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Liver--ast265 alt517
- Thread starter Tomo
- Start date
Well, that qualifies you as a grade III, grade IV if you have any associated consitutional symptoms.
First, stop any gear you are doing and anything else that may put stress on your liver. That means no rec. drugs, no alcohol, no Tylenol or Tylenol containing products etc.
Drink lots of fluids and reduce your workout intensity. If you start to have any symptoms (fever, lethargy, myalgias, stomache pain, especially upper right quadrant, jaundice, etc.) do not work out at all and call your doc.
Despite what many would like to believe, your liver is not very good at regenerating itself after significant assault. You liver is being assaulted if your LFT values are that high. It needs a break now.
Last, get another LFT done in two weeks unless your doc says otherwise. Again, if you have any symptoms, call your doc.
Good luck and what gear were you on? (I am assuming you were on)
First, stop any gear you are doing and anything else that may put stress on your liver. That means no rec. drugs, no alcohol, no Tylenol or Tylenol containing products etc.
Drink lots of fluids and reduce your workout intensity. If you start to have any symptoms (fever, lethargy, myalgias, stomache pain, especially upper right quadrant, jaundice, etc.) do not work out at all and call your doc.
Despite what many would like to believe, your liver is not very good at regenerating itself after significant assault. You liver is being assaulted if your LFT values are that high. It needs a break now.
Last, get another LFT done in two weeks unless your doc says otherwise. Again, if you have any symptoms, call your doc.
Good luck and what gear were you on? (I am assuming you were on)
4oomg test enanthate, and 75 mg eod fina- I'll stop immediately.
Just want to say to snarf thank you bro- I feel bad that I did this
Is there any hope for rejuvenation?
BTW billirubin 2.1
cholesterol 289
Triglycerides 363
hdl 15
vldl 72
ldl 201
Thats very high also, plus an echo discovered left ventricle hypertrophy. Coulsd these things have an effect --tomo
Just want to say to snarf thank you bro- I feel bad that I did this
Is there any hope for rejuvenation?
BTW billirubin 2.1
cholesterol 289
Triglycerides 363
hdl 15
vldl 72
ldl 201
Thats very high also, plus an echo discovered left ventricle hypertrophy. Coulsd these things have an effect --tomo
Hmm, kinda surprised your LFTs spiked like that on this cycle. How many weeks in were you and have you ever had your LFTs checked in the past? Were they elevated at all?
Don't get too worried about your lipids while on. Elevated lipids (cholesterol, trigycerides) take years to do damage. A 8-12 week cycle is not a big deal if they are slightly elevated. Yours are high, but if you stop the cycle, they have not had time to do any long term damage. The important thing is that they drop back down once you are off.
The echo in the left ventricle could be a sign of problems. Prolonged use of AAS can cuase your heart to hypertrophy jus tlike your skeletal muscles. The problem with this is as your heart gets bigger, it gets less efficient, which causes it to work harder, whcih causes it to continue to get larger. This is a vicious cycle that results in congestive heart failure. The only cure for that is a heart transplant. I would consult a cardiologost. You might need some cardio imaging to see the extant of the growth and the cardio will give you better advice than I can. What I do know is that you need to let your heart normalize. This means no gear and moderate training with light cardio. However, you need to get the cardiogram to really know what to do at this point.
There is a chance that the echo was there all the time and was never picked up before. I don't want to scare you, but you should have it looked out. You don't want to wait and wish you had.
Good luck and stay healthy.
Don't get too worried about your lipids while on. Elevated lipids (cholesterol, trigycerides) take years to do damage. A 8-12 week cycle is not a big deal if they are slightly elevated. Yours are high, but if you stop the cycle, they have not had time to do any long term damage. The important thing is that they drop back down once you are off.
The echo in the left ventricle could be a sign of problems. Prolonged use of AAS can cuase your heart to hypertrophy jus tlike your skeletal muscles. The problem with this is as your heart gets bigger, it gets less efficient, which causes it to work harder, whcih causes it to continue to get larger. This is a vicious cycle that results in congestive heart failure. The only cure for that is a heart transplant. I would consult a cardiologost. You might need some cardio imaging to see the extant of the growth and the cardio will give you better advice than I can. What I do know is that you need to let your heart normalize. This means no gear and moderate training with light cardio. However, you need to get the cardiogram to really know what to do at this point.
There is a chance that the echo was there all the time and was never picked up before. I don't want to scare you, but you should have it looked out. You don't want to wait and wish you had.
Good luck and stay healthy.
