November 2013 FAQs
November 2013 FAQs Heading link
What are the most recent recommendations for occupational postexposure prophylaxis(PEP)?
What are the most recent recommendations for occupational postexposure prophylaxis (PEP)?
The Centers for Disease Control (CDC) first published guidelines for postexposure prophylaxis (PEP) of human immunodeficiency virus (HIV) in healthcare providers (HCP) in 1990.1 These guidelines were then revised and published by the United States Public Health Service (PHS) in 1996 with a subsequent 3 revisions, the most recent one in 2005. 2 The newest set of guidelines seeks to improve upon some of the confusing characteristics of the previous versions. The previous guidelines required a level of risk to be established based on characteristics of the exposure and the source patient. This categorical risk would then determine the number of antiretrovirals in the PEP regimen. The list of recommended drugs also included older antiretrovirals with more toxic and prevalent side effect profiles. The new guidelines eliminate the recommendation to determine the level of risk, include newer medications that can be considered for use, and provides an option for concluding follow-up HIV testing for exposed personnel in shorter than 6 months. These new guidelines are the direct result of a working group that consisted of the CDC, Food and Drug Administration (FDA), Health Resources and Services Administration, National Institutes of Health (NIH), and an expert panel.3 Though the transmission rates are low in the event of healthcare exposure, approximately 0.3% for percutaneous injury4 and 0.09% for non-intact skin or mucous membrane contact5, it is important for healthcare systems to develop policies for the implementation of these guidelines in the event of an occupational exposure.
The guidelines define a HCP as, “all paid and unpaid persons working in healthcare settings who have the potential for exposure to infectious materials, including body substances (eg, blood, tissue, and specific body fluids), contaminated medical supplies and equipment, and contaminated environmental surfaces.”3 The exposures that put HCP most at risk include percutaneous injuries such as needlesticks and any cuts to the skin or contact of mucous membranes or non-intact skin with blood, tissue, or other potentially infectious body fluids. Of note, semen and vaginal secretions are not considered vectors for transmission in this setting. Fluids of concern are mostly limited to blood or any bodily fluids that are visibly bloody. Other fluids of concern include: cerebrospinal fluid, synovial fluid, pleural fluid, peritoneal fluid, pericardial fluid, and amniotic fluid. Risk has been shown to be increased in those HCP exposed to larger quantities of blood or from source patients with high HIV titers.6 Source patients with undetectable HIV viral loads, however, do not eliminate the concern for transmission or the need for PEP.
In the case of a known drug-resistant HIV source patient, an expert in HIV should later be consulted; however, initiation of PEP should not be prolonged. Empiric therapy can be started and adjusted.3 Resistance should be suspected in source patients whose CD4 counts have declined or viral loads increased while on drug therapy at any point during the course of their treatment. Resistance testing of the source patient at the time of exposure, however, is not a practical option because results will not be back in time to start the initial PEP regimen.
Antiretrovirals for Postexposure Prophylaxis
None of the antiretrovirals (ARVs) approved for the treatment of HIV has ever been formally approved by the FDA for use in PEP. All recommended drugs were chosen based on their tolerability and proven efficacy in the treatment of HIV. The current recommendation per the guidelines is a 3-drug regimen for a total of 4 weeks.3 The general consensus is that patients on ARVs for PEP tolerate the regimen more poorly than using these agents for the treatment of HIV, so it is even more important that the chosen regimen minimize the potential drug toxicities. Also, when possible, the prescriber should preemptively prescribe any medications that might help ameliorate any known side effects of the drug regimen to increase the likelihood of medication adherence. A thorough analysis of any potential drug-drug interactions between the PEP regimen and any prescribed, over-the-counter (OTC), or herbal supplements the HCP may be currently taking should be performed by the prescriber and/or the pharmacist. This is especially important if the HCP is placed on a protease inhibitor (PI) or non-nucleoside reverse transcriptase inhibitor (NNRTI) as these 2 drug classes have the greatest potential for these interactions. Of note, the preferred drug regimen is safe to use in pregnant patients and is minimally found in the breast milk, but to avoid drug transmission to the infant, breast-feeding may need to be ceased while on the medications.
Table. Preferred Drug Regimen for Postexposure Prophylaxis.3
Drug Dose Considerations Emtricitabinea 200 mg PO daily Rash, hyperpigmentation of skin Tenofovira 300 mg PO daily Nephrotoxicity: should not be administered to patients with acute or chronic kidney injury or eGFR <60 Raltegravir 400 mg PO twice daily Insomnia, nausea, fatigue, headache, and severe skin and hypersensitivity reactions
a As Truvada.
