Evidence based pediatrics - part 8 pdf

21. Siegel SR, Siegel B, Sokoloff BZ, Kanter MH. Urinary infection in infants and preschool children. Five-year follow-up. Am J Dis Child 1980;134(4):369–72. 22. Wettergren B, Hellstrom M, Stokland E. Six year follow-up of infants with bacteriuria on screen- ing. Br Med J 1990;301:845–8. 23. Hoberman A, Wald ER, Penchansky L, et al. Enhanced urinalysis as a screening test for urinary tract infection [see comments]. Pediatrics 1993;91(6):1196–9. 24. Hellerstein S. Recurrent urinary tract infections in children. Pediatr Inf Dis 1982;1(4):271–81. 25. Boehm JJ, Haynes JL. Bacteriology of “midstream catch” urines. Studies in newborn infants. Am J Dis Child 1966;111(4):366–9. 26. Pryles C. Percutaneous bladder aspiration and other methods of urine collection for bacteriologic study. Pediatrics 1965;36:128–31. 27. Schlager T, Dunn M, Dudley S, Lohr J. Bacterial contamination rate of urine collected in a urine bag from healthy non-toilet trained male infants. J Pediatr 1990;116:738–9. 28. Schlager T, Hendley J, Dudley S. Explanation for false-positive urine cultures obtained by bag techniques. Arch Pediatr Adolesc Med 1995;149:170–3. 29. McCarthy J, Pryles C. Clean voided and catheter neonatal urine specimens. Arch Dis Child 1963:473–7. 30. Lohr J, Portilla M, Geuder T, et al. Making a presumptive diagnosis of urinary tract infection by using a urinalysis performed in an on-site laboratory. J Pediatr 1993;122:22–5. 31. Webb K, Patten C, McLean L. A comparison of the filtracheck-UTI and dipstick urinalysis in the diagnosis of pediatric urinary tract infections. Ambulatory Pediatric Association Annual Meeting, Washington, May 5, 1997. 32. Kramer M, Tange S, Drummond K, Mills E. Urine testing in young febrile children: a risk-bene- fit analysis. J Pediatr 1994;125:6–13. 33. Anonymous. American Academy of Pediatrics. Practice parameter: the diagnosis, treatment, and evaluation of the initial urinary tract infection in febrile infants and young children. Pediatrics 1999;103:843–52. 34. Wiswell T, Smith F, Bass J. Decreased incidence of urinary tract infections in circumcised male infants. Pediatrics 1985;75:901–3. 35. Herzog L. Urinary tract infections and circumcision: a case control study. Am J Dis Child 1989;143:348–50. 36. Bachur R, Caputo G. Bacteremia and meningitis among infants with urinary tract infections. Pediatr Emerg Care 1995;11:280–4. 37. Ginsburg C, McCracken G. Urinary tract infection in young infants. Pediatrics 1982;69:409–12. 38. Smellie JM, Ransley PG, Normand IC, et al. Development of new renal scars: a collaborative study. Br Med J (Clinical Research Ed.) 1985;290(6486):1957–60. 39. Winter A, Hardy B, Alton D, et al. Acquired renal scars in children. J Urol 1983;129:1190–4. 40. Anonymous. South Bedfordshire Practitioners’ Group. - Development of renal scars in children: missed opportunities in management. Br Med J 1990;301:1082–4. 41. Winberg J, Bollgren I, Lakkenius G. Clinical pyelonephritis and local renal scarring: a selected review of pathogenesis, prevention, and prognosis. Pediatr Clin North Am 1982;29:801–14. Urinary Tract Problems in Primary Care 321 42. Stokland E, Hellstrom M, Jacobsson B, et al. Renal damage one year after first urinary tract infec- tion: role of dimercaptosuccinic acid scintigraphy. J Pediatr 1996;129:815–20. 43. Berg U, Johansson S.Age as a main determinant of renal functional damage in urinary tract infec- tion. Arch Dis Child 1983;58:963–9. 44. Benador D, Benador N, Slosman D, et al. Are younger children at highest risk of renal sequelae after pyelonephritis? Lancet 1997;349:17–9. 45. Hoberman A, Wald E, Hickey R, et al. Oral versus initial intravenous therapy for urinary tract infections in young febrile children. San Fransisco, CA: Pediatric Academic Societies Meeting; May 4, 1999. 46. Avner E, Ingelfinger J, Herrin J, et al. Single-dose amoxicillin therapy of uncomplicated pediatric urinary tract infections. J Pediatr 1983;102:623–7. 47. McCracken G, Ginsburg C, Namasonthi V, et al. Evaluation of short term antibiotic therapy in children with uncomplicated urinary tract infection. Pediatrics 1981;67:796–801. 48. Moffatt M, Embree J, Grimm P, Law B. Short-course antibiotic therapy for urinary tract infec- tions in children. Am J Dis Child 1988;142:57–61. 49. Smellie J, Katz G, Gruneberg R. Controlled trial of prophylactic treatment in childhood urinary- tract infection. Lancet 1978:175–8. 