Pigmented Contact Dermatitis Resulting from Self-medication for Postherpetic Neuralgia.

Sir,

Herpes zoster is caused by reactivation of varicella zoster virus in dorsal root ganglia. Reactivation occurs due to decrease in virus-specific cell-mediated immunity resulting from aging or immunosuppression.[1] Complications of herpes zoster can be classified as cutaneous, neurological, or visceral complications. Postherpetic neuralgia (PHN) is defined as persistence of pain more than 30 days after healing of lesions. It is the most common complication of herpes zoster and can be disabling. Approximately 10% of individuals develop PHN and incidence of PHN increases in elderly.[2] Other complications which have been described are encephalitis, myelitis, cranial nerve palsies, pneumonitis, hepatitis, or acute retinal necrosis.[3] Cutaneous complications of herpes zoster can be cutaneous dissemination, superadded bacterial infection, scarring, keloid formation, pigmentary abnormalities, or granuloma annulare. We report an unusual cutaneous complication of herpes zoster which resulted from persistent treatment resistant PHN.

A 64-year-old female with no known comorbidities presented with complaints of dark discoloration of face for last 1 year. She developed herpes zoster ophthalmicus on left side 3 years ago which was followed by corneal ulceration in left eye leading to corneal opacity, and she continued to have persistent pain in left side of face which was stabbing in nature and severe enough to disturb her sleep. She was treated with capsule Pregabalin, Nortriptyline, and Jaipur block with which she had partial relief, she continued to apply counterirritant balm to soothe her pain. She started developing insidious onset gradually progressive darkish discoloration of skin of face for last 1 year. Examination revealed diffuse hyperpigmentation of upper face and reticular pattern of pigmentation in lower face. She also had patchy scarring alopecia and depigmentation on left side of forehead along with corneal opacity in left eye. Rest of dermatological examination was within normal limits. Dermoscopic examination using polarized light showed bluish-gray colored granules of pigment suggestive of the presence of pigment in deep dermis. Histopathological examination revealed basal cell vacuolization, melanophages in superficial and deep dermis, and superficial perivascular infiltrate [Figure 1a-c]. Diagnosis of pigmented contact dermatitis (PCD) was made, the patient was told to stop application of balm, apply tacrolimus ointment twice daily and her pain medicines were optimized for better control of PHN.

Figure 1

(a) Diffuse hyperpigmentation involving forehead and left side of face, corneal opacity, scarring alopecia and depigmentation over left side of forehead. (b) Dermoscopy (Heine Delta 20) – grayish to bluish granules seen in linear pattern (arrow shows granules). (c) Histopathology (H and E, ×40) - Basal vacuolation, melanophages in superficial and deep dermis and superficial perivascular infiltrate (arrow shows melanophages in dermis)

PCD is a noneczematous type of contact dermatitis. It is proposed that low-level persistent contact with chemicals result in cytolytic reaction at basement membrane resulting in pigment incontinence.[4] Patch testing and repeat open application test can be used to identify culprit chemical causing PCD.[5] Histopathology and recently dermoscopy can aid in diagnosis of this entity. Topical calcineurin inhibitors and avoidance of chemicals have been used for management of PCD.

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Conflicts of interest

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