This document discusses testosterone deficiency in males. It begins by introducing testosterone as the principal male sex hormone, playing a key role in male reproductive tissue development and secondary sexual characteristics. It then discusses levels of testosterone in adult males versus females, and the measurement and variations of testosterone levels. Common causes that can alter sex hormone-binding globulin and affect testosterone measurements are outlined. The document also covers primary and secondary testosterone deficiency, defining each and providing examples of causes. Androgen insensitivity syndrome is discussed as another cause of testosterone deficiency due to defects in androgen target organs. Age-related declines in testosterone are reviewed, along with studies on the prevalence of testosterone deficiency in aging males. Diagnosing
Hypogonadism is a decreased functional activity of the gonads that results in a failure of the testes to produce androgen, sperm, or both. It can occur at any age, with consequences depending on when it starts - before birth, before puberty, or after puberty. There are two types, primary involving the testes and secondary involving the hypothalamus or pituitary gland. Causes include genetic conditions, tumors, infections, physical damage to the testes from conditions like mumps, and certain medications or medical treatments that can damage the testes.
This document provides information on evaluating and treating delayed puberty. It defines delayed puberty and discusses the main causes, which include constitutional delay of puberty, hypogonadotropic hypogonadism, and hypergonadotropic hypogonadism. Evaluation involves assessing medical history, physical exam including Tanner staging, lab tests of hormone levels, bone age, and imaging if needed. Treatment depends on the underlying cause, and may include observation, sex hormone therapy, or treating any underlying medical conditions.
The document discusses prolactin, a hormone produced by the pituitary gland. It describes the factors that regulate prolactin secretion, such as estrogen and dopamine. The main functions of prolactin include stimulating breast development and lactation. The document also covers disorders of low or high prolactin, and their potential causes and symptoms. Diagnosis involves medical history, exams, and blood tests to measure prolactin and other hormone levels. Treatment depends on the underlying cause but may include dopamine agonists or surgery for pituitary tumors.
Male hypogonadism is caused by androgen deficiency which can negatively impact organ functions and quality of life. The goal of testosterone replacement therapy is to restore hormone levels to the normal range and alleviate symptoms. Common treatment options include injections, patches, gels, and implants which can restore sexual function, muscle strength, and bone density. Therapy requires monitoring for side effects like prostate issues or blood clots. Gonadotropins may also be used to stimulate testosterone production and spermatogenesis in hypogonadotropic hypogonadism.
This document discusses normal sexual differentiation and disorders of sexual differentiation (DSD). It begins by outlining the three main steps in normal sexual differentiation: establishment of chromosomal sex at fertilization, development of gonads into testes or ovaries, and subsequent differentiation of internal and external genitalia due to gonadal endocrine functions. It then discusses how gender is assigned based on genetic sex, external genitalia, gonads/reproductive organs, and psychosocial factors. The majority of the document focuses on DSDs, including definitions, causes such as congenital adrenal hyperplasia and gonadal differentiation disorders, associated genetic and physical characteristics, evaluations including history, exams, imaging and hormonal assays, and examples of
Primary hypogonadism is caused by testicular dysfunction resulting in low testosterone and sperm production. It can be caused by genetic conditions like Klinefelter syndrome, infections, trauma, or chemotherapy/radiation exposure. Physical exam may show small, soft testes and low body hair with high FSH and LH levels. Treatment is testosterone replacement therapy. Secondary hypogonadism results from pituitary or hypothalamic dysfunction, with proportionate low testosterone and sperm production and low or normal FSH and LH levels.
This document discusses male gonadal function and dysfunction, including causes and treatment of hypogonadism. It covers primary hypogonadism conditions like Klinefelter syndrome and secondary causes such as tumors or drugs. Diagnosis involves measuring testosterone, LH and FSH levels. Treatment options for hypogonadism include testosterone replacement therapy via patches, gels or injections, with monitoring of side effects like prostate issues.
The document discusses diseases of the gonads. It begins with a plan to cover topics such as normal sexual differentiation of the gonads, anatomy and physiology of male and female gonads, sexual development in boys and girls, and congenital violations of sexual differentiation. Specific conditions discussed include male hypogonadism, Klinefelter's syndrome, Turner syndrome, hermaphroditism, cryptorchidism, and anorchism. Causes of primary hypogonadism are also reviewed.
Hypogonadism is a decreased functional activity of the gonads that results in a failure of the testes to produce androgen, sperm, or both. It can occur at any age, with consequences depending on when it starts - before birth, before puberty, or after puberty. There are two types, primary involving the testes and secondary involving the hypothalamus or pituitary gland. Causes include genetic conditions, tumors, infections, physical damage to the testes from conditions like mumps, and certain medications or medical treatments that can damage the testes.
This document provides information on evaluating and treating delayed puberty. It defines delayed puberty and discusses the main causes, which include constitutional delay of puberty, hypogonadotropic hypogonadism, and hypergonadotropic hypogonadism. Evaluation involves assessing medical history, physical exam including Tanner staging, lab tests of hormone levels, bone age, and imaging if needed. Treatment depends on the underlying cause, and may include observation, sex hormone therapy, or treating any underlying medical conditions.
The document discusses prolactin, a hormone produced by the pituitary gland. It describes the factors that regulate prolactin secretion, such as estrogen and dopamine. The main functions of prolactin include stimulating breast development and lactation. The document also covers disorders of low or high prolactin, and their potential causes and symptoms. Diagnosis involves medical history, exams, and blood tests to measure prolactin and other hormone levels. Treatment depends on the underlying cause but may include dopamine agonists or surgery for pituitary tumors.
Male hypogonadism is caused by androgen deficiency which can negatively impact organ functions and quality of life. The goal of testosterone replacement therapy is to restore hormone levels to the normal range and alleviate symptoms. Common treatment options include injections, patches, gels, and implants which can restore sexual function, muscle strength, and bone density. Therapy requires monitoring for side effects like prostate issues or blood clots. Gonadotropins may also be used to stimulate testosterone production and spermatogenesis in hypogonadotropic hypogonadism.