D
DaddyX
Guest
fina fucked me up pretty good with my counts
Quadsweep: Not directly in the medical care field but I work in the pharmaceutical industry and have been involved with drugs in the cardiovascular, pain management, HIV, oncology, and various other fields. One drug I deal with extensively has a high degree of hepatotoxicity, so I deal with elevated LFT issues all the time.
Seth Roberts
New member
liver values
Elevated ALT and AST values do not necessarily mean liver toxicity. They will often be elevated in atheletes and people who do regular strenuous exercise. You need to have CK levels done as well as GGT. If your AST, ALT and CK levels are elevated with no elevation in GGT then it is most likely exercise induced. If your GGt levels are also elevated then you have liver toxicity. Bilirubin can also be an indicator, but can be elevated without liver toxicity as well -- especialy if your red blood cell count is high.
I am not saying that you shouldn't be worried, just that more tests should be done. Also, left ventricular hypertrophy is common in athletes. If function is normal then there isn't too much to worry about--did the doc order more cardiovascular tests to be done? stress test etc...?.
Here are a couple references:
J Am Osteopath Assoc. 2001 Jul;101(7):391-4. Related Articles, Links
Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis?
Pertusi R, Dickerman RD, McConathy WJ.
Department of Medicine, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107-2699, USA.
The use of anabolic steroids among competitive athletes, particularly bodybuilders, is widespread. Numerous reports have noted "hepatic" dysfunction secondary to anabolic steroid use based on elevated serum aminotransferase levels. The authors' objective was to assess whether primary care physicians accurately distinguish between anabolic steroid-induced hepatotoxicity and serum aminotransferase elevations that are secondary to acute rhabdomyolysis resulting from intense resistance training. Surveys were sent to physicians listed as practicing family medicine or sports medicine in the yellow pages of seven metropolitan areas. Physicians were asked to provide a differential diagnosis for a 28-year-old, anabolic steroid-using male bodybuilder with an abnormal serum chemistry profile. The blood chemistries showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels. In the physician survey (n = 84 responses), 56% failed to mention muscle damage or muscle disease as a potential diagnosis, despite the markedly elevated CK level of the patient. Sixty-three percent indicated liver disease as their primary diagnosis despite normal GGT levels. Prior reports of anabolic steroid-induced hepatotoxicity that were based on aminotransferase elevations may have overstated the role of anabolic steroids. Correspondingly, the medical community may have been led to emphasize anabolic steroid-induced hepatotoxicity and disregard muscle damage when interpreting elevated aminotransferase levels. Therefore, when evaluating enzyme elevations in patients who use anabolic steroids, physicians should consider the CK and GGT levels as essential elements in distinguishing muscle damage from liver damage.
PMID: 11476029 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
3: Clin J Sport Med. 1999 Jan;9(1):34-9. Related Articles, Links
Anabolic steroid-induced hepatotoxicity: is it overstated?
Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.
The Department of Biomedical Science, University of North Texas Health Science Center, Fort Worth 76107-2699, USA.
OBJECTIVE: There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders. DESIGN: This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis. PARTICIPANTS: The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls. MAIN OUTCOME MEASURES: The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. RESULTS: In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT. CONCLUSION: Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.
PMID: 10336050 [PubMed - indexed for MEDLINE]
Elevated ALT and AST values do not necessarily mean liver toxicity. They will often be elevated in atheletes and people who do regular strenuous exercise. You need to have CK levels done as well as GGT. If your AST, ALT and CK levels are elevated with no elevation in GGT then it is most likely exercise induced. If your GGt levels are also elevated then you have liver toxicity. Bilirubin can also be an indicator, but can be elevated without liver toxicity as well -- especialy if your red blood cell count is high.
I am not saying that you shouldn't be worried, just that more tests should be done. Also, left ventricular hypertrophy is common in athletes. If function is normal then there isn't too much to worry about--did the doc order more cardiovascular tests to be done? stress test etc...?.
Here are a couple references:
J Am Osteopath Assoc. 2001 Jul;101(7):391-4. Related Articles, Links
Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis?
Pertusi R, Dickerman RD, McConathy WJ.
Department of Medicine, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107-2699, USA.
