SEJARAH DAN ANGKA KEJADIAN PENYAKIT SELIAK DI DUNIA

PREVALENCE AND HISTORY OF CELIAC DISEASE IN THE WORLD
.
Widodo Judarwanto

PICKY EATERS CLINIC JAKARTA INDONESIA
Jl Taman Bendungan Asahan 5 Jakarta Indonesia
Phone : 62-21-70081995 – 70081995
email :
wido25@hotmail.com , http://pickyeatersclinic.blogspot.com

.
BACKGROUND
  • Coeliac disease is a permanent, lifelong inflammatory disease of the upper small intestine and result from gluten ingestion in genetically susceptible individuals. This causes damage to the lining of the intestines. This leads to poor absorption of important nutrients including iron, folic acid, calcium, and fat-soluble vitamins. Gluten is a protein found mainly in wheat and to a lesser extent in rye, oats and barley. Hence the alternative name for the condition is Gluten-sensitive Enteropathy. Coeliac Disease is closely related to dermatitis herpetiformis. In dermatitis herpetiformis, skin rash and a similar small intestinal enteropathy to that of coeliac disease are typically present, and both respond to withdrawal of gluten1,4,6
  • The disease is associated with human leukocyte antigen (HLA) alleles DQA1*0501/DQB1*0201, and in the continued presence of gluten the disease is self-perpetuating.2 The typical intestinal damage characterized by loss of absorptive villi and hyperplasia of the crypts completely resolves on elimination of gluten-containing grains from the patients’ diet. CD represents a common cause of malabsorption in western countries with apparent geographic variation in incidence.

HYSTORICAL

  1. In the second century AD, Aretaeus from Cappadocia described what is believed to be the first report of a gastrointestinal condition resembling CD.3
  2. Approximately 1700 years later, the connection between the ingestion of certain cereals and the onset of gastrointestinal symptoms typical of CD was established.4
  3. For the past 18 centuries, CD has been perceived as a disease whose clinical presentation was quite uniform. The case identification was entirely based on the search for symptoms such as chronic diarrhea, abdominal distension, and weight loss (or poor weight gain) occurring in young children a few weeks/months after the introduction of solid food to their diet. Therefore, early epidemiologic studies targeted the pediatric population experiencing this typical clinical presentation of the disease.
  4. Most gastroenterologists recognise that Samuel Gee’s description of coeliac disease in 1888 is now an uncommon presentation – but most general practitioners’ image of coeliac disease is still of this classic form. In the past 5 decades, a substantial number of epidemiologic studies have been conducted in Europe to establish the frequency of CD, and interesting controversies have arisen.
  5. One of the oldest epidemiologic studies on CD conducted in 1950 established that the cumulative incidence of the disease in England and Wales was 1/8000, while an incidence of 1/4000 was detected in Scotland.5 The diagnosis at that time was entirely based on the detection of typical symptoms and confirmed by complicated and sometimes nonspecific tests.
  6. The awareness of the disease greatly increased in the 1960s when more specific tests for malabsorption and the pediatric peroral biopsy technique became available.6
  7. In the middle 1970s reached peaks of 1/450-500 was reported in studies from Scotland.7
  8. This increased incidence of CD urged changes in the dietary habit, based on the hypothesis that delayed exposure to gluten could prevent the onset of the disease.
  9. For the first time in 25 years a decrease in the incidence of CD was reported in the United Kingdom and Ireland8 after a late introduction of gluten in the infants’ diet. Unfortunately, this decrease was deceptive, because subsequent screening studies demonstrated that the reduction of typical cases in infants was counterbalanced by the increase of atypical forms of CD with the onset of the symptoms occurring in older children or in adults.9
  10. In the past 10 to 15 years, we learned that the clinical expression of CD is more heterogeneous than previously thought.10 Besides the classical gastrointestinal form, a series of other clinical manifestations of the disease have been described, thanks to the advent of innovative serologic screening tests such as antigliadin and antiendomysium (EmA) antibodies assays. The combined use of serum antigliadin immunoglobulin G (highly sensitive) and immunoglobulin A (highly specific) and the confirmation with the EmA test resulted in a reliable screening algorithm to study the epidemiology of CD.11 Based on the use of these new tools, we have learned that the clinical presentation of CD is more protean then previously thought, including previously unrecognized atypical and asymptomatic forms. Moreover, these studies demonstrated that CD is not limited to the pediatric population, but the disease may become clinically apparent during adulthood after years of silent disease.
  11. The European experience taught that, despite common genetic and environmental factors, the clinical presentation of CD in neighboring countries may greatly diverge and could justify the different prevalence of the disease previously reported.13 A similar explanation seems to account for the rare prevalence of CD previously reported in the United States.14 Recent studies conducted by using more appropriate experimental designs and powerful screening tools demonstrated that CD in the United States is as frequent as in Europe in both risks groups15 and the general population.16, Similar results were obtained in Africa,17 and Asia,18 continents where CD was considered a rare disorder. Combined together, these studies revealed that CD is one of the most frequent genetically-based diseases of humankind32 occurring in 1 out of every 100 to 300 individuals in the general population worldwide.26
  12. In the future, a multidisciplinary research effort to understand the pathogenesis of CD is currently taking place worldwide. This effort is fueled by the appreciation that CD represents a unique example of an autoimmune disease in which the environmental factor(s) that induces the immune response has been identified. Therefore, scientists view CD as a model to tackle key questions on the pathogenic mechanisms involved in other autoimmune diseases (ie, multiple sceloris, diabetes mellitus, rheumatoid arthritis, etc) whose environmental triggers are still unknown.20
  13. Future directions in an advanced state of development (ie, engineering gluten-free grains), others (ie, the search for the CD genes) are extremely challenging and will require an international task force to generate meaningful data. 19

