Cr250owner
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got some vic's i'd like too pop but i just started taking methadrol, and i know drinking is not recommended because of the liver, but is taking vicodin alright? i'm thinking no?
SwoleInNY
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Don't do it. If youre taking the vicodin for an injury you should wait until that injury is resolved before you cycle. If you are taking it recreationally then you can hold off untill your liver has recovered from superdrol. There is no reason to be taking both of these substances at the same time.
pdigs
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people are all liver crazy on this forum, vicodins fine a couple wont matter. now if u were popin 50 at one time thats somethin else, might wanna hold off. the whole liver thing on this site is overrated. i know people that have drank a liter vodka everyday for 20yrs that have liver problems.... a couple vicodin on a cycle wont do ****
Trauma1
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Vicodin/Lortab/Lorcet/Hydrocet = Hydrocodone/APAP(Acetaminophen or Tylenol)
The tylenol concentration can be different depending on the script for vicodin, however that far from matters anyway.
Tylenol is metabolized extensively via the hepatic(liver) route and will cause liver stress. Taking this in addition to superdrol IS A BAD IDEA.
In short.......don't take it.
The tylenol concentration can be different depending on the script for vicodin, however that far from matters anyway.
Tylenol is metabolized extensively via the hepatic(liver) route and will cause liver stress. Taking this in addition to superdrol IS A BAD IDEA.
In short.......don't take it.
Trauma1
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Wow.....you truly are clueless. :fool2:
pdigs
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if your just looking for high, find some oxycontins and snort em. might be a little pricey though hehe
pdigs
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ya... just as clueless as somebody worried about there liver and doing steroids:fool2:. makes alot of sense doesnt it
Cr250owner
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yea i was just gonna take em for fun, i guess i'll just hold off.
since were talking about thiss...
would smokin bud effect anything during a cycle?
since were talking about thiss...
would smokin bud effect anything during a cycle?
Trauma1
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I'm sure you mean "Their" liver.
Not to mention the fact that this post makes absolutely no sense at all.....
MuscleBound1337
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Opiates aren't liver toxic, but most painkillers are combined with other stuff like acetomenophen which is really toxic. I took 4 grams of tylenol a day for 2 weeks and I ended up in the hospital.
Trauma1
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Yup - Anything over 3 grams/day for any significant time period is a very bad idea.
Now i'm curious, so i'll ask. Why were you taking 4 grams/day of tylenol?
MuscleBound1337
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Well I had mono. My throat was killing me and i had a fever for 2 weeks so I went to the ER on night when It was really bad and they said they would test me for Mono and call me back if I had it later that night. They prescribed antibiotics for strep even tho they tested for strep and said i didn't have it. Well after two more days of taking the antibiotics I just got more sick. I couldn't even keep water down, so I was really dehydrated, like I felt high almost. So I drop by the ER again and there like oh yeah you have mono from those tests we took. Oh well that's nice. They were going to release me with vics and corticosteriods after they gave me 2 liters of fluid IV. But they did bloodword to see my liver function and they saw my ski high levels. Mono itself can give you crappy liver function, but taking it with the tylenol couldn't have helped. They insisted on admiting me to the hospital. The put me on NAC IV. I told them I could just go home and take that **** myself but they admitted me anyways.
Trauma1
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Yeah Epstein Barr(Mono) can cause significant hepatic and spleen involvement. Coupled with huge doses of tylenol, that isn't good.
Well i hope all is well now brother.
That's some story though. I'm not sure why they coulnd't give you your mono spot(tests for mononucleosis) result that night. It doesn't take too long to run the test. However, it takes a good amount of time for this antibody test to pop up positive anyway. Often people have mono, but the mono spot reads negative initially. This is due to insufficient detectable antibody levels that correlate with new onset of the illness.
MuscleBound1337
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Yeah. After a night in the hospital they decided I was well enough to leave. The original plan was 2 or 3 nights to receive the 'tylenol antidote' as they called it. All I saw on the bag was NAC.. But they followed up with bloodwork 2 weeks after and then again in another 2 weeks. I started taking milk thistle when I got home and after 4 weeks I was within normal limits again. I had a crazy experience with that illness. It was so weird. I knew some **** was going on with my doctor, every time I saw that guy he was acting weirder and weirder. About a month after I had my last bloodwork, they found him (my doctor) in the woods naked looking for a bear. And then a week later he shot himself.
Trauma1
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Yeah IV N-Acetyl Cysteine(NAC) or Mucomyst is the treatment for tylenol toxicity. Glad to hear everything is ok now.
Crazy about the doctor though. Believe it or not, the doctor that delievered my brother and I commited suicide years after that i came to find out per my mom. Crazy sh*t huh lol.
LatsRus
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man i dont get it - these doc's wtf!! i had mono about 6 months ago, and my doc told me to take ibuprofin over tylenal, because of toxicity, and so i did and that worked, went through a whole bottle in 3 weeks. i kno others tho that their doc TOLD them to take tylenal, i coudlnt believe it.
A_I_Sports_Nutrition
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This is very poor advice
jcp2
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I pretty much have to agree with this. Superdrol though is the one thing out thier today where i can't get a good feel as per the liver toxicity. Meaning i am not sure if it is worse than anything legal or illegal on the market. One thing on this board, i have a hard time weeding out true toxicity and just info that gets passed on and on and on that is most likely not correct. That being said if something is so toxic that you can't take a tylenol with it, why the **** would anyone take it.
pmiller383
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If you are not dedicated enough to put your recreational away during a cycle, you should not be doing a cycle period. Cannabis can lower testosterone if frequently used therefore you are going to cut your cycle short. Granted it may only be a little bit but none the less if you are serious to run a cycle you should want to maximize the benefits of the cycle. Do I think the occasional bong load on a weekend is going to hurt you, no but judging by you two post I am lead to believe you enjoy chemical alteration to your body and sense. Just figure out why you are doing the cycle in the first place and that should help you answer your questions. I don't mean to come of negative in this post so my apologies if I did. Good Luck!
pdigs
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i dont mean to give "bad" advice, if i did im sorry. im an optimistic and realist by nature. ive been in and out of drug treatment centers, had my problems in the past.... and let me tell u ive seen alot of stuff. the liver can take a massive ammount of abuse, stuff thats not even in the same range as a ph cycle or 4grams of tylonol... i myself have taken 25gs of tylonol at once, liver hurt for a day but i was fine. to do significate damage to ur liver it takes prolonged abuse for many years, not a one month prohormone cycle believe me. thats why i have to roll my eyes when i see all these overdone precautions taken on this site... im sorry but people blow it way out of proportion... YOUR NO GOING TO GO TO THE HOSPITAL FOR ODING ON STEROIDS lol. if u take it all into account... u could do a a ph cycle with absolutly no liver support and absolutely no pct.... and 99 times out of 100 ull be fine and thats the truth, u wont die from liver failure. basic rule of thumb... if ur prone to gyno, ull probably have a better chance of gyno. if ur prone to hairloss, u might lose ur hair..yes, there are things to help it true but its not a for sure chance of preventing it... i still take precautions as well dont get me wrong, but i cant take all the "oh my god that will kill ur liver mentality" on the site. besides, if ur so worried about ur liver and body function, why do steroids to begin with?
