Bloods on a cruise

Does that answer it if they all come high does high CPK automatically mean there is no liver issue present or do I need further labs like the 2 I mentioned above

Ggt would be good it's used to help determine long term liver damage. If the others come back high but that comes back normal then you know that your body just needs a little break to catch back up. Bilirubin would be helpful too.
 
1) GGT would be good it's used to help determine long term liver damage.

2) If the others come back high but that comes back normal then you know that your body just needs a little break to catch back up.

3) Bilirubin would be helpful too.

1) Since no single transaminase elevation has the required sensitivity or specificity to DIAGNOSE the cause of hepatic injury, appropriate testing almost always mandates the use of several assays in conjunction with someone capable answering the question; What are U looking for?

This includes an ability to define terms such as "long term" - "liver damage" since roughly 10% of biopsy confirmed patients with Chronic Hep C or non-alcohol related fatty liver disease have NORMAL transaminase levels.

Consequently some hepatologists use GGT levels to help confirm ETOH (and a few other drugs) as the origin of hepatic cholestasis, but -- other transaminase ratios can provide similar information

2) Im unaware of this prognostic relationship bc it implies transaminase levels can be used to measure the degree of hepatic dysfunction, when hepatic enzyme changes are a better reflection of Hepatocyte integrity or the sludging of bile, as in cholestasis.

3) although useful when obtained in conjunction with other hepatic blood tests, selective testing such as a serum bilirubin lacks the degree of sensitivity or specificity ("accuracy" is the less precise collective lay term) to differentiate or diagnose the varied causes of hepatic injury.

So what LFTs should be obtained in those using AAS.

1) first understand the changes caused by AAS typically BEGIN to rise at around week FOUR

2) and tend to decline at around week SIX, providing the offending agent is discontinued

3 NO SINGLUAR TEST and I MEAN NONE provide the degree of accuracy required to diagnose AAS related hepatic injury

4) consequently several assays must be used IN CONJUNCTION with HISTORICAL factors to enhance the diagnostic accuracy.

5) obtaining "a bunch of tests" wo knowing how to interpret the results is usually an absolute waste of time and money --- so unless one has A LOT of both -- abnormalities require the assistance of a HCP IME.

And why is the latter generally a wise decision? Bc many cyclists have or have had a noteworthy lifestyle :) and are "at risk" for other causes of hepatic injury exclusive of AAS use

6) So what assays do I find are most useful to SCREEN for the presence of AAS related hepatic changes in PATIENTS I KNOW!

- AST
- ALT
- Bilirubin

- ALP is added in those patients
with suspected EXTRA-hepatic cholestasis like gallstones and perhaps on occasion I'll add a GGT for those with suspected INTRA-hepatic cholestasis, drugs being the more likely etiology OR in those with "mixed" transaminase changes

Sorry about the prolonged post but I hope it will aid a few.

Jim
 
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1) Since no single transaminase elevation has the required sensitivity or specificity to DIAGNOSE the cause of hepatic injury, appropriate testing almost always mandates the use of several assays in conjunction with someone capable answering the question; What are U looking for?

This includes an ability to define terms such as "long term" - "liver damage" since roughly 10% of biopsy confirmed patients with Chronic Hep C or non-alcohol related fatty liver disease have NORMAL transaminase levels.

Consequently some hepatologists use GGT levels to help confirm ETOH (and a few other drugs) as the origin of hepatic cholestasis, but -- other transaminase ratios can provide similar information

2) Im unaware of this prognostic relationship bc it implies transaminase levels can be used to measure the degree of hepatic dysfunction, when hepatic enzyme changes are a better reflection of Hepatocyte integrity or the sludging of bile, as in cholestasis.

3) although useful when obtained in conjunction with other hepatic blood tests, selective testing such as a serum bilirubin lacks the degree of sensitivity or specificity ("accuracy" is the less precise collective lay term) to differentiate or diagnose the varied causes of hepatic injury.

So what LFTs should be obtained in those using AAS.

1) first understand the changes caused by AAS typically BEGIN to rise at around week FOUR

2) and tend to decline at around week SIX, providing the offending agent is discontinued

3 NO SINGLUAR TEST and I MEAN NONE provide the degree of accuracy required to diagnose AAS related hepatic injury

4) consequently several assays must be used IN CONJUNCTION with HISTORICAL factors to enhance the diagnostic accuracy.

5) obtaining "a bunch of tests" wo knowing how to interpret the results is usually an absolute waste of time and money --- so unless one has A LOT of both -- abnormalities require the assistance of a HCP IME.

And why is the latter generally a wise decision? Bc many cyclists have or have had a noteworthy lifestyle :) and are "at risk" for other causes of hepatic injury exclusive of AAS use

6) So what assays do I find are most useful to SCREEN for the presence of AAS related hepatic changes in PATIENTS I KNOW!

- AST
- ALT
- Bilirubin

- ALP is added in those patients
with suspected EXTRA-hepatic cholestasis like gallstones and perhaps on occasion I'll add a GGT for those with suspected INTRA-hepatic cholestasis, drugs being the more likely etiology OR in those with "mixed" transaminase changes

Sorry about the prolonged post but I hope it will aid a few.