50. Lohr J, Nunley D, Howards S, Ford R. Prevention of recurrent urinary tract infections in girls. Pediatrics 1977;59:4. 51. Savage D,Howie G, Adler K. Controlled trial of therapy in covert bacteriuria in childhood. Lancet 1975;1:358–61. 52. Lindberg U. Asymptomatic bacteriuria in school girls. V. The clinical course and response to treat- ment. Acta Paediatr Scand 1975;64:718–24. 53. Hanson E, Hansson S, Jodal U. Trimethoprim-sulphadiazine prophylaxis in children with vesico- ureteric reflux. Scand J Infect Dis 1989;21:201–4. 54. Järvelin M, Huttunen N, Seppänen J, et al. Screening of urinary tract abnormalities among day and nightwetting children. Scand J Urol Nephrol 1990;24:181–9. 55. Byrd R, Weitzman M, Lanphear N, Auinger P. Bed-wetting in US children: epidemiology and related behavior problems. Pediatrics 1996;98:414–9. 56. Swithinbank L, Carr J, Abrams P. Longitudinal study of urinary symptoms in children. Scand J Urol Nephrol 1994;163(Suppl):67–73. 57. Verhulst F, van der Lee J, Akkerhuis G, et al. The prevalence of nocturnal enuresis: do DSM III criteria need to be changed? A brief research report. J Child Psychol Psychiatr Allied Discipl 1985;26(6):989–93. 58. Fergusson D, Horwood L. Nocturnal enuresis and behavioral problems in adolescence: a 15-year longitudinal study. Pediatrics 1994;94:662–8. 59. Moffat M, Kato C, Pless I. Improvements in self-concept after treatment of nocturnal enuresis: randomized controlled trial. J Pediatr 1987;110:647–52. 60. Petersen KE, Andersen OO. Treatment of nocturnal enuresis with imipramine and related prepa- rations. A double blind trial with a placebo. Acta Paediatr Scand 1971;60(2):244. 322 Evidence-Based Pediatrics 61. Mishra PC, Agarwal VK, Rahman H. Therapeutic trial of amitryptyline in the treatment of noc- turnal enuresis—a controlled study. Ind Pediatr 1980;17(3):279–85. 62. Meadow R, Berg I. Controlled trial of imipramine in diurnal enuresis. Arch Dis Child 1982;57(9):714–6. 63. Martin GI. Imipramine pamoate in the treatment of childhood enuresis. A double-blind study. Am J Dis Child 1971;122(1):42–7. 64. Lines DR. A double-blind trial of amitriptyline in enuretic children. Med J Austral 1968;2(7):307–8. 65. Laybourne PCJ, Roach NE, Ebbesson B, Edwards S. Double-blind study of the use of imipramine (Tofranil) in enuresis. Psychosomatics 1968;9(5):282–5. 66. Lake B. Controlled trial of nortriptyline in childhood enuresis. Med J Austral 1968;2(14):582–5. 67. Kardash S, Hillman ES, Werry J. Efficacy of imipramine in childhood enuresis: a double-blind control study with placebo. Can Med Assoc J 1968;99(6):263–6. 68. Agarwala S, Heycock JB. A controlled trial of imipramine (‘Tofranil’) in the treatment of child- hood enuresis. Br J Clin Pract 1968;22(7):296–8. 69. Forsythe WI, Merrett JD. A controlled trial of imipramine (‘Tofranil’) and nortriptyline (‘Alle- gron’) in the treatment of enuresis. Br J Clin Pract 1969;23(5):210–5. 70. Smellie J, McGrigor V, Meadow S, et al. Nocturnal enuresis: a placebo controlled trial of two anti- depressant drugs. Arch Dis Child 1996;75. 71. Moffatt M, Harlos S, Kirshen A, Burd L. Desmopressin acetate and nocturnal enuresis: how much do we know? Pediatrics 1993;92:420–5. 72. Aladjem M, Wohl R, Boichis H, et al. Desmopressin in nocturnal enuresis. Arch Dis Child 1982;57(2):137–40. 73. Pedersen P, Hejl M, Kjoller S. Desamino-D-arginine vasopressin in childhood nocturnal enure- sis. J Urol 1985;133:65–6. 74. Post EM, Richman RA, Blackett PR, et al. Desmopressin response of enuretic children. Effects of age and frequency of enuresis. Am J Dis Child 1983;137(10):962–3. 75. Terho P. Desmopressin in nocturnal enuresis. J Urol 1991;145:818–20. 76. Wille S. Comparison of desmopressin and enuresis alarm for nocturnal enuresis. Arch Dis Child 1986;61(1):30–3. 77. Miller K, Klauber G. Desmopressin acetate in children with severe primary nocturnal enuresis. Clin Ther 1990;12:357–66. 78. Pedersen PS, Hejl M, Kjoller SS. Desamino-D-arginine vasopressin in childhood nocturnal enure- sis. J Urol 1985;133(1):65–6. 79. Janknegt A, Smans A. Treatment with desmopressin in severe nocturnal enuresis in childhood. J Urol 1990;66:535–7. 80. Wagner WG, Matthews R. The treatment of nocturnal enuresis: a controlled comparison of two models of urine alarm. J Dev Behav Pediatr 1985;6(1):22–6. 81. Rappaport L. Prognostic factors for alarm treatment. Scandi J Urol Nephrol 1997;183(Suppl):55–7;discussion 57–8. Urinary Tract Problems in Primary Care 323 82. Lynch NT, Grunert BK, Vasudevan SV, Severson RA. Enuresis: comparison of two treatments. Arch Phys Med Rehab 1984;65(2):98–100. 