Iron Lungz
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I agree, T1...
Just my opinion.
And to the OP... You seem like you just want to get high. The way I see it, just do it, get sick or die, and there will be one less sorry-ass in this world for my tax dollars to support.
Just my opinion.
hurdlemaker
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just smoke u jackasses
Trauma1
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Oh my dear god........ :shakes head: :blink:
jcp2
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Please refute this comment, i want to hear some real info the other way. I can only base my thoughts on the medical community. All the steroids out their have been used for mediicinal purposes and all were used for extensive periods, i have never found much on long term liver sides from these drugs. The most i have found were liver issues with anadrol use that were all reversed upon the drug use being terminated. All people on this board ever tell me is that they have done their research and so should I, i have been reading studies since the majority of them were 14 or 15. From actual observation in real world scenarios and real world studies i cannot find any trend in liver damage from steroid use. What i am asking for is someone to Please show me what they are constantly talking about. I am completely open minded, i just want the info.
Rhyno
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Found one so far. This is from the MD forum:
Normal values for AST and ALT are 40 and 45 (IU/L)respectively. Now elevated liver values aren't always the best indicator for liver damaged, but when a person's ALT levels are almost seven times what is normal, you know something is up. Imho, if you brought those levels to a doctor, he would probably go ape sh*t.
jcp2
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Yeah, i beleive that. I also do beleive that the values are not a very good indicator of real long term damage. I also posted something somewhere about not being able to get my hands around the toxicity of superdrol because it is hard to find some real world info. IMO if this product is as bad as these results say it is, this is something that should not be sold otc. I need to go home tonight and see if i can dig up some numbers associate with anadrol and anavar usage as the are probably the most prevelant real steroids i will be able to find. I also want to see ranges for accutane as well. I wish i had alot of the studies i used to have on my harddrive because finding alot of **** again is a real pain in the ass.
dkkon1
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It all comes down to risk vs. reward. If its worth the slight chance of you having problems to get a buzz, then do it. But if thats not a risk youre willing to take, well then don't take it.
futurepilot
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Simple as pie.
Trauma1
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Here is a few threads i posted in a few months back:
http://anabolicminds.com/forum/steroids/85322-help-first-cycle.html
http://anabolicminds.com/forum/steroids/78245-some-more-bloodwork.html
http://anabolicminds.com/forum/steroids/85322-help-first-cycle.html
http://anabolicminds.com/forum/steroids/78245-some-more-bloodwork.html
Trauma1
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This is a great read guys:
Steroids with Michael Scally, MD
Oral Anabolic Steroids, Liver Enzyme Tests and Liver Function
by Michael C. Scally, M.D.Author of eBook Human Experimentation in Anabolic Steroid Research by Michael Scally, M.D.
Harvard Medical School - M.D.; Harvard-M.I.T. Program In Health Science & Technology
Massachusetts Institute of Technology, B.S. Chemistry/LIfe Sciences
Dr. Scally early on recognized the lack of research and treatment for individuals using anabolic-androgenic steroids (AAS). He has remained as the sole physician by reputation and publication to actively pursue and advocate the proper use of AAS to optimize health. Dr. Scally has personally cared for thousands of individuals using AAS. His protocol for Anabolic Steroid Induced Hypogonadism has been presented before the Endocrine Society, American Association of Clinical Endocrinologists, American College of Sports Medicine, & International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV.
Question:
Do oral steroids have long-term effects on liver function long after they have been discontinued? I have done quite a few cycles of anadrol and dianabol in the past. But I haven’t done any oral AAS, prohormones, legal or otherwise in several years and my liver function tests are still elevated (AST and ALT). They are about double the top of the normal range. Can any other factors account for this e.g. dietary supplements, genetics, intense physical exercise, heavy childhood use of NSAIDs?
Response:
Mild elevations in liver chemistry tests such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST) can reveal serious underlying conditions or have transient and benign etiologies. There are no controlled clinical trials examining the optimal approach for evaluating serum liver chemistries. The American Gastroenterological Association guideline regarding the evaluation and management of abnormal liver chemistry tests proposes a practical, algorithmic approach when the history and physical examination do not reveal the cause.
The history should be thorough, with special attention given to the use of medications, vitamins, herbs, drugs, and alcohol; family history; and any history of blood-product transfusions.[1] In addition to liver chemistries, an initial serologic evaluation includes a prothrombin time; albumin; complete blood count with platelets; hepatitis A, B, and C serologies; and iron studies. The most common causes of elevated aminotransferase levels include alcohol-related liver injury, chronic hepatitis B and C, autoimmune hepatitis, hepatic steatosis (fatty infiltration of the liver), nonalcoholic steatohepatitis, hemochromatosis, Wilson's disease, alpha1-antitrypsin deficiency, and celiac sprue.
Depending on the etiology, management strategies may include cessation of alcohol use, attention to medications, control of diabetes, and modification of lifestyle factors such as obesity. If elevations persist after an appropriate period of observation, further testing may include ultrasonography, other serum studies, and in some cases, liver biopsy.[2] Isolated alterations of biochemical markers of liver damage in a seemingly healthy patient often represent a challenge even for the experienced clinician and usually set off a battery of further, costly tests and consultations that may ultimately prove unnecessary.
The liver is the largest and most metabolically complex organ in humans. The liver receives a dual blood supply. The portal vein drains the splanchnic, viscera, circulation and provides 75% of the total blood flow. The hepatic artery provides the remaining 25%. The hepatic vein carries all efferent blood to the inferior vena cava. Rich supplies of lymphatic vessels also drain the liver.
The liver is a complex organ with interdependent metabolic, excretory, and defense functions. Hepatocytes make up the bulk of the organ. Sinusoidal lining cells comprise at least four distinct populations: endothelial cells, Kupffer's cells, perisinusoidal fat-storing cells and pit cells. Endothelial cells are responsible for endocytosis of molecules and particles, and play a role in lipoprotein metabolism. Spindle-shaped Kupffer's cells are tissue macrophages. Perisinusoidal fat-storing cells (Ito cells) store vitamin A. Pit cells are large, granular lymphocytes, which function as natural killer cells.
