Official Newsletter of the Utah Poison Control Center
I N T H I S I S S U E
TOXICOLOGY TODAY A program of the University of Utah College of Pharmacy
2014 • VOLUME 16 • ISSUE 1
T O D A Y
by Amberly R. Johnson, PharmD, BS, Fellow in Applied and Clinical Toxicology, Rachel Woolston, PharmD & Cynthia Din, PharmD
IntroductionPoisoning and over-
doses involving calcium-channel blocker (CCB), beta-blocker (BB), and tricyclic antidepressants (TCA) poisonings are as-sociated with significant morbidity and mortality and may be refractory to standard treatment. In this article, we review two new therapies, high dose insulin euglycemia therapy (HIE) and lipid rescue, for use when standard treatments fail.
High Dose Insulin Euglycemia Therapy (HIE)Toxicity of Calcium Channel Blockers and Beta-Blockers
Overdoses of calcium channel blockers (CCB) and beta-blockers (BB) may produce hypoten-sion and bradycardia, and in severe overdoses, conduction disturbances and cardiovascular
shock. Calcium channel blockers hinder the abil-ity of calcium to enter cells by antagonizing voltage-sensitive calcium channels. This effect is seen most prominently in the myocardial cells but also in the β-cells of the pancreas and smooth muscle result-ing in impaired myo-cardial conduction and contractility and hyperglycemia.1 Beta blocker toxicity is similar to CCB toxicity but without hyperglycemia. Propranolol exerts ad-ditional toxicity through sodium channel block-ade, and it and other lipophilic beta-blockers may produce seizures and more pronounced CNS depression.2
Mechanism of Action of High Dose Insulin Euglycemia Therapy
Insulin likely provides benefit by enhancing glucose uptake in the myocardium. While under normal circum-stances, the heart uses fatty acid oxidation to meet its energy require-ments; under stressed conditions, the heart
prefers glucose.3 Insulin increases inotropy and promotes vasodilation,3 which may restore car-diac output and improve critical organ perfusion.3 This mechanism only oc-curs at supratherapeutic insulin doses.3
Treatment and Dosing Recommendations
High dose insulin eu-glycemia therapy (HIE) is an off-label use often initiated in conjunction with or after traditional treatments such as fluid resuscitation, atropine, glucagon, and vasopres-sors.1,3,4 The UPCC recommends HIE along with traditional sup-portive measures in patients with evidence of depressed myocardial activity. There are cur-rently no standard dos-ing recommendations,
HigH Dose insulin anD lipiD Rescue
Outreach Education: � E-Cigarettes
Poison Pearls: � Antidotes for Methotrexate Toxicity
Meet the UPCC Staff: � Amber Johnson
Toxin in the News
but doses of regular insulin range from 0.1 units/kg/hr IV to 10-15 unit/kg/hr IV.4-13 The UPCC recom-mends a bolus of 1 unit/kg regular insulin followed by an infusion of 0.5 units/kg/hour. Reassess patient’s cardiac function in 15-30 minutes and increase infu-sion to 1-2 units/kg/hour if no improvement in 30 minutes. Dextrose should be infused to maintain a blood glucose of 100-200 mg/dL. Contact the UPCC to receive a copy of our Fast Fax for help in manag-ing a specific patient.See Appendix: Table 1
Safety/Adverse EffectsHypoglycemia may oc-
cur; however HIE therapy is generally well tolerated.3 One case review reported hypoglycemic events in five of twelve patients receiv-
ing HIE.16 In another case series of seven patients who received HIE, no patients experienced hypoglyce-mia.17 Insulin therapeutic errors with minimal hypo-glycemic events occurred in three case reports.13-15 Engebretsen et al14 described one episode of hypoglycemia (57 mg/dL) in a patient inadvertently given insulin 16.7 units/kg/h. No hypoglycemic events were reported by Place et al13 or Stellpflug et al15; however, large dextrose requirements (485 grams over 36 hours) were needed to maintain euglycemia in a patient who inadvertently received insulin 21.8 units/kg/h.15
Hypokalemia may also occur as insulin shifts po-tassium (cont. on pg. 3)
EmErgEnt thErapiEs in toxicology: high DosE insulin anD lipiD rEscuE
2
TOXICOLOGY TODAY A publication for Health Professionals.
