Article: Oral Anabolic Steroids, Liver Enzyme Tests, and Liver Function!

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    Article: Oral Anabolic Steroids, Liver Enzyme Tests, and Liver Function!


    This is a very good read that i think you'd all enjoy. I'll answer any questions about bloodwork and such that you may have to the best of my abilities.

    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

    Factor: Time of day

    AST: 45% variation during day; highest in afternoon, lowest at night

    ALT: No significant difference between 0900 and 2100;

    Comment: similar in liver disease and health


    Factor: Day-to-day

    AST: 5–10% variation from one day to next

    ALT: 10–30% variation from one day to next

    Comment: Similar in liver disease and health, and in elderly and young


    Factor: Race/gender

    AST: 15% higher in African-American men

    ALT: No significant difference between African-American, other women


    Factor: BMI (body mass index)

    AST: 40–50% higher with high BMI

    ALT: 40–50% higher with high BMI

    Comment: Direct relationship between weight and AST, ALT


    Factor: Meals

    AST: No effect

    ALT: No effect


    Factor: Exercise

    AST: 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

    ALT: Effect of exercise seen predominantly in men; minimal difference in women (<10%). Enzymes increase more with strength training


    Factor: Specimen storage

    AST: Stable at room temp for 3 days, in refrigerator for 3 weeks (<10% decrease); stable for years frozen (10–15% decrease)

    ALT: Stable at room temperature for 3 days, in refrigerator for 3 weeks (10–15% decrease); marked decrease with freezing/thawing

    Comment: Stability based on serum separated from cells; stable for 24 h in whole blood, marked increase after 24 h


    Factor: Hemolysis, hemolytic anemia:

    AST: Significant increase

    ALT: Moderate increase attributable to release from red cell

    Comment: Dependent on degree of hemolysis; usually several fold lower than increases in lactate dehydrogenase (LDH)


    Factor: Muscle injury:

    AST: Significant increase

    ALT: Moderate increase

    Comment: 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.
    Last edited by Trauma1; 06-27-2008 at 12:55 PM.

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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.

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    I skimmed through it, and read some of the conclusives. Awesome find T1... I will get into hard in a little bit.

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    Quote Originally Posted by DAdams91982 View Post
    I skimmed through it, and read some of the conclusives. Awesome find T1... I will get into hard in a little bit.

    Adams
    Thanks brudda.

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    that is so much information - dang. its even hard to understand when reading the main points. it is good info tho.
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    Quote Originally Posted by LatsRus View Post
    that is so much information - dang. its even hard to understand when reading the main points. it is good info tho.
    If you have any specific questions, i'll try to decipher it for you in laymens terms.

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    good read.
    although i needed the cliff notes.
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    thanks T1, I skimmed it too (I'm at work) but I've bookmarked this to come back to tonight!
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    Quote Originally Posted by Trauma1 View Post
    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.

    This has been part of my point all along. This is also common knowledge among people who have read on this subject at all unlike most of the people here who have tried to make me look foolish by the constant crys "do your own homework"
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    Trauma i think i responded to the other study in the other post. I will find it later.
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    Quote Originally Posted by jcp2 View Post
    This has been part of my point all along. This is also common knowledge among people who have read on this subject at all unlike most of the people here who have tried to make me look foolish by the constant crys "do your own homework"
    I didn't say, nor do i belive you to be foolish. I understand what you are saying, however the information contained in this excerpt can also be just as misleading as it is helpful.

    I don't necessarily agree with how some of this article is written or presented either. I base my statements on both research and real life experiences/scenarios. I hate to say it, but this article tends to play a very leniant perspective overall on A.A.S use and reflective hepatic involvement. imo.

    Remember, this is just one article and one doctors views on the topic matter. There are definite ways to help differentiate between true hepatic cause vs. differential cause. However, often in medicine things aren't always as they seem, and can present in a very a-typical fashion.

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    ya i need cliff notes to understand that.
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    Quote Originally Posted by witt51 View Post
    ya i need cliff notes to understand that.
    I'll break it down for you guys later.

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    try to make some drawings and pictures or better yet a little cartoon explaining it better.j/k
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    Quote Originally Posted by Trauma1 View Post
    I didn't say, nor do i belive you to be foolish. I understand what you are saying, however the information contained in this excerpt can also be just as misleading as it is helpful.

