Peripheral ulcerative keratitis (PUK) as initial manifestation in a patient with asymptomatic human immunodeficiency virus (HIV) infection is rarely reported. Herein, we describe HIV vasculitis presenting as PUK in an otherwise healthy HIV-infected patient.
A 40-year-old married female presented with right eye redness, blurring of vision and pain since 1 month with no history of trauma, discharge, watering or contact lens wear without any complaints in left eye and no significant systemic history. The best corrected visual acuity was 20/40 and 20/20 in the right and left eyes, respectively. On slit lamp examination, the right eye showed a crescentic lesion involving the nasal corneal margin from 1 to 5 o′clock in the clockwise direction with associated stromal thinning; conjunctival involvement in the form of nodular lesion with dilated tortuous vessels and underlying scleral thinning [Fig. 1]. Ocular adnexa, corneal sensations and dilated fundus examination of both eyes were normal.
With an impression of PUK, the patient was advised the following investigations: erythrocyte sedimentation rate (ESR), rheumatoid arthritis factor, antineutophil cytoplasmic antibody, Venereal Disease Research Laboratory test, counselled enzyme-linked immunoassay (ELISA) for HIV, X-ray chest, Mantoux test and rheumatologist opinion. Corneal scraping was subjected to Gram and Giemsa stains, KOH mount and culture and sensitivity, and was reported to be negative.
Rheumatology opinion showed no clinical evidence of collagen vascular disorder. All blood investigations, Mantoux test (4 mm induration), ESR (15 mm) and X-ray chest were normal. ELISA for HIV was reported to be positive. The patient was started on lubricant drop and referred to the HIV clinic. CD4 counts (110 cells/cu mm) and viral load by polymerase chain reaction (PCR) (163,960 copies/mL) were done and the patient was started on anti-retroviral therapy (ART) – (zidovudine 300 mg BD, lamivudine 150 mg BD and efavirenz 600 mg OD). Impression cytology of the lesion showed inflammatory cells (neutrophils and lymphocytes) suggesting an active disease process. Scraping was repeated and PCR done for herpes simplex virus 1 and 2 and herpes zoster virus, and was negative. The lesion that initially showed worsening after starting ART (immune recovery response) showed almost complete resolution over the next 2 months, with minimal residual subconjunctival scarring [Fig. 2].
PUK with central retinal vein occlusion and PUK secondary to ocular surface infection with herpes zoster virus have been previously reported in the literature as presenting feature of HIV infection. Our patient had no history of chicken pox, no evidence of herpes zoster or any systemic condition known to be associated with PUK in HIV infection. Vasculities in HIV infection is an uncommon but important pathogenic factor that might manifest as organ-based disease process. HIV vasculopathy is an indirect effect of HIV infection via the immune complex-mediated mechanism or direct infection of vascular/perivascular tissue. Negative serological and microbiological tests, simultaneous involvement of cornea, conjunctiva and sclera, acute inflammatory cells on impression cytology, a high viral load with low CD4 counts and excellent resolution with ART led us to suspect HIV vasculopathy as a possible pathogenesis in our patient. Further research will help us determine the exact pathogenesis in these types of cases.
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