Freakenstien
07-19-2016, 05:39 AM
My doc is open minded and Im going to try to help guide him through what i need..
Im going in for my initial bloods before I go back on.. Can anyone tell me if I have missed anything in regards to getting bloods done..
BIOAVAILABLE TESTOSTERONE
Where we actually get the “bang” for the hormonal buck, so to speak. This is the actual amount the body has available for use, as the concentration of hormone available within the capillary beds approximates the sum of the Free Testosterone plus that which is loosely bound to carrier proteins, primarily albumin. If Bio T is not readily available, Free T may be a second choice substitute, as Bio T and Free T serum concentrations are well correlated.
ESTRADIOL
There are several reasons why this assay is VERY important, and should not be ignored in ANY hypogonadism work-up (or subsequent regimen). First, you definitely need to draw a baseline. Next, elevated estrogen can, in and of itself, explain hypogonadal symptoms. If E is elevated, controlling serum concentrations (usually with an aromatase inhibitor, which prevents conversion of T into E) may suffice in clearing the symptoms of hypogonadism. And finally, rechecking it after beginning the initial dose of testosterone will give the astute physician valuable information as to how the patient’s individual hormonal system functions, as well as making sure estrogen does not elevate inappropriately secondary to the testosterone supplementation.
I don’t waste time and money drawing estrone and estriol. E2 is the player of interest here. Unless you specify a ‘sensitive’ assay for male patients, the lab will run the Rapid Estradiol for fertility studies in females, which is useless for our purpose here. Quest Diagnostics calls this their Estradiol by Extraction Method.
Some practitioners believe that it is only the T/E ratio which is significant, and therefore, as long as E “appropriately” rises with elevations in T, all is well. However, the absolute concentration of E is of concern, too, especially in light of new information pointing to elevated estrogen as cause, or adjunctively encouraging, several serious disease processes, including prostate and colon cancer.
LH
As everyone knows, it is LH which stimulates the Leydig cells of the testes to produce testosterone. A caveat, however: LH has a half-life of only about 30 minutes. When you combine this fact with the absolute pulsatile nature of its pituitary release, care must be taken to not place too much weight upon a single draw. A luxury would be to acquire serial draws, say, twenty minutes apart. However, such would be both inconvenient and probably prohibitively expensive for the patient. The most important reason to assay the gonadotrophins is to differentiate between primary and secondary (hypogonadotrophic) hypogonadism.
FSH
The eight hour half-life of this hormone makes it a better marker for gonadotrophin production. It is also less an acute phase reactant to varying serum androgen and estrogen levels than LH. Greatly elevated FSH levels could signal a gonadotrophin-secreting pituitary tumor.
Of note, I run FSH (but not LH) on the follow-up labs, the new third generation (“sensitive”) assay, to determine the magnitude of HPTA suppression secondary to androgen therapy. It also provides valuable information for those patients undergoing TRT who are interested in the state of their fertility.
PROLACTIN
A very important hormone, and must not be overlooked on initial work-up. Approaching five percent of hypogonadotrophic hypogonadism is associated with hyperprolactinemia, due to inhibition of hypothalamic release of LHRH. Its serum concentration must be maintained within physiological range (meaning neither too high nor too low). Greatly elevated hyperprolactinemia, or hyperprolactinemia plus a Total Testosterone less than 150ng/dL, equals a trip to an Endocrinologist for an MRI of the sella turcica.
CORTISOL
True Anti-Aging medicine must be well-familiarized with the ins and outs of this hormone, the only one our bodies cannot live without. Elevated levels can cause secondary (hypogonadotrophic) hypogonadism. I try controlling elevated cortisol with Phosphatidylserine, 300mg QD, with good results. It is just as important to watch for depressed cortisol levels, as well. The assay of choice for that condition is a 24-hour urine.
CBC
This is just good medicine. Ruling out anemia is important, of course, as it may be a cause for the fatigue which brought the patient into your office. You also want to establish baseline H&H, for those rare cases where polycythemia becomes a problem (and we are reminded smokers are at increased risk for polycythemia). Above 18.0/55.0 TRT is withheld, and therapeutic phlebotomy recommended.
