Abstract
PurposeTo describe and analyze the microstructural changes in herpetic stromal keratitis (HSK) observed in vivo by spectral-domain ocular coherence tomography (SD-OCT) at different stages of the disease.MethodsA prospective, cross-sectional, observational, and comparative SD-OCT analysis of corneas with active and inactive keratitis was performed, and the pathologic differences between the necrotizing and non-necrotizing forms of the disease were analyzed.ResultsFifty-three corneas belonging to 43 (81.1%) women and 10 (18.8%) men with a mean age of 41.0 years were included for analysis. Twenty-four (45.3%) eyes had active keratitis, and 29 (54.7%) had inactive keratitis; the majority (83.0%) had the non-necrotizing form. Most corneas (79.1%) with active keratitis showed stromal edema and inflammatory infiltrates. Almost half of the active lesions affected the visual axis, were found at mid-stromal depth, and had a medium density. By contrast, corneas with inactive keratitis were characterized by stromal scarring (89.6%), epithelial remodeling (72.4%), and stromal thinning (68.9%). In contrast to non-necrotizing corneas, those with necrotizing HSK showed severe stromal scarring, inflammatory infiltration, and thinning. Additionally, most necrotizing lesions (77.7%) affected the visual axis and had a higher density (P = 0.01).ConclusionActive HSK is characterized by significant epithelial and stromal thickening and the inactive disease manifests epithelial remodeling at sites of stromal thinning due to scarring. Necrotizing keratitis is characterized by distorted corneal architecture, substantial stromal inflammatory infiltration, and thinning. In vivo SD-OCT analysis permitted a better understanding of the inflammatory and repair mechanisms occurring in this blinding corneal disease.
Highlights
IntroductionMicrostructural Changes in Herpetic Stromal Keratitis; Rodriguez-Garcia et al the stromal form representing almost one-third (29.5%) of all cases.[1, 2] Herpetic stromal keratitis (HSK) accounts for up to 44% of recurrences, and the risk for recurrent infection increases after multiple attacks of keratitis.[3, 4] HSK represents a significant burden of ocular disease, being the most feared presentation of herpetic corneal infection due to its severe damage to the cornea.[5] Most cases of HSK present as non-necrotizing.[6] Non-necrotizing HSK or immune stromal keratitis is characterized by stromal inflammation leading to scarring, thinning, and vascularization of the cornea.[7, 8] The direct viral antigen stimulation of HSV-1-specific CD4αβ T-lymphocytes probably drives stromal inflammation
spectral-domain ocular coherence tomography (SD-OCT) scanning was performed on 53 corneas of patients with unilateral Herpetic stromal keratitis (HSK)
In the inactive keratitis group, 25 (86.2%) corneas belonged to women and only 4 (13.7%) to men with a younger mean age of 39.9 years
Summary
Microstructural Changes in Herpetic Stromal Keratitis; Rodriguez-Garcia et al the stromal form representing almost one-third (29.5%) of all cases.[1, 2] Herpetic stromal keratitis (HSK) accounts for up to 44% of recurrences, and the risk for recurrent infection increases after multiple attacks of keratitis.[3, 4] HSK represents a significant burden of ocular disease, being the most feared presentation of herpetic corneal infection due to its severe damage to the cornea.[5] Most cases of HSK present as non-necrotizing.[6] Non-necrotizing HSK or immune stromal keratitis is characterized by stromal inflammation leading to scarring, thinning, and vascularization of the cornea.[7, 8] The direct viral antigen stimulation of HSV-1-specific CD4αβ T-lymphocytes probably drives stromal inflammation. Other likely pathogenic mechanisms are autoantigens unmasked and mimicked by HSV-1 corneal infection, bystander cytokine activation of CD4αβ T-cells, or a combination of all these mechanisms.[9,10,11] On the other hand, the necrotizing form is characterized by ulcerations, dense leukocytic stromal infiltration, and necrosis that may rapidly progress to corneal perforation.[9, 10] Both viral antigens and replicating virions have been implicated in the pathogenesis of this form of keratitis.[12, 13]
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