O U T R E A C H E D U C A T I O N
P O I S O N P E A R L S
E-cigarettes are devices that are designed to deliver nicotine or other substances in vapor form. They essentially consist of 2 pieces: 1) rechargeable heating element and 2) replace-
able cartridge. The safety and efficacy of e-cigarettes have not been fully studied at this time.
The FDA has con-ducted some limited studies on a sampling of these products. Sig-nificant quality control issues were found. Some labeled as having no nicotine contained
nicotine and sev-eral with the same label emitted markedly different amounts of nicotine.
The lack of studies raises the following concerns:
ʶ How much nicotine or other chemicals are being inhaled during use?
ʶ What are the potential risks of using e-cigarettes?
ʶ Are there any benefits associated with these products?
There are too many unknowns at this time to understand the safety and potential value of these products.
As e-cigarettes have grown in popularity,
the Utah Poison Control Center has seen a rapid rise in pediatric poisoning exposures to these products. From 2012 to 2013, pedi-atric poisoning exposures to e-cigarettes had increased 350%, while poisoning exposures to regular cigarettes increased 35%. Symptoms from poisoning can include drooling, vomit-ing, agitation, cardiac arrhythmia, and convulsions.
Many products come in a variety of candy flavorings, making them appealing to children. Even a small amount of liquid in a spent cartridge can cause toxicity in a child. If these products are used around children, it is important to keep all parts out of reach.
What Do WE KnoW about E-cigarEttEs?
by Thomas G. Martin, MD, MPH Medical Director & Paul Hinckley, PharmD 2014 Candidate
When used as a rescue agent, leucovorin is administered 24 hours after treatment with high dose MTX to save healthy cells without reducing the antitumor activity of MTX.1
In the case of a MTX overdose, leucovorin is administered as soon as possible. For the
treatment of an acute MTX overdose, 1 mg of leucovorin is given for every mg of MTX, every 6 hours, until the serum MTX concentration is < 0.01 µmol/L in those not on MTX and < 0.05 – 0.1 umol/L in those on MTX for chemotherapy. Because of the calcium content of the prepara-tion, the infusion rate in adults should not exceed 160 mg/minutes. Higher doses of leucovorin may
be warranted if the patients renal function is poor or worsening or serum levels of MTX are not declining.1 Levoleucovorin is an alternative to leucovorin. The dose is ½ the dose of leucovorin. Leucovorin should not be given intrathecally. One death has been reported in a child after intrathecal injection.
of patients who develop toxic MTX concen-trations (>1 µmol/L) due to impaired renal clearance.2 Glucarpidase is a recombinant enzyme (carboxypeptidase G2) that is cloned from Pseudomonas. Glucarpidase lowers MTX concentrations by rapidly hydrolyzing
extracellular MTX into inactive metabolites (DAMPA and glutamate). This allows for non-hepatic metabolism and extra renal clearance of MTX .3 Glucarpidase has been available under compassionate use since 1993 and gained FDA approval in January 2012.
Glucarpidase decreases serum MTX concentrations within 15 minutes of infu-sion, thus reducing organ toxicity. Leucovorin rescue is indicated with glucapidase, however it should not be given within 2 hours of the glucarpidase infusion (before or after) as it is a substrate of glucarpidase.2-5 The dose is 50 U/kg infused intravenously over 5 minutes. Glu-carpidase has also been used as an antidote for an inadvertent intrathecal MTX (IT) overdose at a dose of 2000 units IT, as soon as possible. The acquisition cost of glucarpidase is $26,775 per 1000-unit vial.6
antiDotEs for mEthotrExatE toxicity
References1. Stoller RG, Hande KR, Jacobs SA, Rosenberg SA, Chabner BA.
Use of plasma pharmacokinetics to predict and prevent methotrex-ate toxicity. N Engl J Med. Sep 1977;297(12):630-634.
2. Inc. BI. Glucarpidase (Voraxase) Full Prescribing Information. BTG International Inc.; 2013:11.
3. Green JM. Glucarpidase to combat toxic levels of methotrexate in patients. Ther Clin Risk Manag. 2012;8:403-413.
4. Widemann BC, Schwartz S, Jayaprakash N, et al. Efficacy of Glu-carpidase (Carboxypeptidase G2) in Patients with Acute Kidney Injury After High-Dose Methotrexate Therapy. Pharmacotherapy. Oct 2013.
5. Widemann BC, Balis FM, Shalabi A, et al. Treatment of accidental intrathecal methotrexate overdose with intrathecal carboxypepti-dase G2. J Natl Cancer Inst. Oct 2004;96(20):1557-1559.