Institutions should develop clear protocols that are easily available and distributed appropriately for HCP PEP.3 These protocols should effectively outline such details as what service will serve as expert consultation, such as infectious diseases. It should also include labs to be drawn for both the initial source patient and exposed provider, and the initial PEP regimen should be readily available and provided. Counseling should be available to the exposed provider as well as a mechanism for provider follow-up. Exposure prevention remains the best way for decreasing the exposure of HCP to bloodborne pathogen infections and should also be addressed by the protocol.
Figure. Algorithm for human immunodeficiency virus postexposure prophylaxis.3
Abbreviations: HCP, healthcare provider; HIV, human immunodeficiency virus; PEP, postexposure prophylaxis; PHS, Public Health Service.
The 2013 guidelines for occupational exposure to HIV for healthcare providers published by the United States PHS contain 2 major changes from the 2005 guidelines: they eliminate the need for risk stratification, recommending all PEP include a 3-drug regimen, and provide an option for a 4-month total follow-up for providers who are exposed.3 These guidelines are meant to streamline the process of providing PEP to HCP exposed to HIV. The first-line regimen recommended is emtricitabine, tenofovir, and raltegravir for 4 weeks. Source patients should be evaluated for any resistance, and expert consultation should be utilized in tailoring the regimen if resistance is found. Drug toxicities should be minimized by providing medications that help ameliorate known side effects, evaluating all potential drug-drug interactions, and providing regular follow-up for the HCP. Protocols should be put into effect at all institutions and made easily available in the event an occupational exposure occurs.
1. Centers for Disease Control and Prevention. Public Health Service statement on management of occupational exposure to human immunodeficiency virus, including considerations regarding zidovudine postexposure use. MMWR Recomm Rep 1990;39(RR-1):1-14.
2. Panlilio AL, Cardo DM, Grohskopf LA, Heneine W, Ross CS; US Public Health Service. Updated U.S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for postexposure prophylaxis. MMWR Recomm Rep 2005;54(RR-9):1-17.
3. Kuhar DT, Henderson DK, Struble KA, Heneine W, Thomas V, Cheever LW, Gomaa A, Panlilio AL; US Public Health Service Working Group. Updated US Public Health Service Guidelines for the Management of Occupational Exposures to Human Immunodeficiency Virus and Recommendations for Postexposure Prophylaxis. Infect Control Hosp Epidemiol 2013;34(9):875-92.
4. Bell DM. Occupational risk of human immunodeficiency virus infection in healthcare workers: an overview. Am J Med 1997; 102(5B):9-15.
5. Ippolito G, Puro V, De Carli G; Italian Study Group on Occupational Risk of HIV Infection. The risk of occupational human immunodeficiency virus infection in health care workers: Italian multicenter study. Arch Intern Med 1993;153(12):1451-1458.
6. Mast ST, Woolwine JD, Gerberding JL. Efficacy of gloves in reducing blood volumes transferred during simulated needlestick injury. J Infect Dis 1993; 168(6):1589-1592.
Benjamin Hammer, PharmD
University of Illinois at Chicago
What are the safety concerns with electronic cigarettes (“e-cigarettes”),and do they have a role in smoking cessation?
What are the safety concerns with electronic cigarettes (“e-cigarettes”), and do they have a role in smoking cessation?
The growing popularity of electronic cigarettes (or “e-cigarettes”) raises public health concerns, as well as concerns from health care providers unsure of their place in smoking cessation. The latest data from the Centers for Disease Control and Prevention (CDC) in 2011 suggest that about 21% of adult smokers have used e-cigarettes, which is double the 2010 figures.1 Particularly concerning is the fact that these trends are very similar in adolescents.2 In a survey of children in grades 6 to 12, the CDC found that the number of students who had ever used an e-cigarette doubled between 2011 and 2012. About 10% of the students who reported e-cigarette use had never even smoked a traditional cigarette. This statistic raises concerns that e-cigarettes may function as gateway products to traditional cigarettes, especially in light of their widespread distribution and lack of regulation. While the popularity of e-cigarettes continues to increase, lack of long-term safety data and limited efficacy data limit the ability to make recommendations for or against their use as smoking cessation agents. The remainder of this article will review the available safety information and a randomized controlled trial on e-cigarettes for smoking cessation.
