Tryptase in Acute Appendicitis: Unveiling Allergic Connections through Compelling Evidence

Author:

Carvalho Nuno12ORCID,Carolino Elisabete3ORCID,Ferreira Margarida12ORCID,Coelho Hélder4,Santos Catarina Rolo5ORCID,Barreira Ana Lúcia1ORCID,Henriques Susana1,Cardoso Carlos6ORCID,Moita Luís78,Costa Paulo Matos12ORCID

Affiliation:

1. Serviço Cirurgia Geral, Hospital Garcia de Orta, 2805-267 Almada, Portugal

2. Faculdade Medicina, Universidade Lisboa, 1649-028 Lisboa, Portugal

3. H & TRC—Health & Technology Research Centre, ESTeSL—Escola Superior de Tecnologia da Saúde, Instituto Politécnico de Lisboa, 1549-020 Lisboa, Portugal

4. Serviço de Anatomia Patológica, Hospital Garcia de Orta, 2805-267 Almada, Portugal

5. Serviço de Cirurgia Geral, Hospital de Nossa Senhora do Rosário, 2830-003 Barreiro, Portugal

6. Dr. Joaquim Chaves Laboratório de Análises Clínicas, 1495-068 Algés, Portugal

7. Innate Immunity and Inflammation Lab., Instituto Gulbenkian de Ciência Oeiras, 2780-156 Oeiras, Portugal

8. Instituto de Histologia e Biologia do Desenvolvimento, Faculdade Medicina, Universidade Lisboa, 1649-028 Lisboa, Portugal

Abstract

The aetiology of acute appendicitis (AA), the most frequent abdominal surgical emergency, is still unclarified. Recent epidemiologic, clinical and laboratorial data point to an allergic component in the pathophysiology of AA. Mastocytes participate in the Th2 immune response, releasing inflammatory mediators from their granules upon stimulation by IgE-specific antigens. Among the well-known mediators are histamine, serotonin and tryptase, which are responsible for the clinical manifestations of allergies. We conducted a prospective single-centre study to measure histamine and serotonin (commercial ELISA kit) and tryptase (ImmunoCAP System) concentrations in appendicular lavage fluid (ALF) and serum. Consecutive patients presenting to the emergency department with a clinical diagnosis of AA were enrolled: 22 patients with phlegmonous AA and 24 with gangrenous AA The control group was composed of 14 patients referred for colectomy for colon malignancy. Appendectomy was performed during colectomy. Tryptase levels were strikingly different between histological groups, both in ALF and serum (p < 0.001); ALF levels were higher than serum levels. Tryptase concentrations in ALF were 109 times higher in phlegmonous AA (APA) (796.8 (194.1–980.5) pg/mL) and 114 times higher in gangrenous AA (AGA) (837.4 (272.6–1075.1) pg/mL) than in the control group (7.3 (4.5–10.3) pg/mL. For the diagnosis of AA, the discriminative power of serum tryptase concentration was good (AUC = 0.825), but discriminative power was weak (AUC = 0.559) for the differential diagnosis between APA and AGA. Mastocytes are involved in AA during clinical presentations of both phlegmonous and gangrenous appendicitis, and no significant differences in concentration were found. No differences were found in serum and ALF concentrations of histamine and serotonin between histological groups. Due to their short half-lives, these might have elapsed by the time the samples were collected. In future research, these determinations should be made immediately after appendectomy. Our findings confirm the hypersensitivity type I reaction as an event occurring in the pathogenesis of AA: tryptase levels in ALF and serum were higher among patients with AA when compared to the control group, which is in line with a Th2 immune response and supports the concept of the presence of an allergic reaction in the pathogenesis of acute appendicitis. Our results, if confirmed, may have clinical implications for the treatment of AA.

Funder

Joaquim Chaves Lab

Publisher

MDPI AG

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