This document discusses normal sexual differentiation and disorders of sexual differentiation (DSD). It begins by outlining the three main steps in normal sexual differentiation: establishment of chromosomal sex at fertilization, development of gonads into testes or ovaries, and subsequent differentiation of internal and external genitalia due to gonadal endocrine functions. It then discusses how gender is assigned based on genetic sex, external genitalia, gonads/reproductive organs, and psychosocial factors. The majority of the document focuses on DSDs, including definitions, causes such as congenital adrenal hyperplasia and gonadal differentiation disorders, associated genetic and physical characteristics, evaluations including history, exams, imaging and hormonal assays, and examples of
Primary hypogonadism is caused by testicular dysfunction resulting in low testosterone and sperm production. It can be caused by genetic conditions like Klinefelter syndrome, infections, trauma, or chemotherapy/radiation exposure. Physical exam may show small, soft testes and low body hair with high FSH and LH levels. Treatment is testosterone replacement therapy. Secondary hypogonadism results from pituitary or hypothalamic dysfunction, with proportionate low testosterone and sperm production and low or normal FSH and LH levels.
This document discusses male gonadal function and dysfunction, including causes and treatment of hypogonadism. It covers primary hypogonadism conditions like Klinefelter syndrome and secondary causes such as tumors or drugs. Diagnosis involves measuring testosterone, LH and FSH levels. Treatment options for hypogonadism include testosterone replacement therapy via patches, gels or injections, with monitoring of side effects like prostate issues.
The document discusses diseases of the gonads. It begins with a plan to cover topics such as normal sexual differentiation of the gonads, anatomy and physiology of male and female gonads, sexual development in boys and girls, and congenital violations of sexual differentiation. Specific conditions discussed include male hypogonadism, Klinefelter's syndrome, Turner syndrome, hermaphroditism, cryptorchidism, and anorchism. Causes of primary hypogonadism are also reviewed.
FSH, LH, and testosterone are hormones that regulate reproductive functions. FSH acts on the ovaries and testes to stimulate gamete production. LH triggers ovulation in females and supports testosterone production in males. Testosterone promotes male sexual development and secondary sex characteristics. The hormones work by binding to receptors on target cells and activating intracellular signaling cascades. Abnormal levels can cause diseases like polycystic ovarian syndrome or Klinefelter syndrome.
This document discusses male hypogonadism, defined as a decrease in sperm production or testosterone production by the testes. It describes primary hypogonadism, caused by testicular issues, and secondary hypogonadism, caused by pituitary or hypothalamic issues. Causes of primary hypogonadism include Klinefelter's syndrome, infections, drugs, trauma, and genetic mutations. Investigation involves measuring serum testosterone, SHBG, FSH, and LH levels along with other tests. Treatment depends on whether the hypogonadism is primary or secondary based on hormone level patterns.
The document discusses sexual differentiation and disorders of sexual development (DSDs). It covers the three stages of sexual differentiation, gonadal development, factors influencing testicular and ovarian development, and internal and external genital development. It then discusses various DSDs including congenital adrenal hyperplasia, androgen insensitivity syndrome, gonadal dysgenesis, and true hermaphroditism. Evaluation and management of ambiguous genitalia in newborns is also covered.
Congenital Adrenal Hyperplasia (CAH)
For 5th Year Medical Students and Endocrinology Modules and Master and MD Degree Internal Medicine and Endocrinology
By Dr Usama Ragab Youssif
References: Oxford Handbook of Endocrinology & Diabetes
Male gonadal function and dysfunction (male hypogonadism). Emphasis where made on the causes, types of male hypogonadism, diagnosis and treatment methods.
This document discusses the diagnosis and management of hypogonadism in primary care. It defines primary and secondary hypogonadism and describes how to diagnose based on lab tests of testosterone, LH and FSH levels. For a case of hypogonadotrophic hypogonadism, the patient has a history of undescended testicles and removal of one testis, and has been on testosterone injections for over 10 years. Key aspects of management in primary care include monitoring PSA, bone density, liver function and lipids during testosterone treatment, and discontinuing treatment if no improvement after 6 months or if contraindications arise.
Congenital adrenal hyperplasia (CAH) is caused by deficiencies in enzymes involved in cortisol production, leading to increased corticotropin levels and adrenal hyperplasia. The most common type (90% of cases) is due to 21-hydroxylase deficiency, causing cortisol and aldosterone deficiency or excess androgen levels. In females this causes virilization of external genitalia. Treatment involves glucocorticoid and mineralocorticoid replacement and surgery to correct ambiguous genitalia in females. Less common types involve 11β-hydroxylase and 17α-hydroxylase deficiencies, also resulting in hypertension and androgen excess.
This study analyzed mutations in the CYP21A2 gene in Pakistani patients with congenital adrenal hyperplasia (CAH). CAH is caused by defects in enzymes involved in cortisol synthesis and results in virilization in females and salt-wasting in both sexes. The study identified CYP21A2 mutations in Pakistani CAH patients and correlated genotypes to phenotypes. Major findings included several common mutations that matched clinical severity and helped explain the diversity of CAH presentations. Relating genetic mutations to clinical features could improve prenatal diagnosis and management of CAH in Pakistan.
This document discusses sex hormones, including estrogens, progesterone, antiestrogens, and antiprogestins. It provides details on the natural and synthetic forms of estrogens and progesterone, their receptors, mechanisms of action, regulation, and uses. The key points are:
- Estrogens and progesterone are secreted by the ovaries and play important roles in the female reproductive system and other body processes.
- They act through nuclear receptors and genomic/nongenomic signaling pathways to regulate gene expression.
- Selective estrogen receptor modulators (SERMs) can act as agonists or antagonists depending on the tissue.
- Progestins and antiestrogens/antiprogestins are
This document summarizes congenital adrenal hyperplasia (CAH), which is caused by a deficiency in the 21-hydroxylase enzyme. This leads to a deficiency in cortisol and aldosterone, causing salt-wasting in infants. It also causes prenatal androgen excess in females, resulting in virilization of the external genitalia. Prenatally, this causes enlarged clitoris and fused labia in females. Postnatally, both sexes experience signs of androgen excess like accelerated growth and premature epiphyseal closure. The document outlines the various clinical features and complications of both the cortisol/aldosterone deficiency and androgen excess aspects of CAH.
Delayed Puberty Topics in Adolescent Gynecology Delayed Puberty Topics in A...MedicineAndHealth14
This document discusses delayed puberty in adolescent girls. It begins by outlining normal pubertal development and defining delayed puberty. Delayed puberty is then classified into three categories: hypergonadotropic hypogonadism (43%), hypogonadotropic hypogonadism (31%), and eugonadism (26%). For evaluation and management, the document recommends obtaining a history, physical exam, initial labs (TSH, prolactin), and a progestational challenge to determine gonadotropin levels and identify underlying causes. Treatment strategies aim to correct the underlying pathology, prevent disease complications, and provide sex steroids.
