Thygeson Superficial Punctate Keratitis Clinical Presentation
- Author: Robert S Duszak, OD, FAAO; Chief Editor: Hampton Roy Sr, MD more...
History
Patients with TSPK often report bilateral tearing, burning, photophobia, foreign body sensation, and ocular irritation during exacerbations.
During the inactive stages of the disease, patients may have no complaints.
Physical
TSPK is characterized by a bilateral, recurrent, focal, epithelial keratitis without associated conjunctival or stromal inflammation.[2, 3, 4, 5, 6] The classic corneal lesion in active TSPK is a conglomerate of coarse, oval shaped, slightly raised, whitish gray dots that stain minimally with fluorescein. The lesions tend to accumulate centrally in the cornea, and 1-50 lesions may be present (averaging about 20 lesions per flare-up).[7]
Corneal sensitivity is typically normal or only slightly decreased, but it is never completely absent as in herpes simplex keratitis.[2]
Although a conjunctival response is typically not seen, a minimal reaction by way of conjunctival injection may be noted.[3, 8]
Causes
The exact etiology of TSPK is unclear.
Associations with various viral infections, including the adenovirus, herpes simplex virus, and varicella zoster virus, have been made.[9, 10] In 1953, Braley and Alexander provided questionable results suggesting a virus may be responsible for TSPK, and, in 1974, Lemp et al were able to isolate the varicella zoster virus from a corneal surface, albeit a 10-year-old boy.[9, 10] In more recent studies using polymerase chain reactions, the varicella zoster virus was not detected in eyes with TSPK, providing doubts this virus is the causative agent.[11, 12, 13]
HLA-DR3, an antigen associated with immune response genes and multiple autoimmune disorders, has some association with TSPK as well. It has been proposed that this antigen may alter the immune response of individuals with TSPK, yielding the prolonged course of the disease and its hallmark of exacerbations and remissions.[3]
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