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Androgen Deficiency Syndrome: A Rational Approach to Male Hypogonadism
During a routine physical examination, a 65-year-old man wants to find out if he has “Low T.” He complains of fatigue, decreased libido, and erectile dysfunction (ED) for the past five years. He has a history of type 2 diabetes, hypertension, hyperlipidemia, obstructive sleep apnea, and chronic low back pain. His current medications include metformin, glipizide, lisinopril, atorvastatin, and hydrocodone for back pain. Given these clinical features, the next step will be to find out if he has hypogonadism (androgen deficiency).
The Endocrine Society defines hypogonadism as a clinical syndrome in which the testes produce insufficient testosterone as a consequence of an interruption of the hypothalamic-pituitary-testicular axis. Although prevalence is high in older men, the Endocrine Society does not recommend screening the general population for hypogonadism.1 Rather, screening should be limited to patients with clinical conditions associated with high prevalence of hypogonadism. Of note, approximately 30% of adults with type 2 diabetes have a subnormal testosterone concentration.2
Q: What is pertinent in the history?
The first step in evaluation of hypogonadism is a detailed history. Signs and symptoms such as decreased libido, hot flashes, decreased shaving frequency, breast enlargement/tenderness, and decreased testicular size are highly suggestive of hypogonadism. Other, less specific signs and symptoms include dysthymia, poor concentration, sleep disturbances, fatigue, reduction in muscle strength, and diminished work performance.
If these signs and symptoms are present, the likelihood of hypogonadism is high and further evaluation is needed.1,3 Note any history of alcoholism, liver problems, and testicular trauma or surgery.
A detailed medication history is also important. Some medications, such as opiates, can affect the release of gonadotropins. Among men taking long-term opiates for chronic noncancer pain, the prevalence of hypogonadism is 75%.4 Other drugs, such as spironolactone, can block the androgen effect and lead to hypogonadism.1
Recent reports have suggested an association between testosterone replacement therapy and increased cardiovascular events, making a detailed cardiovascular history essential.5,6 One study found that men ages 75 and older with limited mobility and other comorbidities who used testosterone gel had an increased risk for cardiovascular events.7 Therefore, clinicians need to be cognizant of this risk when considering testosterone therapy for their patients.
On the next page: Physical exam, lab tests, and treatments >>
Q: What does the physical exam reveal?
In hypogonadotropic hy pogonadism, physical examination does not usually provide much information, as compared to congenital hypogonadal syndromes (eg, Klinefelter and Kallmann syndromes). However, small testicular volume and/or gynecomastia would indicate hypogonadism.
Q: What lab tests should be ordered?
Serum total and free testosterone should be measured, preferably by liquid gas chromatography. The sample should be drawn before 10 am to limit the effects of diurnal variation. If the total testosterone is less than
300 ng/dL, a second morning sample should be drawn and tested. Serum prolactin, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), complete blood count, prostate-specific antigen (PSA), comprehensive metabolic panel, and ferritin should also be measured.
There is generally little benefit to testosterone therapy when total testosterone is greater than 350 ng/dL.8 The level of testosterone at which hypogonadal symptoms manifest and testosterone replacement provides improvement is yet to be determined. Buvat et al suggest that men with total testosterone levels less than 230 ng/dL usually benefit from therapy.8 If the total testosterone level is less than 150 ng/dL in the setting of secondary hypogonadism (low to low-normal LH/FSH) or if prolactin is elevated, MRI of the sella is recommended to rule out pituitary adenoma.1
Q: Once the diagnosis is confirmed, what treatment should you recommend?
The goal of therapy for confirmed hypogonadism is to normalize the testosterone level. Testosterone replacement therapy may help to improve libido, fatigue, muscle strength, and bone density. However, in the elderly (particularly those older than 70), these therapeutic benefits have not been proven. Therefore, before initiating therapy, the clinician should discuss in detail the risks versus the benefits of testosterone replacement for a particular patient.
Simple lifestyle modifications, such as weight loss and exercise, have been shown to increase total and free testosterone levels.3,8 For patients with obstructive sleep apnea (OSA), a known risk factor for hypogonadism, compliance with CPAP therapy has been associated with modest improvement in testosterone level. If it is appropriate for the patient to discontinue use of certain medications, such as opiates, he or she may experience an improvement in testosterone level as a result.
If the patient’s testosterone levels remain low after these changes have been implemented, consider testosterone therapy. Testosterone products currently available in the United States include transdermal preparations (gel, patch), intramuscular injection, and subcutaneous pellets.