CMP
Again, just good medicine. Baseline for sodium (which may elevate initially secondary to androgen supplementation) is important. We also want to see LFT’s, as elevations in same secondary to androgen supplementation are listed as a possible side effect in the product literature (although I have yet to see this actually happen). I like the BUN/creatinine ratio as a marker for hormonal hemo-concentration, and also it gives me a hint of how compliant the patient will be (because I always tell them to make sure to drink plenty of water while fasting for the test).
Lipid Panel
This is drawn to provide your bragging rights when you drop the CHOL 30 points, thanks to your own good administration of TRT. You should expect to see lowered TRIG and LDL’s, too. Be advised, this will not happen if you choose to elevate their androgens above the top of “normal” range, i.e. providing what amounts to an anabolic steroid cycle. Of course, this would no longer constitute TRT, as the practitioner would then be choosing to damage the health and well-being of the patient.
HDL does frequently drop a bit, but that is believed to be due to increased REVERSE cholesterol transport; so much of the plaque is, after being scavenged from the lining of the CV system by HDL, now being chewed up by the liver. Androgens also elevate hepatic lipase, and this may have an effect. The important thing to keep in mind is that TRT inhibits foam cell formation.
PSA
For all patients over 40. Even though prostate CA is rare in men under the age of fifty, we don’t want it happening on our watch, do we? At this time, rises in PSA above 0.75 are a contraindication to TRT (until follow-up by a Urologist). You may find that, at the initiation of TRT in older men, when serum androgen levels are accelerating, PSA may, too. This is especially true when transdermal delivery systems are employed, because they more greatly elevate DHT. Once T levels have stabilized, PSA drops back down to roughly baseline. You won’t really see gross elevations in PSA secondary to TRT administration in younger patients. New TRT patients need to be cautioned, and reminded, to abstain from sexual relations prior to the draw, as they may now be enjoying greatly elevated amounts of same.
I get a PSA up front on my over 40 patients, at the one month follow-up in my more senior patients, and every six months after that. DRE (Digital Rectal Exam) is recommended twice per year as well, although the American Academy of Clinical Endocrinologists backs “every six to twelve months” in their 2002 Guidelines for treating hypogonadotrophic patients with TRT.
Im going in for my initial bloods before I go back on.. Can anyone tell me if I have missed anything in regards to getting bloods done..
BIOAVAILABLE TESTOSTERONE
Where we actually get the “bang” for the hormonal buck, so to speak. This is the actual amount the body has available for use, as the concentration of hormone available within the capillary beds approximates the sum of the Free Testosterone plus that which is loosely bound to carrier proteins, primarily albumin. If Bio T is not readily available, Free T may be a second choice substitute, as Bio T and Free T serum concentrations are well correlated.
ESTRADIOL
There are several reasons why this assay is VERY important, and should not be ignored in ANY hypogonadism work-up (or subsequent regimen). First, you definitely need to draw a baseline. Next, elevated estrogen can, in and of itself, explain hypogonadal symptoms. If E is elevated, controlling serum concentrations (usually with an aromatase inhibitor, which prevents conversion of T into E) may suffice in clearing the symptoms of hypogonadism. And finally, rechecking it after beginning the initial dose of testosterone will give the astute physician valuable information as to how the patient’s individual hormonal system functions, as well as making sure estrogen does not elevate inappropriately secondary to the testosterone supplementation.
I don’t waste time and money drawing estrone and estriol. E2 is the player of interest here. Unless you specify a ‘sensitive’ assay for male patients, the lab will run the Rapid Estradiol for fertility studies in females, which is useless for our purpose here. Quest Diagnostics calls this their Estradiol by Extraction Method.
Some practitioners believe that it is only the T/E ratio which is significant, and therefore, as long as E “appropriately” rises with elevations in T, all is well. However, the absolute concentration of E is of concern, too, especially in light of new information pointing to elevated estrogen as cause, or adjunctively encouraging, several serious disease processes, including prostate and colon cancer.
LH
As everyone knows, it is LH which stimulates the Leydig cells of the testes to produce testosterone. A caveat, however: LH has a half-life of only about 30 minutes. When you combine this fact with the absolute pulsatile nature of its pituitary release, care must be taken to not place too much weight upon a single draw. A luxury would be to acquire serial draws, say, twenty minutes apart. However, such would be both inconvenient and probably prohibitively expensive for the patient. The most important reason to assay the gonadotrophins is to differentiate between primary and secondary (hypogonadotrophic) hypogonadism.
