Therefore, repeated measurements are necessary to confirm a low testosterone level and a diagnosis of hypogonadism should never be based on a single testosterone level. There is marked variability in testosterone levels not only between individuals but also within an individual. Food intake can reduce total testosterone acutely by as much as 25%, explaining the importance of a fasting blood sample. As testosterone release is diurnal, with the highest levels in the early morning, blood samples should be taken close to 8 am. Patients should be well or medically stable, without acute decompensation of any underlying comorbidity. The initial diagnostic test in suspected androgen deficiency is measurement of fasting morning total testosterone in men with consistent symptoms and signs. Total testosterone is the mainstay of biochemical diagnosis of androgen deficiency.
#Marked decrease of the male hormone testosterone free#
Bioavailable testosterone refers to albumin-bound and free testosterone. Of the total circulating testosterone, 60% is tightly bound to SHBG, 38% is loosely bound to albumin and only 2% is free. *Alcohol excess typically causes mixed (combined primary and secondary) hypogonadism. Mutations in androgen biosynthesis enzymesĬOPD, chronic obstructive pulmonary disease CTX, chemotherapy ESRF, end stage renal disease RTX, radiotherapy HH, hypogonadotropic hypogonadism T2DM, type 2 diabetes mellitus
Causes of androgen deficiency 8 Partial/transientĪndrogen deprivation therapy (GnRH agonists) Signs and symptoms include incomplete or delayed sexual development (if hypogonadism occurs before or during puberty), reduced libido, decreased spontaneous erections, breast discomfort, loss of body hair, reduced shaving, very small (especially 4 ng/ml without urological evaluation is a contraindication to testosterone treatment. Clinical assessment should be focused on eliciting symptoms and signs of androgen deficiency and on identifying clues to the underlying aetiology ( Table 1 8). Given that hypogonadism is primarily a clinical diagnosis supported by consistent biochemical findings, a thorough history and examination are essential. 1 In practice this diagnosis is often difficult, especially in older obese men with chronic disease, as symptoms and signs are often non-specific and because there is no evidence-based, universally agreed pathological testosterone cut-off level. The diagnosis of androgen deficiency should be made only in men with consistent symptoms and signs, and unequivocally and repeatedly low serum testosterone levels. 6 Indeed, a normal testosterone level can be considered to be a sensitive biomarker of good health. 5 However, the age-dependent decrease in testosterone levels is accelerated by accumulation of comorbidities, especially obesity. Most older men have testosterone levels within the reference range and there is recent evidence from Australia that healthy ageing alone may not be associated with marked decreases in testosterone levels. As levels of sex hormone binding globulin (SHBG) rise with age by 1–2% per year, the decline in free testosterone level is greater and is 2–3% per year. In contrast to women who experience a sudden drop in oestradiol levels around the time that menses ceases, the age-related drop in testosterone in men is more gradual at 0.5–2.0% per year from early adulthood onwards.
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