role of otc/rx meds in falsepositive EtG...tylenol otc/ssris rx

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agree dan,cp450/udpgt mostimportant... tylenol is the big otc culprit to interfere with also the big rx culprit as a goup are the ssris.five out of the top ten meds written in ths country are ssris,probably a lot of folks in this group are on them,and they mess with liver function big time...i do not think any one needs to stop rx without md help/taper but just to give people a heads up that ssris can have a role in false positive EtG...regaerds,r SSRIs are metabolized extensively by the liver cytochrome P450 isoenzyme system (i.e., citalopram via CYP3A4 and CYP2C19) and caution must be taken when using higher doses of SSRIs DiBona <danieldibona@...> wrote: The second major pathway for toxin elimination (chemicals, medications) is UDP-glucuronosyltransferase (UDPGT). As with cytochrome P-450 there are an equally large number of isoforms comprising this chemical deactivation and elimination system (1A1 thru 1A7 and 1B1 thru 2B15 are

the most studied). For EtG production, isoforms UGT1A1 and UGT2B7 are most responsible. They are also the most inducible isoforms, and are responsible for most of the toxin elimination requiring the addition of glucuronic acid to molecules-such as opiates, bilirubin, acetaminophen and on and on. Robins thoughts about grapefuit are intriquing. Grapefruit (alkaloids, I think) is complex stuff with significant impact upon our bodies, more so in other individuals. I am not well, but it’s now on my list of “interesting things to find out about”. Anyone turning up positive with EtG has to eliminate acetaminophen and virtually every other chemical entering your body (only if it’s safe to stop taking), whether it has alcohol in it or not. Some medications are conjugated to ethanol (called ethynil, as with estrogens in OCPs) that is released during normal processing. Though in amounts previously not forensically significant. In our cases of zero tolerance, these pills in an upregulated UGT person could produce levels of urine EtG reported on this group website. In my situation, I discovered a required medication of mine, recently started, is a specific and potent inducer (amplifier/upregulator) of UGT1A1 and 2B7-but here’s the kicker; stuff like this gets studied with hepatic

microsomes (ground up liver in a test tube). It’s often rat livers, so it’s hard to convince anyone on your own the sanity of your explanation. Even with me being an academic M.D., I retain someone else to do the explaining for me. I hate it, it costs a lot, but it certainly is more effective. I’m significantly moved by the ethics, politics, economics and personal impact EtG misuse foments. It represents a new brand of tyranny in my way of thinking. The rapid role out and penetration of testing already initiated virtually gurantees this groups growth. The damages are real, and to me, nauseating. I’m convinced not only will the tide turn, but that a

big wave will happen first. This groups grown by about thirty members in the past couple of weeks. The number of posts has logarithmically escalated (and we should not let up on this; everyone needs to keep posting). Right now there are mainly nurses, pharmacists, a few physicians, some legal entanglements and “lurkers” comprising this group. In the coming months, without a dramatic and sustained retraction effort by the testing companies we’ll begin seeing airline pilots, truckers, military and intelligence officers, etc. I doubt we’ll see many lawyers. And when we do (and I am CONVINCED we will), the first contacts should be considered with extreme suspicion and negative prejudice. It’s not beyond the testing companies to retain representation and point them our direction. As for me, I’ll need to hear the Lorie and seal of approval before I would talk to any attorney. Dan -----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of robin murraySent: Wednesday, September 27, 2006 6:55 PMEthylglucuronide Subject: Re: interaction of ingested substances with endogenous etoh may cause false positive EtG The primary site of drug metabolism is the liver, the organ that plays a major role in metabolism, digestion, detoxification, and elimination of substances from the body. Enzymes in the liver are responsible for chemically changing drug components into substances known as metabolites. Metabolites are then bound to other substances for excretion through the lungs, or bodily fluids such as saliva, sweat, breast milk, and urine, or through reabsorption by the intestines. The primary mode of excretion is through the kidneys.

