marijuana with liver complications?

Discussion in 'Medicinal Marijuana' started by reesescups99, Oct 8, 2010.

  1. reesescups99

    reesescups99 New Member

    Hey all,

    Recently I was released from the hospital due to liver complications. It is believed that this was an auto-immune hepatitis from an acne medication. My ALT liver enzymes were extremely high (2500) if that means anything to anyone. When the problem was recognized, I was started on Prednisone and mercaptopurine which has significantly helped my health and with that, my blood levels have slowly been returning to normalcy.

    A doctor (who would be honest with me no matter what he thought of marijuana) has told me that it is a BAD idea. His reasoning seems more of a precautionary thing rather than a specific medical reason. His thinking is that maybe the hepatitis was spurred initially from a marijuana reaction, and that if so it could cripple my health once again. Does this seem plausible to anybody?

    What affects does marijuana have on the liver that we know for sure? Also, would there be any problems interaction wise with those 2 medications I am on.

    Thanks in advance for any help!
  2. Dedbr

    Dedbr Domestic War Veteran


    Mercaptopurine Tablets USP, 50 mg Rx only
    Mercaptopurine is a potent drug. It should not be used unless a diagnosis of acute lymphatic leukemia has been adequately established and the responsible physician is experienced with the risks of Mercaptopurine and knowledgeable in assessing response to chemotherapy.
    Mercaptopurine Description

    Mercaptopurine was synthesized and developed by Hitchings, Elion, and associates at the Wellcome Research Laboratories.
    Mercaptopurine, known chemically as 6H-purine-6-thione, 1,7-dihydro-, monohydrate, is an analogue of the purine bases adenine and hypoxanthine. Its structural formula is:
    Mercaptopurine is available in tablet form for oral administration. Each scored tablet contains 50 mg Mercaptopurine and the inactive ingredients corn starch, hypromellose, lactose (anhydrous), lactose (monohydrate), magnesium stearate, potato starch, sodium starch glycolate, and stearic acid.
    Each tablet meets the requirements of Test 2 for Dissolution in the USP monograph for Mercaptopurine Tablets, USP.
    Mercaptopurine - Clinical Pharmacology

    Mechanism of action

    Mercaptopurine (6-MP) competes with hypoxanthine and guanine for the enzyme hyphoxanthine-guanine phosphoribosyltransferase (HGPRTase) and is itself converted to thioinosinic acid (TIMP). This intracellular nucleotide inhibits several reactions involving inosinic acid (IMP), including the conversion of IMP to xanthylic acid (XMP) and the conversion of IMP to adenylic acid (AMP) via adenylosuccinate (SAMP). In addition, 6-methylthioinosinate (MTIMP) is formed by the methylation of TIMP. Both TIMP and MTIMP have been reported to inhibit glutamine-5-phosphoribosylpyrophosphate amidotransferase, the first enzyme unique to the de novo pathway for purine ribonucleotide synthesis. Experiments indicate that radiolabeled Mercaptopurine may be recovered from the DNA in the form of deoxythioguanosine. Some Mercaptopurine is converted to nucleotide derivatives of 6-thioguanine (6-TG) by the sequential actions of inosinate (IMP) dehydrogenase and xanthylate (XMP) aminase, converting TIMP to thioguanylic acid (TGMP).
    Animal tumors that are resistant to Mercaptopurine often have lost the ability to convert Mercaptopurine to TIMP. However, it is clear that resistance to Mercaptopurine may be acquired by other means as well, particularly in human leukemias.
    It is not known exactly which of any one or more of the biochemical effects of Mercaptopurine and its metabolites are directly or predominantly responsible for cell death.

    Clinical studies have shown that the absorption of an oral dose of Mercaptopurine in humans is incomplete and variable, averaging approximately 50% of the administered dose. The factors influencing absorption are unknown. Intravenous administration of an investigational preparation of Mercaptopurine revealed a plasma half-disappearance time of 21 minutes in pediatric patients and 47 minutes in adults. The volume of distribution usually exceeded that of the total body water.
    Following the oral administration of 35S-6-Mercaptopurine in one subject, a total of 46% of the dose could be accounted for in the urine (as parent drug and metabolites) in the first 24 hours. There is negligible entry of Mercaptopurine into cerebrospinal fluid.
    Plasma protein binding averages 19% over the concentration range 10 to 50 mcg/mL (a concentration only achieved by intravenous administration of Mercaptopurine at doses exceeding 5 to 10 mg/kg).
    A reduction in Mercaptopurine dosage is required if patients are receiving both Mercaptopurine and allopurinol (see PRECAUTIONS and DOSAGE AND ADMINISTRATION).
    Metabolism and Genetic Polymorphism