83. El-Anany FG, Maghraby HA, Shaker SE, Abdel-Moneim AM. Primary nocturnal enuresis: a new approach to conditioning treatment. Urology 1993;53:405–8. 84. Elinder G, Soback S. Effect of Uristop on primary nocturnal enuresis. A prospective randomized double-blind study. Acta Paediatr Scand 1985;74(4):574–8. 85. Sukhai R, Harris A. Combined therapy of enuresis alarm and desmopressin in the treatment of nocturnal enuresis. Eur J Pediatr 1989;148:465–7. 86. Fordham KE, Meadow SR. Controlled trial of standard pad and bell alarm against mini alarm for nocturnal enuresis. Arch Dis Child 1989;64(5):651–6. 87. Monda J, Husmann D. Primary nocturnal enuresis: a comparison among observation, imipramine, desmopressin acetate and bed-wetting alarm systems. J Urol 1995;154:745–8. 88. Bradbury M. Combination therapy for nocturnal enuresis with desmopressin and an alarm device. Scand J Urol Nephrol 1997;183(Suppl):61–3. 89. Anonymous. American Academy of Pediatrics, Task Force on Circumcision. Circumcision Policy Statement. Pediatrics 1999;103:686–93. 90. To T, Feldman W, Dick P, Tran M. Pediatric health services utilization: circumcision. In: Goel V, Williams J, Anderson G, et al, editors. Patterns of health care in Ontario: the ICES practice atlas. Ottawa: Canadian Medical Association;1996. p. 294–7. 91. Anonymous. Fetus and Newborn Committee, Canadian Pediatric Society. Neonatal circumcision revisited. Can Med Assoc J 1996;154:769–80. 92. Fergusson D, Lawton, JM., Shannon, FT. Neonatal circumcision and penile problems: an 8-year longitudinal study. Pediatrics 1988;81:537–41. 93. Herzog L, Alvarez S. The frequency of foreskin problems in uncircumcised children. Am J Dis Child 1986;140:254–256. 94. Oster J. Further fate of the foreskin: incidence of preputial adhesions, phimosis, and smegma among Danish schoolboys. Arch Dis Child 1968;43:200–3. 95. Fergusson D, Horwood L, Shannon F. Factors related to the age of attainment of nocturnal blad- der control: an 8-year longitudinal study. Pediatrics 1986;78:884–90. 96. Wiswell T, Hachey W. Urinary tract infections and the uncircumcised state: an update. Clin Pedi- atr 1993;32. 97. Rushton H, Majd M. Pyelonephritis in male infants: how important is the foreskin? J Urol 1992;148:733–6. 98. Young J, Percy C, Asine A. Surveillance, epidemiology, and end results, incidence and mortality data 1973-77. Natl Cancer Inst Monogr 1981;57:17. 99. Frisch M, Frus S, Kjaer S, Melbye M. Falling incidence of penile cancer in an uncircumcised pop- ulation (Denmark 1943-90). Br Med J 1995;311:1471. 100. Maden C, Sherman K, Beckmann A, et al. History of circumcision, medical conditions, and sex- ual activity and risk of penile cancer. J Natl Cancer Inst 1993;85:19–24. 101. Hellberg D, Valentin J, Eklund T, Milsson S. Penile cancer: is there an epidemiological role for smoking and sexual behavior? Br Med J 1987;295:1306–8. 324 Evidence-Based Pediatrics 102. Brinton L, Li J, Rong S, et al. Risk factors for penile cancer: results from a case-control study in China. Intl J Cancer 1991;47:504–9. 103. Seed J, Allen S, Mertens T. Male circumcision, sexually transmitted disease, and risk of HIV. J AIDS Hum Retrovirol 1995;8:83–90. 104. Tyndall M, Ronald R, Agoki E, et al. Increased risk of infection with human immunodeficiency virus type 1 among uncircumcised men presenting with genital ulcer disease in Kenya. Clin Infect Dis 1996;23:449–53. 105. Kreiss J, Hopkins S. The association between circumcision and human immunodeficiency virus infection among homosexual men. J Infect Dis 1993;168:1404–08. 106. Pepin J, Quigley M, Todd J. Association between HIV-2 infection and genital ulcer diseases among male sexually transmitted disease patients in Gambia. AIDS 1992;6:489–93. 107. Simonsen J, Cameron D, Gakinya N. Human immunodeficiency virus infection among men with sexually transmitted diseases: experience from a center in Africa. N Engl J Med 1988;319:274–8. 108. Bwayo J, Plummer F, Omau M. Human immunodeficiency virus infection in long-distance truck drivers in East Africa. Arch Intern Med 1994;154:1291–6. 109. Moses S, Plummer F, Bradley J, et al. The association between the lack of male circumcision and the risk for HIV infection: a review of the epidemiological data. Sex Trans Dis 1994;21:201–10. 110. De Vincenzi I, Mertens T. Male circumcision: a role in HIV prevention? [editorial]. AIDS 1994;8:153–60. 