Papel dos Neuropéptidos nas Manifestações Gastrointestinais Associadas à Mastocitose Sistémica e Semelhanças com a Síndrome do Intestino Irritável
DOI:
https://doi.org/10.24950/rspmi.2022.01.301Palavras-chave:
Diarreia, Mastócitos, Mastocitose Sistémica, Neuropéptidos, Péptido Intestinal Vasoativo, Síndrome do Intestino Irritável, Substância P, Trato GastrointestinalResumo
A mastocitose sistémica (MS) é uma neoplasia mieloproliferativa rara caracterizada pela proliferação extracutânea de mastócitos clonais na medula óssea ou em outros sítios extramedulares, com ou sem envolvimento cutâneo. As manifestações gastrointestinais (GI), consistindo em dor abdominal, diarreia e má absorção com vários graus de gravidade, são frequentes em pacientes com MS e podem resultar da infiltração direta do trato GI e/ou da libertação de mediadores produzidos por estas células. A síndrome do intestino irritável (SII) é um distúrbio funcional do intestino caraterizado por dor abdominal crónica e recorrente, desconforto associado à defecação e alterações dos hábitos intestinais. A interação entre o sistema imunológico e os neuropéptidos e a intensificação de uma resposta inflamatória da mucosa com um aumento nas células imunológicas é uma característica chave da SII. Evidências anteriores mostram que há um aumento do número de mastócitos na mucosa intestinal e do cólon de doentes com SII. Os mastócitos estão presentes no tracto GI e sua ativação foi associada a alguns neurotransmissores pró-secretores, como a substância P e o peptídeo intestinal vasoativo, na proximidade de nervos entéricos, sugerindo uma via regulatória bidirecional com controlo da ativação dos mastócitos. A investigação sobre o papel dos mastócitos entéricos na MS e na SII ainda é escassa, bem como sua ligação com os neuropéptidos. Da mesma forma, são necessárias mais evidências sobre a interação entre mastócitos e neuropéptidos para compreender melhor a fisiopatologia das manifestações GI associadas à MS e à SII, e as fronteiras entre estas patologias. Nesta revisão, colocamos a hipótese dos sintomas GI em doentes com MS e em doentes com SII terem mecanismos e mediadores semelhantes, com um foco especial no papel do MC da mucosa e neuropéptidos.
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