Fatigue in Mastocytosis: A Case Series.
Clin Ther
; 41(4): 625-632, 2019 04.
Article
em En
| MEDLINE
| ID: mdl-30797624
ABSTRACT
PURPOSE:
Accumulating evidence suggests that fatigue in chronic inflammatory diseases is generated in the brain by mechanisms involving proinflammatory cytokines. We recently reported a high prevalence of fatigue in patients with mastocytosis, a condition with a constant activation of mast cells and release of a variety of bioactive substances. This observation indicates that mast cells somehow could be involved in the biological mechanisms that generate fatigue. In this case series, we aim to describe how typical triggering factors of mastocytosis attacks, as reported by patients, are accompanied by increased fatigue. Possible mechanisms by which mast cells may contribute to the pathophysiology of fatigue are discussed.METHODS:
Seven patients with mastocytosis were interviewed regarding triggers and clinical symptoms and signs of mastocytosis, including the presence and severity of fatigue. Fatigue severity during and between attacks was assessed using the fatigue Visual Analog Scale (fVAS).FINDINGS:
The most important reported triggers were heat and/or cold, exercise, food, alcohol, and psychological stress. The median fatigue Visual Analog Scale scores were 80 (range 40-91) during attacks and 40 (range 30-72) between attacks Fatigue reportedly impaired social and recreational activities in all 7 patients, and influenced occupational activities in 6. IMPLICATIONS This case series illustrates that fatigue is common and severe among patients with mastocytosis. Fatigue increases during attacks, which may indicate that mast cell-derived substances are directly involved in the pathophysiology of fatigue. Mast cells could be an underestimated cellular actor in fatigue and other conditions and thus may represent a potential therapeutic target.Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Mastocitose
/
Fadiga
/
Mastócitos
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article