The document discusses normal sexual differentiation and disorders of sexual differentiation. It describes the process of normal sexual differentiation including chromosomal, gonadal, ductal, and genital differentiation. It also discusses several common disorders of sexual differentiation including congenital adrenal hyperplasia, androgen insensitivity syndrome, mixed gonadal dysgenesis, and others. Specific conditions discussed in more detail include Klinefelter syndrome, Turner syndrome, XX maleness, and mixed gonadal dysgenesis.
details of klinfelter syndrome, noonan syndrome and diseases of pitutary and diseases of hypogonadism and cause of hypogonadism and primary hypogonadism and secondary hypogonadism
This document provides information about low testosterone from the Department of Urology Education. It defines testosterone and its role in male development. It states that testosterone levels naturally decline after age 30. Low testosterone is defined as less than 300 ng/dL. Potential causes of low testosterone include injury, disease, and obesity. Treatment options discussed include gels, patches, injections, buccal tablets, and pellets which all aim to supplement testosterone levels. Risks of treatment include increased red blood cell count and accelerated prostate growth.
This document provides an overview of male infertility, including its definition, causes, evaluation, and treatment options. It discusses factors that can cause infertility, such as varicocele, genetic disorders, hormonal imbalances, and problems with sperm production or transport. The evaluation of male infertility involves assessing medical history, performing a physical exam, analyzing semen samples, and testing for hormonal and genetic abnormalities if indicated. Treatment depends on the underlying cause but may include surgery, hormone therapy, assisted reproduction techniques like IVF, or empiric supplements for some issues.
Additional important history:
- Family history of precocious or early puberty
- Developmental milestones
- Medications/supplements
Examination:
- Bone age X-ray
- Pelvic/abdominal ultrasound
- MRI brain
Differential diagnosis:
- Central precocious puberty
- Peripheral precocious puberty (e.g. McCune-Albright syndrome)
- Pseudoprecocious puberty
Investigations:
- LH, FSH, estradiol
- Chromosome analysis
- MRI to rule out CNS pathology
Final diagnosis: Central precocious puberty likely due to early activation of hyp
This document discusses sex hormones, specifically estrogens. It notes that estrogens are synthesized in the ovaries and other reproductive organs. The three main types of estrogens are estrone, estradiol, and estriol. Estradiol is the most potent estrogen and plays important roles in sexual development and differentiation between males and females. The document provides details on the structure, biosynthesis, metabolism, and effects of estrogens on various body systems.
This document provides an overview of the diagnosis and management of male infertility. It discusses evaluating the patient's history including reproductive, medical, surgical, medication/toxin exposure and family histories. Physical exam and lab tests including semen analysis and hormones are also important. Common causes of male infertility discussed include varicocele, cryptorchidism, infections, cancers, medications/toxins and genetic factors. Lifestyle factors that can impact fertility are also addressed.
Male hypogonadism is a condition where the body does not produce enough of the male sex hormone testosterone. There are two types: primary, where the problem originates in the testicles, and secondary, where it is caused by issues with the hypothalamus or pituitary gland in the brain. Untreated hypogonadism can lead to complications like abnormal genitalia, infertility, erectile dysfunction, and osteoporosis. Diagnosis involves hormone testing, semen analysis, and imaging, while treatment is testosterone replacement therapy.
This document discusses male menopause, obesity, and metabolic disorders. It provides an introduction to male menopause symptoms and assessments. It also discusses obesity and metabolic disorders, hormone replacement therapy, and conclusions. The author's background and expertise are in urology, with a focus on male menopause, prostate laser surgery, and other procedures. Men with conditions like obesity and diabetes are at higher risk of experiencing testosterone deficiency.
FSH, LH, and testosterone are hormones that regulate reproductive functions. FSH acts on the ovaries and testes to stimulate gamete production. LH triggers ovulation in females and supports testosterone production in males. Testosterone promotes male sexual development and secondary sex characteristics. The hormones work by binding to receptors on target cells and activating intracellular signaling cascades. Abnormal levels can cause diseases like polycystic ovarian syndrome or Klinefelter syndrome.
This document discusses male hypogonadism, defined as a decrease in sperm production or testosterone production by the testes. It describes primary hypogonadism, caused by testicular issues, and secondary hypogonadism, caused by pituitary or hypothalamic issues. Causes of primary hypogonadism include Klinefelter's syndrome, infections, drugs, trauma, and genetic mutations. Investigation involves measuring serum testosterone, SHBG, FSH, and LH levels along with other tests. Treatment depends on whether the hypogonadism is primary or secondary based on hormone level patterns.
The document discusses sexual differentiation and disorders of sexual development (DSDs). It covers the three stages of sexual differentiation, gonadal development, factors influencing testicular and ovarian development, and internal and external genital development. It then discusses various DSDs including congenital adrenal hyperplasia, androgen insensitivity syndrome, gonadal dysgenesis, and true hermaphroditism. Evaluation and management of ambiguous genitalia in newborns is also covered.
Congenital Adrenal Hyperplasia (CAH)
For 5th Year Medical Students and Endocrinology Modules and Master and MD Degree Internal Medicine and Endocrinology
By Dr Usama Ragab Youssif
References: Oxford Handbook of Endocrinology & Diabetes
Male gonadal function and dysfunction (male hypogonadism). Emphasis where made on the causes, types of male hypogonadism, diagnosis and treatment methods.
This document discusses the diagnosis and management of hypogonadism in primary care. It defines primary and secondary hypogonadism and describes how to diagnose based on lab tests of testosterone, LH and FSH levels. For a case of hypogonadotrophic hypogonadism, the patient has a history of undescended testicles and removal of one testis, and has been on testosterone injections for over 10 years. Key aspects of management in primary care include monitoring PSA, bone density, liver function and lipids during testosterone treatment, and discontinuing treatment if no improvement after 6 months or if contraindications arise.
Congenital adrenal hyperplasia (CAH) is caused by deficiencies in enzymes involved in cortisol production, leading to increased corticotropin levels and adrenal hyperplasia. The most common type (90% of cases) is due to 21-hydroxylase deficiency, causing cortisol and aldosterone deficiency or excess androgen levels. In females this causes virilization of external genitalia. Treatment involves glucocorticoid and mineralocorticoid replacement and surgery to correct ambiguous genitalia in females. Less common types involve 11β-hydroxylase and 17α-hydroxylase deficiencies, also resulting in hypertension and androgen excess.