FSH
The eight hour half-life of this hormone makes it a better marker for gonadotrophin production. It is also less an acute phase reactant to varying serum androgen and estrogen levels than LH. Greatly elevated FSH levels could signal a gonadotrophin-secreting pituitary tumor.
Of note, I run FSH (but not LH) on the follow-up labs, the new third generation (“sensitive”) assay, to determine the magnitude of HPTA suppression secondary to androgen therapy. It also provides valuable information for those patients undergoing TRT who are interested in the state of their fertility.
PROLACTIN
A very important hormone, and must not be overlooked on initial work-up. Approaching five percent of hypogonadotrophic hypogonadism is associated with hyperprolactinemia, due to inhibition of hypothalamic release of LHRH. Its serum concentration must be maintained within physiological range (meaning neither too high nor too low). Greatly elevated hyperprolactinemia, or hyperprolactinemia plus a Total Testosterone less than 150ng/dL, equals a trip to an Endocrinologist for an MRI of the sella turcica.
CORTISOL
True Anti-Aging medicine must be well-familiarized with the ins and outs of this hormone, the only one our bodies cannot live without. Elevated levels can cause secondary (hypogonadotrophic) hypogonadism. I try controlling elevated cortisol with Phosphatidylserine, 300mg QD, with good results. It is just as important to watch for depressed cortisol levels, as well. The assay of choice for that condition is a 24-hour urine.
CBC
This is just good medicine. Ruling out anemia is important, of course, as it may be a cause for the fatigue which brought the patient into your office. You also want to establish baseline H&H, for those rare cases where polycythemia becomes a problem (and we are reminded smokers are at increased risk for polycythemia). Above 18.0/55.0 TRT is withheld, and therapeutic phlebotomy recommended.
CMP
Again, just good medicine. Baseline for sodium (which may elevate initially secondary to androgen supplementation) is important. We also want to see LFT’s, as elevations in same secondary to androgen supplementation are listed as a possible side effect in the product literature (although I have yet to see this actually happen). I like the BUN/creatinine ratio as a marker for hormonal hemo-concentration, and also it gives me a hint of how compliant the patient will be (because I always tell them to make sure to drink plenty of water while fasting for the test).
Lipid Panel
This is drawn to provide your bragging rights when you drop the CHOL 30 points, thanks to your own good administration of TRT. You should expect to see lowered TRIG and LDL’s, too. Be advised, this will not happen if you choose to elevate their androgens above the top of “normal” range, i.e. providing what amounts to an anabolic steroid cycle. Of course, this would no longer constitute TRT, as the practitioner would then be choosing to damage the health and well-being of the patient.
HDL does frequently drop a bit, but that is believed to be due to increased REVERSE cholesterol transport; so much of the plaque is, after being scavenged from the lining of the CV system by HDL, now being chewed up by the liver. Androgens also elevate hepatic lipase, and this may have an effect. The important thing to keep in mind is that TRT inhibits foam cell formation.
PSA
For all patients over 40. Even though prostate CA is rare in men under the age of fifty, we don’t want it happening on our watch, do we? At this time, rises in PSA above 0.75 are a contraindication to TRT (until follow-up by a Urologist). You may find that, at the initiation of TRT in older men, when serum androgen levels are accelerating, PSA may, too. This is especially true when transdermal delivery systems are employed, because they more greatly elevate DHT. Once T levels have stabilized, PSA drops back down to roughly baseline. You won’t really see gross elevations in PSA secondary to TRT administration in younger patients. New TRT patients need to be cautioned, and reminded, to abstain from sexual relations prior to the draw, as they may now be enjoying greatly elevated amounts of same.
I get a PSA up front on my over 40 patients, at the one month follow-up in my more senior patients, and every six months after that. DRE (Digital Rectal Exam) is recommended twice per year as well, although the American Academy of Clinical Endocrinologists backs “every six to twelve months” in their 2002 Guidelines for treating hypogonadotrophic patients with TRT.