6. Ashley, L. N. (2013, March 19). Glucarpidase (Voraxaze). Formulary Drug Review. Available at: www.pharmacytimes.com/publications/health-system-edition/2013/March2013/Glucarpidase-Voraxaze
Check out this FDA fact sheet for more information about dietary supplements. http://www.fda.gov/downloads/Food/DietarySupplements/UCM240978.pdf
3 TOXICOLOGY TODAY www.utahpoisoncontrol.org
(cont. from pg. 1)Emergent Therapies intracellularly. In one case report,17 two patients treated with HIE had potassium concentrations < 3.5 mEq/mL, and in an-other report,16 eight patients had potassium concentrations < 3.0 mEq/mL. No significant arrhythmias were recorded in either case series.16,17
Lipid RescueLipophilic Drug Toxicity
Lipid emulsion is used as a component of total parenteral nutrition and for the preven-tion and treatment of essential fatty acid deficiency (EFAD).18 Lipid rescue is used off-label in the treatment of local anesthetic-induced cardiac toxicity and for lipophilic drug overdose, unresponsive to conventional resuscitation. Lipid rescue first proved useful in reversing systemic toxicity associated with
bupivacaine in animal studies19,20 and eventu-ally in humans.21,22 A number of case reports have documented the benefit of lipid rescue in the treatment of calcium channel blocker,23 beta blocker,24 tricyclic antidepressant,25 and other lipophilic drug poisonings.26 Intralipid® 20% is the concentration most commonly used for treating acute toxicities in the US.
Mechanism of Action of Lipid RescueLipid emulsions form a lipid partition in
the serum and likely act as a “lipid sink.” It is thought that lipophilic drugs are extracted from the plasma and tissues into the lipid sink, thereby reducing toxicity by decreasing the concentration of drug at the active site. 26-28 Lipid rescue may also improve myocardial fatty acid oxidation by increasing fatty acid uptake by the mitochondria and improving ATP synthesis.27,28 Lipid rescue may also sta-bilize the myocardial membrane and increase ionotropy by promoting calcium entry via voltage-dependent calcium channels.27
T O X I N S I N T H E N E W S
Treatment and Dosing RecommendationsSupporting literature and clinical experi-
ence have led to guidelines for the use of lipid rescue in poisoning emergencies unre-sponsive to conventional resuscitation. Use of lipid rescue therapy should not replace stan-dard ACLS procedures. The American Col-lege of Medical Toxicology’s (ACMT) guide-line is a modification of previously published guidelines and recommends lipid rescue in patients with serious hemodynamic instabil-ity, with or without cardiac arrest, from a drug with a high degree of lipid solubility.29 Large volume of distribution and positive partition constant (log P) predict higher lipid extraction efficiency.30 ACMT recommends an initial bolus of Intralipid® 20% 1.5 mL/kg IV over 2-3 minutes, followed by 0.25 mL/kg/min IV for maintenance.29
Safety/Adverse EffectsLipid rescue is generally well tolerated. The
most common adverse events include pan-creatitis (increased amylase levels, increased lipase levels)31-33 and interferences with a va-riety of laboratory tests due to lipemia.31-34 A rare case of bronchospasm has been report-ed.32 Intralipid® 20% is contraindicated if a patient has hyperlipidemia, any disturbance of normal fat metabolism, acute pancreatitis, or severe allergies to eggs.18
See Appendix: Table 2
SummaryPoisonings and overdoses involving CCB,
BB, and other myocardial depressants may be refractory to standard treatments. HIE is considered by many toxicologists to be indicated early in the therapy of severe CCB toxicity. Lipid rescue should be considered in any acute cardiovascular poisoning that is unresponsive to standard resuscitative measures, especially for lipophilic agents like local anesthetics. Currently, health care professionals can post their experiences with lipid rescue on www.lipidrescue.org under “Post Your Cases.”