    I don't necessarily agree with how some of this article is written or presented either. I base my statements on both research and real life experiences/scenarios. I hate to say it, but this article tends to play a very leniant perspective overall on A.A.S use and reflective hepatic involvement. imo.

    Remember, this is just one article and one doctors views on the topic matter. There are definite ways to help differentiate between true hepatic cause vs. differential cause. However, often in medicine things aren't always as they seem, and can present in a very a-typical fashion.

    I don't mean you trauma, but their are alot of people who think pubmed is the local bar at the medschool down the street. Obviously thier is a risk for certain liver issues, but i said in another post facts need to be laid out so people can make informed decisions. I still feel the biggest risk factors when it comes to steroids are long term HDL levels, and hypertension. I actually know someone on the message boards who passed away from steroid use, and it wasn't from his liver.
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    Quote Originally Posted by jcp2 View Post
    I don't mean you trauma, but their are alot of people who think pubmed is the local bar at the medschool down the street. Obviously thier is a risk for certain liver issues, but i said in another post facts need to be laid out so people can make informed decisions. I still feel the biggest risk factors when it comes to steroids are long term HDL levels, and hypertension. I actually know someone on the message boards who passed away from steroid use, and it wasn't from his liver.
    I agree. Reading an abstract for pubmed is one thing, however actually understanding and applying what you read there is a whole different story.

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    Quote Originally Posted by witt51 View Post
    try to make some drawings and pictures or better yet a little cartoon explaining it better.j/k
    I can make some bad azz stick figure cartoons!.......Actually, i lie.

    Trip is the better artist by far. I can whail away on the old guitar though.

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    good post trauma, short and simple:
    physicians should consider the CK and GGT levels as essential elements in distinguishing muscle damage from liver damage.

    if you want to see how your liver is after a cycle remember this.
    I will
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    Quote Originally Posted by jcp2 View Post
    I don't mean you trauma, but their are alot of people who think pubmed is the local bar at the medschool down the street. Obviously thier is a risk for certain liver issues, but i said in another post facts need to be laid out so people can make informed decisions. I still feel the biggest risk factors when it comes to steroids are long term HDL levels, and hypertension. I actually know someone on the message boards who passed away from steroid use, and it wasn't from his liver.

    I'd agree with you. And from what I have seen liver issues are vastly overplayed based on my personal bloodwork. Granted I am only one examlpe, so take it fwiw.
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    Good information J. Seems like when it comes to oral AAS many times people stand on 1 of 2 sides of the extreme. Some guys act like the liver will regenerate no matter what and others seem to wanna believe that methyl AAS will kill someone stat. I think if someone's healthy to begin with, and they cycle responsibly they'll be fine. But some people seem to think it's ok to run 3 or more oral cycles per year, which's destructive. With potently toxic methyls like Anadrol or Superdrol the cycle length and dosage are critical.

    I've seen some case studies on A&E recently - involving a past history of Anadrol use and one involving Dbol. In both studies the use was limited to Olympic sporting events and both individuals ceased usage of AAS for the remainder of their lives after they stopped competing. Neither individual had any negative symptoms anytime soon after halting their usage of AAS with the exception of elevated lipids & liver enzymes which was temporary. But both developed 'hard spots', or scar tissues on their liver in which they lived perfectly with for years, completely symptom free. Both individuals died at relatively young ages from liver disease, but years after they stopped using AAS. Neither individual were avid drinkers, nor acetaminophen abusers, etc. and were both otherwise very healthy.

    Now obviously something in these cases had to be extreme. And in responsible users with the appropriate knowledge this can easily be avoided. But I don't think enough people are aware of how the liver can develop scar tissue, and slowly get worse. Once this scar tissue increases people can live with it completely symptom free for years before it’s too late. One super extreme run of a potent oral, or a run that may have lasted a bit too long, and who knows. And even though the liver's an incredibly amazing organ, once it's pushed too far too long - excessive scar tissue can develop. In which case there's basically nothing medically that can be done to save the individual.

    Once pushed to this stage, the only chance one would have be a liver transplant - and the chances of this are probably one in a billion. Healthy liver demand is so high in some countries a healthy liver can sell for anywhere from $20,000 to six figures on the black market. With the extreme amount of methyl abuse that’s occurred in recent years partially due to the OTC industry and the mindset of ‘if it’s OTC it’s safe’ - I think the fallout in years to come will be more severe than people realize.
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    ziquor i would need to see a case study. the media likes to say lyle alzado died of steroid use as well. I also need so know if it was state sponsored doping, i read something on that as well. The nice thing about peer reviewed is just that. I am definately not denying the fact. But it just sounds strange. I have not heard of one proplem from all the guys Arnolds age and a little older and they ate quite a bit of dbol from my understanding.
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    The short term studies I have read on drol seem to indicate low hepatoxic effects even at relatively high doses. I believe these were short terms situations however...

