This isn’t directly related to dry eye disease. But many people with DED also have epithelial basement membrane dystrophy (also called map dot fingerprint dystrophy) and in mild phases, it often goes undiagnosed, so I like to highlight it now and then. (If you have a history of waking with sharp eye pain and eye watering, for example, this is something to ask your doctor about.)

This study suggests anti-inflammatory therapy may be appropriate for people with corneal dystrophies.

Distinct ocular surface soluble factor profile in human corneal dystrophies. Shetty R et al, Ocul Surf. 2019 Nov 19.

PURPOSE:
Corneal dystrophies (CD) are classified as rare eye diseases that results in visual impairment and requires corneal transplant in advanced stages. Ocular surface inflammatory status in different types of CD remains underexplored. Hence, we studied the levels of tear soluble factors in the tears of patients with various types of corneal dystrophies.
METHODS:
17 healthy subjects and 30 CD subjects (including epithelial, stromal and endothelial CD) were included in the study. Schirmer's strips were used to collect the tear fluid in all subjects. 27 soluble factors including cytokines, chemokines, soluble cell adhesion molecules and growth factors were measured in the eluted tears by multiplex ELISA or single analyte sandwich ELISA.
RESULTS:
Percentages of subjects with detectable levels of tear soluble factors were significantly higher in CD compared to controls. Significant higher level of IL-2 was observed in both epithelial and stromal CD. IL-4, TGFβ1 and IgE were significantly higher in stromal CD. VCAM, IL-13 and Fractalkine were significantly elevated in epithelial and macular CD. IL-1α, IL-8, IL-12, ANG, Eotaxin, MCP1, RANTES, ICAM1, L-selectin and P-selectin were significantly higher in epithelial CD. TGFBIp was significantly elevated in lattice CD and endothelial CD.
CONCLUSION:
Distinct set of the tear soluble factors were dysregulated in various types of CD. Increase in tear inflammatory factors was observed in majority of the CD subjects depending on their sub-types. This suggests a plausible role of aberrant inflammation in CD pathobiology. Hence, modulating inflammation could be a potential strategy in improving the prognosis of CD.