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References Case Reports inflammatory disorders including sickle cell retinopathy, References Eales' disease, Beh�et' s disease, diabetes, talc 1. Jampol LM, Ebroon DA, Goldbaum MH. Peripheral retinopathy, retinopathy of prematurity, dominant proliferative retinopathies: an update on angiogenesis, exudative vitreoretinopathy and, occasionally, retinal etiologies and management. Surv OphthalmoI1994;38:519-40. detachment. However, the above diagnoses were felt to 2. Greven eM, Weaver RG, Owen J, Slusher MM. Protein S be unlikely. Caucasian race and normal haemoglobin deficiency and bilateral branch retinal artery occlusion. Ophthalmology 1991;98:33-4. electrophoresis excluded sickle cell retinopathy; 3. Bonnet M. Peripheral neovascularisation complicating unilateral findings and absence of evidence for drug rhegmatogenous retinal detachments of long duration. abuse argued against talc retinopathy; unilateral Graefes Arch Clin Exp OphthalmoI1987;225:59�2. findings, an absent family history and a normal birth 4. Elner SG, Elner VM, Diaz-Rohena R, Freeman H, Tolentino PI, weight made retinopathy of prematurity and familial Albert DM. Anterior proliferative vitreoretinopathy: clinicopathologic, light microscopic, and ultrastructural exudative vitreoretinopathy unlikely; and normal blood findings. Ophthalmology 1988;95:1349-57. sugar, blood pressure and digital 5. Wiedemann P. Growth factors in retinal diseases: proliferative ophthalmodynamometry did not support other possible vitreoretinopathy, proliferative diabetic retinopathy, and causes of peripheral neovascularisation. retinal degeneration. Surv Ophthalmol 1992;36:373--84. There was no evidence to suggest that systemic RD. Bourke vascular or coagulation abnormalities played a role in the R.J. Cooling development of retinal neovascularisation, and the only Vitreoretinal Service abnormal finding was a slightly raised protein S level. Moorfields Eye Hospital London, UK This is unlikely to be significant, because, although low protein S levels can be associated with retinal vascular J.P. Bolger thrombosis,2 there is no reported association between Lister Hospital Stevenage thrombosis and high protein S. Herts, UK We may be witnessing the development of an inflammatory disorder such as Eales' disease. However, R.D. Bourke � Royal Brisbane Hospital the combination of lack of progression during 3 years of Herston Road observation, absence of bilateral findings and lack of Brisbane 4029 inflarilmatory signs such as vitreous cells or retinal Australia vascular sheathing, is very atypical. Fax: (07) 3253 5433 The unilateral development of retinal neovascularisation within 3 months of a penetrating ocular injury raises the possibility that trauma played an Sir, aetiological role. To the best of our knowledge this Allergic contact dermatitis reactions to corticosteroids development has not previously been reported, although in periorbital inflammation and conjunctivitis it is not unprecedented for retinal neovascularisation to Delayed hypersensitivity to corticosteroids in topical develop in extensive retinal detachment and proliferative preparations is increasingly recognised by vitreoretinopathy.3,4 Indeed, it is surprising that dermatologists as a cause of contact dermatitis. neovascularisation is not more commonly encountered in Allergic contact dermatitis is diagnosed by patch proliferative vitreoretinopathy (PVR) associated with testing, an investigative tool first described in 18961 and penetrating ocular trauma, given the presence of similar today performed according to a standard protoco1.2 In growth factors in ocular neovascularisation and PVR.5 It our department more than 1000 patients are patch tested is possible that the inflammatory and wound healing annually. We have found that nearly 6% of patients have response, in combination with vitreous traction at the a relevant, allergic reaction to topical corticosteroids,3 impact site in this case, influenced the balance of most commonly tixocortol-21-pivalate (a marker of angiogenic factors in favour of neovascularisation in this hydrocortisone allergy4), hydrocortisone butyrate or eye. In addition, 3600 retinal traction from the posterior budesonide. vitreous insertion may have contributed to retinal Over a period of 18 months we have investigated 40 ischaemia, although, conversely, vitreous traction may patients with persistent periorbital inflammation. In 3 of have resulted from retinal ischaemia inducing a these patch tests to corticosteroid preparations were fibrovascular response. positive and subsequent avoidance has been associated The unexpected development of unilateral peripheral with resolution. retinal neovascularisation following posterior segment penetration emphasises the need for peripheral retinal Case reports examination in the follow-up of such patients. The exact pathogenesis of unilateral peripheral retinal Case 1 A 52-year-old man with no previous history of neovascularisation in this case remains debatable. skin disease presented a I-month history of painful red However, the chronological sequence and the absence of eye secondary to trauma. A diagnosis of conjunctivitis an identifiable cause despite exhaustive investigations was made and when this failed to respond to either and prolonged follow-up implicate a stimulatory role for chloramphenicol or Fucidin (Leo) drops from his general posterior penetrating ocular trauma. practitioner, he was referred to an ophthalmologiSt. 