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Male Hypogonadism: Quick Reference for Residents

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Male Hypogonadism: Quick Reference for Residents Male hypogonadism: Quick Reference for Residents Soe Naing, MD, MRCP(UK), FACE Endocrinologist Associate Clinical Professor of Medicine Director of Division of Endocrinology Medical Director of Community Diabetes Care Center UCSF-Fresno Medical Education Program Version: SN/8-21-2017 Male hypogonadism From Harrison's Principles of Internal Medicine, 19e and Up-To-Date accessed on 8-21-2017 Testosterone is FDA-approved as replacement therapy only for men who have low testosterone levels due to disorders of the testicles, pituitary gland, or brain that cause hypogonadism. Examples of these disorders include primary hypogonadism because of genetic problems, or damage from chemotherapy or infection (mump orchitis). However, FDA has become aware that testosterone is being used extensively in attempts to relieve symptoms in men who have low testosterone for no apparent reason other than aging. Some studies reported an increased risk of heart attack, stroke, or death associated with testosterone treatment, while others did not. FDA cautions that prescription testosterone products are approved only for men who have low testosterone levels caused by a medical condition. http://www.fda.gov/Drugs/DrugSafety/ucm436259.htm 2 Hypothalamic-pituitary-testicular axis Schematic representation of the hypothalamic-pituitary- testicular axis. GnRH from the hypothalamus stimulates the gonadotroph cells of the pituitary to secrete LH and FSH. LH stimulates the Leydig cells of the testes to secrete testosterone. The high concentration of testosterone within the testes is essential for spermatogenesis within the seminiferous tubules. FSH stimulates the Sertoli cells within the seminiferous tubules to make inhibin B, which also stimulates spermatogenesis. Testosterone inhibits GnRH secretion, and inhibin B inhibits FSH secretion. GnRH: gonadotropin-releasing hormone; FSH: follicle-stimulating hormone; LH: luteinizing hormone. 3 Causes of male hypogonadism. From Current Medical Diagnosis & Treatment 2016 > Endocrine Disorders Hypogonadotropic (Low or Normal LH) Hypergonadotropic (High LH) Aging Aging Alcohol Antitumor chemotherapy Chronic illness Bilateral anorchia Congenital syndromes Idiopathic Constitutional delay Klinefelter syndrome Cushing syndrome Leprosy Drugs Lymphoma Estrogen Male climacteric GnRH agonist (leuprolide) Mumps Myotonic dystrophy Ketoconazole Noonan syndrome Marijuana Orchitis Prior androgens Radiation therapy Spironolactone Sertoli cell-only syndrome Hemochromatosis Testicular trauma Hypopituitarism Tuberculosis Hypothyroidism Uremia Idiopathic Kallmann syndrome 17-Ketosteroid reductase deficiency Major medical or surgical illnesses Malnourishment Obesity (BMI > 30) Prader-Willi syndrome BMI, body mass index; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone. Clinical features and diagnosis of male hypogonadism Hypogonadism in a male refers to a decrease in one or both of the two major functions of the testes: sperm production or testosterone production. These abnormalities can result from disease of the testes (primary hypogonadism) or disease of the hypothalamus or pituitary (secondary hypogonadism). The distinction between these disorders, which will be described below, is made by measurement of the serum concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH): ● The patient has primary hypogonadism if the serum testosterone concentration and/or the sperm count are below normal and the serum LH and/or FSH concentrations are above normal. ● The patient has secondary hypogonadism if the serum testosterone concentration and/or the sperm count are below normal and the serum LH and/or FSH concentrations are normal or low. 4 In primary hypogonadism, spermatogenesis tends to be impaired to a greater degree than Leydig cell function, at least in its early stages. In contrast, both functions are impaired to the same degree with secondary hypogonadism. Spermatogenesis cannot be increased in men with primary hypogonadism because of damage to the seminiferous tubules. However, successful pregnancies have now been reported with men with primary hypogonadism, including men with Klinefelter syndrome, using sperm extracted from the testes with subsequent in vitro fertilization by intracytoplasmic sperm injection. In contrast, men with secondary hypogonadism can often have spermatogenesis restored with gonadotropin therapy or pulsatile gonadotropin-releasing hormone (GnRH) therapy (if pituitary function is normal and the patient has access to a center that provides this therapy). CLINICAL FEATURES — The clinical features of male hypogonadism depend upon the age of onset, severity of testosterone deficiency, and whether