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Facial hyperpigmentation caused by diltiazem hydrochloride
Nina Desai1, Andrew F Alexis, Vincent A DeLeo
1Department of Dermatology, St. Luke's-Roosevelt Hospital Center, New York, New York 10025, USA.
Diltiazem hydrochloride, a member of the calcium channel blocker family of antihypertensive medications, has been found to produce many cutaneous reactions, such as photodistributed hyperpigmentation. We report a 53-year-old black woman who presented with facial darkening that began 6 months after starting diltiazem. Areas were not responsive to topical bleaching creams. Biopsy showed postinflammatory pigment alteration with a largely burned-out lichenoid dermatitis. The results of all laboratory evaluations were negative, including complete blood cell count, antinuclear antibodies, anti-Ro antibodies, and anti-La antibodies. Patch testing and photo-patch testing to numerous drugs including diltiazem were negative. Phototesting revealed a normal minimal erythema dose to UVA but a slightly reduced minimal erythema dose to UVB. Diltiazem was then stopped and hydralazine hydrochloride was started. While UVA has been thought to be the main culprit in drug-induced photosensitive reactions, this case demonstrates that UVB may possibly play a role in diltiazem-induced photodistributed hyperpigmentation.
Diltiazem hydrochloride, a member of the calcium channel blocker family of antihypertensive medications, has been found to produce many cutaneous reactions, such as photodistributed hyperpigmentation. We report a 53-year-old black woman who presented with facial darkening that began 6 months after starting diltiazem. Areas were not responsive to topical bleaching creams. Biopsy showed postinflammatory pigment alteration with a largely burned-out lichenoid dermatitis. The results of all laboratory evaluations were negative, including complete blood cell count, antinuclear antibodies, anti-Ro antibodies, and anti-La antibodies. Patch testing and photo-patch testing to numerous drugs including diltiazem were negative. Phototesting revealed a normal minimal erythema dose to UVA but a slightly reduced minimal erythema dose to UVB. Diltiazem was then stopped and hydralazine hydrochloride was started. While UVA has been thought to be the main culprit in drug-induced photosensitive reactions, this case demonstrates that UVB may possibly play a role in diltiazem-induced photodistributed hyperpigmentation.
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