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It is known that celiac disease is characterized by a huge variety of clinical forms ranging from classical ones to silent forms, potential ones and to an increased number of cases of gluten-sensitivity. The latter is an abnormal non-allergic sensibility to gluten. Clinical manifestations can be very different without a severe intestinal damage (Marsh/Oberhuber 0-I) and this condition seems to benefit from a gluten free diet. Cases of gluten-sensitivity appear very interesting in the search of histological markers with elevated specificity, which are able to identify slight and early gluten dependent enteropathy, especially in at risk patients for celiac disease even before classical autoantibodies appear: for instance, this is the case of intraepithelial lymphocytes T-cell receptor gamma delta and mucosal deposits of class IgA anti transglutaminase antibodies. Other studies are investigating transglutaminase isoenzimes (different from tissue one), that can be identified in patients with gluten dependent symptoms without classical autoantibodies. Forms of gluten allergy have a different pathogenesis from celiac disease and are represented by "backer's asthma" or by classical allergy to wheat proteins. Clinical manifestations can vary from anaphylactic reactions to dermatological, respiratory and intestinal symptoms. Also in these cases the therapeutic approach is based on gluten free diet.

A celiac disease update review and a case report are presented, especially concerning a Clinical Pathology Laboratory approach. Implemented basic research, case finding strategy and information technologies are the key tools for a better understanding of the multi-etiological features of this disease. By these tools it will be achieved appropriateness in diagnosing and monitoring of the related clinical pictures.

Objectives: Data on the follow-up of a group of subjects with serum antiendomysial antibodies (EMA) and normal mucosal architecture at the intestinal biopsy are reported. Clinical problems concerning possible evolution of potential celiac disease (CD) towards gluten-induced histological damage are discussed., Methods: Eleven patients belonging to high-risk groups for CD (5 with type-1 diabetes, 2 with familiarity for CD and 4 with symptoms suggesting CD) who had a normal intestinal biopsy, despite positive antiendomysial test, were followed-up. Antigliadin and antitransglutaminase antibodies (anti-tTG) and HLA genotyping were also assessed. According to clinical and serological data a second biopsy was performed in six of them., Results: At the time of the first normal biopsy, all patients were positive for EMA and 5/8 for anti-tTG. Five of 6 subjects genotyped were HLA-DQ2+ or DQ8+. Six patients were rebiopsed after 1 to 4 years. Three had mucosal atrophy, 1 had mild increase of intraepithelial lymphocytes and 2 were morphologically normal., Conclusions: Subjects with antiendomysial antibodies and normal intestinal biopsy deserve clinical and serological follow-up to reduce the time of possible latency of CD. Although good predictors of progression of the disease are not still available, antiendomysial antibodies assessment and HLA genotyping may help to suggest individuals at higher risk to develop gluten-induced enteropathy. This study confirms that subjects with persistent signs of gluten sensitivity and normal biopsy should be re-examined.

Wheat, oat, rye and barley flours are toxic for celiac patients. Prevalence and incidence of Celiac Disease (CD), quite variable from country to country, are very high in Austria (1 out of 476 born alive) and low in France (1 out of 41.667 born alive). This difference is probably due to its multifactorial genesis. In a multicentric Italian study, histocompatibility antigens of HLA complex II were typed in 460 CD children. DR3 was present in 63% of the cases (Relative Risk = RR: 6.8), DR7 in 67% (RR: 3.8) and DR3/DR7 in 22.5% (RR: 10.5), while in 7.7 of patients both antigens were absent. Therefore in a certain percentage of CD patients these risk antigens are absent, while in the normal population they can be present. The probability of CD increases when HLA DR3 and DR7 are present (but their absence cannot exclude the disease. The main etiological factor is gluten and its fractions (B, B1, B2, fraction 9 etc.). It seems that breast feeding can prevent or delay the onset of CD, while the age at gluten introduction does not modify the risk. Pathogenetic mechanisms are still under discussion: 3 theories are under investigation. 1) Enzymatic theory: a proteolytic enzyme for gluten digestion could be lacking. This theory is not yet proven, while Bruce et al. found in the jejunal mucosa of CD patients an elevation of a transglutaminase, which binds the gluten to enterocytes. Its level does not seem to vary with the diet. 2) Lectinic theory: the gluten bind the enterocyte membrane by a lectinic mechanism and damage it.(ABSTRACT TRUNCATED AT 250 WORDS)