there is a decrease in one or both of the two major functions of the testes: sperm production and testosterone production. There are several possible clinical manifestations of testosterone deficiency, which are determined by its time of onset during reproductive development. There are two main clinical manifestations of impaired spermatogenesis: infertility and decreased testicular size. Signs and symptoms of adult male hypogonadism Prepubertal onset Postpubertal onset Primary Secondary Primary Secondary Symptoms Low energy + + + + Low libido + + + + Physical findings Small testes + + + ± Small phallus + + – – Decreased body/facial hair + + ± ± Decreased muscle mass + + ± ± Eunuchoid proportions + + – – Gynecomastia + ± + – Symptoms and physical findings in adults who have untreated hypogonadism grouped by whether the hypogonadism is of prepubertal or postpubertal onset and whether it is primary or secondary. 5 DIAGNOSIS — The diagnosis is based upon the presence of signs and symptoms of male hypogonadism and unequivocally low serum total testosterone concentrations between 8 and 10 AM on at least two occasions. Candidates for testing — Population screening for male hypogonadism has not been shown to be cost- effective and is not recommended. Instead, we suggest case detection by measuring serum testosterone in situations in which the prevalence of hypogonadism is high, as suggested by the Endocrine Society guidelines. ● Diseases of the sellar region ● Medications that affect testosterone production, such as high-dose glucocorticoids for a prolonged period and sustained-release opioids ● Human immunodeficiency virus (HIV)-associated weight loss ● End-stage renal disease and maintenance hemodialysis ● Moderate-to-severe chronic obstructive lung disease ● Infertility ● Osteoporosis or low-trauma fracture, especially in a young man ● Type 2 diabetes mellitus Men with acute or subacute illness should not be assessed for hypogonadism, as they will have a transient functional secondary hypogonadism. 6 Initial evaluation — The evaluation and diagnosis of male hypogonadism are usually straightforward. The clinician obtains clues to the possible presence of hypogonadism from the history and physical examination and confirms the diagnosis by appropriate laboratory testing. Initial laboratory testing is based upon measuring the products of the testes (testosterone and sperm) and the pituitary hormones that control their production (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]). Testosterone is produced by the Leydig cells of the testes under stimulation of LH. Sperm are produced in the seminiferous tubules under stimulation principally by the high concentration of testosterone in the testes but also by FSH. Testosterone, in turn, inhibits both LH and FSH secretion, the latter via conversion to estradiol. FSH is also inhibited by inhibin, a product of the Sertoli cells of the seminiferous tubules. Evaluation of the male with possible hypogonadism (From Up-To-Date accessed on 2-12-2016) T: testosterone; LH: luteinizing hormone; FSH: follicle-stimulating hormone; PRL: prolactin; T4: thyroxine; Fe: iron; MRI: magnetic resonance imaging. * This algorithm applies to the evaluation of outpatients. Men with acute or subacute illness should not be assessed for hypogonadism, as they will have a transient functional secondary hypogonadism. ¶ Iron and transferrin are measured to assess the possibility that hemochromatosis is the cause of secondary hypogonadism. When an MRI should be performed depends upon several factors. One is the patient's serum T relative to his age. A male <40 years with a serum T <250 ng/dL warrants an MRI but in a male >60 years, a value of <150 ng/dL would be necessary to warrant it. An MRI should also be performed if other pituitary hormones are abnormal, eg, if serum prolactin is elevated or if serum T4 and/or early morning cortisol are below normal. 7 Evaluation of hypogonadism. (From Harrison's Principles of Internal Medicine, 19e > Disorders of the Testes and Male Reproductive System) GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; T, testosterone. SUMMARY AND RECOMMENDATIONS FOR DIAGNOSIS: ● Hypogonadism in a male refers to a decrease in either or both of the two major functions of the testes: sperm production and testosterone production. These abnormalities may result from disease of the testes (primary hypogonadism) or disease of the pituitary or hypothalamus (secondary hypogonadism). ● Failure to undergo or complete puberty indicates deficient testosterone secretion. ● Symptoms that could indicate hypogonadism in an adult male are decreases in energy, libido, muscle mass, and body hair, as well as hot flashes, gynecomastia, and infertility. ● Population screening for male hypogonadism has not been shown to be cost-effective and is
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