The liver plays a central role in carbohydrate, protein, and fat metabolism. It stabilizes glucose level by taking up and storing glucose as glycogen (glycogenesis), breaking glycogen down to glucose (glycogenolysis), and forming glucose from noncarbohydrate sources (gluconeogenesis). The liver synthesizes the majority of proteins that circulate in the plasma, including albumin and most of the globulins other than gamma globulins. It is responsible for synthesizing and secreting bile and plasma proteins, including clotting factors. The liver is the site of most amino acid interconversions and catabolism. Amino acid deamination produces urea and esterification of fatty acids produces triglycerides. The liver packages triglycerides with cholesterol, phospholipids, and an apoprotein into a lipoprotein. The lipoprotein enters blood for utilization or storage in adipocytes. Most cholesterol synthesis takes place in the liver.
The liver detoxifies noxious substances arriving from the splanchnic (viscera) circulation, preventing them from entering the systemic circulation. This particularly makes the liver susceptible to drug-induced injury. The liver converts some lipophilic compounds into more water-soluble agents and others to less active agents. In conjunction with the spleen, it is involved in the destruction and reclamation of spent red blood cells.
Prior to a discussion of liver pathology, it is important to have an understanding in the interpretation of laboratory tests. Normal refers to a theoretical frequency distribution for a set of variable data, usually represented by a bell-shaped curve symmetrical about the mean. Laboratory values for a reference range are from a group of healthy individuals with no known factors (medications, illness, genetics, etc.) that would influence the outcome of the testing. The reference range for a particular laboratory test is dependent upon a given subpopulation (e.g., male, female, or children) and the testing laboratory or manufacturer. Federal regulations require laboratories to adhere to certain standards. "Prior to reporting patient test results, the laboratory must verify or establish, for each method, the performance specifications for the following performance characteristics: accuracy; precision; analytical sensitivity and specificity, if applicable; the reportable range of patient test results; the reference range(s) (normal values); and any other applicable performance characteristic."[3] The normal reference range typically refers to the mean or average +2 standard deviations.[4] Interpretation of results is being either within, normal, for a value falling within this bell-shaped curve (reference range) or outside, abnormal, the reference range. Accordingly, 2.5% of normal patients have "abnormal" aminotransferase levels.
A basic tenet, standard practice, of medicine is that interpretation of results is within the framework of a patient's medical condition and treatment, the overall health of the patient.[5] Physicians are taught to think about clinical testing in terms of the clinical significance (particularly, predictive value) of a given test in a given situation. All tests have strengths and limitations for their use in reaching a certain diagnosis or making a causal inference. The risk of a test is seldom inherent in the test itself, but rather is a function of the context in which use of the test is providing information for medical decision-making. Many factors affect test results including sex, medications, overall health of the individual, temporal influences, and variations in laboratory techniques. Thus, in terms of diagnosis, interpretation of a diagnostic test is in the context of history, examination, other tests, and other relevant medical considerations.[6] The proper and correct interpretation for a test is within the situational context.
Levels of serum liver enzymes are indications of hepatocyte integrity or cholestasis rather than liver function. A change in serum protein levels or clotting times may be associated with a decrease in liver functioning mass, although neither is specific for liver disease. No single or simple test assesses overall liver pathology. Use of several screening tests improves the detection of hepatobiliary abnormalities, differentiates the basis for clinically suspected disease, and determines the severity of liver disease (hepatocytes (hepatocellular dysfunction), the biliary excretory apparatus (cholestasis), and the vascular system (portal hypertension)).
The widespread availability and use of serum blood chemistries for screening both symptomatic and asymptomatic patients has resulted in a dramatic increase in the number of normal and abnormal liver chemistry tests requiring interpretation by physicians. A number of review articles on the evaluation of abnormal liver function tests are available on the internet.[7] Aminotransferases (transaminase) include alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Both are exquisitely sensitive indicators of hepatocellular injury and provide the best guide to hepatocellular necrosis/inflammation.[8]
ALT (8-37 IU/L) is present in hepatocytes (liver cells) and is reliable for routine screening for liver disease. It is also called serum glutamate pyruvate transaminase (SGPT) or alanine aminotransferase (ALAT). When a cell is damaged, it leaks this enzyme into the blood, where it is measured. ALT rises dramatically in acute liver damage, such as viral hepatitis or paracetamol (acetaminophen) overdose. The highest level of ALT is in the liver, and levels of this enzyme are accordingly more specific indicators of liver injury. The magnitude of the elevation has no prognostic value and does not correlate with the degree of liver damage.
AST (10-34 IU/L), also called serum glutamic oxaloacetic transaminase (SGOT) or aspartate aminotransferase (ASAT/AAT) is similar to alanine transaminase (ALT) in that it is another enzyme associated with liver parenchymal cells. AST is present, in decreasing order of concentration, in the liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes, and erythrocytes. AST levels thus rise in MI, heart failure, muscle injury, CNS disease, and other nonhepatic disorders. AST is relatively nonspecific, but high levels indicate liver cell injury. In most liver diseases, the AST increase is less than that of ALT (AST/ALT ratio < 1).
Both aminotransferases are normally present in serum at low levels, usually less than 30 to 40 IU/L. The normal range varies widely among laboratories. The following table lists factors affecting AST and ALT serum activity, other than liver injury.[9] Release of both enzymes into the blood occurs in increasing amounts with liver cell membrane damage. Necrosis of liver cells is not required for the release of the aminotransferases. In fact, there is poor correlation between the degree of liver-cell damage and the level of the aminotransferases. The magnitude of elevation covers a very wide range. Levels <100 IU are common and nonspecific, and often have no clinical significance; levels of 100-300 IU are seen in numerous mild/moderate inflammatory processes. In acute viral or drug hepatitis aminotransferase levels are typically in the 500-1,500 IU range, but in alcoholic hepatitis they are usually <300 IU, even if the disease is severe. Values >3,000 IU usually are seen only in acute toxic necrosis or severe hypoxia ("shock liver," "ischemic hepatitis"); in both disorders levels typically plummet within two to three days, whereas values fall more slowly in viral hepatitis. Aminotransferase levels are variable in biliary obstruction but usually remain <200 IU, except with acute passage of common duct stone, characterized by a sudden rise to hepatitic levels and a rapid fall over the next one to two days.