111. Gee S, Ansell J. Neonatal circumcision: a ten-year overview with comparison of Gomco clamp and Plastibell device. Pediatrics 1976;58:824–7. 112. Harkavy K. The circumcision debate. Pediatrics 1987;79:649–50. 113. Taddio A, Katz J, Ilersich A, Karen G. Effect of neonatal circumcision on pain response during subsequent routine vaccination. Lancet 1997;349:599–603. 114. Ganiats T, Humphrey J, Taras H. Routine neonatal circumcision: a cost-utility analysis. Med Deci- sion Making 1991;11:282–93. 115. Lawler F, Bisonni R, Holtgrave D. Circumcision: a decision analysis of its medical value. Fam Med 1991;23:587–93. Urinary Tract Problems in Primary Care 325 CHAPTER 18 Allergy Adelle Roberta Atkinson, RN, BSc, MD, FRCPC, FAAP  Allergic diseases are an extremely common cause of both acute and chronic illness in chil- dren. They are among the most common reasons why a child is brought to the attention of a primary-care practitioner. 1 This translates into a great deal of morbidity and burden of ill- ness on society. The purpose of this chapter is to discuss the major allergens within the realm of pediatric allergy as well as the approach to the diagnosis and management of immunoglobulin E (IgE) -mediated hypersensitivity within those allergenic groups. The emphasis is on the evidence available for diagnostic tests and treatment strategies to aid the practitioner in making informed clinical decisions. Controversies which affect the primary- care practitioner are also discussed. The allergies important in pediatrics include food, drug, and environmental allergies. Each of these areas will be introduced in the following section with special attention paid to areas of controversy. FOOD ALLERGY Hippocrates is credited with one of the first written accounts of an IgE-mediated (urticar- ial) reaction to food, specifically milk. 2 In 1921, Prausnitz and Kustner elucidated that the phenomenon responsible for an “allergic” reaction was present in serum and could be transferred to a nonsensitive individual. 2 With the introduction of the double-blind, placebo-controlled oral food challenge in 1976, the study of food allergy began its scien- tific journey. 3 Adverse reactions to food include toxic and nontoxic reactions. Toxic reactions can occur in anyone, with the reaction being a direct result of the properties of the food ingested, for example, toxins secreted by Salmonella. Nontoxic reactions depend specifically on the sus- ceptibility of the host and can be immune mediated (allergy) or non–immune mediated (intolerance). Intolerances account for the majority of adverse food reactions; however, it is the IgE-mediated immune response that will be the focus of this section. 2 Immunoglobulin E-mediated responses to food hypersensitivity take the form of cutaneous eruptions (urticaria/angioedema, atopic dermatitis), respiratory symptoms (rhinoconjunctivitis, asthma), very specific gastrointestinal complaints (oral allergy syndrome, allergic eosinophilic gastroenteritis), and anaphylaxis. 4 Surveys of both children and adults reveal that approximately 25 percent of the popu- lation believe they have a food allergy. 4 The prevalence of true food allergy, however, is far less and quoted by Sampson to be approximately 5 percent of children less than 3 years of age and 1.5 percent of the general population. 4 What is also clear is that children with atopic dermatitis have a higher incidence of food allergy than the general population, and the more severe their dermatitis, the greater is the chance that they have a food allergy. 2 The most common food allergens include cow’s milk, chicken egg, legumes (specifically peanuts and soyabeans), tree nuts (almonds, Brazil nuts, cashew nuts, filberts, hickory nuts, pecan, pine nuts, pistachios, and walnuts), fish, crustaceans (lobster and shrimp), mollusk (mussels and scallops), and cereal grains. 2 The Peanut The peanut deserves special mention as it is one of the most allergenic foods in children. 2 The peanut is a member of the legume family and therefore not related to other nuts. Allergic reactions to peanuts can be life threatening. Therefore, patients with this allergy must take great care in avoiding eating peanuts and all products potentially containing peanuts. However, even when one is extremely careful, there is unfortunately a great deal of accidental exposure especially in foods such as baked goods, in which the allergen can be hidden. 