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Authors Wessells H, Penson DF, Cleary P, et al.

Review Date Jul 2011

Citation Journal of Urology 2011;185:1828-1834

 

Background

Men with diabetes develop erectile dysfunction (ED) 10 to 15 years earlier than men in the general population. Other studies have demonstrated associations between glycemic control and ED in men with diabetes. This study could take this finding further by seeing if a reduction in glycemia can reduce the risk of ED.

 

Aim

To determine whether intensive glycemic therapy reduces the risk of erectile dysfunction in men with type 1 diabetes enrolled in the Diabetes Control and Complications Trial.

 

Methods

The Diabetes Control and Complications Trial (DCCT) randomised 761 men with type 1 diabetes to intensive or conventional glycemic therapy at 28 sites between 1983 and 1989, of whom 366 had diabetes for 1 to 5 years and no microvascular complications (primary prevention cohort), and 395 had diabetes for 1 to 15 years with non-proliferative retinopathy or microalbuminuria (secondary intervention cohort). Subjects were treated until 1993, and subsequently followed in the Epidemiology of Diabetes Interventions and Complications (EDIC) study. In 2003 the authors conducted an ancillary study using a validated assessment of erectile dysfunction (the IIEF) in 571 men (80% of the EDIC cohort): 291 from the primary prevention cohort and 280 from the secondary prevention cohort of the DCCT. ED was defined using a single question from the IIEF to encompass both sexually active and sexually inactive men.

 

Results

Of the participants in the ED study, 23% reported erectile dysfunction. The prevalence was significantly lower in the intensive therapy vs conventional treatment group (from DCCT) in the secondary intervention cohort (12.8% vs 30.8%, p = 0.001) but not in the primary prevention cohort (17% vs 20.3%, p = 0.49).

The risk of erectile dysfunction in both primary prevention and secondary intervention cohorts was directly associated with mean HbA1c measured during the DCCT, and during the combined period of the DCCT and EDIC. Age, peripheral neuropathy and lower urinary tract symptoms were other risk factors for ED from multivariable analyses.

 

Conclusion

A period of intensive therapy significantly reduced the prevalence of erectile dysfunction measured 10 years later among those men in the secondary intervention cohort but not in the primary prevention cohort. Higher HbA1c was significantly associated with risk of ED in both cohorts. These findings provide further support for early implementation of intensive insulin therapy in young men with type 1 diabetes.

 

Points to Note
  1. This study provides evidence that tight glycaemic control in Type 1 diabetes can reduce the risk of ED in the longer term, particularly in men with microvascular complications.
  2. Some limitations of the study include: 25% of the original DCCT cohort was not included in the ED study; a single item of the IIEF was used to define ED perhaps introducing imprecision in the measure; ED was assessed only at a single point in time (up to 20 years following enrolment into the DCCT).
  3. The lack of effect of intensive therapy on the later prevalence of ED in the primary prevention cohort is hard to explain but the authors propose that it might be due to the fact that this cohort had shorter duration of diabetes, lower baseline HbA1C, younger age and a lower prevalence of ED. However, adjusting for these factors in a multivariable model failed to explain the difference.
  4. It is thought that advanced glycation end products, a product of long-term hyperglycaemia, may be involved in many diabetic complications and this might explain some of the cohort differences.
  5. The association of the prevalence of ED with mean HbA1C levels over the duration of follow up, in both cohorts, confirms findings from other studies showing increased risk of ED associated with poor glycaemic control in men with type 1 diabetes. 

 

Website: www.ncbi.nlm.nih.gov/pubmed/21420129