This study analyzed mutations in the CYP21A2 gene in Pakistani patients with congenital adrenal hyperplasia (CAH). CAH is caused by defects in enzymes involved in cortisol synthesis and results in virilization in females and salt-wasting in both sexes. The study identified CYP21A2 mutations in Pakistani CAH patients and correlated genotypes to phenotypes. Major findings included several common mutations that matched clinical severity and helped explain the diversity of CAH presentations. Relating genetic mutations to clinical features could improve prenatal diagnosis and management of CAH in Pakistan.
This document discusses sex hormones, including estrogens, progesterone, antiestrogens, and antiprogestins. It provides details on the natural and synthetic forms of estrogens and progesterone, their receptors, mechanisms of action, regulation, and uses. The key points are:
- Estrogens and progesterone are secreted by the ovaries and play important roles in the female reproductive system and other body processes.
- They act through nuclear receptors and genomic/nongenomic signaling pathways to regulate gene expression.
- Selective estrogen receptor modulators (SERMs) can act as agonists or antagonists depending on the tissue.
- Progestins and antiestrogens/antiprogestins are
This document summarizes congenital adrenal hyperplasia (CAH), which is caused by a deficiency in the 21-hydroxylase enzyme. This leads to a deficiency in cortisol and aldosterone, causing salt-wasting in infants. It also causes prenatal androgen excess in females, resulting in virilization of the external genitalia. Prenatally, this causes enlarged clitoris and fused labia in females. Postnatally, both sexes experience signs of androgen excess like accelerated growth and premature epiphyseal closure. The document outlines the various clinical features and complications of both the cortisol/aldosterone deficiency and androgen excess aspects of CAH.
Delayed Puberty Topics in Adolescent Gynecology Delayed Puberty Topics in A...MedicineAndHealth14
This document discusses delayed puberty in adolescent girls. It begins by outlining normal pubertal development and defining delayed puberty. Delayed puberty is then classified into three categories: hypergonadotropic hypogonadism (43%), hypogonadotropic hypogonadism (31%), and eugonadism (26%). For evaluation and management, the document recommends obtaining a history, physical exam, initial labs (TSH, prolactin), and a progestational challenge to determine gonadotropin levels and identify underlying causes. Treatment strategies aim to correct the underlying pathology, prevent disease complications, and provide sex steroids.
The document discusses normal sexual differentiation and disorders of sexual differentiation. It describes the process of normal sexual differentiation including chromosomal, gonadal, ductal, and genital differentiation. It also discusses several common disorders of sexual differentiation including congenital adrenal hyperplasia, androgen insensitivity syndrome, mixed gonadal dysgenesis, and others. Specific conditions discussed in more detail include Klinefelter syndrome, Turner syndrome, XX maleness, and mixed gonadal dysgenesis.
details of klinfelter syndrome, noonan syndrome and diseases of pitutary and diseases of hypogonadism and cause of hypogonadism and primary hypogonadism and secondary hypogonadism
This document provides information about low testosterone from the Department of Urology Education. It defines testosterone and its role in male development. It states that testosterone levels naturally decline after age 30. Low testosterone is defined as less than 300 ng/dL. Potential causes of low testosterone include injury, disease, and obesity. Treatment options discussed include gels, patches, injections, buccal tablets, and pellets which all aim to supplement testosterone levels. Risks of treatment include increased red blood cell count and accelerated prostate growth.
This document provides an overview of male infertility, including its definition, causes, evaluation, and treatment options. It discusses factors that can cause infertility, such as varicocele, genetic disorders, hormonal imbalances, and problems with sperm production or transport. The evaluation of male infertility involves assessing medical history, performing a physical exam, analyzing semen samples, and testing for hormonal and genetic abnormalities if indicated. Treatment depends on the underlying cause but may include surgery, hormone therapy, assisted reproduction techniques like IVF, or empiric supplements for some issues.
Additional important history:
- Family history of precocious or early puberty
- Developmental milestones
- Medications/supplements
Examination:
- Bone age X-ray
- Pelvic/abdominal ultrasound
- MRI brain
Differential diagnosis:
- Central precocious puberty
- Peripheral precocious puberty (e.g. McCune-Albright syndrome)
- Pseudoprecocious puberty
Investigations:
- LH, FSH, estradiol
- Chromosome analysis
- MRI to rule out CNS pathology
Final diagnosis: Central precocious puberty likely due to early activation of hyp
This document discusses sex hormones, specifically estrogens. It notes that estrogens are synthesized in the ovaries and other reproductive organs. The three main types of estrogens are estrone, estradiol, and estriol. Estradiol is the most potent estrogen and plays important roles in sexual development and differentiation between males and females. The document provides details on the structure, biosynthesis, metabolism, and effects of estrogens on various body systems.
This document provides an overview of the diagnosis and management of male infertility. It discusses evaluating the patient's history including reproductive, medical, surgical, medication/toxin exposure and family histories. Physical exam and lab tests including semen analysis and hormones are also important. Common causes of male infertility discussed include varicocele, cryptorchidism, infections, cancers, medications/toxins and genetic factors. Lifestyle factors that can impact fertility are also addressed.
Male hypogonadism is a condition where the body does not produce enough of the male sex hormone testosterone. There are two types: primary, where the problem originates in the testicles, and secondary, where it is caused by issues with the hypothalamus or pituitary gland in the brain. Untreated hypogonadism can lead to complications like abnormal genitalia, infertility, erectile dysfunction, and osteoporosis. Diagnosis involves hormone testing, semen analysis, and imaging, while treatment is testosterone replacement therapy.
This document discusses male menopause, obesity, and metabolic disorders. It provides an introduction to male menopause symptoms and assessments. It also discusses obesity and metabolic disorders, hormone replacement therapy, and conclusions. The author's background and expertise are in urology, with a focus on male menopause, prostate laser surgery, and other procedures. Men with conditions like obesity and diabetes are at higher risk of experiencing testosterone deficiency.