The Utah Poison Control Center is here to assist you. We are a team of medical toxicolo-gists, pharmacists, and nurses with extensive experience and specialized training in toxi-cology providing 24 hour, 7 day a week free consultation to Utah. Please call us if you are treating any severe or unusual overdose or have any questions about HIE or lipid rescue therapy, at 1-800-222-1222. (cont. on pg. 4)
FDA regulates dietary supplement products as well as supplement ingredients. FDA is responsible for taking action against any dietary supplement found to be unsafe. Last year FDA initiated several recalls involving supplements and provided safety alerts on many others.The most serious recalls involved the following products:
ʶ Maxiloss Weight Advanced Softgels, PerfectBody Solutions, and Burn 7: FDA testing found these products contain sibutramine. Sibutramine is a serotonin-norepinephrine reuptake inhibitor approved in 1997 for management of obesity and removed from the market in 2010 for safety reasons.
ʶ Oxy Elite Pro, Jack3D, and VERSA-1 (any supplement containing dimethyl-amylamine (DMAA): DMAA is an amphetamine derivative most commonly found in supplements promising weight loss, muscle building and performance enhancement. It is quite dangerous and has been associated with a variety of cardiovascular problems: short-ness of breath, tightening of the chest, and even heart attack in young persons. Given the known biological activity of DMAA, the ingredient may be particularly dangerous when used with caffeine. Other synonyms for DMAA include methylhexanamine, 1,3-DMAA, 1,3-dimethylamylamine, 1,3-dimethylpentylamine, amino-4-methylhexane, 2-hexanamine, 4-methyl-2-hexanamine, 4-methyl-2-hexylamine, 4-methyl- (9CI), di-methylamylamine, geranamine, methylhexanamine, methylhexanenamine, pelargonium graveolens extract, and geranium extract. Oxy Elite Pro and VERSA-1 replaced their products with aegeline, which is not an FDA approved ingredient and has been associated with serious liver damage. Users are urged to discard any remaining products containing DMAA.
FDA is unable to test and identify all products marketed as dietary supplements that have potentially harmful ingredients. Consumers are cautioned to check with their health care pro-vider before starting any new supplement. If someone experiences negative side effects from a supplement they should check with their health care provider or call the poison control center at 1-800-222-1222.
Contact Us: [email protected] Poison Control Center30 South 2000 East, Suite 4540Salt Lake City, Utah 84112
AMBER JOHNSON, pharmD joined the UPCC staff in July 2013 as a fellow-in-training.
Amber was born and raised in Payson, Utah, but did her undergraduate work at the south-ern end of the Utah, receiving an Associate of Arts degree from Dixie State College and a Bachelors of Science degree in biology from Southern Utah University. Amber worked at ARUP Laboratories for many years before she wanted to be a pharmacist. She recently graduated from the University of Utah with her PharmD in 2013. Amber is excited for the opportunity she has to be the fellow at the UPCC because she loves toxicology and also gets to help people. In her free time, she enjoys traveling and spending time with her son, Mason, playing soccer, skiing, draw-ing, learning to make new kinds of foods, and hanging out with her family, friends, and pets. Her clinical interests include illicit drugs of abuse.
References1. Shepherd G, Klein-Schwartz W. High-dose insulin therapy for calcium-channel
blocker overdose. The Annals of pharmacotherapy. May 2005;39(5):923-930.2. Shepherd G. Treatment of poisoning caused by beta-adrenergic and calcium-chan-
nel blockers. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists. Oct 1 2006;63(19):1828-1835.
3. Engebretsen KM, Kaczmarek KM, Morgan J, Holger JS. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning. Clinical toxicol-ogy. Apr 2011;49(4):277-283.
4. Kerns W, 2nd. Management of beta-adrenergic blocker and calcium chan-nel antagonist toxicity. Emergency medicine clinics of North America. May 2007;25(2):309-331; abstract viii.
5. Boyer EW, Shannon M. Treatment of calcium-channel-blocker intoxica-tion with insulin infusion. The New England journal of medicine. May 31 2001;344(22):1721-1722.
6. Marques M, Gomes E, de Oliveira J. Treatment of calcium channel blocker intoxication with insulin infusion: case report and literature review. Resuscitation. May 2003;57(2):211-213.
7. Rasmussen L, Husted SE, Johnsen SP. Severe intoxication after an intentional overdose of amlodipine. Acta anaesthesiologica Scandinavica. Sep 2003;47(8):1038-1040.
8. Stellpflug SJ, Fritzlar SJ, Cole JB, Engebretsen KM, Holger JS. Cardiotoxic over-dose treated with intravenous fat emulsion and high-dose insulin in the setting of hypertrophic cardiomyopathy. Journal of medical toxicology : official journal of the American College of Medical Toxicology. Jun 2011;7(2):151-153.