Factor
AST
ALT
Comments
Time of day
45% variation during day; highest in afternoon, lowest at night
No significant difference between 0900 and 2100; similar in liver disease and health
Day-to-day
5–10% variation from one day to next
10–30% variation from one day to next
Similar in liver disease and health, and in elderly and young
Race/gender
15% higher in African-American men
No significant difference between African-American, other women
BMI (body mass index)
40–50% higher with high BMI
40–50% higher with high BMI
Direct relationship between weight and AST, ALT
Meals
No effect
No effect
Exercise
Threefold increase with strenuous exercise
20% lower in those who exercise at usual levels than in those who do not exercise or exercise more strenuously than usual
Effect of exercise seen predominantly in men; minimal difference in women (<10%). Enzymes increase more with strength training
Specimen storage
Stable at room temp for 3 days, in refrigerator for 3 weeks (<10% decrease); stable for years frozen (10–15% decrease)
Stable at room temperature for 3 days, in refrigerator for 3 weeks (10–15% decrease); marked decrease with freezing/thawing
Stability based on serum separated from cells; stable for 24 h in whole blood, marked increase after 24 h
Hemolysis, hemolytic anemia
Significant increase
Moderate increase attributable to release from red cell
Dependent on degree of hemolysis; usually several fold lower than increases in lactate dehydrogenase (LDH)
Muscle injury
Significant increase
Moderate increase
Related to amount of increase in creatine kinase (CK)
Other biochemical tests of interest are γ-glutamyl transpeptidase (GGT), lactic dehydrogenase (LDH), alkaline phosphatase (ALP), albumin, and bilirubin. Corresponding changes in the serum levels of these markers assist in defining the etiology. γ-Glutamyl transpeptidase (GGT), also known as γ-glutamyltransferase, is present in the liver, pancreas, and kidney. GGT transfers the γ-glutamyl group from one peptide to another or to an L-amino acid. GGT levels (0-51 IU/L) are elevated in diseases of the liver, biliary tract, and pancreas with obstruction of the common bile duct. Drug use and alcohol (acute and chronic) ingestion also elevate GGT. GGT may be elevated with even minor, sub-clinical levels of liver dysfunction. Alkaline phosphatase (ALP) is an enzyme in the cells lining the biliary ducts of the liver. ALP levels (44-147 IU/L) in plasma will rise with large bile duct obstruction, intrahepatic cholestasis, or infiltrative diseases of the liver. ALP is also present in bone. Serum γ-glutamyl transpeptidase (GGT) activity correlates closely with the activities of alkaline phosphatase (ALP) in various forms of liver disease. Maximum elevations of the enzyme activities are observed in diseases that affect the biliary tract. Compared with ALP, GGT is generally increased to a greater extent and is thus the most sensitive indicator of biliary-tract disease.
Lactic dehydrogenase (LDH) is commonly included in routine analysis, is insensitive as an indicator of hepatocellular injury, but is better as a marker for hemolysis, myocardial infarction (heart attack), or pulmonary embolism. LDH can be quite high with malignancies involving the liver. Albumin (3.9-5.0 g/dL) is a protein made specifically by the liver, and can be measured cheaply and easily. It is the main constituent of total protein; the remaining fraction is called globulin (including the immunoglobulins). Bilirubin is a breakdown product of heme (a part of hemoglobin in red blood cells). The liver is responsible for clearing the blood of bilirubin. Bilirubin is taken up into hepatocytes, conjugated (modified to make it water-soluble), and secreted into the bile, which is excreted into the intestine. Increased total bilirubin causes jaundice, and can signal a number of problems.
Elevated serum aminotransferase levels, especially aspartate aminotransferase levels, may be caused by disorders that affect organs or tissues other than the liver, with the most common being striated muscle. Conditions or activities that can cause such elevations include subclinical inborn errors of muscle metabolism; acquired muscle disorders, such as polymyositis; and exercise. If striated muscle is the source of increased aminotransferase levels, serum levels of creatine kinase will be elevated to the same degree or to an even higher degree.
Creatine kinase (CK), also known as phosphocreatine kinase or creatine phosphokinase (CPK) is an enzyme that catalyses the conversion of creatine to phosphocreatine. In tissues that consume ATP rapidly, especially skeletal muscle, but also brain and smooth muscle, phosphocreatine serves as an energy reservoir for the rapid regeneration of ATP. Clinically, creatine kinase is assayed in blood tests as a marker of myocardial infarction (heart attack), rhabdomyolysis (muscle breakdown), and in acute renal failure. Numerous studies have evaluated changes in CK activity after exercise and found that it differs markedly according to exercise conditions. In isometric muscle contraction exercise, peak serum CK activity is observed relatively early, 24-48 hours after exercise, whereas it is seen 3-7 days after exercise in eccentric muscle contraction exercise, and a biphasic pattern is observed in weight training.
Toxic effects of AAS on the liver are primarily due to 17α-alkylated steroids and reported to include increased enzyme activities, cholestasis, peliosis hepatis adenoma, and even case reports of carcinoma.[10] The use of anabolic steroids is common among athletes, particularly bodybuilders. Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels have been overstated. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. Levels of both aspartate aminotransferase (AST) and alanine aminotransferase (ALT) may increase with strenuous exercise. 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.
Steroids with Michael Scally, MD
Oral Anabolic Steroids, Liver Enzyme Tests and Liver Function
by Michael C. Scally, M.D.Author of eBook Human Experimentation in Anabolic Steroid Research by Michael Scally, M.D.
Harvard Medical School - M.D.; Harvard-M.I.T. Program In Health Science & Technology
Massachusetts Institute of Technology, B.S. Chemistry/LIfe Sciences
Dr. Scally early on recognized the lack of research and treatment for individuals using anabolic-androgenic steroids (AAS). He has remained as the sole physician by reputation and publication to actively pursue and advocate the proper use of AAS to optimize health. Dr. Scally has personally cared for thousands of individuals using AAS. His protocol for Anabolic Steroid Induced Hypogonadism has been presented before the Endocrine Society, American Association of Clinical Endocrinologists, American College of Sports Medicine, & International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV.
Question:
Do oral steroids have long-term effects on liver function long after they have been discontinued? I have done quite a few cycles of anadrol and dianabol in the past. But I haven’t done any oral AAS, prohormones, legal or otherwise in several years and my liver function tests are still elevated (AST and ALT). They are about double the top of the normal range. Can any other factors account for this e.g. dietary supplements, genetics, intense physical exercise, heavy childhood use of NSAIDs?
Response:
Mild elevations in liver chemistry tests such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST) can reveal serious underlying conditions or have transient and benign etiologies. There are no controlled clinical trials examining the optimal approach for evaluating serum liver chemistries. The American Gastroenterological Association guideline regarding the evaluation and management of abnormal liver chemistry tests proposes a practical, algorithmic approach when the history and physical examination do not reveal the cause.
