The masks of allergy undone by IVT.
What is allergy?
Allergy is a hyperactive IgE immune-mediated response to a substance (allergen), which is not typically thought to be dangerous but is seen by the body's immune system as an invader. Common allergens include pollens, animal dander, foods, molds, dust, insects, insect stings, metals (especially nickel), and drugs.
In the allergic cascade, when a B cell recognizes an allergen, it produces IgE antibodies. These antibodies circulate via the bloodstream; some of them attach to the surfaces of mast cells and basophils present in the nasal passages, lungs, skin, and digestive tract. When an allergen is encountered again, it binds to the IgE antibodies on a cell's surface, causing the cell to release multiple inflammatory mediators including histamine. These inflammatory mediators produce allergy symptoms, which vary from mild to severe and life threatening (see sidebar on allergy symptoms, page 14).
How big is the problem?
Allergic diseases affect over 50 million Americans and costs the healthcare system over $18 billion annually. (1) Many patients do not have the opportunity for specialist care. In the United States, for example, one in seven is unlikely to receive specialist care because of the expense. (2)
The burden of allergy extends beyond the financial cost. According to the American Academy of Allergy, Asthma, and Immunology (AAAAI), allergies are responsible for 3.8 million lost work and school days each year. Allergy can lower the quality of life, restrict participation in outdoor sports, decrease on-the-job productivity, and unfavorably influence school performance. The time lost from school may negatively affect grades, academic achievement, self-esteem, and future life successes. (3) Given the symptoms of allergy, it is not surprising schoolwork suffers. "Allergic kids may not sleep well, often sleeping with their mouths open," says Terrence E. Zipfel, MD, East Liverpool ENT and Allergy in Ohio. "It can be hard for them to stay attentive and focused on school when they are tired and itching, and have congested nasal and aural passages, and watery eyes."
The allergy march
The allergy march describes a characteristic progression of allergic diseases in atopic individuals (persons with a genetic predisposition for allergy) through childhood (see Figure 1). As shown in the figure, the allergy march frequently begins with atopic dermatitis, recurrent wheezing, and gastrointestinal distress during the first and second years of life. Upper-respiratory symptoms (sinusitis and/or rhinitis) can appear between ages three and seven, with otitis media and conjunctivitis as frequent co-morbidities. The allergy march culminates in asthma, which usually manifests between the ages of seven and 15. (5-7)
[FIGURE 1 OMITTED]
Figure 1 also illustrates why one mother's description of her family's experience is not uncommon: "My daughter was the colic queen. With all the ear infections she had, we were afraid to keep giving antibiotic courses, so we had ear tubes put in. I did not know those conditions [colic and ear infections] could be linked. But since she now has asthma, you could be on to something! Nobody ever suggested an allergy test."
The National Center for Health Statistics cites that the incidence of asthma increased 160% in children up to four years of age between 1980 and 1998. The incidence of asthma in all age groups increased 100% during that same period. Every day in America, 14 people die of asthma. (8) As Moller, et al, (9) showed in 2002, however, early identification of childhood allergies and immunotherapy may halt the allergy march and reduce morbidity due to allergies. Two other studies (10) (11) demonstrated that early use of the anti-histamines cetirizine and ketotifen could also stop the onset of asthma in infants with atopic dermatitis. These three studies speak strongly to the importance of early intervention, which relies on early and accurate diagnosis.
Pathway to diagnosis
Although new allergies can arise at any age (even in adults), allergic disease is frequently observed as a common, chronic illness of childhood, and a primary-care physician or pediatrician is typically the first to evaluate potentially allergic children. The low allergist-to-patient ratio, the high cost of allergist care, and the increasing number of patients should provide strong incentive for primary-care physicians to be fully involved in allergy diagnosis and management.
Health-maintenance organizations (HMOs) mandate that primary-care physicians perform the initial patient evaluation (which may include diagnostic testing) to determine if referral to a specialist is needed. The primary-care physician frequently starts the diagnostic process that will differentiate allergic from non-allergic disease. In vitro testing (IVT) is a convenient, reproducible, and reliable tool for this process. It requires no special training for interpretation by primary-care physicians, and it agrees well with the results garnered from skin testing (ST) that would otherwise have to be performed in the specialist's office. (12-15)
Considering the studies cited above, it is no wonder that the guidelines of both the AAAAI, (16) and European Academy of Allergology and Clinical Immunology, or EAACI, (17) recommend that diagnosis of allergy in children should occur as early as possible and that identification of the offending allergen(s) be achieved through diagnostic testing. In fact, the diagnostic guidelines mandate three specific elements:
* patient's clinical history;
* clinical findings and symptoms; and
* diagnostic tests: in vivo (skin test, food challenge) and/or in vitro testing (IVT).