Background and Safety
Although the components of an e-cigarette differ between brands, most contain a cartridge of nicotine solution (a mixture of nicotine and various solvents), a tube resembling a traditional cigarette, pen, or other common item, and a small battery that functions to heat the cartridge.3 The heating element vaporizes the cartridge solution, allowing the user to inhale the nicotine vapor. In some cases, mint, chocolate, or even fruit flavors are added to the cigarettes. Critics argue that these flavors can attract children to the products. Interestingly, manufacturers can bypass significant Food and Drug Administration (FDA) oversight and sell their products with few restrictions, since e-cigarettes are not considered drug products.4 The D.C. Circuit Court of Appeals upheld this ruling, stating that e-cigarettes are to be regulated as tobacco products, provided that manufacturers refrain from marketing their products as therapeutic agents.
Inconsistent product quality is also an issue with electronic cigarettes.3 Two brands of e-cigarettes claiming to contain 16 mg and 18 mg of nicotine per cartridge each actually had a much lower amount upon laboratory analysis; approximately one sixth to one quarter of the amount claimed. Proponents of e-cigarettes claim that the products contain fewer additives than traditional cigarettes, a claim that the FDA’s Center for Drug Evaluation tested in 2009.5 From an analysis of the liquid contents of 2 brands of cartridges, diethylene glycol, carcinogenic nitrosamines, and tobacco impurities were among the findings. The FDA points out that this was a preliminary analysis and due to the limited sample size, the results cannot be generalized to all marketed e-cigarettes. European e-cigarettes were found to contain formaldehyde, nitrosamines, and trace metals, although all at lower concentrations than traditional cigarettes.6
Role in Smoking Cessation
In terms of smoking cessation potential, few randomized controlled trials have compared e-cigarettes to traditional cigarettes. However, one study in New Zealand compared e-cigarettes, nicotine-free placebo e-cigarettes, and nicotine patches for smoking cessation.7 In the investigator-blinded, randomized controlled trial, 657 participants who wished to quit smoking underwent block randomization into 3 groups. Investigators used a 4:4:1 ratio of e-cigarettes to patches to placebo e-cigarettes. The primary endpoint assessed was continuous smoking abstinence 6 months after randomization. Smoking abstinence was self-reported, and all participants who claimed abstinence were given a carbon monoxide breath test for confirmation. Multiple secondary outcomes were assessed, including adverse events in all groups, reduction in the number of cigarettes smoked per day, and the time to relapse in e-cigarette and nicotine patch users.
An intention-to-treat analysis found that 7.3% of the 289 participants in the e-cigarette group and 5.8% of 295 participants in the nicotine patch group maintained smoking abstinence 6 months after randomization (p=0.46).7 Compared to e-cigarettes, 4.1% of the 73 participants in the placebo cigarette group were abstinent at 6 months (p=0.44). The only statistically significant difference in smoking abstinence was found at 1 month, when 23.2% of e-cigarette users and 15.9% of nicotine patch users remained abstinent (p=0.03). In terms of secondary outcomes, the mean difference in number of cigarettes smoked per day between e-cigarette and patch users was 2 cigarettes per day, with more cigarettes smoked by patch users (p<0.0001). The time to relapse was about 35 days for e-cigarettes users, double the time to relapse in patch users.
A greater proportion of adverse events occurred in the e-cigarette group than in the patches group, but the investigators found that there was no difference in the incidence rate ratio of events between the patch group and the e-cigarettes group (1.05, 95% confidence interval 0.82 to 1.34; p=0.7). 7 Twenty percent of adverse events in the e-cigarette group were considered serious as compared to 12% of events in the patch group. Only 1 adverse event in the study was definitely linked to study treatment, and it occurred in a participant using patches.
Because the quit rates for participants in all groups were lower than anticipated, the power calculation could not show that e-cigarettes are superior to either nicotine patches or placebo e-cigarettes.7 The investigators concluded that e-cigarettes have similar efficacy to nicotine patches in helping smokers quit. The decrease in the mean number of cigarettes smoked per day by e-cigarettes users could be related to the fact that the e-cigarettes mimic the look and feel of traditional cigarettes.
