“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
The central role of hyperglycemia has been demonstrated in a range of studies. Mean HbA1c was approximately 1% higher in men with newly diagnosed type 2 diabetes who went on to develop DSP 10 years later, than in those who did not[33]. The risk of developing DSP (as measured by the odds ratio) has been calculated to rise by approximately 10-15% for every I mmol/l rise in fasting plasma glucose or every 1% rise in HbA1c[6,17]. The importance of hyperglycemia has of course been confirmed in interventional studies. The DCCT demonstrated that intensive glycemic control led to a 64%reduction in the five-year risk of developing DSP [2] in patients with type 1 diabetes. In the similar but smaller Stockholm Diabetes Intervention Study, symptoms of DSP developed in only 14% of those who were intensively treated, compared to 32% in the conventional treatment arm [95]. The effect of glucose lowering in type 2 diabetes is less clear. In the large UKPDS study, strict glycemic control had no significant impact on the development of DSP over the first 12 years [46]. Among the relatively small number of subjects who were followed to 15 years, a significant risk reduction was apparent, but only in those in the main study. Amongst the overweight subjects, whose intensive therapy was primarily with metformin, there was no impact of intensive therapy at all on DSP [96].
In the Rochester Diabetic Neuropathy Study, mean HbA1, severity of diabetic retinopathy, and a term calculated mean In (24-hour proteinuria multiplied by duration of diabetes) were the main covariates for severity of DSP at the 7-year follow-up [97].
Thus, the etiological link between hyperglycemia and DSP seems sound, but while it is clear that glucose lowering protects against the development of neuropathy in type 1 diabetes, the case is not yet proven in type 2 diabetes.
DSP, like the other specific diabetic complications,