Omdal Roald, Mellgren Svein Ivar, Norheim Katrine Brække
Clinical Immunology Unit, Department of Internal Medicine, Stavanger University Hospital, Stavanger.
Department of Clinical Science, Faculty of Medicine, University of Bergen.
Rheumatology (Oxford). 2021 Jul 1;60(7):3099-3106. doi: 10.1093/rheumatology/kez027.
Chronic fatigue, pain and depression are common in patients with primary Sjögren's syndrome. These phenomena mutually affect each other and have a considerable impact on the patients' quality of life. While pain is usually regarded as a fairly somatic phenomenon, both fatigue and depression have traditionally been regarded as more-or-less of psychological origin. There is an increasing understanding that this picture is multifaceted; that there is a genetic foundation, and that biological mechanisms regulate the clinical expression through activation of evolutionary, deeply conserved neuronal pathways in the brain. This pattern is evident not only in primary Sjögren's syndrome, but also in other systemic inflammatory autoimmune diseases, in cancer and in neurodegenerative diseases like Parkinson's disease. This article will mainly focus on the biology of pain and fatigue. We describe how these factors influence each other, and act with the overarching purpose of defending the organism against harm and danger.
慢性疲劳、疼痛和抑郁在原发性干燥综合征患者中很常见。这些现象相互影响，对患者的生活质量有相当大的影响。虽然疼痛通常被视为一种相当躯体化的现象，但疲劳和抑郁传统上都或多或少被认为源于心理因素。人们越来越认识到这种情况是多方面的；存在遗传基础，并且生物机制通过激活大脑中进化上高度保守的神经元通路来调节临床表型。这种模式不仅在原发性干燥综合征中明显，在其他全身性炎症性自身免疫性疾病、癌症以及帕金森病等神经退行性疾病中也很明显。本文将主要关注疼痛和疲劳的生物学机制。我们描述了这些因素如何相互影响，并以保护机体免受伤害和危险为总体目的发挥作用。