Once the patient's allergies have been diagnosed, treatment may include one or more of the following:
* pharmacotherapy; and
* immunotherapy (allergy shots).
Accurate diagnosis is a must. The hallmark symptoms of allergic rhinitis--sneezing, runny nose, watery and itchy eyes, and nasal congestion--also characterize other upper-respiratory diseases. One of the main reasons to diagnose and treat early allergies, such as sinusitis or rhinitis, is to prevent the development of asthma. Americans spend over $3 billion per year on antihistamines to treat the symptoms of allergy. Yet, a recent study found that 64% of the patients diagnosed with allergic rhinitis and treated with antihistamines had negative allergen-specific IgE tests. (18) This study underscores that diagnostic testing is integral to the accurate diagnosis and treatment of allergy.
Improvements in testing
Traditionally in the United States, in vivo diagnostic tests (e.g., ST and food challenge) have been the preferred clinical choice used by the allergist for confirming the diagnosis of allergy and the identification of specific allergens. These methods have proven to be reliable the hands of a trained allergist, but for certain types of allergies such as peanut or insect venoms (e.g., bee and wasp), in vivo tests may result in life-threatening anaphylaxis. In vitro tests can yield significant quantitative clinical data for most allergies without putting patients at risk.
In general, in vitro allergen-specific IgE (sIgE) tests have been more readily accepted and widely used in Europe than in the United States, and the EACCI position is that IVT and ST are generally of equal diagnostic value. (19) While many U.S. allergists still prefer skin tests, the technological improvements made to in vitro testing have made it a reliable test for identification of sIgE, and it is gaining increased acceptance, especially among primary-care physicians who may not have the specialist training necessary to perform skin testing.
Some doctors are still unfamiliar with advances in IVT for allergen-specific IgE. Improvements in the past two decades have transformed IVT to a sensitive and precise methodology for generating reliable results. Primary and continuing medical education are at least partly to blame as they often impart information drawn from literature that is one to two decades old. For example, a pediatric textbook (20) published in 2000 states: "The radioal-lergosorbent test (RAST) determines antigen-specific IgE concentration in serum ... In vitro methods of determining sIgE to several allergens simultaneously have been marketed as screening tests for allergy. The few published data evaluating such methods indicate that they are relatively insensitive and may fail to identify more than 30% of children with allergy."
Although the text goes on to acknowledge that subsequent methodologies were somewhat improved, it illustrates the dissemination to physicians of out-of-date information that all current IVT methodologies are as clinically unreliable as the original commercial RAST test. Using RAST as a generic term for sIgE measurement by IVT has blurred the distinction between older and newer technologies and may be responsible for confusion that affects clinical practice and professional guidelines. (21), (22) Consequently, some doctors--unaware that earlier concerns have been ameliorated or resolved by modern technology--perpetuate misconceptions about the quality and clinical utility of currently available assays.
Exploring the evolution of sIgE assays from the development of the original RAST in the 1960s and the second-generation enzyme and fluorescent immunoassay systems of the 1990s, to FDA-cleared third-generation systems introduced since 2000 may help in the battle against the many masks of allergies.
The original RAST measured radioactive counts per second (CPS) emitted from an isotopically labeled antibody. While this test was highly sensitive and specific, the results could be considered only semi-quantitative because no fully characterized calibration material was available. In addition, the original RAST was too cumbersome and time-consuming for routine use in the clinical reference laboratory.
Although early attempts at commercialization and automation had rather poor sensitivity, yielding up to 50% false negatives, interest in the technology continued. Nalebuff and Fadal showed that better sensitivity could be achieved when the commercial assay was modified by doubling the sample volume, dramatically increasing the incubation time from three to 18 hours, and adding wash steps that reduced the background noise. Six classes were designated on the basis of counts per second (CPS) associated with each dilution and were interpreted using a scale that associated the counts with ST classes. (23) The sensitivity of this modified RAST (mRAST) was enhanced, but at the expense of speed and convenience.
