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Beitragstitel Endothelial decompensation necessitating Descemet's membrane endothelial keratoplasty (DMEK) in a series of patients with Sjögren syndrome
Beitragscode P69
Autor:innen
  1. Algirdas Zabulis Pallas Klinik Olten Präsentierende:r
  2. Christoph Tappeiner Pallas Klinik
  3. David Goldblum Pallas Klinik Olten
Präsentationsform ePoster
Themengebiete
  • External Disease / Cornea
Abstract-Text Purpose: Primary Sjögren syndrome (SS) is a rare autoimmune disorder characterized by chronic lymphocytic infiltration of the exocrine glands, leading to lacrimal gland dysfunction, which in turn leads to dry eye. Although the pathomechanisms causing epithelial damage in dry eye disease associated with SS have been extensively studied, only a few studies have investigated the impact of SS on the corneal endothelium. This case series aimed to shed light on the potential impact of SS on endothelial decompensation.
Methods: This descriptive case series included three female patients with varying degrees of dry eye symptoms due to SS, all of whom had endothelial decompensation requiring treatment with Descemet's membrane endothelial keratoplasty (DMEK). The diagnosis of SS was confirmed using laboratory tests and salivary gland biopsy. Patients underwent evaluations of best-corrected visual acuity (BCVA), slit-lamp microscopy, central corneal thickness (CCT) measurement using spectral domain optical coherence tomography, and endothelial cell count using specular microscopy.
Results: Case 1: A 50-year-old patient presented with mild dryness symptoms and moderate clinical signs of dry eye disease, managed effectively with artificial tears. Before surgery, her BCVA (Snellen decimal) was 0.5, with a CCT of 631 μm. Case 2: 77-year-old patient exhibited moderate dry eye symptoms and signs of moderate superficial punctate keratitis requiring intensive use of artificial tears and ointments. Her preoperative BCVA was 0.25, with a CCT of 576 μm. Case 3: A 72-year-old patient experienced severe dry eye symptoms and had signs including blepharitis, persistent conjunctival hyperemia, massive diffuse superficial punctate keratitis, and corneal filaments. Treatment involved the extensive use of artificial tears, autologous serum, and cyclosporine drops. Preoperatively, the BCVA was 0.1, with a CCT of 779 μm. All three patients had nearly complete loss of endothelial cells, leading to corneal decompensation and swelling, and therefore underwent DMEK treatment. BCVA improved postoperatively (1.0, 0.4, and 0.6, respectively), however had no significant effect on dry eye symptoms, ocular surface signs, or further dry eye treatment.
Conclusions: This case series indicates a potential association between SS and endothelial cell loss. Further studies in larger cohorts are needed to confirm this observation and to clarify the potential pathomechanisms involved.