long acting morphine not helping PLEASE READ

Discussion in 'Fibromyalgia Main Forum' started by sugarpeach, Jul 7, 2008.

  1. sugarpeach

    sugarpeach New Member

    Hello all.
    I have been seeing a new PM doctor since March and before this i was with another Dr. who I had a great relationship in terms of listening taking his time trying dift things etc. unfortunately he is no longer my Doc due to personal problems in his life. So now I am with this new dr. and he is treating me with long acting medications and a small amount of breakthru meds. I had previously tried Avinza with my previous Dr. but it did not help. After many months we finally settled on a mixture of Oxycodone 15mg up to 5x in 24 hrs that was a total of 75 mgs plus Lyrica 150mg at bedtime. worked fine.Still had bad days but was able to do things besides just go to my job.

    This new Dr. started me with Ms Contin 30 mg 2x a day, didnt touch pain so he switched me to OpanaER 60mg didnt help the pain and had terrible anxiety .Since then for past 2 1/2 months He has had me on Kadian. Started at dose of 30mg 2x a day. with 10mg of Hydrocodone every 8 hrs if needed for breakthrough pain . This did not help so he upped the Kadian to 60mg 2x a day and the same amount of hydrocodone. I told him that I dont think that morphine based meds help me b/c when i had a hysterectomy in 2004 it did nothing for the 12 hours I was on it before they switched me to 10mg oral percecet while in the hospital.

    I am still in pain everyday of at least a 5 and thats if I do nothing with my arm or neck. I have 5 bulging discs in my neck.herniated disc in lower back and Thoracic Outlet syndrome from a workers comp injury in 2006 .Plus FM and CFS and addrenal problems etc.

    My question is is there something wrong with me that morphine just doesnt help me or should I go higher. I am taking 120mg of Kadian and 30mg of hydrocodone a day and I am still in pain!!!! This doesnt seem right to me b/c it is double the amount of medicine that worked for me in Feb. Why wont he just treat me with what I was taking before.. I have had 3 epidural injections ,triggerpoint injections, get massage but it isnt working. I feel like I am being mis treated and that he doesnt believe me even though I brought records from prev. Dr, had new MRI of neck had emg's of upper body and lower which both show that i have cervical radiopathy(sp?) in right arm and nueropathy in right leg and foot..Cant feel three toes on that foot. I am a teacher have 3 children and just want to be treated fairly so that I can have some kind of life.

    If anyone can help me with this,offer suggestions or have had problem with long acting morphine meds not working for them I would really appreciate all responses or ideas. Im sorry for ranting its just that I am at the end of my rope and all I want is to be able to live my life, not sit or cry from the pain if I try to do anything physical. Thanks for being here once again. You are all truly courageous, brave, caring and knowledge people who struggle daily with your own problems but always have time to encourage and lend support to others on this board. Peace and hugs to all-Susan
  2. caffey

    caffey New Member

    If I am understanding you correctly I have had the same problem. Do you feel like the morphine is wearing off after so many hrs. We added a a 3rd dose during the day around 2pm ane we increased the dose. That really helped. Then my other docs wanted me to switch over to duragesic pain patchees. That was ok for 6months and then the same problem. Then my pain guy said that for some people they could only go 2 days and not 3. It has been a year now and I feel I have pretty good pain control. I don't know if that helps you or not. So what I am tryi8ng to say is increase the dosage and interval in between with the doc's ok.
  3. PVLady

    PVLady New Member

    You pose a very interesting question... I was reading about people who genetically are slow metabolizers of opiates. This also applies to anti-depressants and many other medications. It is in your genes.

    There is a lab that actually can test you to see which medications work best and also make suggestions to help the doctor adjust your dosage accordingly. Many doctors are using this with their patients now. You might want to check out their website at


    The following info is from their website:

    Pharmacogenetics of Pain

    Do not be surprised if in the next year or two, this kind of DNA testing will be considered as a necessary step before writing a prescription.

    Many common pain medications require activation by CYP2D6 to become effective. Approximately half of patients have genes that alter the function of 2D6.

    Testing for these gene alterations allows for alteration of dosage regimens to compensate for altered metabolism and optimize the safety and efficacy of the opioid family of analgesics.

    Physicians who adopt pharmacogenetic testing into their practice don't know how they were ever able to get along without it.