On the next page: Contraindications, adverse effects, and follow-up >>
Q: What are the contraindications to testosterone therapy?
Testosterone therapy is contraindicated in patients with metastatic prostate cancer and breast cancer. An unevaluated prostate nodule, indurated prostate, PSA greater than 4 ng/mL, elevated hematocrit (>50%), severe lower urinary tract symptoms, poorly controlled congestive heart failure, and untreated severe OSA are associated with moderate to high risk for adverse outcomes; the Endocrine Society has recommended against using testosterone in affected patients.1
Q: What are the adverse effects of testosterone replacement therapy?
Testosterone replacement may worsen symptoms of benign prostatic hyperplasia (ie, urinary urgency, hesitancy, and frequency). Also, testosterone replacement can lead to marked elevation of hemoglobin and hematocrit levels.
Increased cardiovascular events have been associated with androgen replacement, especially in men with prior coronary artery disease. A positive cardiovascular history necessitates discussion with the patient regarding the risks versus the benefits of testosterone replacement therapy.5 In a recent study of obese, hypogonadal men with severe OSA, testosterone therapy was associated with transient worsening of sleep apnea.9
Q: What does monitoring/ follow-up entail?
In patients with long-standing hypogonadism, a lower starting dose of testosterone is recommended, which can be gradually increased. After starting testosterone therapy, patients should be monitored in the first three to six months for total testosterone, PSA, and hematocrit and for improvement of symptoms (ie, fatigue, ED, decreased libido) or worsening of benign prostatic hyperplasia signs/symptoms.
For men ages 40 and older, if the baseline PSA is greater than 0.6 ng/mL, a digital rectal exam (DRE) is recommended prior to initiation of therapy and should be followed in accordance with prostate cancer screening guidelines.1
Patients placed on testosterone cypionate/enanthate IM injections should have their testosterone checked at a midpoint between their injections, with the target testosterone level between 400 and 700 ng/dL.1 For those using gel or transdermal preparations, a morning total testosterone level should be measured.
Urology consultation is recommended if the PSA concentration rises by 1.4 ng/dL within 12 months, if the American Urological Association/International Prostate Symptom Score is greater than 19, or if there is an abnormal DRE.1,8 Treatment with testosterone should be postponed or withheld if the patient’s hematocrit is greater than 54% but may be resumed when it has decreased to normal levels.1
On the next page: References >>
REFERENCES
1. Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2010;95(6):2536-2559.
2. Dandona P, Dhindsa S. Update: hypogonadotropic hypogonadism in type 2 diabetes and obesity. J Clin Endocrinol Metab. 2011;96(9): 2643-2651.
3. Tajar A, Forti G, O’Neill TW, et al. Characteristics of secondary, primary, and compensated hypogonadism in aging men: evidence from the European Male Ageing Study. J Clin Endocrinol Metab. 2010;95(4):1810-1818.
4. Fraser LA, Morrison D, Morley-Forster P, et al. Oral opioids for chronic non-cancer pain: higher prevalence of hypogonadism in men than in women. Exp Clin Endocrinol Diabetes. 2009;117(1):38-43.
5. Vigen R, O’Donnell CI, Baron AE, et al. Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels. JAMA. 2013;310(17): 1829-1836.
6. Finkle WD, Greenland S, Ridgeway GK, et al. Increased risk of non-fatal myocardial infarction following testosterone therapy prescription in men. PloS One. 2014;9(1): e85805.
7. Basaria S, Coviello AD, Travison TG, et al. Adverse events associated with testosterone administration. N Engl J Med. 2010;363(2):109-122.
8. Buvat J, Maggi M, Guay A, Torres LO. Testosterone deficiency in men: systematic review and standard operating procedures for diagnosis and treatment. J Sex Med. 2013;10(1): 245-284.
9. Hoyos CM, Killick R, Yee BJ, et al. Effects of testosterone therapy on sleep and breathing in obese men with severe obstructive sleep apnoea: a randomized placebo-controlled trial. Clin Endocrinol (Oxf). 2012;77(4):
599-607.
