The Leydig germ cells of the testicles are responsible for producing 95 percent of the total testosterone in males. Men’s hypogonadism can result from defects in the hypothalamus-pituitary-testicular (HPG) axis, which can be acquired or congenital. Primary hypogonadism primarily develops in the testes and must be distinguished from secondary hypogonadism (primarily originates in the pituitary or hypothalamus).
Reduced spontaneous erection, reduced nocturnal penile tumescence, loss of libido, and diminished testicle volume are symptoms of hypogonadism that are strongly suggestive. A male’s early-morning testosterone level should fall within the range of 300 ng/dL and 1000 ng/dL. When the morning plasma level of testosterone is less than 300 ng/dL, hypogonadism is identified.
Although testosterone concentrations are within the normal range, clinical judgment can be used to diagnose hypogonadism in patients who have ongoing symptoms of low testosterone. It should be noted that overall testosterone below the fifth percentile is 405.9 ng/dL or less. For older men, the ideal range for levels of testosterone is 500–800 ng/dL, while for younger individuals, the ideal range is 600–900 ng/dL.
Epidemiology
It’s common for hypogonadism to go unreported. Based on specific research, fifty percent of men in their eighties and 40 percent of men over the age of forty-five are hypogonadal.
Every ten years, levels of testosterone have been shown to drop by 100 ng/dL. Race and ethnicity don’t seem to have anything to do with hypogonadism.
Anatomy
Pathophysiology
The stimulation of the anterior pituitary, which releases pulses of LH (luteinizing hormone) into the circulatory, is necessary for the Leydig germ cells in the testicles to produce testosterone. cAMP levels rise when LH attaches to its ligands on Leydig cells. cAMP concentration rises when LH attaches to its ligands on Leydig germ cells.
Two genes, StAR (the steroidogenic acute regulation molecule) as well as CYP11A1, are expressed as cAMP levels rise (the side-chain cleavage enzyme). While CYP11A1 stimulates the transformation of cholesterol into pregnenolone, the progenitor of all sex hormones, StAR promotes the transport of cholesterol from the outer mitochondrial membrane to the mitochondrial inner membrane.
Dehydroepiandrosterone, or DHEA, is produced when 17 alpha-hydroxylation of pregnenolone results in 17 OH pregnenolone. The subsequent transformation of DHEA into Andros enediol produces testosterone.
Etiology
Both inherited and acquired conditions can result in hypogonadism. In pre-pubertal males, ambiguous genitalia, bilateral cryptorchidism, and micropenis are all symptoms of low testosterone. Youngsters undergo karyotype testing to rule out diseases like Klinefelter syndrome and Turner syndrome, which could also cause low testosterone levels.
Klinefelter’s syndrome, mumps orchitis, undescended testes, cancer drugs, normal aging, and hemochromatosis are a few reasons for primary hypogonadism. Kallman syndrome, HIV, pituitary issues, surgery, obesity, trauma, and Pressure-induced hypogonadism are some of the reasons for secondary hypogonadism.
testosterone cypionate: 50-400 mg intramuscularly every 2-4 weeks
testosterone enanthate (generic): 50-400 mg intramuscularly every 2-4 weeks
testosterone undecanoate: Initially 750 mg intramuscularly, repeat after 4 weeks, and then every 10 weeks
Pellet: 150-450 mg subcutaneously every 3-6 months
150 mg of pellet is equivalent to 25 mg of testosterone propionate weekly
Indicated for Hypogonadotropic Hypogonadism in male patients
Prior treatment of 1000-2250 USP IU, 2-3 times each week unless the testosterone reaches the normal range
In the case of persistent azoospermia, increase the dose to 300IU thrice weekly
Continue the treatment upto 18 months for proper response
5-20 mg orally each day
In children, androgens should be used cautiously
Healthcare specialists should only provide the medication, who are well-versed in the adverse effects of bone maturation
For >12 years- testosterone enanthate is indicated to initiate puberty in males, who have reached adolescence
50-200 mg intramuscularly every 2-4 weeks, for 4-6 months
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK532933/
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The Leydig germ cells of the testicles are responsible for producing 95 percent of the total testosterone in males. Men’s hypogonadism can result from defects in the hypothalamus-pituitary-testicular (HPG) axis, which can be acquired or congenital. Primary hypogonadism primarily develops in the testes and must be distinguished from secondary hypogonadism (primarily originates in the pituitary or hypothalamus).
Reduced spontaneous erection, reduced nocturnal penile tumescence, loss of libido, and diminished testicle volume are symptoms of hypogonadism that are strongly suggestive. A male’s early-morning testosterone level should fall within the range of 300 ng/dL and 1000 ng/dL. When the morning plasma level of testosterone is less than 300 ng/dL, hypogonadism is identified.
Although testosterone concentrations are within the normal range, clinical judgment can be used to diagnose hypogonadism in patients who have ongoing symptoms of low testosterone. It should be noted that overall testosterone below the fifth percentile is 405.9 ng/dL or less. For older men, the ideal range for levels of testosterone is 500–800 ng/dL, while for younger individuals, the ideal range is 600–900 ng/dL.
It’s common for hypogonadism to go unreported. Based on specific research, fifty percent of men in their eighties and 40 percent of men over the age of forty-five are hypogonadal.
Every ten years, levels of testosterone have been shown to drop by 100 ng/dL. Race and ethnicity don’t seem to have anything to do with hypogonadism.
