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      Crystalline deposition in the cornea and conjunctiva secondary to long-term clofazimine therapy in a leprosy patient

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          Abstract

          Dear Editor, The continuous introduction of new systemic medications and dosing changes in current drug regimens has resulted in ever-increasing reports of ocular toxicities.[1] We report an unusual side-effect of long term therapy with clofazimine, which caused numerous polychromatic crystalline deposits within the cornea and conjunctiva in a leprosy patient. A 30-year-old woman, case of lepromatous leprosy with recurrent type II lepra reaction, on tablet clofazimine 100 mg/ day was referred to us from dermatology clinic for brownish discoloration of conjunctiva. She was diagnosed as a case of lepromatous leprosy three years ago and started on multi drug therapy-multi bacillary (MDT-MB), which included clofazimine 50 mg/day and 300mg/ month as pulse dose. She was not on any other medication. After three months of treatment, she developed type II lepra reaction and was treated with clofazimine and corticosteroids. The dose of clofazimine was 300 mg/day for two months, which was tapered over the next three months. Over the next two years, she developed two more episodes of type II lepra reaction for which she had again received reactional doses of clofazimine. Estimated cumulative dose of clofazimine was 891.0 gm. Her best corrected visual acuity was 20/50 in both eyes. On slit lamp examination, brownish-red discoloration of peripheral cornea and conjunctiva in inter-palpebral region was noted [Fig. 1]. There were multiple polychromatic crystalline deposits scattered diffusely over peripheral cornea and conjunctiva of both eyes [Figs. 2 and 3]. The lens had Grade 2 nuclear sclerosis in both eyes but no similar deposits. Fundoscopy was normal in both eyes. She also had reddish-brown discoloration of skin. Clofazimine therapy was stopped after two months as treatment of type II lepra reaction was completed. On follow-up after 6 months of discontinuing clofazimine, best corrected visual activity was 20/50 in both eyes and the conjunctival and corneal crystalline deposits had decreased along with conjunctival discoloration [Fig. 4]. The absence of any other known cause of crystalline corneal deposits confirmed long-term clofazimine therapy as a cause of crystalline deposition in the cornea and conjunctiva. Figure 1 Brownish-red discoloration of peripheral cornea and conjunctiva Figure 2 Polychromatic crystalline deposits over conjunctiva () represents crystalline deposits Figure 3 Polychromatic crystalline deposits over cornea. () represents crystalline deposits Figure 4 Follow-up at 6 months Corneal stromal deposition may develop from a number of medications such as clofazimine, gold, immunoglobulins, indomethacin, phenothiazines, retinoids, sparfloxacin, and silver. The deposits of drugs and drug metabolites within corneal stroma may be predominantly pigmented, crystalline, or refractile.[1] Crystalline deposits in cornea are reported following exogenous immunoglobulin therapy and the crystals appear in mid periphery in annular fashion.[2] Gokhale observed multiple refractile crystalline deposits in the corneal stroma following prolonged topical sparfloxacin therapy.[3] Corneal and conjunctival changes have been reported previously in association with clofazimine therapy. Kaur et al., observed conjunctival pigmentation in 46% and corneal pigmentation in 53% patients treated with clofazimine for 6–24 months.[4] Our patient had polychromatic crystalline deposits along with brownish-red discoloration in bulbar conjunctiva and peripheral cornea, which did not affect the vision. Careful literature search revealed that only one such case is reported by Font et al.,[5] having estimated cumulative dose of clofazimine of 219 gm as compared to 891 gm in our patient In the case reported by Font et al., ultrastructural study of conjunctival biopsy demonstrated that many of fibroblasts and macrophages contained rectangular or rhomboidal empty spaces corresponding to crystals, which ranged from 1.5 to 7 μm in length.[5] In greater than 1% of patients on clofazimine therapy diminished vision and ocular dryness, burning, itching, and irritation have been reported, which were absent in our case. Craythorn et al.,[6] reported macular pigmentary abnormalities but in our patient macula was normal. Further studies of clofazimine-treated patients are necessary in order to determine the frequency and spectrum of corneal and conjunctival abnormalities associated with the drug. It is suggested that patients being treated with clofazimine should undergo periodic ophthalmic examination. Clofazimine-induced crystalline keratopathy should be included in the differential diagnosis of crystalline deposits of cornea and conjunctiva.

