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| REVIEW ARTICLE |
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| Year : 2018 | Volume
: 5
| Issue : 2 | Page : 45-48 |
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Erectile dysfunction in type 2 diabetics: Does it need more attention?
Jayanta Chakraborty1, Semanti Chakraborty1, Rita Maitra Chakraborty2
1 Department of Endocrinology, Vivekanand Institute of Medical Sciences, Kolkata, West Bengal, India
2 Visiting Pediatrician, Vivekanand Institute of Medical Sciences, Kolkata, West Bengal, India
| Date of Web Publication | 11-Oct-2018 |
Correspondence Address:
Dr. Jayanta Chakraborty
Department of Endocrinology, Vivekananda Institute of Medical Sciences, 99, Sarat Bose Road, Kolkata - 700 026, West Bengal
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jina.jina_32_17
The obesity, metabolic syndrome, type 2 diabetes, and non-alcoholic fatty liver disease are the menace of this century. Their complications are also tantamount to peril. Erectile dysfunction which affects large number of type 2 diabetics is uncared for and requires more attention before it would cause irreversible damage. The present article will discuss the importance of more research on this subject.
Keywords: Erectile dysfunction in diabetes, prevention of erectile dysfunction in diabetes, therapy of erectile dysfunction in diabetes
How to cite this article:
Chakraborty J, Chakraborty S, Chakraborty RM. Erectile dysfunction in type 2 diabetics: Does it need more attention?. J Integr Nephrol Androl 2018;5:45-8 |
How to cite this URL:
Chakraborty J, Chakraborty S, Chakraborty RM. Erectile dysfunction in type 2 diabetics: Does it need more attention?. J Integr Nephrol Androl [serial online] 2018 [cited 2023 Oct 1];5:45-8. Available from: http://www.journal-ina.com/text.asp?2018/5/2/45/243119 |
| Introduction | |  |
Globally, an estimated 422 million adults were living with diabetes in 2014 compared to 108 million in 1980. The global prevalence of diabetes has nearly doubled since 1980, rising from 4.7% to 8.5% in the adult population. This reflects an increase in associated risk factors such as being overweight or obese. Over the past decade, diabetes prevalence has risen faster in low- and middle-income countries than in high-income countries.[1]
Worldwide epidemic of type 2 diabetes will take a toll of 552 million by 2030.[2]
Diabetes can be delayed or prevented in people who are overweight and have impaired glucose tolerance. Diet and physical activity interventions are more effective than medication.[1] It is recommended that adults aged 18–64 years should do at least 150 min of moderate-intensity aerobic physical activity (e.g., brisk walking, jogging, and gardening) spread throughout the week or at least 75 min of vigorous-intensity aerobic physical activity throughout the week or an equivalent combination of moderate- and vigorous-intensity activity.[1]
| The Relevance of this Review | | |
Some of the complications of diabetes are adequately taken care of, as its major macrovascular complications increase mortality significantly and microvascular complications increase morbidity. Although patients are more concerned about erectile dysfunction (ED) than minor effort intolerance and it may unveil occult advanced coronary artery disease,[3],[4] ED which is due to both macrovascular and microvascular involvement along with some contribution of higher neurological function derangement has not been taken proper care.
Public awareness program for ED in diabetes is still lacking when compared to CAD, retinopathy, neuropathy, nephropathy, or diabetic foot. This is utmost necessary as timely reversal or control of glycemic status is the only effective intervention of this condition, at present, which grossly lacks effective treatment once it is in advance state.
The prevalence of ED in diabetics is 35%–75% as compared to 26% in general nondiabetic population.[5]
The etiopathogenesis of ED in diabetes is multifactorial. Starting from higher neurologic functional derangement to local reflex arc somatic or autonomic neuropathy, we will now discuss one by one.
First, one should take relevant drug history which can cause ED, such as beta-blockers, spironolactone, thiazide diuretics, clonidine, methyldopa, and ketoconazole.
Second, local examination for Peyronie's disease and pelvic trauma should be done and if present referred to andrologist.
Third, physicians usually exclude endocrine disorders which could cause ED, by estimating testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, and thyroid function tests. According to the endocrine society clinical practice guidelines measurement of morning total testosterone level by a reliable assay as the initial diagnostic test of testosterone.
Moreover, confirmation of the diagnosis is done by repeating the measurement of morning total testosterone, and in some men in whom total testosterone is near the lower limit of normal or in whom sex hormone-binding globulin abnormality is suspected the same is done by measurement of free or bioavailable testosterone level.[6] About 25%–40% type 2 diabetic men (T2DM) have low testosterone concentrations in association with inappropriately low or normal LH and FSH concentrations, and diagnosis of hypogonadotropic hypogonadism (HH) can be established. About 4% of T2DM have subnormal testosterone concentrations with elevated, LH and FSH concentrations, which can be associated with primary testes dysfunctions.[7] This low testosterone level not only may have causal relation with ED but also increases cardiovascular mortality.[8]
The mechanisms involved in testosterone deficiency in diabetes include low levels of the sex hormone-binding globulin due to insulin resistance, increased aromatase activity in visceral adipose tissue leading to an augmented conversion of testosterone to estradiol,[2] leptin resistance causing reduced secretion of LH and testosterone, and increased levels of inflammatory mediators, which may suppress the secretion of gonadotropin releasing, hormone, and lLH.[7] Circulating antipituitary antibodies were first detected by Kobayashi et al. in sera from 91 patients with type 2 diabetes at a relatively high frequency (24.2%).[9]
Others suggested a possible autoimmune pathogenesis of HH in type 2 diabetic patients, as indicated by the presence of antipituitary antibodies at high titers, as compared with age-matched controls.[10]
Hence, the pathogenesis of low testosterone state has not yet been evaluated conclusively, but not only it may be responsible for ED but also it may increase insulin resistance and cardiovascular mortality.