Semiautomated, quantitative immunoassays, first marketed in the 1990s, greatly improved the quality and practicality of IVT. In some assays, sensitivity was improved by the replacement of paper disks with other substrates, making it possible to increase the amount of sIgE captured and boost the CPS, (23) while chemical signal-detection methods (i.e., fluorescence) greatly improved assay sensitivity and time-to-first-result.
The World Health Organization International Reference Preparation was used to construct multipoint calibration curves, making standardized quantitative measurement possible. Results were reported in total serum IgE (kU/L). In the eyes of allergy specialists, this constellation of improvements justified designating these systems as second-generation. (12), (24)
Because many second-generation assays proved to have far better specificity and sensitivity than first-generation assays, researchers and allergists could finally recognize IVT's potential for providing useful clinical information, especially because of its quantitative nature. Background noise, however, prevented the quantitative measurement of very low levels of sIgE below 0.35 kU/L (the technological limit of most second-generation systems), which presented an obstacle to further improvements in clinical sensitivity.
Second-generation systems lacked the low-end precision required to quantify sIgE below 0.35 kU/L, and clinicians--of necessity--adopted this technological limitation as the de facto diagnostic cutoff. Consequently, a sample with an sIgE below this artificial cutoff was considered to be negative. Researchers suspected that at least some allergens could evoke a response at much lower sIgE levels, although they were unable to investigate this hypothesis without an assay that could accurately and reliably measure sIgE below 0.35 kU/L. Obstacles to investigating the effects of lower levels of sIgE were removed with the introduction of an assay system which, among other advances, added a zero calibrator and optimized low-end precision. (25), (26) The assay runs on fully-automated, continuously loading, random access immunoassay systems. The assay employs a liquid-allergen matrix replacing the solid-phase capture media of all other sIgE assays. Use of a liquid matrix significantly enhances binding kinetics and sensitivity of the assay through the preservation of antigen conformation, and the reduction of non-specific binding. (27-29) The liquid matrix improves reaction kinetics, sensitivity, low-end precision and diagnostic accuracy.
Because the assay has a detection limit of 0.1 kU/L and functional sensitivity of 0.20 kU/L, it has made it possible to study the significance of low levels of sIgE. Thus far, sIgE levels as low as 0.23 kU/L have been shown to evoke some venom allergy responses. (15) Biagini, et al, (30) showed that for the diagnosis of latex allergy, diagnostic performance at the 0.1 kU/L or greater cutoff level was superior over second-generation systems. In addition, Dr. Biagini's study found the new assay system represented a technological advance, with enhanced speed and less operator intervention.
A case study by Grunwald, et al, (31) demonstrates the potential clinical value of detecting very low levels of sIgE. In this study, a man who had suffered an anaphylactic response to the sting of an unknown insect had a negative ST for honeybee and wasp venom. Using the third-generation system, this patient was subsequently found to have honeybee venom sIgE present at a concentration of 0.23 kU/L (a level approximately 33% lower than the lowest readable level of sIgE in second-generation systems). He was diagnosed with and successfully treated for honeybee-venom allergy.
Third-generation testing has three major improvements:
* It is quantitative--it can detect low levels.
* It is automated and accurate--similar to clinical chemistry immunoassay.
* Its test antigens are better defined and standardized.
Improvements in methodology, automation, and performance justify the classification of this system as a third-generation assay. Time to first result has been reduced to 65 minutes. Individual tests can be run on an as-needed basis, preventing batching delays. Automation and barcode scanning eliminate manual bench work, reducing human error to a minimum.
In vitro sIgE testing is a valuable, reliable tool for allergists and primary-care physicians because it facilitates early accurate diagnosis and appropriate therapeutic interventions with the capacity to serve the ever-increasing numbers of patients. Early diagnosis makes it possible to practice avoidance and begin treatment that can halt the progression of the allergy march, potentially preventing the development of asthma and improving the quality of life for countless children and adults. It also has the potential for reducing the cost-burden of allergy for patients, the healthcare industry, and the insurance industry. Third-generation testing is fully automated and quantitative, making it an excellent system for attaining these goals.