5 It has always been believed that unlike some other food allergies, allergy to peanuts is not outgrown. In a longitudinal study by Bock in 1989, a group of patients who were posi- tive to peanuts by history and skin prick test accidentally ingested it up to 14 years after test- ing. None tolerated it. 6 More recent work by Hourihane in 1998 has shown that there may be some patients with very few other allergies who do, in fact, lose their peanut allergy over time. This study was in a case-control format, and the patient numbers were small with only 15 in each group. 7 The concept of losing sensitivity to peanuts is intriguing and further study in this area will be of great value. The peanut is ubiquitous in our society. Therefore, allergy to this seemingly innocuous legume is worthy of serious and ongoing study. Egg Hypersensitivity and Administration of the MMR Vaccine There has been ongoing controversy and concern over the years about the safety of admin- istering the MMR vaccine to children with documented hypersensitivity to egg protein. Given that the incidence of egg allergy in the pediatric population is reported to be approx- imately 0.5 percent, 8 there is the potential for a significant number of children to have their vaccination either delayed or omitted. There are numerous good studies in the literature showing the safety of administering the MMR vaccine to egg-allergic children. 8–10 Freigang and colleagues, in 1994, published one of the largest studies on the administration of the MMR vaccine to 500 egg-allergic children. Early on in the study, they abandoned skin testing (after 120 patients) as it did not appear to have any relationship to the final reaction to the immunization. 9 There was no anaphy- laxis described in any patients and only 5 patients had minor local reactions to the vaccina- tion. 9 In 1995, James and colleagues published another study combining all the experience of giving the MMR vaccine to egg-allergic children described in the literature since 1963. The results showed that 99.75 percent of children who are allergic to eggs and have a positive skin test can receive the vaccine in the usual way without any severe anaphylactic reactions. 8 On the basis of good evidence, the National Advisory Committee on Immunization has changed the recommendations in the fifth edition of the Canadian Immunization Guide. They are as follows: 1. Given that the Yellow Fever and influenza vaccines are prepared from viruses grown in embryonated eggs, they should not be given unless the risk of the disease outweighs the small risk of a systemic hypersensitivity reaction. 2. Egg allergy is no longer considered a contraindication to immunization with MMR. Children with a history of egg allergy may be immunized in the routine manner with- out prior testing. As an additional measure of safety, however, it may be prudent to observe them for 30 minutes after immunization for any signs of an allergic reaction. 3. A previous anaphylactic reaction to a vaccine containing measles-mumps-rubella is an absolute contraindication to receiving the vaccine a subsequent time. 4. If an individual who has had a prior anaphylactic reaction to a vaccine requires reim- munization, yellow fever or influenza vaccine prepared in embryonated chicken eggs the American Academy of Pediatrics “Report of the Committee on Infectious Diseases” also 328 Evidence-Based Pediatrics agrees and recommends that the MMR can be administered to children with a history of egg allergy. 10a It is also recommended that if an individual has a history of anaphy- lactic hypersensitivity to hen’s eggs, skin testing and a graded challenge can be consid- ered. If a graded challenge is to be conducted it should be done in an appropriately equipped facility by skilled personnel who are both familiar with the procedure itself and the treatment of anaphylaxis. 11 Clearly, the institution of these guidelines, which are based on good evidence, will begin to ensure an increase in immunization rates in our population. They will also result in a decrease in morbidity and discomfort in the patient caused by unnecessary testing and graded immunizations and decrease in parental anxiety (see also Chapter 3 on immuniza- tion). PENICILLIN ALLERGY AND CROSS-REACTIONS Penicillin was discovered by Fleming in 1928 12 and since that time has become the most widely prescribed antibiotic in the world. 