The history should be thorough, with special attention given to the use of medications, vitamins, herbs, drugs, and alcohol; family history; and any history of blood-product transfusions.[1] In addition to liver chemistries, an initial serologic evaluation includes a prothrombin time; albumin; complete blood count with platelets; hepatitis A, B, and C serologies; and iron studies. The most common causes of elevated aminotransferase levels include alcohol-related liver injury, chronic hepatitis B and C, autoimmune hepatitis, hepatic steatosis (fatty infiltration of the liver), nonalcoholic steatohepatitis, hemochromatosis, Wilson's disease, alpha1-antitrypsin deficiency, and celiac sprue.
Depending on the etiology, management strategies may include cessation of alcohol use, attention to medications, control of diabetes, and modification of lifestyle factors such as obesity. If elevations persist after an appropriate period of observation, further testing may include ultrasonography, other serum studies, and in some cases, liver biopsy.[2] Isolated alterations of biochemical markers of liver damage in a seemingly healthy patient often represent a challenge even for the experienced clinician and usually set off a battery of further, costly tests and consultations that may ultimately prove unnecessary.
The liver is the largest and most metabolically complex organ in humans. The liver receives a dual blood supply. The portal vein drains the splanchnic, viscera, circulation and provides 75% of the total blood flow. The hepatic artery provides the remaining 25%. The hepatic vein carries all efferent blood to the inferior vena cava. Rich supplies of lymphatic vessels also drain the liver.
The liver is a complex organ with interdependent metabolic, excretory, and defense functions. Hepatocytes make up the bulk of the organ. Sinusoidal lining cells comprise at least four distinct populations: endothelial cells, Kupffer's cells, perisinusoidal fat-storing cells and pit cells. Endothelial cells are responsible for endocytosis of molecules and particles, and play a role in lipoprotein metabolism. Spindle-shaped Kupffer's cells are tissue macrophages. Perisinusoidal fat-storing cells (Ito cells) store vitamin A. Pit cells are large, granular lymphocytes, which function as natural killer cells.
The liver plays a central role in carbohydrate, protein, and fat metabolism. It stabilizes glucose level by taking up and storing glucose as glycogen (glycogenesis), breaking glycogen down to glucose (glycogenolysis), and forming glucose from noncarbohydrate sources (gluconeogenesis). The liver synthesizes the majority of proteins that circulate in the plasma, including albumin and most of the globulins other than gamma globulins. It is responsible for synthesizing and secreting bile and plasma proteins, including clotting factors. The liver is the site of most amino acid interconversions and catabolism. Amino acid deamination produces urea and esterification of fatty acids produces triglycerides. The liver packages triglycerides with cholesterol, phospholipids, and an apoprotein into a lipoprotein. The lipoprotein enters blood for utilization or storage in adipocytes. Most cholesterol synthesis takes place in the liver.
The liver detoxifies noxious substances arriving from the splanchnic (viscera) circulation, preventing them from entering the systemic circulation. This particularly makes the liver susceptible to drug-induced injury. The liver converts some lipophilic compounds into more water-soluble agents and others to less active agents. In conjunction with the spleen, it is involved in the destruction and reclamation of spent red blood cells.
Prior to a discussion of liver pathology, it is important to have an understanding in the interpretation of laboratory tests. Normal refers to a theoretical frequency distribution for a set of variable data, usually represented by a bell-shaped curve symmetrical about the mean. Laboratory values for a reference range are from a group of healthy individuals with no known factors (medications, illness, genetics, etc.) that would influence the outcome of the testing. The reference range for a particular laboratory test is dependent upon a given subpopulation (e.g., male, female, or children) and the testing laboratory or manufacturer. Federal regulations require laboratories to adhere to certain standards. "Prior to reporting patient test results, the laboratory must verify or establish, for each method, the performance specifications for the following performance characteristics: accuracy; precision; analytical sensitivity and specificity, if applicable; the reportable range of patient test results; the reference range(s) (normal values); and any other applicable performance characteristic."[3] The normal reference range typically refers to the mean or average +2 standard deviations.[4] Interpretation of results is being either within, normal, for a value falling within this bell-shaped curve (reference range) or outside, abnormal, the reference range. Accordingly, 2.5% of normal patients have "abnormal" aminotransferase levels.
A basic tenet, standard practice, of medicine is that interpretation of results is within the framework of a patient's medical condition and treatment, the overall health of the patient.[5] Physicians are taught to think about clinical testing in terms of the clinical significance (particularly, predictive value) of a given test in a given situation. All tests have strengths and limitations for their use in reaching a certain diagnosis or making a causal inference. The risk of a test is seldom inherent in the test itself, but rather is a function of the context in which use of the test is providing information for medical decision-making. Many factors affect test results including sex, medications, overall health of the individual, temporal influences, and variations in laboratory techniques. Thus, in terms of diagnosis, interpretation of a diagnostic test is in the context of history, examination, other tests, and other relevant medical considerations.[6] The proper and correct interpretation for a test is within the situational context.
Levels of serum liver enzymes are indications of hepatocyte integrity or cholestasis rather than liver function. A change in serum protein levels or clotting times may be associated with a decrease in liver functioning mass, although neither is specific for liver disease. No single or simple test assesses overall liver pathology. Use of several screening tests improves the detection of hepatobiliary abnormalities, differentiates the basis for clinically suspected disease, and determines the severity of liver disease (hepatocytes (hepatocellular dysfunction), the biliary excretory apparatus (cholestasis), and the vascular system (portal hypertension)).
The widespread availability and use of serum blood chemistries for screening both symptomatic and asymptomatic patients has resulted in a dramatic increase in the number of normal and abnormal liver chemistry tests requiring interpretation by physicians. A number of review articles on the evaluation of abnormal liver function tests are available on the internet.[7] Aminotransferases (transaminase) include alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Both are exquisitely sensitive indicators of hepatocellular injury and provide the best guide to hepatocellular necrosis/inflammation.[8]
ALT (8-37 IU/L) is present in hepatocytes (liver cells) and is reliable for routine screening for liver disease. It is also called serum glutamate pyruvate transaminase (SGPT) or alanine aminotransferase (ALAT). When a cell is damaged, it leaks this enzyme into the blood, where it is measured. ALT rises dramatically in acute liver damage, such as viral hepatitis or paracetamol (acetaminophen) overdose. The highest level of ALT is in the liver, and levels of this enzyme are accordingly more specific indicators of liver injury. The magnitude of the elevation has no prognostic value and does not correlate with the degree of liver damage.