    . PM poor metabolizer, absent or greatly reduced ability to clear or activate drugs.

    B. IM intermediate metabolizer. Heterozygotes for normal and reduced activity genes.

    C. EM extensive metabolizer. The norm.

    D. UM Ultra Metabolizer. Greatly increased activity accelerating clearance or activation

    I would call this lab at 800 523-3080 and ask about the test for the CYP 2D6 which it appears is for slow metabolizers of opiates.

    I am not a scientist for I cannot explain this very well but the website has alot of information.

    This lab also tests for potential adverse drug reactions.

    Dosage Recommendations


    Specific Dosing Information for Pain Medication

    Interpretive Comments for 2D6, 2C9, and 2C19

    Download Interpretive Comments for 2D6, 2C9, and 2C19

    The information below can help you understand and apply the results of the DNA Prescription Drug Reaction Test currently offered by Genelex. Our tests spot individual genetic variants in the three most important drug metabolizing enzymes: Cytochrome P-450's CYP2D6, CYP2C9, and 2C19.

    More than half of the population has one or more serious defects in the genes coding for these enzymes. Recent research shows that genetic variation in the drug metabolizing system is the singlemost important factor affecting a patient's response to drugs.

    The information Genelex provides can help you determine the appropriateness and dosage of roughly a third of the most commonly prescribed drugs. To determine if medications are metabolized through these pathways, utilize the following drug list.

    Testing places individuals in one of four categories:

    · Extensive metabolizers (EM) represent the norm for metabolic capacity. Genotypes consistent with the EM phenotype include two active forms of the gene producing the drug metabolizing enzyme and therefore posses the full complement of drug metabolizing capacity. Generally, extensive metabolizers can be administered drugs which are substrates of the enzyme following standard dosing practices.

    · Intermediate metabolizers (IM) may require lower than average drug dosages for optimal therapeutic response. In addition, multiple drug therapy should be monitored closely. Genotypes consistent with the IM phenotype are those with only one active form of the gene producing the drug metabolizing enzyme and therefore have reduced metabolic capacity.

    · Poor metabolizers (PM) are at increased risk of drug-induced side effects due to diminished drug elimination or lack of therapeutic effect resulting from failure to generate the active form of the drug. Genotypes consistent with the PM phenotype are those with no active genes producing the drug metabolizing enzyme. These individuals have a deficiency in drug metabolism.

    · Ultra-extensive metabolizers (UM) may require an increased dosage due to higher than normal rates of drug metabolism. Simultaneously treating with medication that inhibits metabolization has also proven effective. Genotypes consistent with UM phenotype include three or more active genes producing the drug metabolizing enzyme and therefore have increased metabolic capacity.

    Cytochrome P-450 2D6
    Phenotype prevalence is 10 % PM, 7% UM, and 35% IM.

    Therapy Modification

    Avoid medications that are altered to their active form through 2D6, such as opioids. (For instance, 10% of a codeine dose is transformed to morphine through demethylation in the liver.) If you are uncertain, contact the drug manufacturer or look up the pharmacology data.

    Reduce dosage 6-10 fold for medications that are administered in their active form and demetabolized through 2D6 as are many antidepressants. (Desipramine, for example, is absorbed from the gastrointestinal tract following oral administration and is extensively bound to tissue and plasma proteins in the order of 90-95%. It is inmetabolized by hydroxylation and by further demethylation in the liver.) If you are uncertain, contact the drug manufacturer or look up the pharmacology data. Therapeutic drug monitoring is recommended for PMs to confirm that steady-state drug concentrations are within the therapeutic target interval.

    Increase dosage 2-5 fold depending on the number of duplications noted in the report. Success has also been achieved by concurrently administering another substrate or an inhibitor of CYP2D6.

    Start IMs at lowest efficacious dose and avoid multiple drug therapy that inhibits or activates through the same pathway.

    Changes in metabolic capacity for an individual does not change the pharmacologic action of the medication. Therefore standard therapeutic drug concentration target intervals can be used to optimize dosage titration. The advantage of knowing the subject's genotype is in predicting the general dosage range for initiation and recognizing changes in time to achieve steady-state for interpretation of blood concentration monitoring.

