Erectile Dysfunction in Diabetes

Erectile Dysfunction in Diabetes

Short Summary

50-year-old male complaining of gradual appearance of erectile dysfunction up to absolute impossibility of even just a single erectile event. His medical history is significant for Type II Diabetes Mellitus and prostatitis. He started taking Cialis, Levitra, and then Viagra without obtaining any benefit. He underwent EMG of the inferior limbs and hematochemical examinations, that revieled signs of diabetic polyneuropathy, and possible superimposed lumbosacral radiculopathy. The possibility to give intracavernous penile injections has been proposed.

Patient’s Questions

1)            Which is the most probable diagnosis for this Erectile Dysfunction? It is possible that Suguan could contribute to this Erectile Dysfunction?
2)            What therapy do you suggest for a persistent resolution of the Erectile Dysfunction?
3)            Prognosis?
4)            Centers of excellence in Italy?

Medical Background

male, 50 years old
Diagnosis : ERECTILE DYSFUNCTION IN DIABETES
Anamnesis:
Patient suffering from Type 2 Diabetes Mellitus for approximately 10 years, currently under pharmacological therapy with hypoglycemizing oral drug (Suguan at a dosage of 1 tablet before dinner) and with self-controls reported to be stable. Prostatitis in October, 2007.
Case history:
For just over 1 year gradual appearance of erectile dysfunction up to the current absolute impossibility of even just a single erectile event.
Due to the persistence of the Erectile Dysfunction condition the patient underwent a specialist’s examination on 07/2008. In this occasion he shows:
–       hormonal screening with results within norm limits (see enclosure on 07/2008);

–       Basal and Dynamic Penile Ecodoppler on 06/2008 is reported: “neither coarse focal lesions nor images referred to IPP plaques are apparently evident. (Induratio Penis Plastica) No signs of fibrosis of the cavernous bodies. Intracavernous injection (ICI) with 10 mcg of PGE1 was performed, obtaining a rigidity of approximately 80%; therefore, the arterial sampling with colour-doppler at the level of the cavernous arteries at 5, 10, 15, 20 and 30 minutes was carried out with systolic peaks velocity apparently within norm limits (max 45 cm/s); the diastolic values are within norm limits during the entire length of the examination (with R.I. 1.00).

–       At the Power Doppler a regular ramification of the helicine arteries is appreciated, therefore, a re-dosing of PGE1 is not carried out.
Conclusions: meaningful signs of artery deficiency in the cavernous area are not apparently visible, while there is no evidence of signs of accelerated venous drainage (cavernous-venous incompetence).”
–       physical examination external genitalia: hyperemic and slightly edematous external urethral meatus.

–       At rectal exploration: prostate like an apricot, parenchymatous, no longer with inflammation signs.
Therefore, the specialist recommended the administration of Cialis 10 mg at a dosage of 1 tablet when needed subject to ECG and cardiological visit. After the cardiological tests were performed, without any evidence of cardiological pathology such as to contraindicate the advised therapy, the patient started taking the prescribed drug without obtaining any benefit. During the last year the medicine dosage was increased, so the drug administered passed from Levitra and, then, to Viagra. At present the patient is taking Viagra 100 mg without ever obtaining any useful result. In the light of such results the possibility to give intracavernous penile injections has been proposed.
On completion of the clinical picture description, besides the enclosures of the latest hematochemical examinations on 08/2008, on 09/2008 and on 12/2008, also the EMG medical report (Electromyography) of the inferior limbs, that the patient underwent on 01/2009 suspecting a diabetic polyneuropathy, is reported: “the examination has revealed signs compatible with a picture of marked distal chronic sensitive-motor polyneuropathy with electrophysiological aspects indicative of a mixed pathology, mainly axonal. Absence of evident electro-miographical signs revealing a possible superimposed lumbosacral radiculopathy.”

Expert’s Opinion

The patient describes rapidly progressing erectile dysfunction over a period of 1 year. His erection hardness is not clearly reported. Clinically, erection rigidity is scored according to the “Erection Hardness Score”(Mulhall JP et al. J Sex Med,2007, 4:1626‐34), with 1 – penis is larger but not hard, 2 – penis is hard but not hard enough for penetration, 3 – penis is hard enough for penetration but not completely hard, and 4 – penis is completely hard and fully rigid. Alternatively, erections are scored on a 0 to 10 scale, with 0 – no enlargement or rigidity, 6– partial rigidity just enough to perform penetration and 10 – full rigidity. It is not clearly described whether a year before the onset of the erectile dysfunction the patient was able to achieve full rigidity and now he cannot achieve any response, or was there slight decline even previously. The rate of erections rigidity decline is important to learn about the cause of this erectile dysfunction and to provide prognosis regarding the progression rate. There is also no mentioning if the erectile dysfunction is only with sexual intercourse or also with an attempt for self‐stimulation.