13 Of great concern is the number of children with a history of “hypersensitivity” to peni- cillin. Not only is the medication inexpensive, but it also has a quite favorable side-effect pro- file, when compared with other antimicrobials. Cutaneous reactions and gastrointestinal symptoms are not uncommon in connection with penicillin use and are often interpreted as allergic reactions. 14 This leads to a significant number of children being referred to both hos- pital and community allergists for evaluation of their sensitivity. Penicillin is highly immunogenic and considered to be the most common drug causing allergic reactions. 15 The prevalence of penicillin allergy in the general population is quoted as being between 1 and 10 percent. 15 The prevalence of adverse reactions to cephalosporins ranges from 1 to 10 percent also. 16 These figures are based on reporting and therefore may turn out to be overestimates of the prevalence, when confirmed via skin testing and oral chal- lenges. There is ongoing concern on the part of physicians treating patients with “hypersensi- tivity” to penicillin about its cross-reactivity with cephalopsorins. This concern has the potential to further reduce the antibiotic choices for given infections. The concern has stemmed from the fact that both penicillin and cephalosporins contain a beta-lactam ring. 12 Earlier in-vitro studies demonstrated antigenic cross-reactivity with little information on the clinical relevence; 12 some authors felt that these studies, in fact, overestimated the risk. 17 As early as 1967, there appeared in the literature published accounts of patients who were penicillin allergic and, when given a cephalosporin they had not encountered previ- ously, had a type I hypersensitivity reaction. 18,19 Most of these early reports were in the form of case reports. The generally accepted rate of cross-reactivity in the literature has varied between 6 and 15 percent. 20 There have not been any randomized controlled trials (RCTs) to further define this percentage, and one study has reported that it is, in fact, safe to admin- ister cephalosporin antibiotics to penicillin-allergic patients. 16 Unfortunately, this particular study used published reports and postmarketing data from pharmaceutical corporations as the basis for the analysis. 16 Solley and colleagues prospectively studied patients with a his- tory of penicillin allergy and both negative and positive skin tests. The group with negative skin tests had a 1.3 percent reaction rate (well within the average quoted for cephalosporin reactions alone), and there were no reactions in the positive skin test group. 21 Given that there have been no RCTs prospectively comparing the incidence of IgE- mediated reactions to cephalosporins in penicillin-allergic patients virus non–penicillin- allergic patients, it is difficult to determine how concerned one should be when consider- ing administation of cephalosporins to penicillin-allergic patients. Although the percent- age may be much lower than is the current teaching, until there is better evidence, one must Allergy 329 be cautious when considering prescribing cephalosporin antibiotics to penicillin-allergic patients. ENVIRONMENTAL ALLERGY Environmental allergies may be manifested clinically as rhinitis, conjunctivitis, or asthma exacerbations. These allergies may be perennial, with or without seasonal exacerbations, or only seasonal. 22 They are IgE-mediated reactions to a variety of aeroallergens. Typical sea- sonal allergens are pollens and molds, while typical perennial aeroallergens include dust mites, molds, animal allergens, and certain occupational allergens. 22 In the United States, the most common indoor allergens are dust mite feces, cockroach (both the insect’s body and feces contain the allergen), and cat dander. The most common outdoor allergens are pollens and fungal spores. 23 Rhinitis is defined as inflammation of the membranes lining the nose. It is character- ized by nasal congestion, rhinorrhea, sneezing, itching of the nose, and/or postnasal drainage. 23 Allergic rhinitis is believed to affect 20 to 40 million people in the United States. Up to 40 percent of children may be affected, with the greater percentage of males. 22 Given the large numbers of patients affected in the population, the morbidity and burden of ill- ness are marked in terms of costs to the health-care system as well as time away from work. 22 DIAGNOSIS OF IMMEDIATE HYPERSENSITIVITY The diagnosis of IgE-mediated reactions to the various allergens described above begins with a thorough history, including very specific questions about each of the potential allergens, timing, and a description of the clinical symptoms. Previous trials of therapy should also be documented. 