9. Yuan TH, Kerns WP, 2nd, Tomaszewski CA, Ford MD, Kline JA. Insulin-glucose as adjunctive therapy for severe calcium channel antagonist poisoning. Journal of toxicology. Clinical toxicology. 1999;37(4):463-474.
10. Herbert J, O’Malley C, Tracey J, Dwyer R, Power M. Verapamil overdosage unresponsive to dextrose/insulin therapy (abstract). Journal of toxicology. Clinical toxicology. 2001;39:293-294.
11. Meyer M, Stremski E, Scanlon M. Successful resuscitation of a verapamil intoxicated child with a dextrose-insulin infusion. Clinical Intensive Care. 2003;14:109-113.
12. Morris-Kukoski C, Biwas A, Para M. Insulin “euglycemia” therapy for ac-cidental nifedipine overdose (abstract). Journal of toxicology. Clinical toxicology. 2000;38:577.
13. Place R, Carlson A, Leikin J, Hanashiro P. Hyperinsulin therapy in the treatment of verapamil overdose. Journal of toxicology. Clinical toxicology. 2000;38:576-577.
14. Engebretsen KM, Holger JS, Harris CR. Therapeutic misadventure of high dose insulin without adverse effects [abstract]. Clinical toxicology. 2008;46:604.
15. Stellpflug SJ, Harris CR, Engebretsen KM, Cole JB, Holger JS. Intentional overdose with cardiac arrest treated with intravenous fat emulsion and high-dose insulin. Clinical toxicology. Mar 2010;48(3):227-229.
16. Holger JS, Stellpflug SJ, Cole JB, Harris CR, Engebretsen KM. High-dose insulin: a consecutive case series in toxin-induced cardiogenic shock. Clinical toxicology. Aug 2011;49(7):653-658.
17. Greene SL, Gawarammana I, Wood DM, Jones AL, Dargan PI. Relative safety of
hyperinsulinaemia/euglycaemia therapy in the management of calcium channel blocker overdose: a prospective observational study. Intensive care medicine. Nov 2007;33(11):2019-2024.
19. Weinberg GL, VadeBoncouer T, Ramaraju GA, Garcia-Amaro MF, Cwik MJ. Pretreatment or resuscitation with a lipid infusion shifts the dose-response to bupivacaine-induced asystole in rats. Anesthesiology. Apr 1998;88(4):1071-1075.
20. Weinberg G, Ripper R, Feinstein DL, Hoffman W. Lipid emulsion infusion rescues dogs from bupivacaine-induced cardiac toxicity. Regional anesthesia and pain medicine. May-Jun 2003;28(3):198-202.
21. Rosenblatt MA, Abel M, Fischer GW, Itzkovich CJ, Eisenkraft JB. Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac arrest. Anesthesiology. Jul 2006;105(1):217-218.
22. Spence AG. Lipid reversal of central nervous system symptoms of bupivacaine toxicity. Anesthesiology. Sep 2007;107(3):516-517.
23. Liang CW, Diamond SJ, Hagg DS. Lipid rescue of massive verapamil overdose: a case report. Journal of medical case reports. 2011;5:399.
24. Dean P, Ruddy JP, Marshall S. Intravenous lipid emulsion in propranolol [cor-rected] overdose. Anaesthesia. Nov 2010;65(11):1148-1150.
25. Harvey M, Cave G. Case report: successful lipid resuscitation in multi-drug over-dose with predominant tricyclic antidepressant toxidrome. International journal of emergency medicine. 2012;5(1):8.
26. Cave G, Harvey M, Graudins A. Intravenous lipid emulsion as antidote: a sum-mary of published human experience. Emergency medicine Australasia : EMA. Apr 2011;23(2):123-141.
27. Weinberg GL. Lipid emulsion infusion: resuscitation for local anesthetic and other drug overdose. Anesthesiology. Jul 2012;117(1):180-187.
28. Rothschild L, Bern S, Oswald S, Weinberg G. Intravenous lipid emulsion in clinical toxicology. Scandinavian journal of trauma, resuscitation and emergency medicine. 2010;18:51.
29. American College of Medical Toxicology (ACMT). Interim Guidance for the Use of Lipid Resuscitation Therapy. 2010; American College of Medical Toxicology. http://acmt.net/cgi/page.cgi?aid=3384&_id=462&zine=show. Updated 2012. Accessed March 14 2014.