Jim

Yeah I would have to say I agree 100% with everything you've said. Without having a persons complete history it is difficult to determine cause of hepatic injury which is why it's ideal for people to have a doctor they know with plenty of pre-lifestyle bloods.

As far as your reference to #2 you are correct in that it could not be used to measure hepatic disfunction. I was interested in the cpk value just to see if maybe it's extremely elevated and there's possible muscle damage from excessive training or such.
 
No one knows for certain, but one things for sure comparing today's lab data from that which was obtained weeks or months ago says next to nothing about causation.

And for someone who is "blasting" oral agents for WEEKS on end to believe subsequent LFTs changes are the result of a "power lifters exercise regimine" rather than toxin mediated hepatocyte injury is ignorant and that's being kind

Nonetheless unless the condition is chronic, such as hepatitis, the assays must ALL be obtained within the same interval as exposure to the offending agent/s
 
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As I said I have never ran dbol for 6 months and if I called you illiterate would be kind too I won't do it since I appreciate your help in telling me which bloods I need thank you
 
As I said I have never ran dbol for 6 months and if I called you illiterate

comparing today's lab data from that which was obtained weeks or months ago says next to nothing about causation.

And for someone who is "blasting" oral agents for WEEKS on end .....

I only hope one day you will understand the importance of READING the posts of others, rather "seeing" what you want to see and coming off as some delusional thin skinned child.

Adios
 
And you clearly don't understand the meaning of your underlined quote or you missed the fact I am not on orals for 1 month now and your phrasing made it sound as if I am still on anyway will post bloods as soon as I can
 
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1)

So what LFTs should be obtained in those using AAS.

1) first understand the changes caused by AAS typically BEGIN to rise at around week FOUR

2) and tend to decline at around week SIX, providing the offending agent is discontinued


Jim

Damn Jim how about a summary of all that stuff dude.

OK :)

Useful tests for those who want to check their LIVER

1) AST
2) ALT (in general ALT elevations exceed that of AST when AAS are the cause)
3) Bilirubin
4) ALP ??? is the fourth assay included in many LFT screening "bundles" ----- but

Enzyme changes that exceed 3 X the upper limit of normal warrant discontinuation of the offending agent, ESPECIALLY if associated with an elevated bilirubin.

Other assays that may be useful include;
1) GGT
2) CPK
3) Alkaline Phosphatase (AKA - - - - -ALP)

GGT ---- is often elevated when drugs (ETOH and "hormones" in particular) are the suspected cause of an elevated ALT

CPK --- may also be elevated when exercise is the primary cause of enzyme elevations
however novice endurance enthusiasts who have limited access to WATER are MUCH more likely to develop CPK changes rather than BB !

ALP --- with a few exceptions changes in ALP suggest a NON-AAS etiology is the source of hepatic injury!


JIM
 
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Damn Jim how about a summary of all that stuff dude.

OK :)

Useful tests for those who want to check their LIVER

1) AST
2) ALT (in general ALT elevations exceed that of AST when AAS are the cause)
3) Bilirubin
4) ALP ??? is the fourth assay included in many LFT screening "bundles" ----- but

Enzyme changes that exceed 3 X the upper limit of normal warrant discontinuation of the offending agent, ESPECIALLY if associated with an elevated bilirubin.

Other assays that may be useful include;
1) GGT
2) CPK
3) Alkaline Phosphatase (AKA - - - - -ALP)

GGT ---- is often elevated when drugs (ETOH and "hormones" in particular) are the suspected cause of an elevated ALT

CPK --- may also be elevated when exercise is the primary cause of enzyme elevations
however novice endurance enthusiasts who have limited access to WATER are MUCH more likely to develop CPK changes rather than BB !

ALP --- with a few exceptions changes in ALP suggest a NON-AAS etiology is the source of hepatic injury!


JIM

Off topic but if I want to send you a pm with a question how would I do that?
 
Off topic but if I want to send you a pm with a question how would I do that?

Unfortunately bc PED forums tend to attract the good AND the bad as in the despondent, destitute, depressed, clowns, trolls, fools, drug seekers (you name it and I've prob received it) bla, bla, bla, I had to to restrict my PM requirements
considerably.

No offense but for those reasons I only accept PM's from "those I follow".

And I only "follow" those I know are "level headed" reasonably well informed members.

JIM
 
And again you have my thanks can you tell me if any of those enzymes have to be taken fasted or does that have impact on results as I had my previous bloods fasted cause of cholesterol too
 
And you can see the new bloods now

Bilirubin 6.4 umol/l (<21)
AST 43 U/l (<44)
ALT 90 U/l (<44)
GGT 20 U/l (5-50.0)
CPK 625 U/l (25-195)
 
Walked by the lab yesterday and went for another test it came to:

AST 48.31 U/l (2-40)
ALT 79.75 U/l (2-40)

I have used 2 different labs hence the difference in ULN... Kind of puzzled by why is ALT high for that long now... Can that happen to be hepatitis considering the ggt and bilirubin value?
 
AST: 25 U/l (<44)
ALT: 44 U/l (<44)
Almost back to normal now.
I have discontinued all multivitamin and other tablet form supplements for 3 days that had my value come down to nearly half. Actually it could have probably had nothing to do with that. Anyway time for superdrol now.
 
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