    Notice the length of time on this one:

    http://www.aidsonline.com/pt/re/aids...195628!8091!-1
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    Quote Originally Posted by Mulletsoldier View Post
    So, you mean, the Thundergod is not being safe?
    I wish you wouldn't name me specifically like this dude! Have some respect. I won't start slinging hash if you don't. There's lots more people using even larger doses than me. If a 165 lb. kid with 1 year of training decides to do Super-Drol @20 mg. for 4 weeks it's o.k., but if I (263 lbs. with 20+ years of natural experience) decide to run Super @ 30 mg. for 3 weeks, it's all of a sudden dangerous. Please Mullet, don't mention my name anymore, and I won't mention yours. Truce? THE THUNDERGOD
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    Quote Originally Posted by thundergod View Post
    I wish you wouldn't name me specifically like this dude! Have some respect. I won't start slinging hash if you don't. There's lots more people using even larger doses than me. If a 165 lb. kid with 1 year of training decides to do Super-Drol @20 mg. for 4 weeks it's o.k., but if I (263 lbs. with 20+ years of natural experience) decide to run Super @ 30 mg. for 3 weeks, it's all of a sudden dangerous. Please Mullet, don't mention my name anymore, and I won't mention yours. Truce? THE THUNDERGOD
    I don't think the 16 year old example is okay, but I don't think you running three methyls for extended periods is okay either. But this isn't our argument thread, so sorry bud.
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    Play nice now guys. I'll get on here later tonight to help break down this article into more simplified terms for my AM peeps.

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    Quote Originally Posted by Trauma1 View Post
    Play nice now guys. I'll get on here later tonight to help break down this article into more simplified terms for my AM peeps.
    No problem T1. I wish everyone was as nice and affable as you. You are a gentlemen sir! And I can't wait for the breakdown. Coming from you, I know it'll be uber informative!!THE THUNDERGOD
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    Nice thread, T1!
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    Quote Originally Posted by B5150 View Post
    Very nice addition. Thanks B!

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    Quote Originally Posted by Ziquor View Post
    Good information J. Seems like when it comes to oral AAS many times people stand on 1 of 2 sides of the extreme. Some guys act like the liver will regenerate no matter what and others seem to wanna believe that methyl AAS will kill someone stat. I think if someone's healthy to begin with, and they cycle responsibly they'll be fine. But some people seem to think it's ok to run 3 or more oral cycles per year, which's destructive. With potently toxic methyls like Anadrol or Superdrol the cycle length and dosage are critical.

    I've seen some case studies on A&E recently - involving a past history of Anadrol use and one involving Dbol. In both studies the use was limited to Olympic sporting events and both individuals ceased usage of AAS for the remainder of their lives after they stopped competing. Neither individual had any negative symptoms anytime soon after halting their usage of AAS with the exception of elevated lipids & liver enzymes which was temporary. But both developed 'hard spots', or scar tissues on their liver in which they lived perfectly with for years, completely symptom free. Both individuals died at relatively young ages from liver disease, but years after they stopped using AAS. Neither individual were avid drinkers, nor acetaminophen abusers, etc. and were both otherwise very healthy.

    Now obviously something in these cases had to be extreme. And in responsible users with the appropriate knowledge this can easily be avoided. But I don't think enough people are aware of how the liver can develop scar tissue, and slowly get worse. Once this scar tissue increases people can live with it completely symptom free for years before it’s too late. One super extreme run of a potent oral, or a run that may have lasted a bit too long, and who knows. And even though the liver's an incredibly amazing organ, once it's pushed too far too long - excessive scar tissue can develop. In which case there's basically nothing medically that can be done to save the individual.

    Once pushed to this stage, the only chance one would have be a liver transplant - and the chances of this are probably one in a billion. Healthy liver demand is so high in some countries a healthy liver can sell for anywhere from $20,000 to six figures on the black market. With the extreme amount of methyl abuse that’s occurred in recent years partially due to the OTC industry and the mindset of ‘if it’s OTC it’s safe’ - I think the fallout in years to come will be more severe than people realize.
    this is an important post that people should remember.