24 A very important detail that may be overlooked is to investigate the extent to which the symptoms interfere with the patient’s life. 24 After a complete physical examina- tion, it is time to decide which tests, if any, will aid in the diagnosis. Allergy testing does not diagnose allergic disease but rather determines the presence or absence of allergen-specific IgE antibodies. 1 These results combined with the clinical presentation aid the physician in diagnosing allergic disease. To properly study a diagnostic tool, there must be a gold standard to which the test can be compared. Ideally, this standard should be able to induce typical signs and symptoms and be reproducible. It must also be done in a double-blind, placebo-controlled fashion. 1 This is possible in some areas of allergy such as food allergy but is more challenging in other areas such as environmental allergies. 1 Skin Prick Testing Skin tests have been used as the major diagnostic tool in allergy since 1865, when they were first introduced by Blackley. 25 There have been some modifications over the years, and it is believed that they may provide important information that can corroborate clinical suspi- cion of a specific allergy. They are simple and time efficient, which explains their global use by trained allergists. 25 Skin prick testing was described in 1924 by Lewis and Grant and became widely used in the 1970s. 25 It involves the placement of a small drop of extract as well as a small drop of both saline and histamine controls on the volar surface of the forearm or the back. A sterile lancet is then used to break the epidermis. Each allergen must be placed 2 cm apart. The area is then observed for clinical reaction for 15 to 20 minutes. 26 For a reaction to be considered positive, there must be a wheal that is at least 3 mm larger than the negative control. 26 Skin prick testing is believed to be the most specific screening method to detect the pres- ence of IgE antibodies in patients with a clinical history of reaction to allergen exposure. 26 Skin prick testing has been demonstrated to be highly reproducible when both inter- and intravariations were calculated, using histamine dihydrochloride. 27 Although the presence of 330 Evidence-Based Pediatrics a positive skin prick test does not necessarily correlate with the presence of clinical symp- toms, there may be a higher incidence of clinically significant allergy with larger reactions. 26 This mode of testing is used in the area of food allergy, environmental allergy, drug allergy, and latex allergy. Testing for Penicillin Allergy Penicillin allergy has been studied extensively. In 1992, the results of a collaborative clinical trial conducted by the National Institute of Allergy and Infectious Diseases were published. The usefulness of four penicillin allergen skin tests in the prediction of IgE-mediated reac- tions following administration of penicillin was assessed. 28 This study demonstrated the high negative predictive value (NPV) of a negative skin test, which has been reproduced else- where. 28–30 The NPV of skin testing to the major and minor determinants of penicillin in patients with a positive history was in the order of 98 to 99 percent. However, as the major- ity of patients who had positive skin tests did not go on to receive oral penicillin, the posi- tive predictive value (PPV) is unknown. The specificity of the test is also quite high, in the order of 99 percent, in this defined group of patients, but again, the sensitivity could not be determined from this data. Despite this lack of data, there are those who believe that the PPV of a skin prick test is high. 30 This assumption is based on the observation made in a number of studies that patients with positive skin tests who were given penicillin, either deliberately or inadvertently, did show a clinical reaction 40 to 100 percent of the time. 21,29,30 These num- bers are small and observed incidentally. However, to determine the PPV of positive skin prick testing to penicillin, further careful studies need to be carried out in a systematic fash- ion. Until these studies are done, the PPV of this test is unclear. A further question to be stud- ied lies in the area of negative skin tests. Given the high NPV of a negative test, should one proceed to an oral challenge or feel safe in giving a proper course of treatment on the basis of the test alone? Pichichero and Pichichero outline that skin testing without an oral chal- lenge may allow room for non–IgE-mediated adverse reactions to be missed. 