After endocrine evaluation, usually investigations are directed to penile circulation, both artery and venous, as integrity of both the systems is necessary for proper erectile function. Normal erections require blood flow into the corpora cavernosa and corpus spongiosum. As the blood accelerates, the pressure within the intracavernosal space increases dramatically to choke off penile venous outflow. This combination of increased intracavernosal blood flow and reduced venous outflow allows a man to acquire and maintain a firm erection.[5]
To evaluate circulation, one should advise nocturnal penile tumescence testing, duplex Doppler imaging, or pudendal artery angiography. A simple test often done at specialist center is intracavernosal injection of alprostadil, and normal response is 30 min of sustained penile erection.[11]
Not only circulation compromise due to atherosclerosis of penile and pudendal arteries is the only vascular factor, derangement of endothelial function is also important determinant. Nitric oxide which is also known as endothelium-derived relaxing factor also plays a significant role. High levels of nitric oxide act as local neurotransmitters and facilitate the relaxation of intracavernosal trabeculae, thereby maximizing blood flow and penile engorgement. Loss of erection, or detumescence, occurs when nitric oxide-induced vasodilation ceases.[5] The final investigation is focused on the pelvic and sacral reflex arc, namely, somatosensory-evoked potential, sacral evoked potential, dorsal penile nerve conduction velocity, and cavernous electromyography.[11] The neural control of erection is by both somatic and autonomic nerves. Activation of sacral parasympathetic pathways elicits penile erection through the release of vasorelaxant neurotransmitters that increase blood flow to the penis and relax the penile erectile tissue. Sympathetic pathways are anti-erectile. The pudendal pathway, responsible for the contraction of the perineal striated muscles, enhances an already present erection.[12]
| Management Controversy – Inadequate and Awkward | | |
As almost 40% of type 2 diabetics above 40 years have some degree of ED, it is a common presenting symptom of type 2 diabetics of this age group. However, only one group of oral drug, namely, phosphodiesterase type 5 (PDE5) inhibitors, is effective without long-term complications, if its contraindications are taken proper care before prescribing. However, it is effective only in 50% of participants. The mechanism of action of these groups of drugs is through nitric oxide, which when liberated by endothelial cells stimulates guanylate cyclase to produce cGMP and reduce intracellular calcium level, which stimulates the relaxation of arterial smooth muscle and augments flow within the corpora. PDE5 present in corpora degrades cGMP, so PDE5 inhibitors potentiate cGMP and sustain erection.[13]
The second group of available drugs is cumbersome and needs local injection in penis such as alprostadil or papaverine. Patient acceptability to this group of drugs is poor.
The third group is intraurethral PGE1 suppository, in the form of pellets for intraurethral insertion, by a plastic applicator. Penile discomfort and pain often prevent its further use.[14]
The last group of the presently available drug is testosterone itself which is terribly and alarmingly misused. Indiscreet use of testosterone suppresses pituitary–gonadal axis and causes more depression of hormone level, not to speak of its potential side effects. Though, there are multitude of its proponents, There are some studies which have shown beneficial effect of testosterone replacement on insulin resistance, lipid profile, and HbA1C.[15] Another group has shown that men with coronary artery disease have lower levels of androgens than with men with normal coronary angiograms. The same group also depicted that low-dose transdermal testosterone therapy improves angina threshold in men with chronic stable angina.[16],[17]
We will now discuss endocrine society guidelines for testosterone therapy in men with androgen deficiency syndromes.
Testosterone therapy could be started in only young men with ED and low testosterone level after failure of standard nonhormonal treatment. Here, again controversy regarding the lowest level of testosterone where treatment should start 200 or 300 ng/dL.
After starting testosterone, urologist should be consulted if the following occurs:
An increase in serum or plasma prostate-specific antigen (PSA) concentration >1.4 ng/mL within any 12-month period of testosterone treatment. PSA velocity of more than 0.4 ng/mL/year using the PSA level after 6 months of testosterone administration as the reference. PSA velocity should be used only if there are longitudinal PSA data for more than 2 years. Detection of a prostatic abnormality on digital rectal examination.[6]
Hence, instead of all these care, testosterone therapy is effective in very meager number of patients, and vast cross-section of patients of type 2 diabetics with failure of PDE5 inhibitors, is taking resort of either indigenous remedies or antidepressants.
Hence, it is time for prevention, widespread awareness, to keep glycosylated hemoglobin in the normal range before it creeps into prediabetic range or if it has already entered the diabetic arena, to keep it under good control to avoid this complication of diabetes.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | World Health Organization. Global Report on Diabetes. Geneva; Switzerland: World Health Organization; 2016.  |
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