Despite the strong design of this study, there are a variety of limitations.7 First, 43 participants in the nicotine patch group were lost to follow up or discontinued the study, compared to 16 in the electronic cigarettes group. Because electronic cigarettes are not for sale in New Zealand, people may have been motivated to participate in the study and then disappointed once they were randomized to the nicotine patch group. Blinding of participants and investigators with a double dummy approach may have eliminated the disparity in dropout rates. Compliance was not measured and it is unclear how the devices were used among participants due to lack of a protocol. Also, due to variation in nicotine content and additives in all e-cigarettes, the type used in this study may or may not be equivalent to the products commercially available in the United States.
The greatest limitation of this study is arguably the inclusion of participants who had previously attempted to quit smoking using patches.7 About 20% of total participants in the study had previously attempted to quit smoking, but the number randomized to each group was not disclosed. Many had already had unsuccessful quit attempts with patches; on the other hand, electronic cigarettes were a new option for quitting. This could have reduced the likelihood that the nicotine patches would be effective in these participants.
The variability among e-cigarettes makes it difficult to draw conclusions about their safety and potential use as smoking cessation agents. Most of the available data suggest that e-cigarettes contain less nicotine and toxic substances than their traditional cigarette counterparts. Recent studies show that potentially hazardous combustion products are found in trace amounts in e-cigarettes vapor, although the clinical significance of these findings has not been established. Given the inconsistency among products, the lack of conclusive safety data, and poor regulatory oversight, it is difficult to justify recommending these products to patients who wish to quit smoking. It has been suggested that the development of an FDA-approved electronic nicotine delivery device with a consistent formulation and favorable safety profile could be a solution. Fortunately, there is active research devoted to e-cigarettes, and new efficacy and safety data will be available in the years to come.
1. About one in five U.S. adult smokers have tried an electronic cigarette. Centers for Disease Control and Prevention website. http://www.cdc.gov/media/releases/2013/p0228_electronic_
cigarettes.html. Updated February 28, 2013. Accessed October 8, 2013.
2. Notes from the field: electronic cigarette use among middle and high school students – United States, 2011-2012. MMWR Morb Mortal Wkly Rep. 2013;62(35):729-730.
3. Cobb NK, Byron MJ, Abrams DB, Shields PG. Novel nicotine delivery systems and public health: the rise of the “e-cigarette.” Am J Public Health. 2010;100(12):2340-2342.
4. Regulation of e-cigarettes and other tobacco products. US Food and Drug Administration website. geo. Updated April 25, 2011. Accessed September 27, 2013.
5. Summary of results: laboratory analysis of electronic cigarettes conducted by FDA. US Food and Drug Administration website. http://www.fda.gov/newsevents/publichealthfocus/ucm173146.htm. Updated July 22, 2009. Accessed October 14, 2013.
6. Goniewicz M, Knysak J, Gawron M, et al. Levels of selected carcinogens and toxicants in vapour from electronic cigarettes [published online March 6, 2013]. Tob Control. doi:10.1136/tobaccocontrol-2012-050859.
7. Bullen C, Howe C, Laugesen M, et al. Electronic cigarettes for smoking cessation: a randomised controlled trial [published online ahead of print September 9, 2013]. Lancet. doi:10.1016/S0140-6736(13)61842-5.
Doctor of Pharmacy candidate, 2015
University of Illinois at Chicago
What data are available to direct dosing of intravenous immunoglobulin G based on total versus ideal or adjusted body weight?
What data are available to direct dosing of intravenous immunoglobulin G based on total versus ideal or adjusted body weight?
Intravenous immunoglobulin (IVIG) is a serum antibody preparation of human immunoglobulin G (IgG) manufactured from pooled human plasma.1 IVIG is Food and Drug Administration (FDA)-approved for the treatment of various primary immunodeficiency syndromes and is also utilized in numerous off-label immune-related conditions.2 Although the dosing of IVIG varies by indication, the administered dose is usually weight-based. Despite the frequent use of weight-based dosing, little data exist to clarify a safe and efficacious dosing weight for IVIG in overweight or obese patients. 3 This lack of data is relevant to pharmacy departments, as unwarranted supratherapeutic dosing may compromise supplies of this costly resource. This article aims to review clinical and pharmacokinetic data, guideline recommendations, practice patterns, and practical considerations relevant to weight-based dosing of IVIG.
