More research needed to better discern differences in graft-versus-host disease, dry eye
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Key takeaways:
- Both conditions may include reduced tear production, epithelial disruption and meibomian gland dysfunction.
- A better understanding of underlying mechanisms is needed to improve treatment.
Although similarities exist between ocular graft-versus-host disease and dry eye disease, more research is needed to improve diagnostic criteria and treatment, according to a review in Clinical & Experimental Ophthalmology.
“Graft-versus-host disease (GVHD) occurs due to complications of allogeneic hematopoietic stem cell transplant,” Nicole B. Kantor, BS, from Bascom Palmer Eye Institute, and colleagues wrote. “GVHD is the most common cause of non-relapse morbidity in stem cell transplant recipients. Despite this, the pathophysiology of GBHD is incompletely understood.”
In a review comparing ocular GVHD and dry eye disease, researchers assessed similarities and differences in pathophysiology, among other factors, between the two conditions.
According to NIH 2014 criteria, ocular GVHD is defined as new ocular sicca, with severity determined by symptom intensity, artificial tear use and the effect on daily living. In addition, grading of meibomian gland and eyelid abnormalities, tear instability, ocular surface inflammation and anatomic features is used to assess dry eye disease.
A Japanese study examining lacrimal gland histology in Sjögren syndrome-associated dry eye and ocular GVHD subtypes found that both conditions include lacrimal gland inflammation, but the sites of inflammatory cell location are different. Results showed that higher levels of CD4+ T cells were found in glands of dry eye patients, although CD8+ T cells were less common in these patients, and that CD34+ fibroblasts were found in all ocular GVHD specimens but not dry eye glands.
The researchers also reported that the conjunctiva is affected in both ocular GVHD and dry eye cases, involving both inflammatory and fibrotic components. T cells were found in the conjunctiva in both dry eye and ocular GVHD subtypes.
Both conditions also present with alterations to the ocular surface microbiome, though for ocular GVHD it is unclear whether this is a contributor or consequence of the disease.
While the two diseases share similar symptom profiles, the severity and duration of symptoms differs.
“While oGVHD and DED have different underlying causes, both diseases share cellular and soluble inflammatory mediators that enter the lacrimal gland, conjunctiva and cornea and drive disease manifestations,” Kantor and colleagues wrote. “While these cellular and soluble mediators have been explored more thoroughly in DED, there are many gaps in the literature in oGVHD that are pivotal to better understanding targetable pathophysiological mechanisms.”
Perspective
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GVHD is a relatively overlooked cause of severe dry eye signs and symptoms. Patients with this condition have nonlocalized ocular surface disease characteristics that extend beyond the traditional classifications of aqueous, lipid or mucin deficiency. Instead, they show signs of severe desiccation throughout each structure of the anterior segment, and achieving relief from symptoms is a major challenge in treating these patients.
In this review of ocular GVHD and its similarities to dry eye disease (DED), authors described the biological and clinical distinctions between GVHD and DED. It’s important to note that, similar to DED, there is no consensus on a single objective or subjective measure for characterizing ocular GVHD. Ocular GVHD presents with similar pathophysiology and clinical signs relative to moderate to severe DED, including T-cell involvement in inflammation, conjunctival goblet cell reductions, decreased tear volume, tear film instability and meibomian gland dysfunction.
The review article identified some of the hallmark signs of ocular GVHD, which are cicatrizing conjunctivitis or pseudomembrane development, diffuse corneal staining, meibomian gland dysfunction, madarosis, decreased corneal nerve sensitivity and decreased tear production. Patients present with many of the same symptoms such as burning, foreign body sensation and decreased vision, but the presence of hematopoietic stem cell transplant should raise suspicion for GVHD as the etiology of DED. Indeed, the two conditions are interconnected, as GVHD is a specific cause of the general umbrella term “dry eye disease.”
The management of both conditions is targeted towards relieving symptoms to improve patients’ quality of life and minimizing or inhibiting ocular surface inflammation. While short-term topical corticosteroid and long-term treatment with topical cyclosporine is common in DED management, long-term corticosteroids, cyclosporine, tacrolimus or autologous serum tears are more commonly used for ocular GVHD management and have proven effective in improving symptoms and reducing severe ocular inflammation.
Both conditions can be managed with punctal plugs and scleral contact lenses. In our clinic, we have found that these cases are best treated with autologous serum or amniotic membrane; scleral shells are a highly useful tool in offering symptom relief and improving vision. In severe cases, systemic comanagement may be indicated, but for these patients, understanding etiology and developing a treatment plan targeting relief for multiple ocular structures concurrently will often yield the most success.
This helpful review article offers a comprehensive overview of this condition and illustrates the need for greater understanding of this challenging condition.
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Kantor NB, et al. Clin Exp Ophthalmology. 2024;doi:10.1111/ceo.14347.
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