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Sheila B. Pinkson practices at Audie L. Murphy VA Hospital in San Antonio and is an Adjunct Assistant Professor in Endocrinology at the University of Texas Health Science Center at San Antonio (UTHSCSA). Devjit Tripathy is a staff physician at Audie L. Murphy VA Hospital in San Antonio and an Associate Professor in the Endocrinology/Diabetes Division at UTHSCSA.
| Clinician Reviews in partnership with |
|
Sheila B. Pinkson practices at Audie L. Murphy VA Hospital in San Antonio and is an Adjunct Assistant Professor in Endocrinology at the University of Texas Health Science Center at San Antonio (UTHSCSA). Devjit Tripathy is a staff physician at Audie L. Murphy VA Hospital in San Antonio and an Associate Professor in the Endocrinology/Diabetes Division at UTHSCSA.
| Clinician Reviews in partnership with |
|
Sheila B. Pinkson practices at Audie L. Murphy VA Hospital in San Antonio and is an Adjunct Assistant Professor in Endocrinology at the University of Texas Health Science Center at San Antonio (UTHSCSA). Devjit Tripathy is a staff physician at Audie L. Murphy VA Hospital in San Antonio and an Associate Professor in the Endocrinology/Diabetes Division at UTHSCSA.
During a routine physical examination, a 65-year-old man wants to find out if he has “Low T.” He complains of fatigue, decreased libido, and erectile dysfunction (ED) for the past five years. He has a history of type 2 diabetes, hypertension, hyperlipidemia, obstructive sleep apnea, and chronic low back pain. His current medications include metformin, glipizide, lisinopril, atorvastatin, and hydrocodone for back pain. Given these clinical features, the next step will be to find out if he has hypogonadism (androgen deficiency).
The Endocrine Society defines hypogonadism as a clinical syndrome in which the testes produce insufficient testosterone as a consequence of an interruption of the hypothalamic-pituitary-testicular axis. Although prevalence is high in older men, the Endocrine Society does not recommend screening the general population for hypogonadism.1 Rather, screening should be limited to patients with clinical conditions associated with high prevalence of hypogonadism. Of note, approximately 30% of adults with type 2 diabetes have a subnormal testosterone concentration.2
Q: What is pertinent in the history?
The first step in evaluation of hypogonadism is a detailed history. Signs and symptoms such as decreased libido, hot flashes, decreased shaving frequency, breast enlargement/tenderness, and decreased testicular size are highly suggestive of hypogonadism. Other, less specific signs and symptoms include dysthymia, poor concentration, sleep disturbances, fatigue, reduction in muscle strength, and diminished work performance.
If these signs and symptoms are present, the likelihood of hypogonadism is high and further evaluation is needed.1,3 Note any history of alcoholism, liver problems, and testicular trauma or surgery.
A detailed medication history is also important. Some medications, such as opiates, can affect the release of gonadotropins. Among men taking long-term opiates for chronic noncancer pain, the prevalence of hypogonadism is 75%.4 Other drugs, such as spironolactone, can block the androgen effect and lead to hypogonadism.1
Recent reports have suggested an association between testosterone replacement therapy and increased cardiovascular events, making a detailed cardiovascular history essential.5,6 One study found that men ages 75 and older with limited mobility and other comorbidities who used testosterone gel had an increased risk for cardiovascular events.7 Therefore, clinicians need to be cognizant of this risk when considering testosterone therapy for their patients.
On the next page: Physical exam, lab tests, and treatments >>
Q: What does the physical exam reveal?
In hypogonadotropic hy pogonadism, physical examination does not usually provide much information, as compared to congenital hypogonadal syndromes (eg, Klinefelter and Kallmann syndromes). However, small testicular volume and/or gynecomastia would indicate hypogonadism.
Q: What lab tests should be ordered?
Serum total and free testosterone should be measured, preferably by liquid gas chromatography. The sample should be drawn before 10 am to limit the effects of diurnal variation. If the total testosterone is less than
300 ng/dL, a second morning sample should be drawn and tested. Serum prolactin, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), complete blood count, prostate-specific antigen (PSA), comprehensive metabolic panel, and ferritin should also be measured.
There is generally little benefit to testosterone therapy when total testosterone is greater than 350 ng/dL.8 The level of testosterone at which hypogonadal symptoms manifest and testosterone replacement provides improvement is yet to be determined. Buvat et al suggest that men with total testosterone levels less than 230 ng/dL usually benefit from therapy.8 If the total testosterone level is less than 150 ng/dL in the setting of secondary hypogonadism (low to low-normal LH/FSH) or if prolactin is elevated, MRI of the sella is recommended to rule out pituitary adenoma.1
Q: Once the diagnosis is confirmed, what treatment should you recommend?
