Tear physiology in dry eye associated with chronic GVHD

Abstract

The purpose of this study was to compare tear physiology characteristics of chronic GVHD (cGVHD)-associated dry eye to dry eye caused by Sjogren's syndrome (SS), a extreme form of aqueous-deficient dry eye, and meibomian gland dysfunction (MGD), the major cause of evaporative dry eye. Tear turnover rate, evaporation and osmolarity along with meibomian gland dropout and lipid layer interferometric patterns were assessed in the right eyes of 12 patients with dry eye associated with cGVHD, 12 age-matched patients with SS and 12 age-sex matched subjects with MGD. In cGVHD, the decrease in tear turnover rate was similar (P ¼ 0.33), but the number of non-functioning meibomian glands was significantly higher (Po0.01) than in SS. Tear evaporation rate in cGVHD dry eye was found to be similar to that in MGD (P ¼ 0.36) and significantly higher than in SS (Po0.01). The lipid layer was most unstable in cGVHD compared with other groups. There was no variation in tear volume across all groups. Although statistical significance was not detected, the mean tear osmolarity (333.51± 14.67mOsm/L) was highest in cGVHD. Major aspects of tear physiology were severely impaired in cGVHDassociated dry eye.

Meibomian Gland Dysfunction in Primary and Secondary Sjögren Syndrome

“…Researchers have reported that subjects with SS have decreased meibum expressibility and quality [38], as well as increased meibomian gland dropout [39, 40] and dysfunction [38, 40, 41]. Further, SS patients have a reduced volume [1, 42], stability [39], lipid layer [39], and surface activity [43] of tears, heightened tear film evaporation [44, 45], ocular surface damage [1, 42], and increased DED symptoms [1, 41]. In effect, as indicated by Akpek et al [46], SS patients have combined aqueous and evaporative DED.…”

“…Such conjunctival inflammation may create a toxic environment, leading to the release of proinflammatory cytokines that impact the terminal duct of the meibomian gland and cause other pathophysiological sequelae on the ocular surface. These effects are known to occur in severe atopy [18], Stevens-Johnson syndrome [19-21], and graft-versus-host disease [22, 23], conditions that are sometimes (e.g., graft-versus-host disease) [24-27], but not necessarily, associated with androgen deficiency.…”

Allogeneic Serum Eye Drops for the Treatment of Dry Eye Patients with Chronic Graft-Versus-Host Disease

“…KCS can also cause conjunctival fibrosis, lid abnormality, atrophy of meibomian glands, loss of eyelashes, and stenosis of the lacrimal punctum. [5][6][7] Therapeutic options include artificial tears, therapeutic contact lenses, punctual plugs, topical or systemic corticosteroids, and other immunosuppressive drugs. 3,6 Previous reports have demonstrated that autologous serum eye drops are effective for treating dry eye disease and have also been used for severe ocular disorders, including Sjogren and non-Sjogren syndrome, ocular surface disorders such as cicatricial pemphigoid syndrome, Steven-Johnson syndrome, and superior limbic keratitis.…”

Autologous platelet lysate for treatment of refractory ocular GVHD

“…6 Pathophysiology is complex, and includes fibroblastic and T-lymphocytic infiltrates in the lacrimal gland with consequent deficiency in lacrimal production owing to fibrosis. 7 DES clinical characteristics resemble those found in some autoimmune diseases (for example, Sjö gren's syndrome). 8 Despite many advances in understanding the pathophysiology, there is a paucity of good-quality studies on therapeutic options for this condition.…”