This document discusses testosterone deficiency syndrome (TDS) and its relationship to prostate cancer. It begins by providing background on testosterone physiology and the prevalence of TDS, which increases with age. It then reports on a study of 705 men who underwent prostate biopsies. The study found that testosterone levels were not related to prostate cancer diagnosis in men with normal testosterone, but were related in men with low testosterone. Specifically, men with testosterone levels below 346 ng/dL who were diagnosed with prostate cancer had even lower testosterone levels on average of 272 ng/dL. The study suggests testosterone levels may be a risk factor for prostate cancer diagnosis only in hypogonadal men.
This document discusses late-onset hypogonadism, also known as andropause, which is characterized by low serum testosterone levels and associated clinical symptoms in older men. It describes the physiology of testosterone and its metabolites like estradiol and dihydrotestosterone. Age-related changes include a decline in total and free testosterone levels and blunting of circadian rhythms. Causes of hypogonadism in older men can be primary testicular issues or secondary to hypothalamic-pituitary problems. Clinical features encompass sexual, muscle, bone and metabolic effects. Diagnosis involves symptoms, low total testosterone levels on two tests, and measuring LH/FSH to distinguish primary versus secondary eti
This document summarizes information about androgen deficiency in aging men (ADAM syndrome). It discusses the physiology of androgens and how levels change with aging. ADAM syndrome, also called late-onset hypogonadism, describes the effects of declining testosterone in older men. Testosterone replacement therapy can improve sexual function, bone density, lean muscle mass, mood and cognition. However, risks include prostate issues and erythrocytosis. Guidelines recommend monitoring prostate-specific antigen and hematocrit for men undergoing testosterone replacement. More research is still needed to fully understand the risks and benefits of testosterone therapy in older men.
OP MED Conf TESTOSTERONE with Anti estrogensMichael Lada
The document discusses the diagnosis and management of hypogonadism. It defines hypogonadism and outlines the key diagnostic steps including medical history, physical exam, and lab tests to distinguish between primary and secondary causes. The primary care management of hypogonadism is also reviewed, including treatment with testosterone and monitoring of side effects.
This document defines and discusses andropause (also known as male menopause), including its definition, symptoms, epidemiology, pathophysiology, effects of testosterone deficiency, monitoring and risks/benefits of testosterone replacement therapy. Some key points are: andropause is characterized by declining testosterone levels and affects quality of life; symptoms include reduced energy, libido and erectile dysfunction; prevalence increases with age, with 20% of men over 60 and 50% of men over 75 having low testosterone; testosterone replacement can improve symptoms in men with very low levels if administered carefully under medical supervision due to risks like prostate issues.
Andropause, also known as male menopause, is defined as a syndrome of age-related low testosterone levels in older men. It is characterized by signs and symptoms that include reduced libido, erectile dysfunction, fatigue, depression and changes in body composition. The prevalence of low testosterone increases with age, affecting up to 49% of men over 80 years old. Testosterone replacement therapy can effectively treat the signs and symptoms of andropause and is generally safe for most men when monitored closely. However, risks include sleep apnea, prostate issues, cardiovascular effects and polycythemia.
Erectile Dysfunction: New Paradigms in Treatment Ranjith Ramasamy
1. Discuss diagnosis of erectile dysfunction
2. Treatments of ED using Viagra, Cialis, Trimix (intracavernosal injections)
3. Evaluate penile prosthesis and implant as ED surgical therapy options
The document discusses andropause, also known as late-onset hypogonadism, which is a common condition characterized by low testosterone levels and associated symptoms in aging men. It defines andropause and discusses the diagnosis of late-onset hypogonadism based on symptoms and low testosterone levels. Potential benefits of testosterone replacement therapy are also summarized, including improved body composition, increased muscle and bone mass, and enhanced sexual function. While testosterone therapy shows potential benefits, the document notes that further large clinical trials are still needed to fully evaluate risks and complex interactions with aging.
This document summarizes the results of two clinical trials that studied the effects of testosterone replacement therapy with and without aromatase inhibition. In the first trial, testosterone therapy increased lean mass and muscle size, and improved sexual function, while excess body fat decreased at higher doses. In the second trial where aromatase was inhibited, body fat increased for all groups. This suggests estradiol prevents fat accumulation. Sexual function also declined more with aromatase inhibition, showing both androgens and estrogens impact this domain. The trials delineated the roles of testosterone and estradiol in various health outcomes.
Hormone replacement therapy (HRT) involves administering hormones to supplement a lack of natural hormones or substitute other hormones. It is primarily used as a medical treatment for post-menopausal symptoms but can also treat hormone deficiencies in men. There are several types of HRT including testosterone replacement therapy, transgender hormone therapy, and menopausal hormone therapy. Menopausal HRT provides benefits like relieving vasomotor symptoms and protects bone and cardiovascular health but also carries risks like increased breast cancer risk.
1) Male hypogonadism is caused by androgen deficiency and can affect multiple organ functions and quality of life. It has various forms that are caused by different factors and have implications for evaluation and treatment.
2) Diagnosis is based on clinical signs and symptoms of androgen deficiency along with low serum testosterone levels on two occasions. Treatment aims to restore testosterone levels to improve quality of life.
3) Testosterone replacement therapy options include oral, injectable, topical, and implant preparations. Risks include side effects and potential impacts on the prostate and cardiovascular and breast health that require monitoring.
This document discusses andropause and sarcopenia, which are age-related declines in testosterone and muscle mass. It provides evidence that testosterone levels and muscle mass begin declining in the late 30s and accelerate after age 70. Intrinsic and extrinsic factors like lower hormone levels and muscle protein breakdown contribute to sarcopenia. The document recommends addressing these issues with a balanced diet, exercise, stress reduction, sleep, and potentially testosterone therapy. It summarizes several studies showing that natural supplements like tongkat ali can safely and effectively increase testosterone levels and muscle mass. The document promotes Andraiz T, a supplement containing these ingredients, to help treat andropause and sarcopenia symptoms.
This document discusses testosterone replacement therapy (TRT). It covers indications for TRT including hypogonadism and symptoms of low testosterone. It describes methods of testosterone delivery including gels, patches, injections, and pellets. It discusses follow up testing and potential risks and side effects of TRT. Adjunctive therapies like HCG are also summarized.
Androgens such as testosterone are responsible for male sexual development. Testosterone is produced in the testes and regulated by LH and FSH. It has pharmacological actions via the androgen receptor and is metabolized in the liver. Therapeutic uses include androgen replacement therapy. Anabolic steroids have similar effects but higher anabolic to androgenic ratios. Antiandrogens like danazol and flutamide work by blocking androgen receptors. PDE5 inhibitors like sildenafil are used to treat erectile dysfunction by increasing nitric oxide signaling.