The stimulation of the anterior pituitary, which releases pulses of LH (luteinizing hormone) into the circulatory, is necessary for the Leydig germ cells in the testicles to produce testosterone. cAMP levels rise when LH attaches to its ligands on Leydig cells. cAMP concentration rises when LH attaches to its ligands on Leydig germ cells.
Two genes, StAR (the steroidogenic acute regulation molecule) as well as CYP11A1, are expressed as cAMP levels rise (the side-chain cleavage enzyme). While CYP11A1 stimulates the transformation of cholesterol into pregnenolone, the progenitor of all sex hormones, StAR promotes the transport of cholesterol from the outer mitochondrial membrane to the mitochondrial inner membrane.
Dehydroepiandrosterone, or DHEA, is produced when 17 alpha-hydroxylation of pregnenolone results in 17 OH pregnenolone. The subsequent transformation of DHEA into Andros enediol produces testosterone.
Both inherited and acquired conditions can result in hypogonadism. In pre-pubertal males, ambiguous genitalia, bilateral cryptorchidism, and micropenis are all symptoms of low testosterone. Youngsters undergo karyotype testing to rule out diseases like Klinefelter syndrome and Turner syndrome, which could also cause low testosterone levels.
Klinefelter’s syndrome, mumps orchitis, undescended testes, cancer drugs, normal aging, and hemochromatosis are a few reasons for primary hypogonadism. Kallman syndrome, HIV, pituitary issues, surgery, obesity, trauma, and Pressure-induced hypogonadism are some of the reasons for secondary hypogonadism.
testosterone cypionate: 50-400 mg intramuscularly every 2-4 weeks
testosterone enanthate (generic): 50-400 mg intramuscularly every 2-4 weeks
testosterone undecanoate: Initially 750 mg intramuscularly, repeat after 4 weeks, and then every 10 weeks
Pellet: 150-450 mg subcutaneously every 3-6 months
150 mg of pellet is equivalent to 25 mg of testosterone propionate weekly
Indicated for Hypogonadotropic Hypogonadism in male patients
Prior treatment of 1000-2250 USP IU, 2-3 times each week unless the testosterone reaches the normal range
In the case of persistent azoospermia, increase the dose to 300IU thrice weekly
Continue the treatment upto 18 months for proper response
5-20 mg orally each day
In children, androgens should be used cautiously
Healthcare specialists should only provide the medication, who are well-versed in the adverse effects of bone maturation
For >12 years- testosterone enanthate is indicated to initiate puberty in males, who have reached adolescence
50-200 mg intramuscularly every 2-4 weeks, for 4-6 months
https://www.ncbi.nlm.nih.gov/books/NBK532933/
medtigo
Hypogonadism
Updated :
August 22, 2023
The Leydig germ cells of the testicles are responsible for producing 95 percent of the total testosterone in males. Men’s hypogonadism can result from defects in the hypothalamus-pituitary-testicular (HPG) axis, which can be acquired or congenital. Primary hypogonadism primarily develops in the testes and must be distinguished from secondary hypogonadism (primarily originates in the pituitary or hypothalamus).
Reduced spontaneous erection, reduced nocturnal penile tumescence, loss of libido, and diminished testicle volume are symptoms of hypogonadism that are strongly suggestive. A male’s early-morning testosterone level should fall within the range of 300 ng/dL and 1000 ng/dL. When the morning plasma level of testosterone is less than 300 ng/dL, hypogonadism is identified.
Although testosterone concentrations are within the normal range, clinical judgment can be used to diagnose hypogonadism in patients who have ongoing symptoms of low testosterone. It should be noted that overall testosterone below the fifth percentile is 405.9 ng/dL or less. For older men, the ideal range for levels of testosterone is 500–800 ng/dL, while for younger individuals, the ideal range is 600–900 ng/dL.
It’s common for hypogonadism to go unreported. Based on specific research, fifty percent of men in their eighties and 40 percent of men over the age of forty-five are hypogonadal.
Every ten years, levels of testosterone have been shown to drop by 100 ng/dL. Race and ethnicity don’t seem to have anything to do with hypogonadism.
The stimulation of the anterior pituitary, which releases pulses of LH (luteinizing hormone) into the circulatory, is necessary for the Leydig germ cells in the testicles to produce testosterone. cAMP levels rise when LH attaches to its ligands on Leydig cells. cAMP concentration rises when LH attaches to its ligands on Leydig germ cells.
Two genes, StAR (the steroidogenic acute regulation molecule) as well as CYP11A1, are expressed as cAMP levels rise (the side-chain cleavage enzyme). While CYP11A1 stimulates the transformation of cholesterol into pregnenolone, the progenitor of all sex hormones, StAR promotes the transport of cholesterol from the outer mitochondrial membrane to the mitochondrial inner membrane.
Dehydroepiandrosterone, or DHEA, is produced when 17 alpha-hydroxylation of pregnenolone results in 17 OH pregnenolone. The subsequent transformation of DHEA into Andros enediol produces testosterone.
Both inherited and acquired conditions can result in hypogonadism. In pre-pubertal males, ambiguous genitalia, bilateral cryptorchidism, and micropenis are all symptoms of low testosterone. Youngsters undergo karyotype testing to rule out diseases like Klinefelter syndrome and Turner syndrome, which could also cause low testosterone levels.
Klinefelter’s syndrome, mumps orchitis, undescended testes, cancer drugs, normal aging, and hemochromatosis are a few reasons for primary hypogonadism. Kallman syndrome, HIV, pituitary issues, surgery, obesity, trauma, and Pressure-induced hypogonadism are some of the reasons for secondary hypogonadism.
https://www.ncbi.nlm.nih.gov/books/NBK532933/
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