The general diagnostics generally to be performed by the general practitioner should include, in addition to routine laboratory parameters (small blood count, creatinine, liver values), a determination of blood lipids (cholesterol, triglycerides) and blood glucose. Since the negative influence of a disturbed lipid metabolism on the smooth enamel body musculature could be demonstrated experimentally and a correlation to vascular erectile dysfunction was also indicated , lipid electrophoresis with determination of the LDL/HDL ratio is also suggested in some cases for better detection of possible lipid metabolism disorders. In order to exclude a still subclinical diabetes mellitus, a supplementation of the fasting blood glucose value by a daily blood glucose profile or a glucose tolerance test appears to be useful.
Endocrinological diagnostics must primarily consider androgen deficiency and hyperprolactinemia. Functional disorders of the thyroid gland (hyperthyroidism, hypothyroidism) and diseases of the adrenal cortex (Cushing's disease, Addison's disease) should also be considered; reference must be made to the relevant reference books for diagnostics in the case of corresponding clinical suspicion.
In the context of the basic diagnosis of androgen deficiency, the determination of gonadotropins (FSH, LH) and testosterone by radioimmunoassay appears to be sufficient. Because of the circadian fluctuations of serum testosterone, blood should be drawn between 7 and 12 am, as testosterone levels plateau at this time . Values between 3 and 9 ng/ml are considered the normal range, and values below 3 ng/ml indicate androgen deficiency. If the testosterone level is still normal and the LH level is high, there may already be a compensated disturbance of Leydig cell function (compensated hypergonadotropic hypogonadism), which may be favorably influenced by testosterone administration. This finding is found, for example, in Climacterium virile, in which libido and potency reduction is dependent on the extent of androgen deficiency. Hypogonadotropic hypogonadism (FSH and LH low) is not testicular in origin. The location of the cause (pituitary gland, hypothalamus) and the therapeutic strategy must be determined by further endocrinologic testing, which should be performed by someone experienced in these issues.
Table 2.5. Laboratory diagnostics in erectile dysfunction.
The aim of the investigation of hyperprolactinemia must be the detection of the prolactin-secreting adenoma of the pituitary gland, which is the most common pituitary tumor. These tumors are clinically noticed primarily by loss of libido and potency. If visual field loss and headache are already present, a macroprolactinoma destroying the sella must be assumed, which may require neurosurgical therapy. Patients with macroprolactinomas were usually older and had tolerated sexual dysfunction for a significantly longer period of time . However, hyperprolactinemia can be triggered by several drugs (see Section 1.4). The mechanism by which erectile function is affected by prolactin is still unclear. A summary of laboratory diagnostics in erectile dysfunction is given in Table 2.5.
Laboratory diagnostics for erectile dysfunction include general diagnostics and the determination of sex hormones. General diagnostics are used to detect vascular risk factors and associated underlying diseases. Hormone status primarily considers testosterone deficiency and hyperprolactinemia.