The family of liver isoenzymes known as cytochrome P-450 are crucial to drug metabolism. These enzymes (labeled CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4) have a catabolic action on substances, breaking them down into metabolites. Consequently, they also act to lower the concentration of medication in the bloodstream. Drug int! eractions can occur when one drug inhibits or induces a P-450 that acts on another drug. An example is nicotine, a drug contained in tobacco, and known to induce P-450s. Individuals with liver disease (e.g., cirrhosis) may also have insufficient levels of P-450 enzymes. As a result, the concentration of drugs metabolized by these enzymes (e.g., amprenavir and other protease inhibitors) remains high and can build up to toxic

levels in the bloodstream. In addition, certain medications and foods, such as grapefruit juice, can inactivate or lessen the metabolic activity of P-450s. Changing the drug dosage can alleviate the problem in some cases. The metabolic rate can vary significantly from person to person, and drug dosages that work quickly and effectively in one individual may not work well for another. Factors such as genetics, environment, nutrition, and age also influence drug metabolism; infants and elderly patients may have a reduced capacity to metabolize certain drugs, and may require adjustments in dosage. Causes and symptoms Drugs that commonly interact with other medications include: Diuretics. Diuretics such as hydrochlorothiazide can reduce serum potassium and sodium electrolyte levels when taken with digoxin and lithium, respectively. Monoamine oxidase inhibitors (MAOIs). MAOI antidepressants can cause convulsions and other serious side effects when used with tricyclic antidepressants (e.g., Imipramine, Nortriptyline), selective serotonin

reuptake inhibitors (SSRIs), or sympathomimetic drugs (e.g., amphetamines). Antibiotics. Anti! biotics may reduce the efficiency of oral contraceptives. Metals. Medications containing metals, such as antacids with aluminum additives and iron supplements, can reduce the absorption of tetracyclines and fluoroquinolones. Drugs that inhibit liver enzyme function. Drugs that slow drug metabolism include ciprofloxacin, erythromycin, fluoxetine, nefazodone, paroxetine, and ritonavir. The therapeutic effect of other medications taken with these drugs may be amplified. Warfarin, a blood thinner, should be used with great caution in individuals taking these

drugs. Foods and beverages that may interact with drugs include: Grapefruit juice. Grapefruit juice inhibits the metabolism of many medications, including cyclosporine, felodipine, nifedipine, nitrendipine, nisoldipine, carbamazepine, triazolam, and midazolam. Foods and beverages with tyramines. Red wine, malted beers, smoked foods (e.g., fish and meats), dried fruits, and aged cheeses may contain tyramines, and can cause a severe and dangerous elevation in blood pressure when taken with MAOI inhibitors (a class of antidepressants). Dairy products. Milk, cream, and other dairy products containing calcium can prevention the absorption of antibiotics such as tetracycline, doxycycline, and ciprofloxacin when they are taken with the drug. In addition, whole milk with vitamin D can cause milk-alkali syndrome in patients taking aluminum hydroxide antacids. Caffeinated beverages. The caffeine contained in coffee and colas can influence drug metabolism. Alcohol. Alcohol is a central nervous system depressant, and should not be taken with other CNS depressants (e.g., antipsychotics, antihistamines). In addition, certain fermented beverages may contain tyramines. This list is not all-inclusive and individuals should always robin murray <remurraymd > wrote: hi julie and karen,you might want to have a look at the UAE endogenous alcohol study that lorie has posted...table one shows exponential variability of BAC with almost all 1553 subjects fron all countries having

max BAC 2-3 mg/dl from time to time during the study period which would translate to the exponential variability of EtG that y'all are having..i would have a careful look at that study the data supports completely what you are saying...also any rx or otc medicine with liver metabolism will skew to false positive EtG...might rx or otc meds have a role?also household cleaners like lysol,maybe?regards,r hartsonkaren <Thartsonbak (DOT) rr.com> wrote: >> I can't find the

cause of my positive etg. I have changed every thing > I consume and use but still test positive. I have had 4 positives in > a row over a month. It makes me think that I have gut fermentation > syndrome. I don't know what to do, please help> >, I too have had 2 pos. etg tests. One for 1000 and one for 1200. I can't find any link to foods or beverages either. I'm getting a bit desperate. I have been clean and SOBER for 4 yrs 2 mos. I have always been very careful of what I eat/drink. Because of these tests I've been pulled from work and my transition status in my diversion program has been revoked. What a nightmare.Please let me know what you find out about the Auto-Brewery Syndrome. I'm tempted to contact my MD for an evaluation.Thnaks,