148 Prednisolone plus neomycin drops were prescribed and Discussion after initial benefit these were associated with marked Allergic contact dermatitis must be considered in those periorbital oedema and inflammation. When these signs patients with periorbital inflammation who fail to persisted and betamethasone valerate drops (0.1%) were improve or deteriorate following treatment. Both the ineffective, contact allergy was suspected and the patient active ingredients and the excipients of topical was referred for patch testing. This revealed delayed medicaments can produce delayed hypersensitivity hypersensitivity to betamethasone valerate and reactions. Patch testing should be undertaken to neomycin (Table 1). Avoidance of these medicaments investigate all relevant, potential allergens including the and the use of topical clobetasone butyrate 0.05% twice components of any ophthalmological or dermatological corticosteroid preparations used by the patient. daily to eyelid skin was associated with rapid recovery. In our first case there was no record of previous corticosteroid use and we believe the patient was Case 2 A 52-year-old woman who had suffered eczema sensitised through contact with eye drops containing as a child and had a contact allergy to perfume betamethasone valerate and neomycin prescribed for demonstrated 7 years previously, presented with a 2 year conjunctivitis. In cases 2 and 3 the persisting history of periorbital eczema and allergic conjunctivitis inflammation was predominantly in the eyelid skin. It is despite fragrance avoidance. This failed to respond to probable that the corticosteroid sensitisation resulted hydrocortisone 0.1% ointment. She had developed a mild from hand-eye transfer of the preparations used for hand eczematous eruption on the hands 3 years previously for dermatitis.5 which she had also used hydrocortisone 0.1% ointment. Patch testing uncovered relevant contact sensitivities allowing us to give avoidance advice which resulted in Patch testing confirmed fragrance allergy and complete resolution of the periorbital problems in all 3 demonstrated allergy to hydrocortisone (Table 1), patients. We feel that ophthalmologists should be aware subsequent avoidance of which has been associated with of the potential for allergy to corticosteroids and the resolution of the eye problem. effectiveness of patch testing in differentiating sensitivities. Delayed hypersensitivity thus Case 3 A 43-year-old woman with 13 years of persistent demonstrated may have important implications for hand eczema tr�ated variously with either subsequent systemic steroid therapy. Systemic hydrocortisone 0.1%, hydrocortisone butyrate 0.1%, hydrocortisone has been shown to induce cutaneous clobetasol 0.05% or alclometasone 0.05%, gave a 6-month reactions at the site of allergic contact dermatitis6 as well history of periorbital inflammation and oedema which as more generalised erythema? had led her to discontinue the use of soft contact lenses. We thank Mr B. Leatherbarrow, consultant ophthalmologist, and This eruption was exacerbated by topical hydrocortisone Dr N. Telfer, consultant dermatological surgeon. and patch testing demonstrated allergy to hydrocortisone and hydrocortisone butyrate (Table 1). References Relevant positive hypersensitivity reactions were noted 1. Jadasshon J. Zur Kenntnis der Arsneiexantheme. Arch to the constituents of eye medicaments in 18 of the Dermatol Forsch 1896;34:103. 2. Pirila V. Chamber test versus patch test for epicutaneous remaining 37 patients. These were to anti-microbials in testing. Contact Dermatitis 1985;1:48-52. 10 patients (aminoglycosides, chloramphenicol, 3. Boffa MJ, Wilkinson SM, Beck MH. Screening for polymixin B and sodium fusidate), preservatives in 7 corticosteroid hypersensitivity. Contact Dermatitis 1996;33:149-51. patients (phenylmercuric acetate and thiomersal) and 4. Wilkinson SM, English JSc. Hydrocortisone sensitivity: a antiseptics in 4 patients (chlorhexidine digluconate and prospective study into the value of tixocortol-21-pivalate and benzalkonium chloride). No contact sensitivity to
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