Body weight is one of the determinants of appropriate IVIG dosing, along with trough serum levels of immunoglobulin G (IgG) and clinical response. 1 Therefore, it is important to consider pharmacokinetic parameters when dosing IVIG. The low volume of distribution (Vd) of IVIG indicates that it minimally distributes into fat.3,4 Therefore, an overweight or obese patient may not necessarily experience subtherapeutic outcomes when IVIG is dosed based on ideal body weight (IBW) or adjusted body weight (ABW). Despite the potential for dosing weight to influence safety and efficacy of IVIG treatment, few investigations have evaluated this factor. The ideal trial evaluating clinical efficacy and safety of different weight-based dosing regimens of IVIG has not been performed. However, some data demonstrate that body weight and body mass index (BMI) do not influence the IVIG dose required to produce a target trough IgG level.4
Khan and colleagues evaluated immunoglobulin therapy in 107 patients with common variable immunodeficiency to evaluate the correlation between IVIG dose and trough levels of IgG when adjusted for patient weight or BMI.4 All patients were on a clinician-determined IVIG replacement dose that was stable for at least 6 months. Patients had mean ± standard deviation (SD) weight of 70.8 ± 14.6 kg and received a mean ± SD annual dose of 383 ± 118 mg/kg every 3 weeks. The analysis found that trough IgG levels were not correlated with the dose of IVIG when adjusted for patient weight (R2=0.06, p=0.1) or BMI (R2=0.04, p=0.1), indicating that dosing based on IBW or ABW may still yield appropriate trough levels of IgG in patients who receive IVIG.
Guidelines and Expert Opinion
Currently, guidelines in the United States for labeled and unlabeled uses of IVIG do not provide recommendations on the most appropriate weight to use when calculating IVIG doses.5-9 However, international guidelines and institutional protocols provide guidance in this area.10-16
Guidelines from the United Kingdom on the use of IVIG recommended dosing of IVIG based on ABW in 2007.11 While these 2007 guidelines supported adjusted doses, this recommendation was removed from the 2008 second edition and the 2011 update, citing the limited evidence to support a firm recommendation.12-13 However, 2008 and 2011 guidelines still provide the formula for dosing based on ABW, stating there is evidence to support this approach. Also, guidelines published in Australia and various Canadian provinces recommend adjustment of IVIG dosing based on ABW.14-16
Citing the pharmacokinetic properties of IVIG presented earlier, Siegel at Ohio State University Medical Center recommends patients with a BMI of 30 kg/m 2 or higher or who weigh greater than 120% of IBW should be dosed based on ABW.10 The ABW is calculated by adding IBW and 40% of the difference between actual and IBW. Similarly, the Hospital Corporation of America (HCA) created a policy requiring all IVIG doses to be based on IBW (except in neonates), rather than total body weight.17
Besides choosing the most appropriate dosing weight, additional steps in dosing IVIG include rounding the dose to be administered in order to avoid product waste.10 For example, doses can be rounded to the nearest whole vial size to avoid discarding product from partially used vials. This practice is included in the HCA IVIG policy.17
A recent comprehensive study of global markets found that the use of IVIG is rapidly growing.18 From 1984 to 2008, the use of IVIG increased by 12% per year, with the United States and Canada being the leading consumers. Furthermore, usage can reasonably be expected to increase based on the rise in obesity, the potential expansion of labeled indications, and continuing widespread use in off-label indications.18-20 Despite the likely rise in demand, the manufacture of IVIG is dependent on supply of human plasma and whole blood; thus, supplies are ultimately limited.1 Institutions have published results of attempts to address such limited supplies.21,22 A pilot study in Australia reported a 3-year cost savings of at least $781,830 and reduced consumption of IVIG by 2.4% to 4.2% after instituting a protocol for dosing IVIG on ABW.21 As such, dosing considerations for IVIG may become increasingly relevant to maximize product stewardship and cost-effectiveness.
There is a paucity of data evaluating the effect of weight-based dosing of IVIG on clinical outcomes, and no data clearly indicate whether actual, ideal, or adjusted body weight is optimal. However, pharmacokinetic studies suggest that dosing based on ABW may be appropriate and this practice is advocated by various international guidelines and required by some institutional policies. As consumption of IVIG continues to increase despite limited supply, stewardship measures including dosing based on ABW or IBW may promote product conservation and cost-effective drug use.
1. Shah S. Pharmacy considerations for the use of IGIV therapy. Am J Health Syst Pharm. 2005;62(16 Suppl 3):S5-S11.
2. Micromedex Healthcare Series [database online]. Greenwood Village, CO: Thomson Reuters (Healthcare), Inc; 2013. http://www.thomsonhc.com/hcs/librarian. Accessed October 19, 2013.
3. Koleba T, Ensom MH. Pharmacokinetics of intravenous immunoglobulin: a systematic review. Pharmacotherapy. 2006;26(6):813-27.
