Endocrine disorders
Endocrine disorders may cause ED and, in some cases, may be one of the few etiologies whose resolution might lead to a ‘cure’. Consequently, such disorders should be routinely sought out in the assessment of men with ED. However, as ED is multifactorial in origin, an endocrine disorder might be only a contributory factor to the problem. Endocrine disorders commonly seen in ED patients include diabetes, thyroid disease, androgen deficiency, and hyperprolactinemia.
Diabetes: Diabetes is the most common endocrine abnormality associated as a risk factor for ED. The prevalence of ED is almost three times higher in diabetic men (28%) than in the nondiabetic population (9.6%). Diabetes is associated w i t h dyslipidemia, neuropathy and smooth muscle dysfunction, all of which are associated with ED. Although there is little evidence that improving glycemic control in diabetics improves their erectile function, there is some evidence that high glycosylated hemoglobin (HbAIC) levels impair smooth muscle function. Thus, there are theoretical grounds for believing that improved diabetic control is advantageous in ED, although this alone will not normally restore erections. Diabetics are a difficult group to treat for ED, as their response rate to drug therapies, such as sildenafil, is lower than in most other groups. Diabetic men also commonly have reduced androgen levels.
Thyroid disease: There is an association between hyper thyroidism and ED. This may be due to a hyperthyroidismrelated increase in sex hormone-binding globulin (SHBG) levels and increased aromatization of testosterone to estrogen. Restoring the euthyroid state may resolve the ED. Androgen deficiency: Androgen deficiency in the adult male becomes more common with increasing age, but its management remains controversial. As well as sexual dysfunction, androgen deficiency is associated with osteoporosis, dyslipidemia, metabolic syndrome and depression. Far from being a benign consequence of aging, it is a significant cause of increased cardiovascular risk. Androgens act at several sites in the sexual response system: within the CNS, peripheral nitrergic nerves, and corpora cavernosa. Androgen deficiency may affect sexual interest, erections, and responsiveness to PDE5 inhibitors.
Identification of androgen deficiency is based upon the identification of its non-specific clinical features and blood testing. Choice of assay is between total, free (unbound to plasma proteins), and bioavailable testosterone (unbound to SHBG). Free testosterone is probably the most reliable assay, as it is not affected by changes in SHBG levels. However, the most reliable direct measure, equilibrium dialysis, is only available in research laboratories; commercial radioimmunoassay are frequently unreliable. Calculated free testosterone is probably the best available surrogate. It can be derived from total testosterone, SHBG and albumin levels; an ou’line calculator can be found at www.issam.ch.
As there is a diurnal variation in testosterone release, samples for testosterone assay should be drawn in the morning, between 08.00 and 11.00. The assay should be repeated after 2 or 3 wrecks, as testosterone is released in a pulsatile manner, as well as with diurnal variation, and the result of a single assay may be misleading.
Men with symptoms of androgen deficiency should be assessed and androgen replacement given on its merits. A screening questionnaire for androgendeficiency symptoms has been published, although it is of low specificity.
There is no evidence that giving testosterone to men with ED and normal androgen levels restores or improves their erectile function. Testosterone should be prescribed under specialist
supervision for men with established hypogonadism. Prior assessment and safety monitoring should be performed accor’ ding to contemporary authoritative guidelines.
Hyperprolactinemia: Hyperprolactinemia is associated with ED, loss of sexual interest and anorgasmia. It is frequently accompanied by androgen deficiency, as high prolactin levels suppress LH production and, consequently, cause hypogonadism.
Hyperprolactinemia should be excluded by blood testing in all men with reduced sexual interest. Moderate elevation of prolactin levels is unlikely to cause ED. Hyperprolactinemia is often due to stress and drugs (notably metoclopramide, chlorpromazine, and several other antipsy’ chotics). Only about one in ten of these men will be found to have a prolactiu’Secreting pituitary tumor, but these must not be missed. Hyperprolactinemia is common in men on dialysis for chronic renal failure. Unless an obvious cause is found and the prolactin levels return to normal, referral to an endocrinologist is advisable.
Tags: Adult Male, Aromatization, Contributory Factor, Diabetic Control, Diabetic Men, Drug Therapies, Dyslipidemia, Ed Patients, Endocrine Disorder, Endocrine Disorders, Glycosylated Hemoglobin, Hyper Thyroidism, Metabolic Syndrome, Neuropathy, Response Rate, Risk Factor, Sex Hormone Binding Globulin, Smooth Muscle Function, Theoretical Grounds, Thyroid Disease