Soyfoo Muhammad, Motulsky Elie, Sarrand Julie
Department of Rheumatology, Hôpital Universitaire de Bruxelles (HUB), 1070 Bruxelles, Belgium.
Department of Ophthalmology, Hôpital Universitaire de Bruxelles (HUB), 1070 Bruxelles, Belgium.
Int J Mol Sci. 2025 Sep 10;26(18):8824. doi: 10.3390/ijms26188824.
Keratoconjunctivitis sicca (KCS), also commonly known as dry eye disease (DED), is one of the most prevalent and crippling features of Sjögren disease (SD), a chronic systemic autoimmune disorder featuring lymphocytic infiltration and progressive impairment of exocrine glands. KCS affects up to 95% of patients with SD and is often the earliest and most persistent manifestation, significantly compromising visual function, ocular comfort, and overall quality of life. Beyond the ocular surface, KCS mirrors a wider spectrum of immune dysregulation and epithelial damage characteristic of the disease, making it a valuable window into the underlying systemic pathology. The pathophysiology of KCS in SD is complex and multifactorial, involving an interplay between autoimmune-mediated lacrimal gland dysfunction, neuroimmune interactions, ocular surface inflammation, and epithelial instability. Tear film instability and epithelial injury result from the aberrant activation of innate and adaptive immunity, involving T and B lymphocytes, pro-inflammatory cytokines, and type I interferon pathways. Despite the clinical significance of KCS, its diagnosis remains challenging, with frequent discrepancies between subjective symptoms and objective findings. Traditional diagnostic tools often lack sensitivity and specificity, prompting the development of novel imaging techniques, tear film biomarkers, and standardized scoring systems. Concurrently, therapeutic strategies have evolved from palliative approaches to immunomodulatory and regenerative treatments, aiming to restore immune homeostasis and epithelial integrity. This review provides a comprehensive update on the pathogenesis, diagnostic landscape, and emerging treatments of KCS in the context of SD.
干燥性角结膜炎(KCS),通常也被称为干眼病(DED),是干燥综合征(SD)最常见且严重的特征之一。干燥综合征是一种慢性全身性自身免疫性疾病,其特点是淋巴细胞浸润和外分泌腺的进行性损害。KCS影响高达95%的干燥综合征患者,且往往是最早出现且最为持久的表现,严重损害视觉功能、眼部舒适度和整体生活质量。除眼表外,KCS反映了该疾病更广泛的免疫失调和上皮损伤特征,使其成为了解潜在全身病理的重要窗口。干燥综合征中KCS的病理生理学复杂且多因素,涉及自身免疫介导的泪腺功能障碍、神经免疫相互作用、眼表炎症和上皮不稳定之间的相互作用。泪膜不稳定和上皮损伤是由先天性和适应性免疫的异常激活导致的,涉及T和B淋巴细胞、促炎细胞因子和I型干扰素途径。尽管KCS具有临床重要性,但其诊断仍然具有挑战性,主观症状和客观检查结果之间常常存在差异。传统诊断工具往往缺乏敏感性和特异性,这促使了新型成像技术、泪膜生物标志物和标准化评分系统的发展。与此同时,治疗策略已从姑息性方法发展为免疫调节和再生治疗,旨在恢复免疫稳态和上皮完整性。本综述全面更新了干燥综合征背景下KCS的发病机制、诊断现状和新兴治疗方法。