Retinal dysfunction and anterior segment deposits in a patient treated with rifabutin

Abstract

ABSTRACT.Purpose: To describe the clinical and electrophysiological findings in a young boy with decreased vision possibly due to retinal damage by rifabutin. Methods: An 8-year-old boy with osteomyelitis was referred due to visual disturbance. During a period of 4 years, the boy was examined six times with electroretinography. Ophthalmological examination included testing of visual acuity, slit-lamp inspection, fundus inspection, fundus photography and kinetic perimetry. Two electrophysiological methods were performed for objective evaluation of retinal function, namely full-field electroretinography and multifocal electroretinography. Results: We found a slightly reduced visual acuity, a slowly increasing amount of yellow-white deposits on the posterior surface of the cornea and on the anterior part of the lens, a normal fundus appearance, and normal visual fields. However, the electroretinogram was abnormal on several occasions during therapy with rifabutin, but returned to normal 3 months after withdrawal of the medication. The multifocal electroretinogram returned to normal after the fullfield electroretinogram had done so. The anterior chamber deposits still remain. Conclusion: Long-term treatment with rifabutin may have a reversible and previously undescribed side-effect on retinal function. The drug may also accumulate irreversibly on the posterior surface of the cornea and on the anterior surface of the lens. We suggest that objective evaluation of retinal function with electrophysiological methods should be performed in patients with visual disturbance during treatment with rifabutin.

Corneal deposits secondary to rifabutin

“…This revealed nine publications with reports of 43 patients with rifabutin‐attributed corneal deposits. To our knowledge, the entirety of the reports in this patient population noted bilateral yellow‐white/yellow‐brown coloured, stellate deposits concentrated predominantly in the peripheral cornea (Table ). Located in the posterior layers of the cornea, they tend to affect the periphery first and later appear centrally.…”

“…Reports have emerged since 1999 of HIV patients presenting with irreversible posterior corneal deposits. Most reports have associated these deposits with long‐term use of rifabutin prescribed for treating or preventing Mycobacterium avium complex (MAC) infections . Conversely, the association of deposits with rifabutin has been refuted by others, showing evidence that similar deposits may present in HIV‐infected patients without known rifabutin use or may present years after discontinuation of rifabutin .…”

Ocular toxicity from systemically administered xenobiotics

“…Moreover, deposition in anterior lens and a reversible retinal dysfunction have been noted. Long-term treatment with rifabutin may also allow the drug to accumulate irreversibly on the posterior surface of the cornea and on the anterior surface of the lens [65,67,68]. Despite many observations, the mechanism underlying the endothelial deposition still remains unclear.…”

Transient Anterior Corneal Deposits in a Human Immunodeficiency Virus-Positive Patient

“…4 In all cases, however, rifabutinassociated corneal deposits were localized to the endothelium, Descemet's membrane, or the posterior stroma, and were present predominantly in the peripheral cornea. Additionally, an increase in density and size of rifabutin-associated corneal deposits over time has been noted by some investigators, 8,9 while others have noted a static behaviour.…”

“…Deposits in these cases have varied in pigmentation from light brown 4 to yellow-brown or golden 4,8,10 to yellow-white, 9 white, 11 or gray-white. 4 In all cases, however, rifabutinassociated corneal deposits were localized to the endothelium, Descemet's membrane, or the posterior stroma, and were present predominantly in the peripheral cornea.…”