The use of anabolic steroids among competitive athletes, particularly bodybuilders, is widespread. Numerous reports have noted "hepatic" dysfunction secondary to anabolic steroid use based on elevated serum aminotransferase levels. The authors' objective was to assess whether primary care physicians accurately distinguish between anabolic steroid-induced hepatotoxicity and serum aminotransferase elevations that are secondary to acute rhabdomyolysis resulting from intense resistance training. Surveys were sent to physicians listed as practicing family medicine or sports medicine in the yellow pages of seven metropolitan areas. Physicians were asked to provide a differential diagnosis for a 28-year-old, anabolic steroid-using male bodybuilder with an abnormal serum chemistry profile. The blood chemistries showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels. In the physician survey (n = 84 responses), 56% failed to mention muscle damage or muscle disease as a potential diagnosis, despite the markedly elevated CK level of the patient. Sixty-three percent indicated liver disease as their primary diagnosis despite normal GGT levels. Prior reports of anabolic steroid-induced hepatotoxicity that were based on aminotransferase elevations may have overstated the role of anabolic steroids. Correspondingly, the medical community may have been led to emphasize anabolic steroid-induced hepatotoxicity and disregard muscle damage when interpreting elevated aminotransferase levels. Therefore, when evaluating enzyme elevations in patients who use anabolic steroids, physicians should consider the CK and GGT levels as essential elements in distinguishing muscle damage from liver damage.
PMID: 11476029 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
3: Clin J Sport Med. 1999 Jan;9(1):34-9. Related Articles, Links
Anabolic steroid-induced hepatotoxicity: is it overstated?
Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ.
The Department of Biomedical Science, University of North Texas Health Science Center, Fort Worth 76107-2699, USA.
OBJECTIVE: There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders. DESIGN: This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis. PARTICIPANTS: The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls. MAIN OUTCOME MEASURES: The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. RESULTS: In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT. CONCLUSION: Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.
PMID: 10336050 [PubMed - indexed for MEDLINE]
B
BrothaBill
Guest
Tomo said:
Ok, I wont touch the lft issue, since I dont directly deal with that issue. I do work in a cardiology group and deal directly with some issues.
1. Cholesterol is too high, consult physician about lowering with lipitor or other drugs. Diet should be changed.
2. Triglycerides too high, diet should be changed. Absolutely no high glycemic foods should be taken, i.e sugar, sugared pop, starches such as potatos, or anything processed like pasta or bread until those numbers are corrected.
3. Those are horrible lipid level percentages and increase your risk of heart disease tremendously, if you dont correct those numbers, you put yourself at high risk for a heart attack. No joke, I see patients with better numbers than that have to undergo coronary artery intervention.
4. LVH is consistent with High bp, If your numbers are high like this its b/c of the high glycemic carbs you are taking-most likely(obviously I havent examined you, so I dont know.) The High triglycerides we often see with high bp. Not going to explain the mechanism here. The edema from water retention will cause this too. The problem is I dont know how severe your LVH is. Is it 11mm or 20mm of your left ventricle. Some people have this naturally called hypertrophic cardiomyopathy. So we must know what is causing this. My experience which is more anecdotal than science is that LV wall thickness returns to normal after cessation of aas. I have often encouraged people I know who take aas to come in for a free screening of their heart and to compare before and after. I do the same here, if anyone wants to have there heart checked PM about coming to Seattle. The issue is this: cause and effect. Was it caused by the aas or just naturally occuring. I feel that something in you health genetic makeup is putting you at risk for the incorrect blood levels. I also feel that due to the history of people that I have examined that appear like you, is that you have too much refined food in your diet. NO PROCESSED FOOD,PASTA, BREAD, ALCOHOL, FRUITS, ANYTHING THAT COULD RAISE YOUR BLOOD SUGAR LEVELS, BASICALLY ANYTHING SWEET OR CARBO LOADED. Then check your blood levels and bp and I guarantee that Itll be lower. I win this bet 9/10 times.
lucias brown-- You are right on my brother. here is how it started
I was feeling heart symptoms, so instead of doing the right thing and going to the doc, I order a heart monitor watch, strange thing is, I'm never below a 100bpm, always around 120bpm even when waking up in the am. So now I go to doc. He checks bp, and its 140/90 checks heart rate at 120. orders echo and gives me a script for diovan. The rest is current history. I am going to follow your advice to the letter . Damn, I am lucky to be a memberr on this board -tomo
I was feeling heart symptoms, so instead of doing the right thing and going to the doc, I order a heart monitor watch, strange thing is, I'm never below a 100bpm, always around 120bpm even when waking up in the am. So now I go to doc. He checks bp, and its 140/90 checks heart rate at 120. orders echo and gives me a script for diovan. The rest is current history. I am going to follow your advice to the letter . Damn, I am lucky to be a memberr on this board -tomo
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