{'fraction_non_alphanumeric': 0.01937269372693727, 'fraction_numerical': 0.0013837638376383763, 'mean_word_length': 5.694444444444445, '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}}
Colonic mast cells: a new target in chronic constipation?

SIRS, We have read with interest the recent publication by Bassotti et al. The authors describe a statistically significant increase of colonic mast cell population in severely constipated patients when compared with controls. The authors suggest this finding as a compensation phenomenon for the impaired propulsive activity of these patients. This study is relevant as an approach for chronic constipated patients. Mast cells have been deeply investigated in systemic mastocytosis, and irritable bowel syndrome patients, 4 but only a few studies have been published regarding chronic constipation, and most of them are related to Chagas’ and Hirschsprung’s disease. The pathogenesis of gastrointestinal symptoms in mastocytosis remains unclear; abdominal pain, diarrhoea, peptic disease and malabsorption are the main clinical manifestations in systemic mastocytosis. Recent investigations have shown that histamine induces the neural hypertrophy and increases mast cells in the gastrointestinal tract. Moreover, mast cells have been recognised as a source of nerve growth factor: in Hirschsprung’s disease, mast cells are increased; investigators speculate as a repair phenomenon of the enteral nervous system. 8 Mast cells influence motor and sensory functions of the human gut, through the interaction with other cell types, such as eosinophils, fibroblasts, etc. Microscopic colitis and eosinophilic gastroenteritis are diseases where the immune system might be affected, and mast cells and eosinophils could play an important role. By contrast, degranulation of mast cells may develop an overproduction of prostaglandin D2, an important factor in the pathogenesis of diarrhoea in these patients. Besides, accumulation of mast cell in the bowel villi may generate architectural alterations and consequently, a dysfunction in the gastrointestinal barrier. The clinical consequences of all these changes warrant further investigations. Finally, colonic transit might be impaired due to multiple causes such as systemic, local or neuroendocrine factors, apart from mast cell accumulation in the colon wall.