetic subjects, but most of these included small samples of highly selected populations subject to referral bias. Thus, the true prevalence of delayed gastric emptying is not known. Using the 13C-octanoic acid breath test, delayed gastric emptying has been shown in 16% of type 1 diabetic subjects without gastrointestinal symptoms, while the rate increased to 43% in those with these symptoms [79]. Several clinic-based studies reported the prevalence of gastrointestinal symptoms in diabetic and nondiabetic subjects [80–82] (Table 3.5). In type 1 diabetic patients only nausea, vomiting, early satiety, and fullness after meals occurred significantly more frequently than in the nondiabetic subjects in some studies. In type 2 diabetic patients nausea, early satiety, fullness after meals, diarrhea, and constipation were significantly more frequent than in the nondiabetic subjects. The prevalence of gastrointestinal symptoms such as dysphagia, heartburn, or bloating was comparable to that seen in nondiabetic subjects. However, there were considerable differences between the studies regarding the prevalence of the individual symptoms. For example, diarrhea was observed in 35% of the type 2 patients studied in Hong Kong vs 7% of those studied in Germany [80–82].
The gallbladder may become atonic in association with autonomic neuropathy, which increases the gallbladder volume by retention of bile. It is unknown whether these changes result in symptoms. It may be that biliary stasis explains the increased risk of gallstones shown by recent epidemiological data. In a population-based study from Tivoli. Rome, the prevalence of diabetes in subjects affected by gallstone disease was significantly higher than in controls matched for sex, age, and body mass index (12% vs 5%) [83].
“Gustatory sweating” refers to sweating over the face and scalp (and sometimes upper trunk), often accompanied by a flush, that follows the ingestion of food or drink. Diabetic gustatory sweating has been reported in a clinic-based study to occur in 69% of patients with nephropathy, 36% with peripheral neuropathy, and 4% of those without either complication [84]. Diabetic gustatory sweating is believed to be triggered by the taste buds as it is not evoked by chewing inert substances, thinking of food, smelling food or by placing food or alcohol in the stomach by a gastric tube. The tongue is the most sensitive area, and even cocainization fails to inhibit gustatory sweating completely. The etiology of diabetic gustatory sweating is uncertain. The hypothesis that it results from aberrant regrowth of parasympathetic fibers leading to a connection between salivation centers and facial sweat glands seems to have been disproved by a series of case reports of immediate cessation of gustatory sweating after renal transplantation [84].
Prevalence
Male erectile dysfunction, defined as “the inability to achieve or maintain an erection sufficient for sexual intercourse” [85], is one of the most common sexual dysfunctions in men. Erectile dysfunction is more common with advancing age, and since the aged population is increasing, its prevalence will continue to rise [86]. Diabetes mellitus is the most frequent organic cause of erectile dysfunction. In the population-based Massachusetts Male Aging Study (MMAS), the age-adjusted prevalence of complete erectile dysfunction was 28% in men with treated diabetes. Minimal, moderate, and complete erectile dysfunction together had a prevalence of 64% in men with treated diabetes [87]. In a recent clinic-based survey in Italy involving 9868 men with diabetes, 45.5% of those aged over 59 years reported erectile dysfunction [88]. Table 3.6 shows that erectile dysfunction is encountered in 20-52% of type 1 and 36-54% of type 2 diabetic patients [61,87-93]. Once erectile dysfunction has developed, it is likely to persist in most patients. Risk factors and clinical correlates include duration of diabetes, glycemic control, each of the chronic diabetic complications, and smoking [88].
Incidence
The MMAS recently reported the incidence of erectile dysfunction after an average follow-up of 8.8 years in a population-based cohort of 847 men aged 40-69 years without erectile dysfunction at baseline. The crude incidence of erectile dysfunction was 26 cases per 1000 man-years (95% CI: 23-30) and increased with age, lower education, diabetes, heart disease, and hypertension. In diabetic patients the incidence of erectile dysfunction was twice as high, 51 cases per 1000 man-years. Population projections for men aged 40-69 years suggest that 617715 new cases of erectile dysfunction in the USA (white males only) are expected annually, a considerable proportion of whom will be diabetic subjects [94].
Whilst debate continues about the precise nature of the pathophysiological changes that eventually result in diabetic neuropathy, there is some agreement over the risk factors associated with its development. The risk factors and risk indicators for DSP and the relative degrees of their association with it are listed in Table 3.7.
Table 3.7 Risk factors and markers of diabetic polyneuropathy
| Type 1 diabetes | Type 2 diabetes | |
|---|---|---|
| Age | + | + |
| Sex | - | - |
| Height | + | (+) |
| Weight | - | (+) |
| Hyperglycemia | ++ | ++ |
| Hypoinsulinemia | n.a. | + |
| Duration of diabetes | ++ | ++ |
| Smoking | + | (+) |
| Alcohol | (+) | (+) |
| Hyperlipidemia | (+) | (+) |
| Hypertension | ++ | (+) |
| Nephropathy | ++ | + |
| Retinopathy | ++ | + |
| CAN | ++ | ++ |
| Macroangiopathy | (+) | (+) |
Association strong, ++; moderate, +; disputed, (+): not found. -; CAN, cardiovascular autonomic neuropathy: n.a., not applicable