The goal of therapy for confirmed hypogonadism is to normalize the testosterone level. Testosterone replacement therapy may help to improve libido, fatigue, muscle strength, and bone density. However, in the elderly (particularly those older than 70), these therapeutic benefits have not been proven. Therefore, before initiating therapy, the clinician should discuss in detail the risks versus the benefits of testosterone replacement for a particular patient.
Simple lifestyle modifications, such as weight loss and exercise, have been shown to increase total and free testosterone levels.3,8 For patients with obstructive sleep apnea (OSA), a known risk factor for hypogonadism, compliance with CPAP therapy has been associated with modest improvement in testosterone level. If it is appropriate for the patient to discontinue use of certain medications, such as opiates, he or she may experience an improvement in testosterone level as a result.
If the patient’s testosterone levels remain low after these changes have been implemented, consider testosterone therapy. Testosterone products currently available in the United States include transdermal preparations (gel, patch), intramuscular injection, and subcutaneous pellets.
On the next page: Contraindications, adverse effects, and follow-up >>
Q: What are the contraindications to testosterone therapy?
Testosterone therapy is contraindicated in patients with metastatic prostate cancer and breast cancer. An unevaluated prostate nodule, indurated prostate, PSA greater than 4 ng/mL, elevated hematocrit (>50%), severe lower urinary tract symptoms, poorly controlled congestive heart failure, and untreated severe OSA are associated with moderate to high risk for adverse outcomes; the Endocrine Society has recommended against using testosterone in affected patients.1
Q: What are the adverse effects of testosterone replacement therapy?
Testosterone replacement may worsen symptoms of benign prostatic hyperplasia (ie, urinary urgency, hesitancy, and frequency). Also, testosterone replacement can lead to marked elevation of hemoglobin and hematocrit levels.
Increased cardiovascular events have been associated with androgen replacement, especially in men with prior coronary artery disease. A positive cardiovascular history necessitates discussion with the patient regarding the risks versus the benefits of testosterone replacement therapy.5 In a recent study of obese, hypogonadal men with severe OSA, testosterone therapy was associated with transient worsening of sleep apnea.9
Q: What does monitoring/ follow-up entail?
In patients with long-standing hypogonadism, a lower starting dose of testosterone is recommended, which can be gradually increased. After starting testosterone therapy, patients should be monitored in the first three to six months for total testosterone, PSA, and hematocrit and for improvement of symptoms (ie, fatigue, ED, decreased libido) or worsening of benign prostatic hyperplasia signs/symptoms.
For men ages 40 and older, if the baseline PSA is greater than 0.6 ng/mL, a digital rectal exam (DRE) is recommended prior to initiation of therapy and should be followed in accordance with prostate cancer screening guidelines.1
Patients placed on testosterone cypionate/enanthate IM injections should have their testosterone checked at a midpoint between their injections, with the target testosterone level between 400 and 700 ng/dL.1 For those using gel or transdermal preparations, a morning total testosterone level should be measured.
Urology consultation is recommended if the PSA concentration rises by 1.4 ng/dL within 12 months, if the American Urological Association/International Prostate Symptom Score is greater than 19, or if there is an abnormal DRE.1,8 Treatment with testosterone should be postponed or withheld if the patient’s hematocrit is greater than 54% but may be resumed when it has decreased to normal levels.1
On the next page: References >>
REFERENCES
1. Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2010;95(6):2536-2559.
2. Dandona P, Dhindsa S. Update: hypogonadotropic hypogonadism in type 2 diabetes and obesity. J Clin Endocrinol Metab. 2011;96(9): 2643-2651.
3. Tajar A, Forti G, O’Neill TW, et al. Characteristics of secondary, primary, and compensated hypogonadism in aging men: evidence from the European Male Ageing Study. J Clin Endocrinol Metab. 2010;95(4):1810-1818.
4. Fraser LA, Morrison D, Morley-Forster P, et al. Oral opioids for chronic non-cancer pain: higher prevalence of hypogonadism in men than in women. Exp Clin Endocrinol Diabetes. 2009;117(1):38-43.
5. Vigen R, O’Donnell CI, Baron AE, et al. Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels. JAMA. 2013;310(17): 1829-1836.
6. Finkle WD, Greenland S, Ridgeway GK, et al. Increased risk of non-fatal myocardial infarction following testosterone therapy prescription in men. PloS One. 2014;9(1): e85805.
7. Basaria S, Coviello AD, Travison TG, et al. Adverse events associated with testosterone administration. N Engl J Med. 2010;363(2):109-122.