The patient had also blood tests; the relevant test for sexual function is testosterone level, which was normal, 6.04 ng/mL.
The patient  also had a penile duplex Doppler ultrasound. This test is a dynamic test and can be fully interpreted only by the examiner. The quality of the test depends on the rigidity achieved, the study technique and the examiner experience. The reported rigidity is 80%, which is adequate for the test. I can base my opinion only on 4 poor quality images and the written report. There is one longitudinal B‐mode penile image, based on which I cannot make any diagnosis. There are 3 transverse sections with color Doppler and wave Doppler and blood flow measurements. Measurement of penile blood flow by Doppler ultrasound is done in longitudinal sections (Golijanin D et al. Int J Impot Res, 2007, 19:37‐42 or Aversa A et al. J Sex Med 2007, 4:1437‐47). It is unclear to me why the measurement was done in this particular way and if the results are affected. Based on my experience I can estimate that if the results are affected, the penile blood flow would be underestimated. As the measured flow is within normal range, even if they are underestimated – we can conclude that the patient had normal penile arterial blood flow, in his arteries on both sides of his penis, during the test. Based on the images, there is not demonstration of veno‐occlusive dysfunction (dysfunction of the veins,which occlude the blood drainage from the penis). The written report is compatible with the images, describing a normal test.
Physical exam was reported as normal, besides hyperemia (redness) and slight edema at the urethral meatus, which should be considered not clinically worrisome.
The next step was treatment with commercially available PDE5 inhibitors, starting with a low dose treatment after cardiology clearance. There is no need for cardiology clearance if the patient is able to perform an effort of 3‐4Mets in a stress test (or walking up 2 flights of stairs) and not taking nitrates (nitroglycerine containing medications). There is no clear advantage to switch from one drug to another. There is a benefit in dose adjustment (maximal dose is recommended), avoiding food with Viagra and Levitra, waiting enough time for absorption (1 hour with Viagra and Levitra, 2 hours with Cialis) and I must emphasize the need for sexual stimulation for the medication to show its effect. Once Viagra 100mg failed to help achieving satisfying erections (if taken on empty stomach, allowing time for absorption and with sexual stimulation), the next reasonable therapeutic step is penile injection therapy.
 
The next step in the evaluation was EMG which was interpreted as showing marked distal chronic sensorymotor neuropathy and possible superimposed lumbosacral radiculopathy. These finding are consistent with nerve damage from Diabetes Mellitus. Patient who has extensive sensory‐motor neuropathy are at risk for loss of penile sensation, which may compromised an attempt to respond to tactile stimuli (touching the penis) and they are very likely to have autonomic nerve damage which may include damage to the erection nerves. I would suggest considering to have biothesiometry, a simple test to assess the penile sensation,as a baseline, to learn the exact extent of the neurologic deficit. The lack of response to Viagra,
Levitra and Cialis, together with normal vascular assessment by Doppler, is very consistent with the described peripheral nerve damage.
To Mr. patient’s questions:
  1. Based on the described findings the most probable diagnosis is erectile dysfunction due to nerve damage. This nerve damage may affect the motor nerves, the sensation nerve and autonomic nerves that mediate the erection process. Diabetic patients are at risk for these types of nerve damage, but they are also at risk for arterial inflow impairment and venous mechanism dysfunction; however, the findings are not supportive of vascular (blood vessels) pathology.
  2. Suguan could not contribute significantly to the development of erectile dysfunction. On the contrary, good control of the blood glucose levels is essential for minimizing progression of diabetic damage to target organs, including nerves. I would suggest a blood test for HbA1C, to trace diabetic control, and Diabetes specialist consult and close monitoring.
  3. Any additional reversible cause of neuropathy should be sought, including vitamin deficiency, cancer, toxins, renal failure, amyloidosis and many other causes of neuropathy. A neurologist will be able to conduct this evaluation.
  4. Given the diagnosis of possible superimposed lumbosacral radiculopathy, an orthopedic consult is warranted, to assess for possible contributing role of spinal nerve root compression. I would believe that this contribution to the clinical picture is not significant.
  5. There is no known treatment to reverse diabetic neuropathy (nerve damage) and to cure the erectile dysfunction. Good diabetic control is essential to slow further progression.
  6. Diabetic men with isolated nerve damage with good vascular function are very good candidates for penile injection therapy. The chances are that the patient will respond beautifully to a low‐dose penile injection therapy. A sex‐therapist will be able to assist him and his partner, if available, to integrate this treatment to his sexual life, if needed. This treatment has been available for over 25 years and is the treatment of choice for the patient for erectile dysfunction.
  7. Prognosis: The damage that has occurred unfortunately cannot be reversed, if the only cause is Diabetes. Hence the importance of neurology consults to search for reversible causes of neuropathy and the importance of good diabetic control to prevent further damage. Unsatisfactory diabetic control may potentially lead to future blood vessels damage, with diminishing response to penile injection therapy. If this point is reached, a penile implant surgery should be considered.
  8. Centers of excellence in Italy: Professor Francesco Montorsi, Universita Vita Salute San Raffaele, Milan, is one of the leading names in Sexual Medicine in Europe and worldwide.