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          Most cited references 6

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          Drug-induced corneal complications.

          To review the common corneal manifestations of systemic medications in order to describe the characteristic clinical features associated with particular systemic drugs, the indications for drug cessation, and the risks for irreversible ocular toxicity. Systemic medications may reach the cornea via the tear film, aqueous humor, and limbal vasculature. The corneal changes are often the result of the underlying chemical properties of medications. Amphiphilic medications (amiodarone, chloroquine, suramin, clofazimine, etc.) may produce a drug-induced lipidosis and development of a vortex keratopathy. Antimetabolites (cytarabine) may lead to a degeneration of basal epithelial cells with formation of epithelial microcysts. Additionally, systemically administered medications and drug metabolites may lead to a stromal or endothelial deposition. Corneal changes may result in reduced visual acuity, photophobia, and ocular irritation, though these symptoms typically resolve following drug cessation. Corneal manifestations of systemic medications are often dose related, and may reflect the potential risk for lenticular or retinal changes. Corneal changes secondary to systemic medications may affect all layers of the cornea. While corneal deposition is typically not an indication for drug cessation, patients receiving particular medications should be monitored for symptoms related to corneal deposition as well as for signs of irreversible ocular toxicity.
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            Polychromatic corneal and conjunctival crystals secondary to clofazimine therapy in a leper.

            A 67-year-old man had a diagnosis of dapsone-resistant lepromatous leprosy. He received clofazimine (Lamprene) at a dosage of 100 mg twice daily. After 3 years of therapy, results of slit-lamp examination disclosed myriad polychromatic crystals diffusely involving the cornea and perilimbal conjunctiva of both eyes. Thick sections (1 micron) from a conjunctival biopsy showed numerous rectangular-to-rhomboidal crystals within stromal fibroblasts and macrophages. By electron microscopy, these cells contained elongated, membrane-bound, cleft-like spaces that corresponded to the sites where crystals had been present previously. Additionally, complex lipid inclusions were observed in mesenchymal cells as well as in endothelial cells and pericytes of blood vessels. The ocular side effects of clofazimine therapy are reviewed. Clofazimine-induced keratopathy should be included in the differential diagnosis of patients with polychromatic crystalline deposits in the corneas. To the best of the authors' knowledge, this complication of clofazimine therapy has not been described previously.
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              Clofazimine-induced bull's-eye retinopathy.

              Bull's-eye retinopathy has multiple associations. We report a case of bull's-eye retinopathy presumed to be secondary to clofazimine (Lamprene) treatment of a 30-year-old patient with acquired immunodeficiency syndrome (AIDS). Pretreatment baseline eye exam of this patient was normal except for bilateral cotton-wool spots. However, follow-up exam 5 months later revealed bilateral anterior pigmentary corneal deposits in a whorl pattern, a presumed infectious retinitis in the left eye, and bilateral annular macular pigmentary abnormalities. The patient was taken off clofazimine treatment, but died 1 month later. The authors suggest that patients being treated with clofazimine be examined for drug-related corneal and retinal lesions.
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                Author and article information

                Journal
                Indian J Ophthalmol
                IJO
                Indian Journal of Ophthalmology
                Medknow Publications (India )
                0301-4738
                1998-3689
                Jul-Aug 2011
                : 59
                : 4
                : 328-329
                Affiliations
                Department of Ophthalmology, Rajiv Gandhi Medical College and C. S. M. Hospital, Thane, Maharashtra, India
                [1 ]Department of Dermatology, Rajiv Gandhi Medical College and C. S. M. Hospital, Thane, Maharashtra, India
                Author notes
                Correspondence to: Dr. Rakesh K. Barot. 12, Jyotinagar CHS., Four Bungalows, Near RTO, Andheri (West), Mumbai – 400 053, Maharashtra, India. E-mail: rakesh_barot23@ 123456yahoo.com
                Article
                IJO-59-328
                10.4103/0301-4738.82012
                3129769
                21666328
                © Indian Journal of Ophthalmology

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Ophthalmology & Optometry

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