This document discusses testosterone and hypogonadism. It begins by defining three types of hypogonadism: primary, secondary, and ADAM (age-related). It then discusses specific causes and considerations for evaluating and diagnosing hypogonadism. Key tests discussed include measuring total testosterone, LH, and symptoms. The document raises questions about treating asymptomatic low T and outlines scenarios for treatment decisions. Benefits and risks of testosterone replacement therapy are weighed. It concludes by discussing an ongoing trial studying effects of TRT on physical functioning in older men.
Andropause, also known as male menopause, is the gradual decline in testosterone levels that occurs in men as they age. Unlike female menopause which is sudden, andropause is a slow process resulting in more subtle symptoms. Low testosterone can negatively impact many organ systems and quality of life. Treatment options include lifestyle changes as well as hormone replacement therapy administered through oral, injectable, or transdermal methods. However, testosterone therapy may increase risks for certain health conditions like sleep apnea and prostate issues.
Discuss the etiologies and the pathophysiology of erectile dysfunction (ED)
Describe the mechanism of action of agents used to treat ED
Recommend pharmacologic and non-pharmacologic treatment for ED
Identify drug interactions and adverse effects of currently used medications for ED
Identify treatment related side effects.
Similar to Testosterone Deficiency in Male by Dr Selim (20)
The document discusses various methods for treating diabetes through replacing or regenerating insulin-producing cells, including pancreas and islet cell transplantation, stem cell therapy, and gene therapy. Pancreas transplantation provides the best outcomes but requires lifelong immunosuppression. Islet cell transplantation has improved but success rates decline over time. Stem cells show promise for treating both type 1 and type 2 diabetes by replenishing beta cells, but challenges remain around immune responses and insulin resistance. Gene therapy also offers potential for treating diabetes by replacing insulin genes or suppressing autoreactive immune cells. Further research is still needed but cell and gene-based therapies may eventually provide cures or better treatment options than current insulin management approaches.
The document discusses gynecomastia, or male breast enlargement. It defines gynecomastia and provides statistics on prevalence. It describes the histology and potential causes, including hormonal imbalances, medications, tumors, and medical conditions. Evaluation involves history, physical exam, and lab tests of thyroid, liver, kidney, and sex hormone levels. Treatment depends on the cause but may include treating the underlying condition, reassurance for self-limited cases, antiestrogens like tamoxifen, or surgery for severe cases.
The document summarizes information about osteoporosis from a lecture by Dr. Shahjada Selim. It discusses how bone remodeling occurs throughout life, leading to peak bone mass and then age-related bone loss. It defines osteoporosis as a disorder causing fragile bones from low bone mass and deteriorated bone structure. Key points include how osteoporosis is diagnosed using BMD tests and fracture risk tools, treatments include medications to reduce fracture risk, and lifestyle changes can help prevent osteoporotic fractures.
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Testosterone Deficiency in Male by Dr Selim
1. TESTOSTERONE
DEFICIENCY IN MALE
Dr Shahjada Selim
Assistant Professor
Department of Endocrinology
Bangabandhu Sheikh Mujib Medical University, Dhaka
Email: selimshahjada@gmail.com, info@shahjadaselim.com
2. • Testosterone (T) is the principal male sex
hormone.
• In men, this anabolic steroid plays a key role
in the development of male reproductive
tissues such as the testis and prostate as well
as promoting secondary sexual
characteristics.
INTRODUCTION:
3. • In adult males, levels of testosterone are
about 7–8 times as great as in adult females.
INTRODUCTION:
4.
5. Testosterone and its Metabolites
Sexual differentiation
Musculature
Bone mass
Erythropoiesis
Psychotropicaction
Potency/libido
Lipid metabolism
Bone mass
Epiphyseal closure
Psychotropicaction
Lipid metabolism
Feedback action
Prostate
Sexual differentiation
Secondaryhair
Sebum production
Prostate
Testosterone
Dihydrotestosterone Oestradiol
6. Binding of testosterone (T)
T firmlyboundto
SHBG
60%
BIOAVAILABLETESTOSTERONE= Albumin-boundT
+FreeT
Free TT looselyboundto
albumin
2%38%
7. T Measurement
T levels vary
– Circadian rhythms & episodic secretion
– Assay variations
– Variations in SHBG concentrations
– Illness, drugs, nutritional deficiency :
transiently low T not defined cut-off values
for normal T levels
7
8. When should you measure testosterone?1
Circadianrhythmoftestosterone
1. NieschlagE & BehreHM.Andrology,Malereproductivehealthanddysfunction(2ndEdition).Springer, Heidelberg;2002.
9. Recommendation
•A serum sample for total
testosterone determination should
be obtained between 0700 and
1100 h (Level 2a, A)
European Journal of Endocrinology (2008) 159 507–514
9
10. 10
CommonAlterations in SHBG
Affect Total and Free TAnalog Levels
• Estrogens
• HIV
• Anabolic steroids
• Acromegaly
• Anticonvulsants• Glucocorticoids/progestins
• Hyperthyroidism• Hypothyroidism
• Hepatitis, cirrhosis• Low protein (nephrotic)
• Aging• Moderate obesity
SHBG
Total T
SHBG
Total T
Bhasin S, et al, J Clin Endocrinol Metab 91:1995-2010, 2006
11. 11
Testosterone Assays
• Affected by changes in SHBG
• Total T
• Free T by analog assay (~all clinical labs)
• Not affected by changes in SHBG
• Calculated free T and bioavailable T from total T
and SHBG
• Free T by equilibrium dialysis
• Bioavailable T by ammonium sulfate precipitation
12. Medications and low T
Decrease Leydig Cell T Production
corticosteroids
ethanol
ketoconazole
Bind to the Androgen Receptor
spironolactone
flutamide
cimetidine
Decrease Gonadotropin Secretion
corticosteroids
ethanol
estrogens & progestins (Megace)
Rx that raise prolactin (opiates, metoclopramide,
psychotherapy medication)
Decreases Conversion of T to DHT
finasteride
12
13. Change of Nomenclature
• Over time name of the condition changes
• Men Andropause> Late onset Hypogonadism
(LOH)>
• Testosterone Deficiency (TD)
• In March 2014, ISSM Testosterone Guideline
Committee in New York opined a new generally
accepted definition, Testosterone Deficiency (TD)
to replace the other inconsistent definition like
• Hypogonadism, (primary, secondary, mixed)
• LOH, androgen deficiency, andropause etc
14. ISSM definition of Testosterone Deficiency
(TD)
• ISSM has defined Testosterone Deficiency
(TD) as
• A clinical & biochemical syndrome
characterized by a deficiency of
testosterone, or testosterone action and
relevant symptoms and signs.