    IMO the toxicity of methylated steroids is overstated but people should not forget that THEY ARE TOXIC, SO PROPER PRECAUTIONS ARE NEEDED.
    4 rules to PREVENT problems:
    1)keep cycles short( 3weeks )
    2)use liver support supps : LIVER PROTECTORS- the list, don't run a cycle without them
    3)give enough time to liver recovery( for 3 weeks I recommend at least 6 weeks to proper recovery)
    4)do blood test at least 3 times a year to see the values of your liver enzymes
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    Quote Originally Posted by jcp2 View Post
    ziquor i would need to see a case study. the media likes to say lyle alzado died of steroid use as well. I also need so know if it was state sponsored doping, i read something on that as well. The nice thing about peer reviewed is just that. I am definately not denying the fact. But it just sounds strange. I have not heard of one proplem from all the guys Arnolds age and a little older and they ate quite a bit of dbol from my understanding.
    It involved myth & fact about AAS and the 2 people who were discussed were 'talked into to' using AAS by their American coach who appeared on the special too. I'll look out to see if it's on again anytime soon. It was actually one of the more honest pieces I've seen and it was in no way bashing AAS. I'm certain with 'responsible' and limited use this would never be an issue. But for some who think oral AAS can be used with little to no regard for safety may be in for tough times ahead.
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    A great read that should be easier for you guys to understand.


    UTH Gastroenterology Grand Rounds - Discussion



    --------------------------------------------------------------------------------

    Final Diagnosis: Drug Induced Cholestasis
    Drug induced cholestasis is a well-known side effect of many performance-enhancing supplements. Often times, these are used discretely by athletes and body builders. Steroids are believed to increase muscle mass by binding to androgen receptors and increasing protein synthesis. It also has an anticatabolic effect in muscle. Gynecomastia occurs from the peripheral conversion of androgens to estradiol (1). (Visual 2) Testosterone first appeared in international sporting competitions after the 1948 Olympics. East German records reported a 0.7 second reduction in a 100m sprint, 7-10 seconds in the 1500m run, 8-15m in a javelin throw (2). Names of common anabolic steroids are oxymetholone, stanozolol, nandrolone, and testosterone.


    Liver Injury

    Liver injury is an increase of ALT or conjugated bilirubin greater than two times the upper limit of normal or a combined increase of AST, alkaline phosphatase, total bilirubin and at least one parameter is greater than two times the upper limit of normal. The AASLD conference in 2000 suggested that an ALT of more than three times the upper limit of normal and a total bilirubin of more than twice the upper limit of normal be used to indicate significant abnormalities on the liver test (3).


    Liver injury is broadly classified into (Visual 1)

    1) hepatocellular injury with increases in ALT

    2) cholestatic with an elevated alkaline phosphatase

    3) mixed with elevated alkaline phosphatase and ALT.


    Pathogenesis

    The cause of the liver injury and subsequent elevations of liver enzymes are drug specific. The various mechanisms include the inhibitions of drug metabolism, disruption of bilirubin transport pumps causing cholestasis, apoptosis via Fas pathways, free radiation formation, and mitochondrial dysfunction. Anabolic steroid –induced jaundice appears to be from interference of bilirubin excretion into the canaliculus via suppression of the Na-K adenosine triphosphatase activity (6). The cholestatic side effects are typically seen in C17 alpha alkylated steroids.


    Clinical presentation/Diagnosis

    Anabolic steroid induced cholestasis typically causes pruritis and jaundice as an initial presenting symptom with elevations in the alkaline phosphatase and bilirubin level. In rare cases, chronic liver injury may lead to the vanishing bile duct syndrome (3). There has been case reports of marked elevation of AST/ALT from steroid use (4).

    Acute hepatotoxicity is associated with malaise, pain, and jaundice. Labs will show an elevation of ALT and a mild increase in alkaline phosphatase levels. Increased PT/INR and encephalopathy may also be seen in patients with liver failure.

