In acute GVHD, chemosis, injection, and pseudomembrane should receive much attention by internists and ophthalmologists.
74 Just before the onset of dry eye, pseudomembrane may occur as a result of changes in immunological conditions.
75 Histopathological findings of pseudomembrane show infiltration of macrophages in the necrotic epithelia,
75 which produce a large amount of cytokines, leading to a cytokine storm on the ocular surface. Macrophages release chemokines such as stromal derived factor-1, which attract fibroblast chemotaxis.
76 According to our earlier reports of lacrimal gland biopsy performed for diagnostic purposes, immunocompetent cells—including T cells and macrophages as well as activated and donor-derived fibroblasts expressing HLA class II and co-stimulatory molecules—interact with T cell infiltrates in pathogenic areas and myxedematous fibrotic areas already exist in the early phases of dry eye (
Fig.).
77,78 Conjunctival fibrosis including fibrovascular tissue, symblepharon, and fornix shortening, all characteristic features of cGVHD-related dry eye.
74,79–81 Other features of ocular surface fibrosis include limbal stem cell deficiency, neovasculization, conjunctivalization, and spontaneous punctal occlusion.
79,80,82,83 The onset of dry eye disease is approximately 6 to 18 months after HSCT.
73,84 Risk factors of dry eye include recipients who are older, higher amounts of CD34
+ cells infused,
85 and female-to-male transplantation.
86,87 Dry eye is the most severe after peripheral blood stem cell transplantation in bone marrow, followed by bone marrow and cord blood transplantation.
88 Glaucoma, cataract, infection, and corneal perforation should be prevented as side effects that occur after topical or systemic corticosteroid administration for preventing or treating GVHD.
89