CE test on THE MASKS OF ALLERGY UNDONE BY IVT
MLO and Northern Illinois University (NIU), DeKalb, IL, are co-sponsors in offering continuing education units (CEUs) for this issue's article on THE MASKS OF ALLERGY UNDONE BY IVT. CEUs or contact hours are granted by the College of Health and Human Sciences at NIU, which has been approved as a provider of continuing education programs in the clinical laboratory sciences by the ASCLS P.A.C.E[R] program (Provider No. 0001) and by the American Medical Technologists Institute for Education (Provider No. 121019; Registry No. 0061). Approval as a provider of continuing education programs has been granted by the state of Florida (Provider No. JP0000496), and for licensed clinical laboratory scientists and personnel in the state of California (Provider No. 351). Continuing education credits awarded for successful completion of this test are acceptable for the ASCP Board of Registry Continuing Competence Recognition Program. After reading the article on page 10, answer the following test questions and send your completed test form to NIU along with the nominal fee of $20. Readers who pass the test successfully (scoring 70% or higher) will receive a certificate for 1 contact hour of P.A.C.E.[R] credit. Participants should allow four to six weeks for receipt of certificates.
The fee for this continuing education test is $20.
All feature articles published in MLO are peer-reviewed.
Learning Objectives and CE questions were prepared by Sharon M. Miller, Professor Emeritus, Northern Illinois University, DeKalb, IL.
1. How many Americans are afflicted annually with allergic disorders?
a. 5 million
b. 1/2 billion
c. 0.05 billion
d. 500 million
2. On a daily basis, allergies can cause
a. decreased productivity on the job.
b. poor school attendance.
c. restriction of outdoor activities.
d. All of the above.
3. Common allergens include all of the following except
a. grass and weed pollens.
b. mold spores.
c. metals, especially titanium.
d. insect venom.
4. Individuals with a genetic predisposition to hyper-responsiveness when exposed to allergens are
5. If unhalted, the patient's allergy march frequently progresses to development of asthma
a. by one to three years of age.
b. in late childhood or early teens.
c. in middle age.
d. after the age of 60.
6. In the United States between 1980 and 1998, the incidence of asthma in children [less than or equal to]4 years of age
b. deceased dramatically due to early diagnosis.
c. increased 160%.
d. remained unchanged.
7. Allergy refers to the body's response to re-exposure to a sensitizing antigen that originally triggered production and cell binding of
8. Once sensitized, subsequent exposure to the specific allergen triggers the release of inflammatory mediators including
9. Cells that directly release inflammatory mediators are
a. basophils and mast cells.
b. macrophages and histiocytes.
c. neutrophils and T cells.
d. B cells and monocytes.
10. The most severe form of allergic response is
b. allergic rhinoconjunctivitis.
c. chronic otitis media.
d. pediatric asthma.
11. Prevalence of food allergies is greatest during what period of life?
a. 12 to 24 months
b. Three to five years
c. Eight to 10 years
d. 12 to 15 years
12. Examples of in vivo diagnostic tests of allergy include food challenges and
13. When diagnosing allergies in children, guidelines of both the AAAAI and the EAACI recommend
a. genotyping of parents and siblings.
b. diagnosis at the earliest age possible.
c. delay diagnostic testing until the immune system matures.
d. immediate initiation of immunomodulation therapy.
14. Diagnosis of IgE-mediated allergic diseases should optimally be based upon
a. patient's detailed clinical history.
b. skin testing to measure sIgE bound to cutaneous mast cells.
c. challenge testing with a suspected antigen when appropriate.
d. laboratory determination of circulating sIgE.
e. All of the above.
15. Generally, in vitro allergen-specific testing has been more readily and widely accepted in Europe than in the United States.
16. A significant drawback to in vivo testing is that it may trigger life-threatening anaphylaxis.
17. Negative allergen-specific IgE tests have been reported in almost--of patients diagnosed with allergic rhinitis and treated with antihistamines.
18. The original radioallergosorbent test (RAST)
a. was developed in the 1940s.
b. was calibrated using a well-characterized standard.
c. used a solid-phase capture medium.
d. was easily integrated into routine clinical laboratory testing.
19. All of the following are true of second-generation IVTs except
a. enzyme and fluorescent immunoassay systems.
b. levels of sIgE < 0.35 kU/L could be quantitated.
c. first marketed in the 1990s.
d. results reported in a continuous scale standardized to the WHO International Reference Preparation for sIgE.
20. Third-generation IVT sIgE testing
a. is fully automated and quantitative.
b. employs a liquid-allergen matrix.
c. has a detection limit of 0.1 kU/L.
d. is believed by the EACCI to be of equal diagnostic value with the ST.
e. All of the above.