AST (10-34 IU/L), also called serum glutamic oxaloacetic transaminase (SGOT) or aspartate aminotransferase (ASAT/AAT) is similar to alanine transaminase (ALT) in that it is another enzyme associated with liver parenchymal cells. AST is present, in decreasing order of concentration, in the liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes, and erythrocytes. AST levels thus rise in MI, heart failure, muscle injury, CNS disease, and other nonhepatic disorders. AST is relatively nonspecific, but high levels indicate liver cell injury. In most liver diseases, the AST increase is less than that of ALT (AST/ALT ratio < 1).
Both aminotransferases are normally present in serum at low levels, usually less than 30 to 40 IU/L. The normal range varies widely among laboratories. The following table lists factors affecting AST and ALT serum activity, other than liver injury.[9] Release of both enzymes into the blood occurs in increasing amounts with liver cell membrane damage. Necrosis of liver cells is not required for the release of the aminotransferases. In fact, there is poor correlation between the degree of liver-cell damage and the level of the aminotransferases. The magnitude of elevation covers a very wide range. Levels <100 IU are common and nonspecific, and often have no clinical significance; levels of 100-300 IU are seen in numerous mild/moderate inflammatory processes. In acute viral or drug hepatitis aminotransferase levels are typically in the 500-1,500 IU range, but in alcoholic hepatitis they are usually <300 IU, even if the disease is severe. Values >3,000 IU usually are seen only in acute toxic necrosis or severe hypoxia ("shock liver," "ischemic hepatitis"); in both disorders levels typically plummet within two to three days, whereas values fall more slowly in viral hepatitis. Aminotransferase levels are variable in biliary obstruction but usually remain <200 IU, except with acute passage of common duct stone, characterized by a sudden rise to hepatitic levels and a rapid fall over the next one to two days.
Factor
AST
ALT
Comments
Time of day
45% variation during day; highest in afternoon, lowest at night
No significant difference between 0900 and 2100; similar in liver disease and health
Day-to-day
5–10% variation from one day to next
10–30% variation from one day to next
Similar in liver disease and health, and in elderly and young
Race/gender
15% higher in African-American men
No significant difference between African-American, other women
BMI (body mass index)
40–50% higher with high BMI
40–50% higher with high BMI
Direct relationship between weight and AST, ALT
Meals
No effect
No effect
Exercise
Threefold increase with strenuous exercise
20% lower in those who exercise at usual levels than in those who do not exercise or exercise more strenuously than usual
Effect of exercise seen predominantly in men; minimal difference in women (<10%). Enzymes increase more with strength training
Specimen storage
Stable at room temp for 3 days, in refrigerator for 3 weeks (<10% decrease); stable for years frozen (10–15% decrease)
Stable at room temperature for 3 days, in refrigerator for 3 weeks (10–15% decrease); marked decrease with freezing/thawing
Stability based on serum separated from cells; stable for 24 h in whole blood, marked increase after 24 h
Hemolysis, hemolytic anemia
Significant increase
Moderate increase attributable to release from red cell
Dependent on degree of hemolysis; usually several fold lower than increases in lactate dehydrogenase (LDH)
Muscle injury
Significant increase
Moderate increase
Related to amount of increase in creatine kinase (CK)
Other biochemical tests of interest are γ-glutamyl transpeptidase (GGT), lactic dehydrogenase (LDH), alkaline phosphatase (ALP), albumin, and bilirubin. Corresponding changes in the serum levels of these markers assist in defining the etiology. γ-Glutamyl transpeptidase (GGT), also known as γ-glutamyltransferase, is present in the liver, pancreas, and kidney. GGT transfers the γ-glutamyl group from one peptide to another or to an L-amino acid. GGT levels (0-51 IU/L) are elevated in diseases of the liver, biliary tract, and pancreas with obstruction of the common bile duct. Drug use and alcohol (acute and chronic) ingestion also elevate GGT. GGT may be elevated with even minor, sub-clinical levels of liver dysfunction. Alkaline phosphatase (ALP) is an enzyme in the cells lining the biliary ducts of the liver. ALP levels (44-147 IU/L) in plasma will rise with large bile duct obstruction, intrahepatic cholestasis, or infiltrative diseases of the liver. ALP is also present in bone. Serum γ-glutamyl transpeptidase (GGT) activity correlates closely with the activities of alkaline phosphatase (ALP) in various forms of liver disease. Maximum elevations of the enzyme activities are observed in diseases that affect the biliary tract. Compared with ALP, GGT is generally increased to a greater extent and is thus the most sensitive indicator of biliary-tract disease.
Lactic dehydrogenase (LDH) is commonly included in routine analysis, is insensitive as an indicator of hepatocellular injury, but is better as a marker for hemolysis, myocardial infarction (heart attack), or pulmonary embolism. LDH can be quite high with malignancies involving the liver. Albumin (3.9-5.0 g/dL) is a protein made specifically by the liver, and can be measured cheaply and easily. It is the main constituent of total protein; the remaining fraction is called globulin (including the immunoglobulins). Bilirubin is a breakdown product of heme (a part of hemoglobin in red blood cells). The liver is responsible for clearing the blood of bilirubin. Bilirubin is taken up into hepatocytes, conjugated (modified to make it water-soluble), and secreted into the bile, which is excreted into the intestine. Increased total bilirubin causes jaundice, and can signal a number of problems.
Elevated serum aminotransferase levels, especially aspartate aminotransferase levels, may be caused by disorders that affect organs or tissues other than the liver, with the most common being striated muscle. Conditions or activities that can cause such elevations include subclinical inborn errors of muscle metabolism; acquired muscle disorders, such as polymyositis; and exercise. If striated muscle is the source of increased aminotransferase levels, serum levels of creatine kinase will be elevated to the same degree or to an even higher degree.
Creatine kinase (CK), also known as phosphocreatine kinase or creatine phosphokinase (CPK) is an enzyme that catalyses the conversion of creatine to phosphocreatine. In tissues that consume ATP rapidly, especially skeletal muscle, but also brain and smooth muscle, phosphocreatine serves as an energy reservoir for the rapid regeneration of ATP. Clinically, creatine kinase is assayed in blood tests as a marker of myocardial infarction (heart attack), rhabdomyolysis (muscle breakdown), and in acute renal failure. Numerous studies have evaluated changes in CK activity after exercise and found that it differs markedly according to exercise conditions. In isometric muscle contraction exercise, peak serum CK activity is observed relatively early, 24-48 hours after exercise, whereas it is seen 3-7 days after exercise in eccentric muscle contraction exercise, and a biphasic pattern is observed in weight training.
Toxic effects of AAS on the liver are primarily due to 17α-alkylated steroids and reported to include increased enzyme activities, cholestasis, peliosis hepatis adenoma, and even case reports of carcinoma.[10] The use of anabolic steroids is common among athletes, particularly bodybuilders. Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels have been overstated. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. Levels of both aspartate aminotransferase (AST) and alanine aminotransferase (ALT) may increase with strenuous exercise. 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.