(Dean et al; J sex Med 2015; 12: 1660-1686)
15. • TD may affect the function of multiple
organ systems, and result in significant
impacts, determine in the quality of life,
including alterations in sexual functions.
(Dean et al; J sex Med 2015; 12: 1660-1686)
16. Clinical picture of testosterone deficiency1
• Decreased muscle
bulk/power
• Abdominal obesity
• Loss of libido
• Hot flushes/palpitations
• Decreased body hair
• Anaemia
• Subfertility
• Subnormal genital size
• Loss of pubic hair
• Erectile dysfunction
• Sexual dysfunction
• Depression
• Reduced well-being
• Low self esteem
• Poor concentration/drive
General body effects
Reproductive system
Emotional Complications
• Osteoporosis
• Raised lipids
• Insulin resistance
• Sarcopaenia
1. NieschlagE andBehreHM.Testosterone:action,deficiency,substitution(3rd Edition).CambridgeUniversityPress;2004.
23. DDx: Secondary TD
Acquired :
1.Hyperprolactinemia
2.GnRH analog therapy
3.Glucocorticoid therapy
4.Critical or Chronic illness
5.Diabetes mellitus
6.Opiates
7.Pituitary mass lesions
8.Infiltrative diseases
9.Sellar surgery or radiation
10.hemochromatosis
24
24. TD DUE TO DEFECTS OF ANDROGEN
TARGET ORGANS
Androgen Insensitivity Syndrome (AIS)
25
25. Androgen insensitivity syndrome (AIS)
• The effects that androgens have on the human
body virilization, masculinization, anabolism,
etc. are the result of androgens bound to
androgen receptors, the androgen receptor
mediates the effects of androgens in the
human body.
• AIS can result if even one of the steps involved
in androgenization is significantly disrupted, as
each step is required in order for androgens to
successfully activate the AR and regulate gene
expression
26
26. Androgen insensitivity syndrome (AIS)
•Laboratory findings include a 46,XY
karyotype and normal or elevated
postpubertal testosterone, LH and
estradiol levels.
27
27. Pathophysiology of LOH
Hypothalamus & aging
1-number of GnRH secreting neurons decreases
2-decrease in the release of neuropeptide Y(an
excitatory peptidergic signal to GnRH secreting
neurons)
3-beta receptors become less functional in aged men
4-hypothalamic norepinephrine content decrease with
aging
5-diminished GnRH impulse strength is the
proximate cause of the relative hypogonadism of
old age.
28
28. Late-onset hypogonadism
• A clinical and biochemical syndrome associated with advancing age
and characterised by typical symptoms and a deficiency in serum
testosterone levels1,2
0
25
50
75
25-34
(n=45)
35-44
(n=22)
45-54
(n=23)
55-64
(n=43)
65-74
(n=47)
75-84
(n=48)
75=100
(n=21)
1. NieschlagE et al. EurUrology2005;48:1-4.
2. VermeulenA et al. JClinEndocrinolMetab1996;81:1821-1826.
SHBG Free T (x100) Testosterone
Hormonelevel(nmol/L)
Age
29. Pathophysiology of LOH
Hypothalamus
Pituitary
Testes
Reduced Leydig cell number
Impaired Leydig cell function
diminished LH feedforward activity on
testosterone secretion
Decreased spermatogenesis
Lower GnRH pulse amplitude
Attenuation of diurnal pulsatility
blunted HPG feedback response
to low testosterone
T
E
LH &
FSH
Increased SHBG
30
30. 31
Longitudinal T Levels with Age
Testosterone
(nmol/L)
Age (Years)
10
12
14
16
18
20
30 40 50 60 70 80 90
(177)
(144)
(151)
(158)
(109)
(43)
Harman SM, et al, J Clin Endocrinol Metab 86:724-731, 2001.
31. TD in Males (HIM) study : 2006
• Based on a TT of <300 ng/dL, 39% of the men
were defined as being hypogonadal; for every 10-
year increase in age, the risk of hypogonadism
increased by 17%
32
32. TD incidence and age (US data)
0
5
10
15
20
25
Overall 48-59 60-69 70-79
Incidence
per1,000person-years
Age(years)
• Expected481,000new casesp.a.in US men 40-69yrs
1. AraujoA et al. JClinEndocrinolMetab2004;89(12):5920-5926.
34. Massachusetts male aging study (MMAS)
•The prevalence rate of androgen
deficiency at study entry, without
consideration of signs or symptoms and
with a cut-off TT of 400 ng/dl was
estimated to be 25.3%; at followup, the
prevalence rate was 39.3%
35
35. But :
•Considering the presence of at
least three signs or symptoms
and TT, the prevalence rates
were 6% at baseline and 12%
at follow-up
36
36. The European Male Aging Study (EMAS)
• Defined by symptoms [poor morning erection,
low sexual desire, and erectile dysfunction (ED)].
and biochemical evidence (TT < 317 ng/dL and
free testosterone < 6.34 ng/dL) the prevalence
of hypogonadism was estimated at 2.1% overall,
increasing from as little as 0.1% in men aged 40
to 49 to 5% in men aged 70 to 79.
37
37. Boston Area Community Health Study
(BACH)
• used a somewhat strict definition of symptomatic
TD and estimated its prevalence at 5.6%
nationwide among men aged 30 to 79 years
38
38. Prevalence of hypogonadism in DM
0
10
20
30
40
50
Free T Total T Bioavailable T
Percentageofpatients
1. DhindsaS et al. JClinEndocrinolMetab2004;89(11):5462-5468.
• n=103 men with type 2 diabetes
39. Hypogonadism in diabetic vs
nondiabetic men with ED1
22.3
34.0
All ages
ED no diabetes Diabetes
0
10
20
30
40
50
30-39 40-49 50-59 60-69 >70
Age (Years)
%Hypogonadism(T<12nmol/L)
p <0.0001
p <0.0001
1. CoronaG et al. EurUrol2004;46(2):222-228.
n=1027men with ED with and without type 2 diabetes mellitus
+ ED
41. Recommendation
• At present, the diagnosis of treatable TD,
requires the presence of symptoms and
signs suggestive of testosterone deficiency
(Level 3, Grade A)
European Journal of
Endocrinology (2008) 159 507–514
42
42. Recommendation
• We recommend making a diagnosis of androgen
deficiency only in men with consistent symptoms
and signs and unequivocally low serum
testosterone levels. (1| OOO)
• CLINICAL PRACTIC GUIDELINE (The Journal of Clinical Endocrinology &
Metabolism 91(6):1995–2010)
43
43. Specific symptoms:
- Incomplete or delayed sexual development
- Reduced sexual desire.
