4. Cheng TL, Wright JL, Pearson-Fields AS, Brenner RA. The spectrum of intox-ication and poisonings among adolescents: surveillance in an urban population. Inj Prev2006;12:129-32.5. McCaig LF, Burt CW. Poisoning-related visits to emergency departments in theUnited States, 1993-1996. J Toxicol Clin Toxicol 1999;37:817-26.6. Mintegi S, Fernandez A, Alustiza J, Canduela V, Mongil I, Caubet I, et al.Emergency visits for childhood poisoning: a 2-year prospective multicenter survey inSpain. Pediatr Emerg Care 2006;22:334-8.7. Lamireau T, Llanas B, Kennedy A, Fayon M, Penouil F, Favarell-Garrigues JC,et al. Epidemiology of poisoning in children: a 7-year survey in a paediatric emergencycare unit. Eur J Emerg Med 2002;9:9-14.8. Marchi AG, Renier S, Messi G, Barbone F. Childhood poisoning: a populationstudy in Trieste, Italy, 1975-1994. J Clin Epidemiol 1998;51:687-95.9. Lovejoy FH Jr, Nizet V, Priebe CJ. Common etiologies and new approaches tomanagement of poisoning in pediatric practice. Curr Opin Pediatr 1993;5:524-30.10. Lamminpaa A, Riihimaki V, Vilska J. Hospitalizations due to poisonings inFinland. J Clin Epidemiol 1993;46:47-55.11. Smith T. Accidents, poisoning and violence as a cause of hospital admissions inchildren. Health Bull (Edinb) 1991;49:237-44.

12. Mattila VM, Makitie I, Pihlajamaki H. Trends in hospitalization for firearms-related injury in Finland from 1990 to 2003. J Trauma 2006;61:1222-7.13. Official Statistics of Finland. Structure of Population and Vital Statistics: WholeCountry and Provinces, 2006. Helsinki: Statistics Finland; 2006.14. Bryant S, Singer J. Management of toxic exposure in children. Emerg Med ClinNorth Am 2003;21:101-19.15. Aro S, Koskinen R, Keskimaki I. Reliability of hospital discharge data concerningdiagnosis, treatments and accidents [in Finnish]. Duodecim 1990;106:1443-50.16. Council Directive 67/548/EEC of 27 June 1967 on the approximation of laws,regulations and administrative provisions relating to the classification, packaging andlabelling of dangerous substances. Official J 1967:0001-98.17. White ML, Liebelt EL. Update on antidotes for pediatric poisoning. PediatrEmerg Care 2006;22:740-6;quiz 7-9.18. Alko Inc. Annual Report and Corporate Social Responsibility Report for 2006.Helsinki: Alko; 2007.19. Lintonen T, Rimpela M, Ahlstrom S, Rimpela A, Vikat A. Trends in drinkinghabits among Finnish adolescents from 1977 to 1999. Addiction 2000;95:1255-63.20. Shepherd G, Klein-Schwartz W. Accidental and suicidal adolescent poisoningdeaths in the United States, 1979-1994. Arch Pediatr Adolesc Med 1998;152:1181-5.

50 Years Ago in The Journal of PediatricsCELIAC DISEASE: RESPONSE TO A GLUTEN FREE DIET

Graven SN and Tomsovic EJ. J Pediatr 1958;53:726-30

There were no grains containing gluten 10 000 years ago and, therefore, presumably there was no celiac disease (CD).With the advent of agriculture, wheat and other gluten-containing grains were developed, providing 1 of the 2 keyelements (the second being the predisposing genes) necessary for the onset of CD. However, it took almost 8000 yearsbefore Aretaeus of Cappadocia reported the first scientific description of CD. Another 2000 years passed before DrWillem Karel Dicke, a Dutch pediatrician, made the connection between gluten and CD soon after World War II.Therefore, little progress was made in understanding this condition at the time of the case reported in 1958. This16-month-old Caucasian girl had the classical celiac crisis, with pallor, lethargy, irritability, weight loss, and protrudingabdomen. The diagnostic tools available at that time were non-specific, including abdominal radiography, nutritionaltests, and detection of steatorrhea. The cornerstone for a proper diagnosis (ie, the intestinal biopsy) was not available,because the first devices to obtain duodenal biopsies were developed only the year before and were not routinelyaccessible. As indicated in this report, the treatment regimen was rather limited, based mainly on skim milk and freshbananas (the so-called “banana babies”). Therefore, the mortality rate was high (up to 35%), and the length ofhospitalization was long (this child was in the hospital for 49 days). In only 50 years, a fraction of time in the 10 000history of CD, we have witnessed revolutionary changes. Once considered rare, it is now clear that CD is one of the mostfrequent genetically based disorders, affecting 0.5% to 1% of the general population worldwide. CD is now classified asan autoimmune disease rather than a food allergy. We now also know that in addition to the typical malabsorptionsymptoms, CD can manifest in a previously unappreciated spectrum of symptoms that potentially can affect any organsystem. The diagnosis is based on very sensitive and specific serological tests and confirmed by using an upper endoscopyperformed in the ambulatory setting. The treatment is based on a variety of gluten-free products, the palatability andvariety of which has increased dramatically during the past few years. Finally, because of the clear role of gluten in causinginflammation and immune-mediated tissue damage, CD represents a unique model for studying autoimmunity anddeveloping new strategies for treatment.

Alessio Fasano, MDMucosal Biology Research Center and Center for Celiac Research

University of Maryland School of MedicineBaltimore, Maryland

10.1016/j.jpeds.2008.05.024

824 Kivistö et al The Journal of Pediatrics • December 2008