Trauma1
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A retrospective study examined the effects of AAS on a population in which the mean time off steroids was 43 months with the minimum length of time 1 year and the maximum 10 years.[11] Blood parameters of 32 male bodybuilders were studied. Fifteen subjects had not been using AAS for at least 12-43 months on average (mean dosage 700 mg for 26 weeks per year over 9 years), 17 subjects were still using AAS (750 mg for 33 weeks per 8 years). The study did not separate out for exercising and nonexercising. Former users had been training for 14.0±4.5 years for 6.0± 2.0 h per week, current users for 11.0 ± 5.0 years for 6.0 ± 1.0 h per week (no statistical difference). The activity of total CK was significantly higher in current users in comparison with former users. There was a significant correlation between total CK activity and AST or ALT (r = 0.87 and 0.67, both P <0.001).
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were higher in current users (65+/-55 and 38+/-27) compared to former users (24+/-10 and 18+/-11; each P<0.001). The values in former users were increased above the upper limit of reference in six (ALT) and three (AST) subjects. All but one (with considerably increased CK activity of 1747 U/l) current user showed increased values for ALT and AST above the upper limit of reference with higher values for ALT than AST in each case. ALT and AST correlated significantly with the extent (duration and weekly dosage) of AAS use (r=0.68 and 0.57; each P<0.01). The GGT was above the upper limit of reference in one former user (43 U/l) and one current user (37 U/l).In 1999, comparison of serum chemistry profiles from (1) bodybuilders using AAS, (2) bodybuilders not using AAS, (3) exercising medical students, (4) nonexercising medical students, and (5) patients with serologic confirmed viral hepatitis was published.[12] The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), and creatine kinase (CK) levels. In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. Creatine kinase (CK) was elevated in all exercising groups. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT.
In a follow-up study, these same investigators using a survey assessed 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.[13] The survey presents 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), creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels. In the physician survey, 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.
In summary, active treatment should steadfastly adhere to the World Health Organization (WHO) guidelines. WHO Grading of abnormality (0 is least severe, IV is most severe) monitors the liver enzymes ALT, AST, GGT and ALP. Recommended action is based on the Grade level. Grade 0 enzyme level is the upper limits normal (ULN) reference range; Grade I > ULN up to 2.5 times ULN, continue treatment but monitor regularly; Grade II > 2.6 up to 5 times ULN, should be closely monitored or managed in a similar manner to those with Grade 3; Grade III > 5 up to 20 times ULN, the dose should be reduced or interrupted and cautiously reinstated when enzymes return to normal or Grade I; Grade IV > 20 times ULN, should be discontinued permanently. Upon discontinuation of AAS with continued transaminase elevations, best recommendation is to follow a diagnostic algorithm for a known cause. It is unwise to consider enzyme elevations in the absence of a diagnosis as nonsignificant and of no concern.
In a group of 100 consecutive blood donors with elevated alanine aminotransferase levels, 48 percent had changes related to alcohol use, 22 percent had fatty liver, 17 percent had hepatitis C, 4 percent had another identified problem, and in the remaining 9 percent, no specific diagnosis was made.
In another study of 149 asymptomatic patients with elevated alanine aminotransferase levels who underwent liver biopsy, 56 percent had fatty liver, 20 percent had non-A, non-B hepatitis, 11 percent had changes related to alcohol use, 3 percent had hepatitis B, 8 percent had other causes, and in 2 percent, no cause was identified.
A recent study assessed 1124 consecutive patients who were referred for chronic elevations in aminotransferase levels. Eighty-one of these patients had no definable cause of the elevation and underwent a liver biopsy. Of these 81 patients, 41 had steatosis, 26 had steatohepatitis, 4 had fibrosis, 2 had cirrhosis, and 8 had normal histologic findings. The patients with histologic evidence of fibrosis and cirrhosis also had evidence of fatty metamorphosis. None of the biopsies yielded a specific diagnosis except those showing steatosis and steatohepatitis.
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were higher in current users (65+/-55 and 38+/-27) compared to former users (24+/-10 and 18+/-11; each P<0.001). The values in former users were increased above the upper limit of reference in six (ALT) and three (AST) subjects. All but one (with considerably increased CK activity of 1747 U/l) current user showed increased values for ALT and AST above the upper limit of reference with higher values for ALT than AST in each case. ALT and AST correlated significantly with the extent (duration and weekly dosage) of AAS use (r=0.68 and 0.57; each P<0.01). The GGT was above the upper limit of reference in one former user (43 U/l) and one current user (37 U/l).In 1999, comparison of serum chemistry profiles from (1) bodybuilders using AAS, (2) bodybuilders not using AAS, (3) exercising medical students, (4) nonexercising medical students, and (5) patients with serologic confirmed viral hepatitis was published.[12] The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), and creatine kinase (CK) levels. In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. Creatine kinase (CK) was elevated in all exercising groups. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT.
In a follow-up study, these same investigators using a survey assessed 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.[13] The survey presents 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), creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels. In the physician survey, 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.
In summary, active treatment should steadfastly adhere to the World Health Organization (WHO) guidelines. WHO Grading of abnormality (0 is least severe, IV is most severe) monitors the liver enzymes ALT, AST, GGT and ALP. Recommended action is based on the Grade level. Grade 0 enzyme level is the upper limits normal (ULN) reference range; Grade I > ULN up to 2.5 times ULN, continue treatment but monitor regularly; Grade II > 2.6 up to 5 times ULN, should be closely monitored or managed in a similar manner to those with Grade 3; Grade III > 5 up to 20 times ULN, the dose should be reduced or interrupted and cautiously reinstated when enzymes return to normal or Grade I; Grade IV > 20 times ULN, should be discontinued permanently. Upon discontinuation of AAS with continued transaminase elevations, best recommendation is to follow a diagnostic algorithm for a known cause. It is unwise to consider enzyme elevations in the absence of a diagnosis as nonsignificant and of no concern.
In a group of 100 consecutive blood donors with elevated alanine aminotransferase levels, 48 percent had changes related to alcohol use, 22 percent had fatty liver, 17 percent had hepatitis C, 4 percent had another identified problem, and in the remaining 9 percent, no specific diagnosis was made.
In another study of 149 asymptomatic patients with elevated alanine aminotransferase levels who underwent liver biopsy, 56 percent had fatty liver, 20 percent had non-A, non-B hepatitis, 11 percent had changes related to alcohol use, 3 percent had hepatitis B, 8 percent had other causes, and in 2 percent, no cause was identified.