- Decrease spontaneous erections
- Breast discomfort of gynecomastia.
- Loss of body (axillary, and pubic) hair reduced
shaving.
- Small < 5 ml or shrinking testicles
- Inability to father children, low to zero sperm count
- Height loss, or bone fracture
- Hot flushes, sweats.
MEASUREMENT OF SERUM TESTOSTERONE IN
PATIENTS WITH CLINICAL MANIFESTATIONS
44. 6 | ISSM Quick Reference Guide on Testosterone Deficiency
for men
Erectile dysfunction, hypoactive sexual desire,
osteoporosis, other potential symptoms or signs of
TD or at-risk patient
History, physical examination
and Morning Total Testosterone
(TT)
Low or borderline low T; T<12nmol/l
(346ng/dL)
Normal T; T>12nmol/l
(346ng/dL)
Repeat TT + LH, SHBG,
PRL
No TD-seek other
causes
T 8-12nmol/l (231-
346ng/dL)
+/- SHBG, bother ++
TD if T<8nmol/l
(<346ng/dL)
Normal T; T>12nmol/l
(<346ng/dL)
High
LH
Low/Normal
LH
Exclude
contraindications
Investigate pituitary + other
causes
Reassess, consider
referral or trial of
TRT
Trial of TRT
Lifestyle
modification
No
identifiable
cause
Identified
cause
Successful
Monitor TT,
FBC
Failure
Review
diagnosis
Manage cause
Figure 1: Flow chart for the processof care for the assessmentand management of testosterone deficiency in adult men
45. Patients with borderline testosterone
levels (8-12 nmol/l)1,2
• Consider additional biochemical tests
• Gonadotrophins, SHBG, prolactin
• Careful consideration of comorbidities
• Calculate free testosterone (see online calculator
at www.issam.ch/freetesto.htm)
• Counsel patient regarding treatment options
1. NieschlagE et al.Eur Urol 2005;48:1-4.
2. BhasinS et al.J ClinEndocrinolMetab2006;91(6):1995-2010.
47. Who should receive testosterone treatment?
• Men with clinical symptoms and testosterone <8
nmol/l1
• Men with clinical symptoms and testosterone 8-12
nmol/l where additional investigations indicate
presence of hypogonadism1
• Older men with significant symptoms
• Long-term risks /benefits have yet to be clearly demonstrated
1. Nieschlag E et al. Int J Androl 2005;28:125-127
48. Who shouldn’t receive testosterone treatment?
Untreated or suspected carcinoma of prostate [PSA
of >4 ng/ml or PSA of 3 ng/ml in patient with high risk
for prostate cancer]
• Moderate to severe symptoms of BPH
• Breast cancer
• Liver tumour
• Significant polycythaemia
• Severe cardiac failure
• Untreated sleep apnoea
49. Treat of TD without Testosterone
• The ISSM Committee recommends that men
who wish to maintain spermatogenesis, fertility ,
and the testosterone volume be referred for
specialist management (e.g., Endocrinologist,
Fertility specialist) until an approved non
testosterone is available.
50. Treat of TD without Testosterone
• Clomiphene Citrate blocks estrogen
receptors in the hypothalamus and pituitary
and increase GnRH, LH, FSH release. But
no consistent effect on seminal parameters
or pregnancy rates.
• Aromatase Inhibitor (AI) is used for 2ndary
hypogonadism as alternative approach to
TRT.
51. Follow Up
• The effect of Testosterone Replacement Therapy
(TRT) on symptoms reduction are assesssed and
enquiry about side effects be made 3, 6 and 12
months after initiating TRT and annually there
after.
• Testes to be covered
• TT (target range is mid point of the reference
range for a young adult)
• Lipid profile
• Hematocrit
• PSA (men above 40 years)
52. Follow-up… conted
• Patient should be monitored every 3-6 months during first
year and at least annually thereafter.
• Each visit careful clinical & andrological evaluation should
be performed.
• Digital Rectal Examination is mandatory (as per the ESSM
guideline)
• PSA, hematocrit mandatory
• Consider prostate biopsy if PSA is more than 4ng/ml, or
PSA concentration>1.4ng/ml within any 12 mo period of
TRT
53. TRT outcomes
• Compared to placebo TRT significantly improved
all aspects of sexual function in the studies of
middle ages and elderly men with low T (T
concentration <12nmol/l, 346ng/dl.
• No EFFECTS observed on TRT if the baseline
Testosterone levels higher than 12 nmol/l
54. TRT outcomes
• More severe hypogonadism more significant or
impressive are the result of improvement.
• Hypogonadism is the main cause of ED in
younger men while it is one of the multifactorial
ED in older ones (like DM, dyslipidemia,
metabolic syndrome, Sp Cord Injury etc)
55. TRT outcomes
• Combination of TRT and PDE5I (sildenafil,
tadalafil ) can be used to improve the outcomes of
PDE5I in hypogonadism.
• TRT is associated with reduction in bone
resorption and increase lumber bone mineral
density.
56.
57.
58. Conclusion: Managing TD
• Sexual function such as libido, erection and
ejaculation are clearly testosterone dependent
with different T-cut off values regarding onset of
clinical symptoms.
• To get maximum effect of TD patients both TRT
and PDE5I (sildenafil, tadalafil) should be given
to get the maximum PDE5I response.
59. Take home message
•No EFFECTS observed on TRT if
the baseline Testosterone levels
higher than 12 nmol/l .
60. Take home message
•Testosterone Deficiency (TD) causes
ED and low libido and after
testosterone replacement therapy both
function improves. Maximum effect
reached after 2-3 months of treatment
with TRT.
61. Take home message
• Oral testosterone (17 alpha methyl
testosterone is not recommended by ISSM
committee on TD due to hepatotoxic side
effects and hepatoma.