Postgraduate Medical Journal | 2021

‘Black eyelid’

 
 

Abstract


© Author(s) (or their employer(s)) 2021. No commercial reuse. See rights and permissions. Published by BMJ. A 22yearold woman presented with blackish discolouration over the left upper eyelid for the past 6 weeks. Initially, the lesions presented as reddish discolouration of the left upper eyelid and later developed into a hyperpigmented macule. She presented to the dermatology out patient department because of increase in size and burning sensation for the past 3 days. A day prior to the onset of the lesion, she had been prescribed oral cotrimoxazole for the treatment of an upper respiratory tract infection by a general physician. She had history of similar lesions occurring over the same site previously on taking cotrimoxazole. On examination, a welldefined hyperpigmented macule was found to involve the entire left upper eyelid region (figure 1). Her ophthalmological examination was within normal limits. Based on the history and the clinical findings, a diagnosis of fixed drug eruption (FDE) to cotrimoxazole confining to the eyelid region was made. FDE is a unique variant of cutaneous drug reaction. The striking feature of FDE is that lesions recur at the exact same site in the skin and mucous membranes on repeated administration of the culprit drug. On discontinuation of the drug, the lesions subside leaving behind a residual hyperpigmentation. The common drugs implicated in causing FDE are cotrimoxazole, nonsteroidal antiinflammatory drugs, tetracyclines, ciprofloxacin, paracetamol, penicillins, metronidazole, sulfasalazine, omeprazole, antiepileptics like barbiturates and carbamazepine. The most common drug causing FDE is cotrimoxazole. Genitalia are the most common site affected by cotrimoxazole. FDE occurs due to delayed type IV hypersensitivity reaction. Cytotoxic CD8+T cells play a major role in pathogenesis by causing epidermal damage in both old inactive and new active lesions of FDE. On exposure to the drug, there is increased expression of ICAM-1 in the keratinocytes of the affected site. This ICAM-1 expression triggers CD8+T cytotoxic cells to produce Interferon-γ that leads to inflammation at the site of reaction. Differential diagnosis for black eyelids include FDE, discoid lupus erythematosus, cutaneous anthrax of eyelids, loxoscelism of eyelids, allergic contact dermatitis of eyelids, mercurial discolouration of eyelids and raccoon eyes. In our case, the patient was advised not use cotrimoxazole again. She was prescribed mild potency topical steroid for the eyelids. Furthermore, the patient was clearly instructed to strictly avoid usage of cotrimoxazole in the future and was provided with a drug card indicating her drug allergy. After the symptoms, subsided aesthetic appearances were of prime consideration. Hence cosmetic camouflage was advised. In our patient, the eyelid was a rare site to be involved by FDE.

Volume None
Pages None
DOI 10.1136/postgradmedj-2020-139109
Language English
Journal Postgraduate Medical Journal

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