    Therapeutic drug monitoring is recommended in patients with metabolic variations. Keep in mind that subjects with metabolic deficiency will have decreased drug clearance and require additional time to achieve steady-state. In contrast, subjects with increased metabolic activity (UMs) have increased drug clearance and will achieve steady-state sooner that extensive metabolizers.

    Cytochrome P-450 2C9 and 2C19

    Phenotype prevalence is 3.7% PM, 38% IM for 2C9. Phenotype prevalence is 3% PM (for Asians 15-21%) for 2C19.

    Therapy Modification

    Reduce dosage 3-5 fold.

    Start IM's at lowest efficacious dose, avoid multiple drug therapy that inhibits or activates through the same pathway.

    Therapeutic drug monitoring in PM and IM subjects is highly recommended. Again standard measures of efficacy (INR for warfarin or therapeutic target interval for phenytoin, for example) can be applied to ensure optimal therapy.


    Linder MW, Valdes R Jr. Pharmacogenetics in the practice of laboratory medicine.
    Mol Diagn. 1999 Dec;4(4):365-79. Review.
    PMID: 10671647 [PubMed - indexed for MEDLINE]

    Interpretive Comments for 1A2

    Download Interpretive Comments for 1A2

    Interpretive Comments for 1A2

    The information below can help you understand and apply the results of the DNA Prescription Drug Reaction Test for CYP1A2 currently offered by Genelex.

    CYP1A2 Interpretation

    Hyperinduction phenotype: 39 - 47% (Japanese, Egyptian, Caucasian)
    Drugs metabolized by this enzyme approximately 5-10%
    Low affinity/high capacity enzyme

    Therapy Modification
    Testing places individuals in one of three categories:

    Normal Induction represents the norm for induction of metabolic activity in the presence of an inducer. Genotypes consistent with the normal induction phenotype include two CYP1A2 *1A alleles.

    Diminished Induction represents a lower than normal level of induction in the presence of an inducer. Genotypes consistent with the diminished induction phenotype are those with either one or two CYP1A2*1C alleles.

    Hyperinduction represents a higher than normal level of induction in the presence of an inducer. Induction may be approximately 40% higher in these patients than in those with the normal induction phenotype.

    Genotypes consistent with the hyperinduction phenotype include one or two CYP1A2*1F alleles. Patients with this phenotype may require an increased dosage of CYP1A2 substrates due to higher than normal rates of drug metabolism in the presence of an inducer.

    Doses of CYP1A2 substrates with a narrow therapeutic range should be decreased immediately on cessation of heavy smoking. A stepwise daily dose reduction of approximately 10% until the fourth day after smoking cessation accompanied by therapeutic drug monitoring has been proposed by Faber et al. Clin Pharmacol Ther.

    [This Message was Edited on 07/08/2008]
  4. msbsgblue

    msbsgblue Member

    Thank you
  5. Janalynn

    Janalynn New Member

    PVLady - thank you for the wonderful information!

    Susan- I totally understand where you're coming from. I tried MSContin with no luck whatsoever. I don't know why. It is very frustrating why some things work, some things don't. BUT we can't help it.

    I am one that barely took a darn Tylenol. I can only take a half of a Xanax before I'm knocked out, yet I can take enough pain medication to knock out a horse and barely have it touch my pain. Part of it must be tolerance. I must develop tolerance quickly.

    I don't drink, only tried drugs once as a teenager and hated it cause it made me feel out of it - so I don't want anything that makes me feel that way. I don't get any high from my medication. The only feeling I used to get was sort of a carsick feeling.

    Trying to get doctors to understand why different meds work better than others when it doesn't seem to make sense is difficult - but as I said, we don't have any control over how our bodies respond. My doctor has shaken her head many times when I've explained how my medication does or doesn't work.

    What I'm trying to say (and probably not very well LOL) is there is nothing wrong with you. We just respond differently to different medications/dosages, the combinations and of course if our pain levels change, well then it's time to start all over again.

    I'd have another nice talk with your doctor. Tell him of your frustration with all of this. Ask to try for 30 days, the medicine that you knew worked.
  6. sugarpeach

    sugarpeach New Member

    Thanks to all of you for taking the time and answering my questions. Cant wait to research some more on the info from PVLady. It is so very helpful to know that it just isnt me. Thanks again caffey and janalynn.Glad this was helpful to others too. Take care.Peace to all. xxoo susan
  7. Ginner

    Ginner New Member


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