Erectile dysfunction (ED) is defined as the inability to obtain or maintain an erection for satisfactory sexual activity and penetration.1 There are many causes (see box), but diabetes mellitus and vascular disease account for the majority of cases.
The likelihood of complete ED is higher in men with heart disease (39 per cent), diabetes (28 per cent) and hypertension (15 per cent) compared with the general population (9.6 per cent).2 With the increasing prevalence of type-2 diabetes, it is likely that this will soon become the major cause of ED.
Initial assessment should include a short history aimed at determining aetiology, bearing in mind that psychological and organic causes often coexist. Gradual onset of ED in all situations, stimulated and involuntary, in the presence of risk factors and normal libido suggests diabetes-related ED.
Sudden-onset ED, either situational or global is suggestive of a psychological cause. Loss of libido should alert clinicians to possible hypogonadism.
Physical examination should include BP and examination of the genitalia. Testes should be examined for size, symmetry and presence of nodules; gynaecomastia should be excluded and secondary sexual characteristics noted.
As a routine, thyroid function, serum testosterone and sex hormone binding globulin (SHBG) are measured, although therapy is typically started before the results are available (see box).
ED in diabetes
The reported prevalence of ED in diabetes is 20-36 per cent.3 People with type-1 diabetes develop ED at a younger age.
Almost half of type-1 patients develop ED by their early forties,4 while studies estimate that 43 per cent of type-2 patients over the age of 53 are likely to have ED.5 Research has shown an increased prevalence of ED associated with longer duration of type-2 diabetes.6
Men with a history of cardiovascular disease (CVD), diabetes or hypertension are four times more likely to have complete ED.2 Many risk factors for CVD are also risk factors for ED. Therefore ED itself is regarded as a risk factor for CVD and may be seen as a marker for occult coronary artery pathology.
The relative risk of MI is increased by sexual intercourse but the absolute risk for an individual is small.
For example, in a patient with a cardiac history, the risk of MI in any hour is 10 in a million, this increases only to 29 in a million in the two hours following sex.
The energy required for sex is said to be equivalent to walking one mile in less than 20 minutes; if patients can cope with this level of exercise, they should be able to take advantage of any treatment success.
Patients who do not have angina and have fewer than three CVD risk factors (excluding age and sex) can be safely treated without further investigation.6
Options for treatment
Weight reduction, exercise and smoking cessation, should be advised for all patients. First-line treatment is with one of the three oral phosphodiesterase-5 (PDE5) inhibitors - sildenafil, tadalafil, or vardenafil.
As most diabetic patients end up on the maximum dosage, it is reasonable to start at this level: sildenafil 100mg, tadalafil 20mg and vardenafil 20mg.
Each agent should be given up to an hour before sexual activity and only one dose should be taken in a 24-hour period. The pharmacokinetics of sildenafil and vardenafil are similar, while tadalafil has a longer half-life (see box). Their efficacy in patients with diabetes is 50-60 per cent and they should be taken on at least eight occasions before being deemed unsuccessful.
PDE5 inhibitors are contraindicated in patients taking nitrous oxide donors, such as nicorandil, where profound hypotension may occur.
Patients on long-acting preparations of nitrates should stop nitrate therapy for at least a week before taking a PDE5 inhibitor.
Adverse effects with PDE5 inhibitors tend to be mild and transient, and include headache and flushing.
Rhinitis can occur in patients taking sildenafil and vardenafil but has not been reported with tadalafil. But myalgia and back pain have been reported in patients taking tadalafil.
Tadalafil and vardenafil are highly specific for PDE5; sildenafil is less so, leading to inhibition of other PDE enzymes. It is the inhibition of PDE6, found in the retina, which results in the visual side-effects reported with sildenafil. These are transient and resolve spontaneously.
There has been concern about a possible link between PDE5 inhibition and non-arteritic anterior ischaemic optic neuropathy (NAION).
The current view is that there is no convincing evidence that NAION occurs more frequently in men taking a PDE5 inhibitor.
It is recommended that any patient with a history of monocular NAION be cautioned that PDE5 inhibitors may increase the risk of NAION in the other eye.
Any man taking PDE5 inhibitor who develops visual problems should stop taking the drug and see an ophthalmologist.
Second-line therapy includes alprostadil, or use of a vacuum device. Alprostadil may be administered as an intracavernosal injection or intraurethral pellet. Success rates in patients who have not responded to a PDE5 inhibitor are 80 and 50 per cent, respectively.7
Intracavernosal injection is the preferred mode of alprostadil administration. Injections can only be used once a week, and patients should be advised about potential side-effects, such as priapism. Penile pain occurs in about one fifth of patients.
Vacuum devices have success rates of about 90 per cent in those not responding to oral therapies. Some men prefer them because they may be used more than once a week; others do not consider an erection with a vacuum device to be 'natural'.
The devices are unsuitable for patients with limited manual dexterity.
Dr Rahim is consultant physician at the Heart of England NHS Trust and Professor Bain is professor of medicine (diabetes) at Singleton Hospital, Swansea NHS Trust and the University of Wales
14 February is National Impotence Day. For more information see www.impotence.org.uk
|Causes of ED|
|Testosterone and SHBG|
|Pharmacokinetics of PDE5 inhibitors|
|Tmax||60 min||45 min||120 min|
|T 1/2||3-4 hour||5 hour||17.5 hour|
|Fatty food (>55% fat)||Reduced||Reduced||No effect|
1. NIH Consensus Conference. Impotence. NIH Consensus Development Panel on Impotence. JAMA 1993; 270: 83-90.
2. Feldman H, Goldstein I, Hatzichristou D et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol 1994; 151: 54-61.
3. Klein R, Klein B, Lee K et al. Prevalence of self-reported erectile dysfunction in people with long-term IDDM. Diabetes Care 1996; 19: 135-41.
4. Fedele D, Bortolotti A, Coscelli C et al. Erectile dysfunction in type 1 and type 2 diabetics in Italy. Int J Epidemiol 2000; 29: 524-31.
5. Bacon C, Hu F, Giovannucci E et al. Association of type and duration of diabetes with erectile dysfunction in a large cohort of men. Diabetes Care 2002; 25: 1,458-63.
6. Jackson G, Betteridge J, Dean J et al. A systematic approach to erectile dysfunction in the cardiovascular patient: a Consensus Statement - update 2002. Int J Clin Pract 2002; 56: 663-71.
7. Mancini M, Raina R, Agarwal A et al. Sildenafil citrate vs intracavernous alprostadil for patients with arteriogenic erectile dysfunction. Int J Impot Res 2004; 16: 8-12.