{'fraction_non_alphanumeric': 0.01937046004842615, 'fraction_numerical': 0.0, 'mean_word_length': 5.312977099236641, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Etiopathogenesis of celiac disease: the attraction and flimsiness of hypotheses].

The pathogenetic mechanisms which induce the intestinal lesions observed in coeliac disease are still unknown. The hypothesis of a primary intestinal peptidase deficiency has not been confirmed. The immunological theory is supported by a large number of findings, but it cannot explain all of the facts. The concept of a surface cell membrane abnormality aims at making up for the previous shortcomings, but it is based on very few unconfirmed data. Although the new pathogenetic theories for auto-immune diseases, and especially coeliac disease, are of considerable interest, experimental confirmation is eagerly awaited. Recently isolated pure toxic gliadin peptides may be of great value to test these new concepts in future research work.