4. Khan S, Grimbacher B, Boecking C, et al. Serum trough IgG level and annual intravenous immunoglobulin dose are not related to body size in patients on regular replacement therapy. Drug Metabolism Letters. 2011;5(2):132-6.
5. Orange JS, Hossny EM, Weiler CR. Use of intravenous immunoglobulin in human disease: a review of evidence by members of the Primary Immunodeficiency Committee of the American Academy of Allergy, Asthma and Immunology. J Allergy Clin Immunol. 2006;117(4 Suppl):S525-53.
6. Bonilla FA, Bernstein IL, Khan DA, et al. Practice parameter for the diagnosis and management of primary immunodeficiency. Ann Allergy Asthma Immuno. 2005;94(5 Suppl 1):S1-63.
7. Neunert C, Lim W, Crowther M. The American Society of Hematology 2011 evidence based practice guideline for immune thrombocytopenia. Blood. 2011 21;117(16):4190-4207.
8. Newburger JW, Takahashi M, Gerber MA. Diagnosis, treatment and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in Young, American Heart Association. Pediatrics. 2004;114(6):1708-1733.
9. Patwas HS, Chaudhry V, Katzberg H, Rae-Grant AD, So YT. Evidence-based guideline: intravenous immunoglobulin in the treatment of neuromuscular disorders: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2012 ;78(13):1009-1015.
10. Siegel J. Immunoglobulins and obesity. Pharmacy Practice News. http://www.pharmacypracticenews.com/ViewArticle.aspx?d=IVIG+FAQs&d_id=401&i=January+2010&i_id=597&a_id=14546 . Accessed September 30, 2013.
11. Wimperis J, Lunn M, Jones A, et al. Clinical guidelines for immunoglobulin use: second edition update. National Health Services website. http://www.ivig.nhs.uk/clinicinfo.html. Updated July 2011. Updated January 2010. Accessed September 30, 2013.
12. Provan D, Nokes TJC, Agrawal S, Winer JB, Wood P. Clinical guidelines for the use of intravenous immunoglobulin. National Health Services website. http://www.ivig.nhs.uk/clinicinfo.html. Updated 2007. Accessed September 30, 2013.
13. Provan D, Nokes TJC, Agrawal S, Winer JB, Wood P. Clinical guidelines for immunoglobulin use. National Health Services website. http://www.ivig.nhs.uk/clinicinfo.html. Updated May 2008. Accessed September 30, 2013.
14. Criteria for clinical use of intravenous immunoglobulin in Australia. National Blood Authority Australia website. http://www.blood.gov.au/ivig-criteria. Updated July 2012. Accessed September 30, 2013.
15. Utilization of intravenous immunoglobulin. Newfoundland Labrador Department of Health and Community Resources website. http://www.health.gov.nl.ca/health/index.html. Accessed September 30, 2013.
16. Intravenous immunoglobulin. British Columbia Provincial Blood Coordinating Office website. http://www.pbco.ca/index.php?option=com_content&task=category&id=18&Itemid=59 . Updated August 2012. Accessed September 30, 2013.
17. IVIG HCA Pharmacy Protocol. ASHP website. http://www.ashp.org/s_ashp/docs/files/DShort_IVIGHCAPharmacyProtocol.doc . Updated 1995. Accessed October 19, 2013.
18. Research and markets: immunoglobulins market to 2019. Wall Street Journal website. http://online.wsj.com/article/PR-CO-20130520-904965.html. Updated May 20, 2013. Accessed October 19, 2013.
19. Loeffler DA. Intravenous immunoglobulin and Alzheimer’s disease: what now. J Neuroinflammation. 2013;10(1):70.
20. Leong H, Stachnik J, Bonk ME, Matuszewski KA. Unlabeled uses of intravenous immune globulin. Am J Health Syst Pharm. 2008;65(19):1815-1824.
21. Aston L, McNae A, Taylor J. The effect of ideal body weight adjusted dosing on the use of intravenous immunoglobulin in Western Australia. Australian Red Cross Blood Service website. http://www.transfusion.com.au. Accessed September 30, 2013.
22. Chow S, Salmasi G, Callum JL, Lin Y. Trimming the fat with an IVIG approval process. Transfus Apher Sci. 2012;46(3):349-52.
Prepared by: Aparna Reddy, PharmD
PGY-2 Drug Information Specialty
University of Illinois at Chicago