Tissue transglutaminase: The Holy Grail for the diagnosis of celiac disease, at last?  

Oleh:

Fasano, Alessio

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Journal of Pediatrics vol. 135 no. 02 (Feb. 1999), page 134-135.
Topik: AEA ; Anti-endomysium antibody; AGA ; Anti-gliadin antibody; CD ; Celiac disease; ELISA ; Enzyme-linked immunosorbent assay; tTG ; Tissue transglutaminase

Ketersediaan

Perpustakaan FK Nomor Panggil: J45.K.1999.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Celiac disease is an autoimmune enteropathy triggered by the ingestion of gluten in genetically susceptible individuals. 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 patient’s diet. CD represents a common cause of malabsorption in western countries, with apparent geographic variation in incidence. Until a few decades ago, the general perception was that the clinical presentation of the disease was quite uniform. The case identification was based entirely on the search for symptoms such as chronic diarrhea, abdominal distension, and weight loss (or poor weight gain) occurring in young children a few months after the introduction of solid foods to their diet. Therefore early epidemiologic studies targeted the pediatric population with this typical clinical presentation of the disease. In the past 10 to 15 years, we have learned that the clinical expression of CD is more heterogeneous than previously thought. Besides the classical gastrointestinal form, a series of other clinical expressions of the disease have been described thanks to the advent of innovative serologic screening tests, such as assays for anti-gliadin antibody and anti-endomysium antibody. The combined use of serum AGA IgG (highly sensitive) and IgA (highly specific) resulted in a reliable screening test with which to study the epidemiology of CD. With the use of this new tool, we have learned that the clinical presentation of CD is more protean than previously thought, including previously unrecognized atypical and asymptomatic forms. Moreover, these studies demonstrated that CD is not limited to the pediatric population but that the onset of disease may occur during adulthood after years with no symptoms. Screening studies conducted in several European countries seem to suggest that the occurrence of CD is comparable throughout the old continent and that the prevalence is one of the highest (~1:250/300) among genetically based diseases. The European experience taught us that despite common genetic and environmental factors, the clinical presentation of CD may greatly diverge even between neighboring countries. Factors such as type of cow’s milk formula, breast feeding, age at gluten introduction, quantity of gluten, quality of cereals, and quantity of wheat gluten may all influence the clinical presentation of the disease. Within the American scientific community, it is generally held that CD is a rare disorder in the United States, which is reflected by the limited number of CD-related scientific papers published from the new continent in the past 30 years. However, by using the screening assays described above, we have recently demonstrated that the prevalence of CD in both the pediatric and adult North American populations is comparable to that reported in Europe. Our results suggest that some of the aforementioned influencing factors are probably operative in the United States and are therefore responsible for atypical forms that are more difficult to identify in common clinical practice.

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