8. Buvat J, Maggi M, Guay A, Torres LO. Testosterone deficiency in men: systematic review and standard operating procedures for diagnosis and treatment. J Sex Med. 2013;10(1): 245-284.
9. Hoyos CM, Killick R, Yee BJ, et al. Effects of testosterone therapy on sleep and breathing in obese men with severe obstructive sleep apnoea: a randomized placebo-controlled trial. Clin Endocrinol (Oxf). 2012;77(4):
599-607.
During a routine physical examination, a 65-year-old man wants to find out if he has “Low T.” He complains of fatigue, decreased libido, and erectile dysfunction (ED) for the past five years. He has a history of type 2 diabetes, hypertension, hyperlipidemia, obstructive sleep apnea, and chronic low back pain. His current medications include metformin, glipizide, lisinopril, atorvastatin, and hydrocodone for back pain. Given these clinical features, the next step will be to find out if he has hypogonadism (androgen deficiency).
The Endocrine Society defines hypogonadism as a clinical syndrome in which the testes produce insufficient testosterone as a consequence of an interruption of the hypothalamic-pituitary-testicular axis. Although prevalence is high in older men, the Endocrine Society does not recommend screening the general population for hypogonadism.1 Rather, screening should be limited to patients with clinical conditions associated with high prevalence of hypogonadism. Of note, approximately 30% of adults with type 2 diabetes have a subnormal testosterone concentration.2
Q: What is pertinent in the history?
The first step in evaluation of hypogonadism is a detailed history. Signs and symptoms such as decreased libido, hot flashes, decreased shaving frequency, breast enlargement/tenderness, and decreased testicular size are highly suggestive of hypogonadism. Other, less specific signs and symptoms include dysthymia, poor concentration, sleep disturbances, fatigue, reduction in muscle strength, and diminished work performance.
If these signs and symptoms are present, the likelihood of hypogonadism is high and further evaluation is needed.1,3 Note any history of alcoholism, liver problems, and testicular trauma or surgery.
A detailed medication history is also important. Some medications, such as opiates, can affect the release of gonadotropins. Among men taking long-term opiates for chronic noncancer pain, the prevalence of hypogonadism is 75%.4 Other drugs, such as spironolactone, can block the androgen effect and lead to hypogonadism.1
Recent reports have suggested an association between testosterone replacement therapy and increased cardiovascular events, making a detailed cardiovascular history essential.5,6 One study found that men ages 75 and older with limited mobility and other comorbidities who used testosterone gel had an increased risk for cardiovascular events.7 Therefore, clinicians need to be cognizant of this risk when considering testosterone therapy for their patients.
On the next page: Physical exam, lab tests, and treatments >>
Q: What does the physical exam reveal?
In hypogonadotropic hy pogonadism, physical examination does not usually provide much information, as compared to congenital hypogonadal syndromes (eg, Klinefelter and Kallmann syndromes). However, small testicular volume and/or gynecomastia would indicate hypogonadism.
Q: What lab tests should be ordered?
Serum total and free testosterone should be measured, preferably by liquid gas chromatography. The sample should be drawn before 10 am to limit the effects of diurnal variation. If the total testosterone is less than
300 ng/dL, a second morning sample should be drawn and tested. Serum prolactin, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), complete blood count, prostate-specific antigen (PSA), comprehensive metabolic panel, and ferritin should also be measured.
There is generally little benefit to testosterone therapy when total testosterone is greater than 350 ng/dL.8 The level of testosterone at which hypogonadal symptoms manifest and testosterone replacement provides improvement is yet to be determined. Buvat et al suggest that men with total testosterone levels less than 230 ng/dL usually benefit from therapy.8 If the total testosterone level is less than 150 ng/dL in the setting of secondary hypogonadism (low to low-normal LH/FSH) or if prolactin is elevated, MRI of the sella is recommended to rule out pituitary adenoma.1
Q: Once the diagnosis is confirmed, what treatment should you recommend?
The goal of therapy for confirmed hypogonadism is to normalize the testosterone level. Testosterone replacement therapy may help to improve libido, fatigue, muscle strength, and bone density. However, in the elderly (particularly those older than 70), these therapeutic benefits have not been proven. Therefore, before initiating therapy, the clinician should discuss in detail the risks versus the benefits of testosterone replacement for a particular patient.