To earn CEUs, see test on page 20.
Upon completion of this article, the reader will be able to:
1. Define atopy and allergy.
2. Identify four common allergens and four symptoms of allergy.
3. State four examples of the impact of allergic disorders on patient quality of life and/or healthcare costs.
4. Describe the pathogenesis of the allergic response.
5. Explain the meaning and clinical significance of the "allergy march."
6. Summarize AAAAI diagnostic criteria for allergy and treatment options.
7. Assess the clinical merits of in vitro and in vivo tests for allergic diseases.
(1.) American Academy of Allergy, Asthma, and Immunology Task Force. The allergy report. http://www.aaaai.org/ar/working_vol1/009.asp. Accessed May 2007.
(2.) Annual Estimates of the Population of the United States, and for Puerto Rico: April 1, 2000 to July 1, 2005 (NT-EST2005-01). Available from: http://www.census.gov/popest/states/NST-ann-est.html. Accessed May 2007.
(3.) Lenney W. The burden of pediatric asthma. Pediatr Pulmonol. 1997;15:13-16.
(4.) Wahn U. The atopic march. http://www.shsweb.co.uk/neocate/prof/docs/focus5.pdf Accessed May. 2007.
(5.) Kulig M, Bergman R, Tacke U, Wahn U, Guggenmoos-Holzmann I. Long lasting sensitization to food during the first two years produces allergic airway disease. The MAS study group, Germany. Pediatr Allergy Immunol. 1998;9:961-967.
(6.) Sigurs N, Hattevig G, Kjellman B, Kjellman NI, Nisson L, Bjorksten B. Appearance of atopic disease in relation to serum IgE antibodies in children followed up from birth for 4 to 15 years. J Allergy Clin Immunol. 1994;94:757-763.
(7.) Allergic Rhinitis and its impact on Asthma. http://www.whiar.org/docs/ARIA_PG.pdf. Accessed May 2007.
(8.) Asthma Introduction. National Safety Council. http://www.nsc.org/EHC/asthma.htm. Accessed May 2007.
(9.) Moller C, Dreborg S, Ferdousi H, Halken S, Host A, Jacobsen L, et al. Pollen immunotherapy reduces the development of asthma in children with seasonal rhinocon-junctivitis (the PAT-study). J Allergy Clin Immunol. 2002;109:251-256
(10.) Warner JO; ETAC Study Group. Early Treatment of the Atopic Child. A double-blinded, randomized, placebo-controlled trial of cetirizine in preventing the onset of asthma in children with atopic dermatitis: 18 months' treatment and 18 months' posttreatment follow-up. J Allergy Clin Immunol. 2001;108:929-937.
(11.) likura Y, Naspitz CK, Mikawa H, Talaricoficho S, Baba M, Sole D, et al. Prevention of asthma by ketotifen in infants with atopic dermatitis. Ann Allergy. 1992;68:233-236.
(12.) Hamilton RG, Adkinson NF Jr. In vitro assays for the diagnosis of IgE-mediated disorders. J Allergy Clin Immunol. 2004;114:213-225.
(13.) Cobbaert CM, Jonker GJ. Allergy testing on the IMMULITE 2000 random-access immunoanalyzer- a clinical evaluation study. Clin Chem Med Lab. 2005;43:772-781.
(14.) Prates S, Morais-Almeida M, Matos V, Loureiro V, Rodado-Pinto J. In vitro methods for specific IgG detection on cow's milk allergy. Allergol Immunopthal(Madr). 2006;34:27-31.
(15.) Ollert M, Weissenbacher S, Rakoski J, Ring J. Allergen-specific IgE measured by a continuous random-access immunoanalyzer:interassay comparison and agreement with skin testing. Clin Chem. 2005;51:1241-1249.
(16.) American Academy of Allergy, Asthma and Immunology Task Force. The allergy report. http://www.aaaai.org/ar/working_vol1/054.asp. Accessed May 2007.
(17.) The European Academy of Allergology and Clinical Immunology. http://www.eaaci.net/site/content.php?artid=650. Accessed May 2007.
(18.) Szeinbach SL, Williams B, Muntendam P, O'Connor RD. Identification of allergic disease among users of antihistamines. J Manag Care Pharm. 2004;10:234-238.