    Variability in Mercaptopurine metabolism is one of the major causes of interindividual differences in systemic exposure to the drug and its active metabolites. Mercaptopurine activation occurs via hypoxanthine-guanine phosphoribosyl transferase (HGPRT) and several enzymes to form 6-thioguanine nucleotides (6-TGNs). The cytotoxicity of Mercaptopurine is due, in part, to the incorporation of 6-TGN into DNA. Mercaptopurine is inactivated via two major pathways. One is thiol methylation, which is catalyzed by the polymorphic enzyme thiopurine S-methyltransferase (TPMT), to form the inactive metabolite methyl-6-MP. TPMT activity is highly variable in patients because of a genetic polymorphism in the TPMT gene. For Caucasians and African Americans, approximately 0.3% (1:300) of patients have two non-functional alleles (homozygous-deficient) of the TPMT gene and have little or no detectable enzyme activity. Approximately 10% of patients have one TPMT non-functional allele (heterozygous) leading to low or intermediate TPMT activity and 90% of individuals have normal TPMT activity with two functional alleles. Homozygous-deficient patients (two non-functional alleles), if given usual doses of Mercaptopurine, accumulate excessive cellular concentrations of active thioguanine nucleotides predisposing them to Mercaptopurine toxicity (see WARNINGS and PRECAUTIONS). Heterozygous patients with low or intermediate TPMT activity accumulate higher concentrations of active thioguanine nucleotides than people with normal TPMT activity and are more likely to experience Mercaptopurine toxicity (see WARNINGS and PRECAUTIONS). TMPT genotyping or phenotyping (red blood cell TPMT activity) can identify patients who are homozygous deficient or have low or intermediate TPMT activity (see WARNINGS, PRECAUTIONS: Laboratory Tests, and DOSAGE AND ADMINISTRATION sections).
    Another inactivation pathway is oxidation, which is catalyzed by Xanthine oxidase (XO) and forms 6-thiouric acid. Xanathine oxidase is inhibited by ZYLOPRIM® (allopurinol). Concomitant use of allopurinol with Mercaptopurine decreases the catabolism of Mercaptopurine and its active metabolites leading to Mercaptopurine toxicity. A reduction in Mercaptopurine dosage is therefore required if patients are receiving both Mercaptopurine and allopurinol (see PRECAUTIONS and DOSAGE AND ADMINISTRATION).
    After oral administration of 35S-6-Mercaptopurine, urine contains intact Mercaptopurine, thiouric acid (formed by direct oxidation by xanthine oxidase, probably via 6-mercapto-8-hydroxypurine), and a number of 6-methylated thiopurines.
    Indications and Usage for Mercaptopurine

    Mercaptopurine is indicated for maintenance therapy of acute lymphatic (lymphocytic, lymophoblastic) leukemia as part of a combination regimen. The response to this agent depends upon the particular subclassification of acute lymphatic leukemia and the age of the patient (pediatric or adult).
    Mercaptopurine is not effective prophylaxis or treatment of central nervous system leukemia.
    Mercaptopurine is not effective in acute myelogenous leukemia, chronic lymphatic leukemia, the lymphomas (including Hodgkin’s Disease), or solid tumors.

    Prednisone is a steroid, I wasn't too worried about your drugs until I read this about
    mercaptopurine . I would surely take it in small hits, one at a time and see how you feel. Hope you get to feeling better. Keep us updated.........:wave:


  3. reesescups99

    reesescups99 New Member

    dedbr - thanks for the quick reply. I was wondering where you found that listing. Based on what my doctor says and my own personal research, I have seen even a speck of the "dangers" of mercaptopurine that your post lists.
  4. Dedbr

    Dedbr Domestic War Veteran

    I just binged it and clicked the first one......:shrug:

    Most patients don't know what their taking, just that Dr. so and so said to take it......:rolleyes:

    The question is, did your doctor get all A's in medical school or C's? :D I've been prescribed meds that were contrary to ones he had given me when I saw him before. Don't trust them about Anthing. Educate yourself about anything your body is taking in. After you learn, grill your physician about his diagnosis and make sure he knows what he's talking about......

    Some of them don't..........:(


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