In men responsible for osteoporosis, muscle atrophy, weight gain and cognition changes.
Male hypogonadism refers to the inability of the testes to produce testosterone, sperm or both.
Can affect men of any age, from fetal development through adulthood.
Adult onset hypogonadism is a clinical and biochemical syndrome characterized by a deficiency of testosterone symptoms and signs secondary to testicular and or hypothalamic-pituitary dysfunction.
Hypogonadism is directly associated with increased risks of metabolic syndrome, CVD risk factors, and CVD and may also contribute to depression, loss of energy, fertility problems, decreased sexual function, osteoporosis, and muscle weakness in men.
Adult onset hypergonadism is clinically distinct from classical primary and secondary hypogonadism and is characterized by testosterone deficiency and the failure to mount an adequate compensatory pituitary response to low levels of testosterone.
In adult onset hypogonadism gonadotropin levels are low or in the normal range.
Annual incidence in men in their 60s is 20% and 30% in men in their 70s.
Associated with undescended testicles in infancy, in fertility, impaired sexual drive, erectile dysfunction, hemochromatosis and genetic processes such as Kallman’s syndrome.
The two major types of male hypogonadism or primary and secondary.
Primary hypogonadism is also known as primary testicular failure and originates from an abnormality in the testicle.
Primary hypogonadism associated with Klinefelter’s syndrome, undescended testicles, hemochromatosis, previous hernia surgery, anti-neoplastic therapy and aging.
Primary hypogonadism is the result of testicular failure to produce adequate levels of testosterone and is identified by low levels of testosterone and elevated gonadotroponin levels LH, and FSH.
Secondary hypogonadism is caused by pituitary gland abnormalities which may be related to inflammatory diseases, and use of certain drugs.
Secondary hypogonadalism is the result of gonadotropin or luteinizing hormone releasing hormone deficiency, which may be congenital or arise from pathological processes including hypothalamic-pituitary dysfunction injury from tumors, trauma, or radiation.
Primary testicular disorders impair both Leydig and seminiferous tubule function, resulting in reduced testosterone synthesis and hypospermatogenesis.
Etiologies of primary testicular disorder impairment including XXY karyotype, Klinefelter syndrome, toxicities such as chemotherapy induced changes, infectious destruction of the testicle as in mumps orchitis, or radiation-induced damage.
The hormonal pattern in primary testicular disorders include a low serum testosterone level with elevated serum gonadotropin levels.
A large number of men with hypogonadism seen in clinical practice have low T levels accompanied by a normal low or level of gonadotropins, suggesting failure at both the testicle and pituitary hypothalamic levels- this is referred to as adult onset hypogonadism.
Effects are variable depending upon the age of life that it occurs.
Hypogonadism in early in fetal development may be associated with hypofuntioning internal and external sex organs.
Hypogonadism during puberty may slow growth and development, muscle development may be impaired, impaired growth of the penis, testicles, body hair and deepening of the voice may not occur, breast tissue may develop and the patient may be tall and have abnormal body proportions.
Associated with weight loss and poor outcomes in cancer patients, and up to 50% of men are hypogonadal at presentation or during treatment.
Deficiency in anabolic hormones is associated with increased morbidity and mortality in male patients with heart failure.
Low circulating testosterone levels affects around 20-30% of male patients with heart failure, related to higher neurohormonal activation, skeletal muscle wasting, and lower functional capacity.
Hypogonadism in adulthood it can be associated with erectile dysfunction, infertility, decreased beard and body hair growth, increased body fat, decrease in muscle size and strength, development of breast tissue and testicle atrophy and decreased bone mass.
Hypogonadal bone loss is among the three leading causes of osteoporosis, which increases with age.
Males may experience hot flashes, decreased sexual drive, irritability, fatigue, and depression.
Symptoms in men include: low libido, fatigue, muscle atrophy, erectile dysfunction, increased abnormal fat, diabetes, hypercholesterolemia, insomnia, impaired ability to concentrate, shyness, depression, gynecomastia, hot flashes, loss of bone mass, irritability, infertility, testicular atrophy, myalgias, night sweats and dry skin.
Symptoms in women include: hot flashes, irritability, anger, decreased libido, in fertility, menstrual abnormalities, loss of body hair, heart disease, loss of bone mass, sleep disturbances, bladder symptomatology with frequency urgency and increased infections, lack of vaginal lubrication, vaginal discharge, breast atrophy and loss of sense of smell.
In men may be due to primary gonadal failure or pituitary or hypothalamic abnormalities.
In men not defined by a specific level of serum testosterone because levels associated with dysfunction vary widely among individuals.
Oral testosterone is no longer used because it is metabolized in the liver and rendered inactive.
Testosterone therapy may take 2 to 3 months to reduce symptoms.
Typically testosterone levels are checked in the morning, since these levels are highest at that time.
Treatment of male hypogonadism includes testosterone injections, patches and topical ointments.
Late-onset hypogonadism also referred to as androgen decline in the aging male (ADAM).
Testosterone levels 500-700 ng per deciliter are adequate for young, healthy man from 20-40 years of age.
Both type 2 diabetes and the metabolic syndrome strongly associated with below normal levels of testosterone.
Low testosterone or androgen deficiency is commonly associated with opioid use.
There is an association of low testosterone levels and renal disease.
Renal disease typically reduces prolactin clearance, which inhibits production of luteinizing hormone, which reduces testosterone production.
Uremia inhibits luteinizing hormone receptors in Leydig cells.
Medications including angiotensin converting enzyme inhibitors, spironolactone, ketoconazol, statin and glucocorticoids all are thought to interfere with the synthesis of sex hormones.