PREVALENCE

  • There is scarcity of data on the incidence of the full spectrum of celiac disease, including classical, atypical, silent and latent forms. Recent studies using serology and small intestinal biopsy suggest that the prevalence of celiac disease in Europe and in the United States is 0.5%-1%. This included both symptomatic and asymptomatic individuals. There is probably a substantial number of undiagnosed cases in the general population (possibly 10 times as many as actually have been diagnosed).20
  • Approximately 3 million people in Europe and another 3 million people in the United States are estimated to be affected by celiac sprue. Celiac sprue is prevalent in European countries with temperate climates. The highest prevalence of celiac sprue is in Ireland and Finland and in places to which Europeans emigrated, notably North America and Australia. In these populations, celiac sprue affects approximately 1 in 100 individuals. The incidence of celiac sprue is increasing among certain populations in Africa (Saharawui population), Asia (India), and the Middle East.21
  • Certain populations have an increased prevalence: first degree relatives (4%-12%), type I diabetes mellitus (3%-8%), and Down sydrome (5%-12%). Furthermore, celiac disease is associated with i.a. IgA deficiency and autoimmune disorders.20

REFERENCE

  1. Hardman CM, Garioch JJ, Leonard JN, Absence of toxicity of oats in patients with dermatitis herpetiformis. N Engl J Med 1997; 337:1884-1887
  2. Sollid L, Thorsby E HLA susceptibility genes in celiac disease: genetic mapping and role in pathogenesis. Gastroenterology 1993; 105:910-922
  3. Thomas C. On the coeliac affection. In: Major RH, ed. Classic Descriptions of Disease. Springfield, IL: Charles C. Thomas; 1945:600-601
  4. Dicke WK. Investigation of the Harmful Effects of Certain Types of Cereals on Patients With Coeliac Disease [doctoral thesis]. The Netherlands: University of Utrecht; 1950
  5. Davidson LSP, Fountain JR Incidence of sprue syndrome with some observation on the natural history. Br Med J 1950; 1:1157-1161
  6. Meeuwisse GW Diagnostic criteria in coeliac disease. Acta Paediatr Scand 1970; 59:461-463
  7. Logan RFA, Rifking EA, Busuttil A, Gilmous HM, Ferguson A Prevalence and `incidence’ of celiac disease in Edinburgh and the Lothian region of Scotland. Gastroenterology 1986; 90:334-342
  8. Stevens FM, Egar-Mitchell B, Cryan E, McCarthy CF, McNicholl B Decreasing incidence of coeliac disease. Arch Dis Child 1987; 62:465-468
  9. Greco L, Maki M, DiDonato F, Visakorpi JK. Epidemiology of coeliac disease in Europe and the Mediterranean area. In: Auricchio S, Visakorpi JK, eds. Common Food Intolerances 1: Epidemiology of Coeliac Disease. Basel, Switzerland: Karger; 1992;2:25-44
  10. Logan RFA. Problems and pitfalls in epidemiological studies of coeliac disease. In: AuricchioS, Visakorpi JK, eds. Common Food Intolerances 1: Epidemiology of Coeliac Disease. Basel, Switzerland: Karger; 1992:14-24
  11. Burgin-Wolff A, Berger R, Gaze H, Huber H, Lentze MJ, Nussle D IgA and IgG gliadin antibody determinations as screening test for untreated coeliac disease in children, a multicentre study. Eur J Pediatr 1989; 148:496-502
  12. Weile B, Krasilnifoff PA Extremely low incidence rate of celiac disease in the Danish population of children. J Clin Epidemiol 1993; 46:661-664
  13. Kristianson B, Ascher H, Odenman I, Sandberg L. The incidence of coeliac disease and changes in gluten consumption. In: Mearin ML, Mulder CJJ, eds. Coeliac Disease. The Netherlands: Kluwer Academic Publisher Netherlands; 1991:107-114
  14. Talley NJ, Valdovinos M, Petterson TM, Carpenter HA, Melton L Jr Epidemiology of celiac sprue: a community-based study. Am J Gastroenterol 1994; 89:843-846
  15. Hill ID, Horvath K, Fasano A Epidemiology of celiac disease. Am J Gastroenterol 1995; 90:163-164
  16. Berti I, Horvath K, Green PHR, Sblattero D, Not T, Fasano A. Prevalence of celiac disease among risk groups and the general population in U.S.A. J Invest Med. 2000;48:206:220A
  17. Catassi C, Ratsh IM, Gandolfi L, Why is coeliac disease endemic in the people of the Sahara? Lancet 1999; 354:647-648
  18. Yachha SK, Mohindra S, Srivastava A, Krishnani N, Saxena A Effects of gluten-free diet on growth and small bowel histology in children with celiac disease in India. J Pediatr Gastroenterol Nutr 2000; 31:S23
  19. Ninth International Symposium on Celiac Disease. J Pediatr Gastroenterol Nutr. 2000;31(suppl):S1-S35
  20. Rewers M. Epidemiology of celiac disease: what are the prevalence, incidence, and progression of celiac disease? Gastroenterology 2005; 128:S47-S51.
  21. Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. Feb 10 2003;163(3):286-92

 

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CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

 

 

 

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

 

 

 

 

 

 

 

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

 

4 thoughts on “SEJARAH DAN ANGKA KEJADIAN PENYAKIT SELIAK DI DUNIA

  1. Lisa

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