    Work up for a drug induced hepatotoxicity includes excluding other precipitating factors (viral, biliary obstruction, alcohol abuse, autoimmune causes, Wilson’s, Hematochromatosis, shock liver, etc). Biliary imaging is important to evaluate for biliary obstruction. A review of the medications should be done to evaluate for potential hepatotoxic medications. (Visual 3)

    When urine is tested for androgen use, the ration of testosterone and epitestosterone (inactive metabolite of testosterone produced by the gonads with little peripheral metabolism of testosterone) is measured. The normal ratio is 1:1. If exogenous testosterone is used, the testosterone:epitestosterone is increased (1).


    Management

    The suspected drug or drugs should be stopped. In most cases, the liver parameters will improve after stopping the offending agent, however the improvement may be delayed or follow a protracted course over the next few weeks/months. Liver dysfunction may also briefly worsen following discontinuation of the offending medication. Cholestyramine or ursodiol may provide symptomatic relief.


    Patient Follow-up

    Patient was diagnosed with drug-induced cholestasis. He was using anabolic steroids and tamoxifen which commonly causes a cholestatic liver disease. Tamoxifen is used by body builders for its anti-estrogen effects to reduce anabolic steroid-induced gynecomastia. The patient was instructed to stop all performance enhancing drugs and start cholestyramine and ursodiol. His jaundice and pruritis gradually improved over the next 2 months.








    --------------------------------------------------------------------------------
    Last edited by Trauma1; 06-27-2008 at 12:57 PM.

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    A good Liver Function break down for you guys:


    Liver Function Tests:

    Liver function tests represent a broad range of normal functions performed by the liver. The diagnosis of liver disease depends upon a complete history, complete physical examination, and evaluation of liver function tests and further invasive and noninvasive tests. Many patients become confused regarding the meaning of a liver function test. This section is designed to describe the basic liver function tests and the meaning for patients.

    The hepatobiliary tree represents hepatic cells and biliary tract cells. Inflammation of the hepatic cells results in elevation in the alanine aminotransferase (ALT), aspartate aminotransferase (AST) and possibly the bilirubin. Inflammation of the biliary tract cells results predominantly in an elevation of the alkaline phosphatase. In liver disease there are crossovers between purely biliary disease and hepatocellular disease. To interpret these, the physician will look at the entire picture of the hepatocellular disease and biliary tract disease to determine which is the primary abnormality.

    Alanine Aminotransferase (ALT):

    ALT is the enzyme produced within the cells of the liver. The level of ALT abnormality is increased in conditions where cells of the liver have been inflamed or undergone cell death. As the cells are damaged, the ALT leaks into the bloodstream leading to a rise in the serum levels. Any form of hepatic cell damage can result in an elevation in the ALT. The ALT level may or may not correlate with the degree of cell death or inflammation. ALT is the most sensitive marker for liver cell damage.

    Aspartate Aminotransferase (AST):

    This enzyme also reflects damage to the hepatic cell. It is less specific for liver disease. It may be elevated and other conditions such as a myocardial infarct (heart attack). Although AST is not a specific for liver as the ALT, ratios between ALT and AST are useful to physicians in assessing the etiology of liver enzyme abnormalities.

    Alkaline Phosphatase:

    Alkaline phosphatase is an enzyme, which is associated with the biliary tract. It is not specific to the biliary tract. It is also found in bone and the placenta. Renal or intestinal damage can also cause the alkaline phosphatase to rise. If the alkaline phosphatase is elevated, biliary tract damage and inflammation should be considered. However, considering the above other etiologies must also be entertained. One way to assess the etiology of the alkaline phosphatase is to perform a serologic evaluation called isoenzymes. Another more common method to asses the etiology of the elevated alkaline phosphatase is to determine whether the GGT is elevated or whether other function tests are abnormal (such as bilirubin)

    Alkaline phosphatase may be elevated in primary biliary cirrhosis, alcoholic hepatitis, PSC, gallstones in choledocholithiasis.

    Gamma Glutamic Transpeptidase (GGT):

    This enzyme is also produced by the bile ducts. However, it is not very specific to the liver or bile ducts. It is used often times to confirm that the alkaline phosphatase is of the hepatic etiology. Certain GGT levels, as an isolated finding, reflect rare forms of liver disease. Medications commonly cause GGT to be elevated. Liver toxins such as alcohol can cause increases in the GGT.

    Bilirubin:

    Bilirubin is a major breakdown product of hemoglobin. Hemoglobin is derived from red cells that have outlived their natural life and subsequently have been removed by the spleen. During splenic degradation of red blood cells, hemoglobin (the part of the red blood cell that carries oxygen to the tissues) is separated out from iron and cell membrane components. Hemoglobin is transferred to the liver where it undergoes further metabolism in a process called conjugation. Conjugation allows hemoglobin to become more water-soluble. The water solubility of bilirubin allows the bilirubin to be excreted into bile. Bile then is used to digest food.