A recent study assessed 1124 consecutive patients who were referred for chronic elevations in aminotransferase levels. Eighty-one of these patients had no definable cause of the elevation and underwent a liver biopsy. Of these 81 patients, 41 had steatosis, 26 had steatohepatitis, 4 had fibrosis, 2 had cirrhosis, and 8 had normal histologic findings. The patients with histologic evidence of fibrosis and cirrhosis also had evidence of fatty metamorphosis. None of the biopsies yielded a specific diagnosis except those showing steatosis and steatohepatitis.
Trauma1
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Ok - That should silence the critics for a bit.
If you guys have any specific questions i'll do what i can to answer them.
If you guys have any specific questions i'll do what i can to answer them.
pdigs
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my god trauma u should be a doctor have u ever considered? i guess in ur case u should take ur own advice and not do steroids because theyre bad for your liver.... which im sure u dont, why would i ever consider a man such as yourself would have double standards. dont try and google own me
Cr250owner
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haha you got me. i do smoke probably more than i should, so as of now i'll cut back/quit till cycles over. and the whole vic thing, i happened to get em for free so i wanna pop em, but i'm not an addict lol i CAN WAIT.
retort50ml
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I've taken as much as 4 grams of Tylenol a day for a couple of years due to severe cervical and thoracic spinal problems. I get blood work every 3 months and my liver values have never been elevated. I'm not commenting on mixing Tylenol with SuperDrol because I've never done it, but making a blanket statement that 4 grams of Tylenol is toxic to the liver is not accurate. It depend on the indidvidual, just like it does with many substances. It is recommended by the FDA not to exceed 4 grams of Tylenol per day.
Jayhawkk
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Steroids will effect your liver and adding other drugs/supps will just keep upping the chance of temp/longterm damage. If this is a chance you're willing to take then it's on you but I can tell you first hand it isn't worth it. It doesn't take years of abuse to have long term damage. Just because you can't feel your liver 'hurt' doesn't mean it isn't damaged. That damage can present itself in a whole grocery list of symptoms. People don't realize what these symptoms are and end up worsening the condition by self medicating the symptoms instead of correcting the cause.
The damage is real and anyone telling you that it isn't has nothing to lose if you go and destroy yourself. You think this dude will lose an ounce of sleep if you **** yourself up?
The damage is real and anyone telling you that it isn't has nothing to lose if you go and destroy yourself. You think this dude will lose an ounce of sleep if you **** yourself up?
jcp2
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So GGT was not above normal limits in all but on user and one non user. The study also goes on to speak about how intense resistance training can be a cause for increased alt/ast. Let me ask you another question, in someone with a truly damaged liver, what are the odds you will have a normal GGT. Part of this seems to state that resistance training needs to be looked at for increase ALT/AST, which everyone on here should know. This also shows me the non steroid using group (who used at one time) could have increased ALT/AST due to resistance training since you are only talking about half the sampling. The study does not show how far over normal range we are talking either. Something that would be useful.
jcp2
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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.
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.
Kristofer68SS
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Trauma1
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The ONLY way to assess true hepatic damage is through a liver biopsy. YES you can in fact have significant hepatic damage with a fairly normal Alk Phos/GGT level(which give indication of biliary involvement).
Some of you are missing the fact that ALT IS HEPATIC SPECIFIC. It can be raised to a small degree through resistance training, however any significant elevation (especially 2-3x the AST) is very concerning for acute(not sub-acute hepatic injury. AST is MUCH more likely to be elevated than ALT through resistance type elevations. Another point to remember is the physical exam is used to correlate the findings and diagnosis. If you are showing physical signs of hepatic/biliary injury you may demonstrate: jaundice, pruritis(itching), pale stools, tea colored urine, confusion(due to elevated ammonia level). You levels don't have to be that far off normal to demonstate some of these symptoms.
Even with long term liver damage, your Hepatic Function may not be all that abnormal. Chronic alcoholics for example typically have massive sclerotic damage, however typically their liver function is either normal or mildly elevated.
Every lab has different values that they consider as a "normal" range for the test they perform. So essentially, it can be slightly different depending on which lab runs the blood.
I have almost 9 years of real life experience in emergency nursing. I've seen many different scenarios that have lead to hepatic injury/failure. I can assure you all this. Once liver tissue is sclerosed, it's VERY DEAD. This does not regenerate.
I think way too many people automatically assume because " I don't have symptoms, so everything must be ok then." That statement couldn't be farther from the truth. Guys, be smart about what you do or you can pay for it down the line.
jcp2
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I agree with what you are saying, specifically about the parts about scirrosis (sic) but even lesions found on liver from steroid use pretty much go away when the drug is discontinued. I have bascially been told i am going to severlyl damage my liver by taking anadrol for 8 weeks without a "liver protector", but what about the people who took it for 6 months at a clip. How come they have not had liver cancer, i mean these drugs were used on a reasonable number of people. I am sure these people had elevated ALT/AST during the duration of treatment, same with accutane use. Were doctors sacrificing future liver function? Comparing someone cycling reasonable amounts of steroids to alchoholics is tough, scirrosis usually does not afflict people for 30 years plus of constant abuse. My uncle was told he would not make 30 by his doctor when he was 25 due to a severly swollen liver, don't know the numbers, due to booze and black beauties, he has never had an issue since. He is now 55. Once Scirrosis sets in their is no looking back, that is when their is no more regeration of the tissue, that is point of no return. But you are not looking at these issues from 6 weeks of an oral steroid.
Trauma1
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In a short term situation you can certainly endure a significant drug induced hepatic injury. Many factors weigh into this such as duration of use, other contributing disease factors, and other substances such as drugs/alcohol use. If it is severe enough, it can definitely lead to an acute hepatic failure.
Make no mistake when i say this. Do you really think that the full story is always disclosed with everyone that uses A.A.S. such as alcohol drug use or other contributing disease factors? People very often don't tell the whole story and are poor historians that often hide the true nature of the pathologic process. I see this in medicine EVERY SINGLE DAY.
Now many people if caught and treated in a timely fashion could recover very well from an acute injury. However, there is no real way to assess longterm complications from damage that may have been done in spite of normal hepatic function.....unless a biopsy is performed.
Jayhawkk
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My doc has me lay off of any strenuous exercise several days prior to getting bloodwork done and has explained that extreme muscle fatigue can cause inflated blood values.
Kristofer68SS
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This is why I hold little value to ALOT of the information that I read, this board and many others included.......and i mean no disrespect, its just the way it has to be.
Trauma1
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I don't blame you at all for feeling that way either. I'm in your boat with that sentiment.
Like i basically summed up in my above statement, take it all for what it's worth.
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