(19.) Host A, Andrae S, Charkin S, Diaz-Vazquez C, Dreborg S, Eigenmann PA, et al. Allergy testing in children: why, who, when and how? Allergy. 2003;58:559-569.
(20.) Sly RM. Textbook of Pediatrics: part XIV, Allergic Disorders. Behrman RE, Kliegman RM, Jenson HB (eds). 16th ed. WB Saunders Co. 2000;650-653.
(21.) American Academy of Allergy, Asthma, and Immunology. The Allergy Report. http://www.aaaai.org/ar/working_vol1/058.asp. Accessed May 2007.
(22.) Li JT. Allergy Testing. Am Family Phys. 2002;66:621-624.
(23.) Gordon BR. In vitro allergy testing: an overview. http://www.nwallergylab.com/bloodallergy.htm. Accessed May 2007.
(24.) Plebani M, Borghesan F, Faggian D. Clinical efficiency of in vitro and in vivo tests for allergic diseases. Ann Allergy Asthma Immunol. 1995;74:23-28.
(25.) Yman L. Allergy. In Wild D, editor. The immunoassay handbook, 2nd edition. London: Nature Publishing Group; 2001;664-80.
(26.) World Health Organization. International reference material. Last updated October 2005. http://www.who.int/bloodproducts/ref_materials/Bim-Oct05.pdf. Accessed May 2007.
(27.) EI Shami AS, Alaba O. Liquid-phase in vitro allergen-specific IgE assay with in situ immobilization. Adv Biosci. 1989;74:191-201.
(28.) Alaba O, EI Shami AS. Evaluation of non-specific IgE binding: comparison of two in vitro allergen assays. Adv Biosci 1989;74:203-214.
(29.) Li TM, Chuang T, Tse S, Hovanec-Burns D, EI Shami AS. Development of a Third-Generation Allergen-Specific IgE Assay on the Continuous Random Access IMMULITE[R] 2000. Poster A-57 American Association for Clinical Chemistry (AACC) 55th Annual Meeting and Clinical Lab Exposition. July 20-24, 2003 Philadelphia, PA, US Clin Chem Lab Med. 2005;43:772-781.
(30.) Biagini R, MacKenzie B, Sammons B, Smith J, Krieg E, Robertson S, Hamilton, R. Latex specific IgE: performance characteristics of the IMMULITE 2000 3gAllergy assay compared with skin testing. Ann Allergy Asthma and Immunol. 2005;97:196-202.
(31.) Grunwald T, Bockisch B, Spillner E, Ring J, Bredhorst R, Ollert MW. Molecular cloning and expression in insect cells of honeybee venom allergen acid phosphatase (Api m 3). J Allergy Clin Immunol. 2006;117:848-854.
RELATED ARTICLE: Allergy symptoms
* Nasal congestion
* Watery eyes
* Persistent cough
* Recurrent ear infections
* Skin rashes
* Diarrhea and vomiting
RELATED ARTICLE: A positive tale for parents of children with allergies
Seeking to educate consumers, specifically parents, about allergies, Siemens Medical Solutions Diagnostics recently produced "Thomas Meets a Zebra: A Child's Allergy Story," authored by Connie Mardis. This children's book provides parents with a tool to help their children who are suffering from allergies. The story is about the consequences of Thomas living with undiagnosed allergy and the benefits of blood testing in the allergy diagnosis process. The book will enable parents to understand the impact of allergies on the lives of their children and make informed decisions on allergy testing methods.
By Connie Mardis, MEd; Tricia Bal, MD; and Roma Levy, MS
Connie Mardis, head of Global Training at Siemens Medical Solutions Diagnostics, has 20+ years' experience in cardiac perfusion, laboratory diagnostics, and education, with extensive work in promoting allergy diagnostics, as well as holding key marketing positions focused on hospital, reference, and physician-office laboratories, both domestically and internationally. Tricia Bal, MD, is a scientific writer at Siemens Medical Solutions Diagnostics. She received her degree from University of Michigan Medical School. Roma Levy, MS, is also a scientific writer for Siemens Medical Solutions Diagnostics, Los Angeles, CA. She holds a BA in biology from Northwestern University and an MA in biology from University of California, Santa Cruz.
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|Title Annotation:||CE IVT|
|Author:||Mardis, Connie; Bal, Tricia; Levy, Roma|
|Publication:||Medical Laboratory Observer|
|Article Type:||Cover story|
|Date:||Jun 1, 2007|
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