    As the liver becomes irritated, the total bilirubin may rise. It is then important to understand the difference between total bilirubin, which has undergone conjugation (that is hepatic cell metabolism), and at portion of bilirubin which has not been metabolized. These two components are called total bilirubin and direct bilirubin. The direct bilirubin fraction is that portion of bilirubin that has undergone metabolism by the liver. When this fraction is elevated, the cause of elevated bilirubin (hyperbilirubinemia) is usually outside the liver. These types of causes are typically gallstones. This type of abnormality is usually treated with surgery (such as a gallbladder removal or choleycystectomy).

    If the direct bilirubin is low, while the total bilirubin is high, this reflects liver cell damage or bile duct damage within the liver itself.

    Albumin:

    Albumin is the major protein present within the blood. Albumin is synthesized by the liver. As such, it represents a major synthetic protein and is a marker for the ability of the liver to synthesize proteins. It is only one of many proteins that are synthesized by the liver. However, since it is easy to measure, it represents a reliable and inexpensive laboratory test for physicians to assess the degree of liver damage present in the in any particular patient. When the liver has been chronically damaged, the albumin may be low. This would indicate that the synthetic function of the liver has been markedly diminished. Such findings suggest a diagnosis of cirrhosis. Malnutrition can also cause low albumin (hypoalbuminemia) with no associated liver disease.

    Prothrombin time (PT):

    Another measure of hepatic synthetic function is the prothrombin time. Prothrombin time is affected by proteins synthesized by the liver. Particularly, these proteins are associated with the incorporation of vitamin K metabolites into a protein. This allows normal coagulation (clotting of blood). Thus, in patients who have prolonged prothrombin times, liver disease may be present. Since a prolonged PT is not a specific test for liver disease, confirmation of other abnormal liver tests is essential. This may include reviewing other liver function tests or radiology studies of the liver. Diseases such as malnutrition, in which decreased vitamin K ingestion is present, may result in a prolonged PT time. An indirect test of hepatic synthetic function includes administration of vitamin K (10mg) subcutaneously over three days. Several days later, the prothrombin time may be measured. If the prothrombin time becomes normal, then hepatic synthetic function is intact. This test does not indicate that there is no liver disease, but is suggestive that malnutrition may coexist with (or without) liver disease.

    Platelet count:

    Platelets are cells that form the primary mechanism in blood clots. They're also the smallest of blood cells. They derived from the bone marrow from the larger cells known as megakaryocytes. Individuals with liver disease develop a large spleen. As this process occurs platelets are trapped with in the sinusoids (small pathways within the spleen) of the spleen. While the trapping of platelets is a normal function for the spleen, in liver disease it becomes exaggerated because of the enlarged spleen (splenomegaly). Subsequently, the platelet count may become diminished.

    Serum protein electrophoresis:

    This is an evaluation of the types of proteins that are present with in a patient's serum. By using an electrophoretic gel, major proteins can be separated out. This results in four major types of proteins. These are 1) albumin, 2) alpha globulins, 3) beta globulins and 4) gammaglobulins. This test is useful for evaluation of patients who have abnormal liver function tests since it allows a direct quantification of multiple different serum proteins. If the gamma globulin fraction is elevated, autoimmune hepatitis may be present. In addition a deficiency in the alpha globulin fraction can result in the diagnosis, or a clinical clue, to A. alpha-1 antitrypsin deficiency. This is a simple blood test that is commonly performed by hepatologists

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    Awesome Inform T1... you are a credit to your family name.

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    Quote Originally Posted by DAdams91982 View Post
    Awesome Inform T1... you are a credit to your family name.

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    As are you my fellow brethren!

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    Quote Originally Posted by Trauma1 View Post
    As are you my fellow brethren!
    LEGENDARY!!!

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    Quote Originally Posted by DAdams91982 View Post
    LEGENDARY!!!

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    I believe that's the word haha!

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    Uber-informative read Trauma!! Thanks for the diligent research and for sharing this wealth of knowledge with the rest of us. You are the epitomy of what this board stands for: Learn, Teach, and Lead!! THE THUNDERGOD
  

  
 

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