Simple lifestyle modifications, such as weight loss and exercise, have been shown to increase total and free testosterone levels.3,8 For patients with obstructive sleep apnea (OSA), a known risk factor for hypogonadism, compliance with CPAP therapy has been associated with modest improvement in testosterone level. If it is appropriate for the patient to discontinue use of certain medications, such as opiates, he or she may experience an improvement in testosterone level as a result.
If the patient’s testosterone levels remain low after these changes have been implemented, consider testosterone therapy. Testosterone products currently available in the United States include transdermal preparations (gel, patch), intramuscular injection, and subcutaneous pellets.
On the next page: Contraindications, adverse effects, and follow-up >>
Q: What are the contraindications to testosterone therapy?
Testosterone therapy is contraindicated in patients with metastatic prostate cancer and breast cancer. An unevaluated prostate nodule, indurated prostate, PSA greater than 4 ng/mL, elevated hematocrit (>50%), severe lower urinary tract symptoms, poorly controlled congestive heart failure, and untreated severe OSA are associated with moderate to high risk for adverse outcomes; the Endocrine Society has recommended against using testosterone in affected patients.1
Q: What are the adverse effects of testosterone replacement therapy?
Testosterone replacement may worsen symptoms of benign prostatic hyperplasia (ie, urinary urgency, hesitancy, and frequency). Also, testosterone replacement can lead to marked elevation of hemoglobin and hematocrit levels.
Increased cardiovascular events have been associated with androgen replacement, especially in men with prior coronary artery disease. A positive cardiovascular history necessitates discussion with the patient regarding the risks versus the benefits of testosterone replacement therapy.5 In a recent study of obese, hypogonadal men with severe OSA, testosterone therapy was associated with transient worsening of sleep apnea.9
Q: What does monitoring/ follow-up entail?
In patients with long-standing hypogonadism, a lower starting dose of testosterone is recommended, which can be gradually increased. After starting testosterone therapy, patients should be monitored in the first three to six months for total testosterone, PSA, and hematocrit and for improvement of symptoms (ie, fatigue, ED, decreased libido) or worsening of benign prostatic hyperplasia signs/symptoms.
For men ages 40 and older, if the baseline PSA is greater than 0.6 ng/mL, a digital rectal exam (DRE) is recommended prior to initiation of therapy and should be followed in accordance with prostate cancer screening guidelines.1
Patients placed on testosterone cypionate/enanthate IM injections should have their testosterone checked at a midpoint between their injections, with the target testosterone level between 400 and 700 ng/dL.1 For those using gel or transdermal preparations, a morning total testosterone level should be measured.
Urology consultation is recommended if the PSA concentration rises by 1.4 ng/dL within 12 months, if the American Urological Association/International Prostate Symptom Score is greater than 19, or if there is an abnormal DRE.1,8 Treatment with testosterone should be postponed or withheld if the patient’s hematocrit is greater than 54% but may be resumed when it has decreased to normal levels.1
On the next page: References >>
REFERENCES
1. Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2010;95(6):2536-2559.
2. Dandona P, Dhindsa S. Update: hypogonadotropic hypogonadism in type 2 diabetes and obesity. J Clin Endocrinol Metab. 2011;96(9): 2643-2651.
3. Tajar A, Forti G, O’Neill TW, et al. Characteristics of secondary, primary, and compensated hypogonadism in aging men: evidence from the European Male Ageing Study. J Clin Endocrinol Metab. 2010;95(4):1810-1818.
4. Fraser LA, Morrison D, Morley-Forster P, et al. Oral opioids for chronic non-cancer pain: higher prevalence of hypogonadism in men than in women. Exp Clin Endocrinol Diabetes. 2009;117(1):38-43.
5. Vigen R, O’Donnell CI, Baron AE, et al. Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels. JAMA. 2013;310(17): 1829-1836.
6. Finkle WD, Greenland S, Ridgeway GK, et al. Increased risk of non-fatal myocardial infarction following testosterone therapy prescription in men. PloS One. 2014;9(1): e85805.
7. Basaria S, Coviello AD, Travison TG, et al. Adverse events associated with testosterone administration. N Engl J Med. 2010;363(2):109-122.
8. Buvat J, Maggi M, Guay A, Torres LO. Testosterone deficiency in men: systematic review and standard operating procedures for diagnosis and treatment. J Sex Med. 2013;10(1): 245-284.
9. Hoyos CM, Killick R, Yee BJ, et al. Effects of testosterone therapy on sleep and breathing in obese men with severe obstructive sleep apnoea: a randomized placebo-controlled trial. Clin Endocrinol (Oxf). 2012;77(4):
599-607.