31 These authors also described that pediatrician-diagnosed adverse reactions to a variety of antibiotics accu- rately predicted IgE sensitivity only 34 percent of the time. 31 In other words, 66 percent of the physician-diagnosed “penicillin allergic” patients were, in fact, not allergic, as confirmed by negative skin testing and oral challenge. 31 The false-positive diagnosis rate may have been even higher as none of the 34 percent of patients with a positive skin test were challenged with oral penicillin. The NPV of skin prick testing for the major and minor determinants of penicillin is high as is the specificity in patients with a history of an adverse reaction to penicillin. However, given the concern of missing a non–IgE-mediated reaction by omitting the oral challenge component, it would appear prudent to take this next step despite this reliability. With respect to the PPV, further work is required to make this determination. If it is, in fact, low, should we change our approach and go directly to an oral challenge in the area of penicillin allergy? Testing for Food Allergy Skin prick testing is widely used in the clinical evaluation of food allergy. Positive results indi- cate the possibility that the patient may have a clinical reaction to that particular food. The PPV, however, is less than 50 percent, while the NPV is greater than 95 percent in a trial that studied children with atopic dermatitis. 32–34 These values were determined through compar- ison with the “gold standard”in the diagnosis of food allergy, the double-blind, placebo-con- trolled food challenge (DBPCFC). 33 Thus, the skin prick test is a way to rule out an IgE-mediated food allergy but is only suggestive of clinical food allergy in the case of a pos- itive test. 32 One must also remember that there are no standardized allergens in this area. 35 Therefore, a variety of extracts as well as fresh foods are often used in the test. Allergy 331 [...]... more specific Anti-ds-DNA antibodies 3 58 Evidence- Based Pediatrics (serum autoantibodies to native double-stranded DNA) are highly specific for SLE ( 98 percent), but less sensitive (50 to 70 percent) Because of the high specificity, a positive anti-dsDNA test is useful to rule in a diagnosis of SLE.49 There are other specific autoantibodies seen in patients with SLE; the anti-Sm (anti-Smith) antibody is... 1994;94 :81 8–25 344 Evidence- Based Pediatrics 49 LaForce C, Dockhorn RJ, Prenner BM, et al Safety and efficacy of azelastine nasal spray (Astelin NS) for seasonal allergic rhinitis: a 4-week comparative multicenter trial Ann Allergy Asthma Immunol 1996;76: 181 8 50 Erffmeyer JE, McKenna WR, Lieberman PL, et al Efficacy of phenylephrine-phenylpropanolamine in the treatment of rhinitis South Med J 1 982 ;75:562–4... corticosteroid therapy in rhinitis J Allergy Clin Immunol 1 988 ;81 : 984 –91 57 Taylor G, Shivalkar PR Disodium cromoglycate: laboratory studies and clinical trial in allergic rhinitis Clin Allergy 1971;1: 189 – 98 58 Pelikan Z, Snoek WJ, Booij-Noord H, et al Protective effect of disodium cromoglycate on the allergen provocation of the nasal mucosa Ann Allergy 1970; 28: 5 48 53 59 Meltzer EO, Orge; JA Bronsky EA, et al Ipratropium... first-line therapy for allergic rhinitis In a double- 336 Evidence- Based Pediatrics blind, randomized, placebo-controlled, multicenter trial azelastine nasal spray was shown to be efficacious in the treatment of seasonal allergic rhinitis, when compared with placebo 48, 49 Both these studies were performed in adults and in children 12 years and over Oral decongestants Oral decongestants are alpha-adrenergic... egg-allergic children Ann Allergy 1994;73: 486 8 10 Fasano MB, Wood RA, Cooke SK, et al Egg hypersensitivity and adverse reactions to measles, mumps, and rubella vaccine J Pediatr 1992;120 :87 8- 8 1 10a American Academy of Pediatrics Active and passive immunization In: Peter G, editor 1997 Red Book: Report of the Committee on Infectious Diseases 24th edition Elk Grove Village, IL: American Academy of Pediatrics, ... al, for the Evidence- Based Medicine Working Group User’s guides to the medical literature VIII How to use clinical practice guidelines A Are the Recommendations Valid? 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