30. French D, Smollin C, Ruan W, Wong A, Drasner K, Wu AH. Partition constant and volume of distribution as predictors of clinical efficacy of lipid rescue for toxicological emergencies. Clinical toxicology. Nov 2011;49(9):801-809.
31. Bucklin MH, Gorodetsky RM, Wiegand TJ. Prolonged lipemia and pancreatitis due to extended infusion of lipid emulsion in bupropion overdose. Clinical toxicology. Nov 2013;51(9):896-898.
32. Cave G, Harvey M, Willers J, et al. LIPAEMIC Report: Results of Clinical Use of Intravenous Lipid Emulsion in Drug Toxicity Reported to an Online Lipid Registry. Journal of medical toxicology : official journal of the American College of Medical Toxicology. Jan 11 2014.
33. Levine M, Brooks DE, Franken A, Graham R. Delayed-onset seizure and cardiac arrest after amitriptyline overdose, treated with intravenous lipid emulsion therapy. Pediatrics. Aug 2012;130(2):e432-438.
34. West PL, McKeown NJ, Hendrickson RG. Iatrogenic lipid emulsion overdose in a case of amlodipine poisoning. Clinical toxicology. May 2010;48(4):393-396.
Table 1: Insulin Doses Used in Case Reports/Reviewsa
Reference (year) Age (yr) CCB/BB Ingested Highest Insulin Dose Used OutcomeBoyer et al (2001)5 34 amlodipine 0.5 units/kg/h Survived
48 diltiazem ER 0.5 units/kg/h Survived
Engebretsen (2008)14 32 amlodipineb
metoprolol16.7 units/kg/hc Survived
Herbert et al (2001)10 58 verapamil Unknown Died
Marques et al (2003)6 75 diltiazemb 0.5 units/kg/h Survived
Meyer et al (2003)11 13 verapamil SR 0.1 units/kg/h Survived
Morris-Kukoski et al (2000)12
5 mo nifedipine 1 unit/kg/h Survived
Place et al (2000)13 49 verapamil SR 10 unit/kg bolusc Survived
Rasmussen et al (2003)7 36 amlodipineb 0.4 units/kg bolus Survived
Stellpflug et al (2010)15 48 nebivololb 21.8 units/kg/hc Survived
Stellpflug et al (2010)8 30 amlodipine metoprolol
10 units/kg/h Survived
Yuan et al (1999)9 37 amlodipineb
atenolol0.5 units/kg/h Survived
14 verapamil SR 0.5 units/kg/h Survived
31 verapamil SR 0.1 units/kg/h Survived
36 verapamil SR 0.3 units/kg/h Survived
50 verapamil SRb 1 unit/kg/h Surviveda Table adapted from Shepherd et al.1 b Co-ingestants in addition to CCB or BB c Therapeutic error
Table 2. Lipid Rescue Adverse EventsReference Intoxicant Total Dose of Intralipid® Adverse EventCave et al32 ropivicaine 300 mL Bronchospasm
olanzapine, ethanol, lithium 1000 mL Elevated amylase levels
propranolol, methocarbamol
1000 mL Laboratory interference
Levine et al33 amitriptyline 1.5 mg/kg x 20.25 mg/kg/min x 30 min
Elevated lipase, possible pancreatitis, laboratory interference
West et al34 amlodipine 2000 mL Laboratory interference
Bucklin et al31 bupropion 4000 mL Elevated lipase and amylase, possible pancreatitis, laboratory interference
A L E R T S
National Poison Prevention Week was held March 16-22nd 2014. Awareness
of the poison problem and poison prevention messages were promoted
throughout the state. Over 88,000 education materials were sent out in conjunction with this event and
hundreds of people were reached via presentations, health fairs, radio and TV
interviews, and newspaper articles during the month of March.
After an FDA warning to the pub-lic not to use it, Pro ArthMax, a dietary supplement for joint, muscle and ar-thritic pain has been withdrawn from market. It contains undeclared active NSAIDS, which can cause adverse effects or allergic reactions in sensitive individu-als.
The following OTC male sexual enhancement products: Boost Ultra, XZone Gold, Sexy Monkey, Triple MiracleZen Platinum, Magic for Men, “New” Extenze, and New XZen Platinum have been voluntarily recalled. These prod-ucts were found to contain undeclared sildenafil and/or tadalafil, which may interact with nitrates and may lower blood pressure to danger-ous levels.
