A Case of Disseminated Superficial Actinic Porokeratosis Successfully Treated With Topical Lovastatin/Cholesterol Gel

Abstract

Disseminated superficial actinic porokeratosis (DSAP) is a disorder of abnormal keratinization for which there is no standard treatment. Treatment modalities that have traditionally been utilized with varying success include ablative therapies, topical pharmacologic treatments, surgical excision, and retinoids. The underlying pathophysiology of DSAP is secondary to genetic mutations in the mevalonate biosynthesis pathway, and thus topical lovastatin/cholesterol presents a promising treatment modality for this condition. We present a case of familial DSAP successfully treated with topical lovastatin/cholesterol gel and provide a brief review of the existing literature surrounding this novel therapy.

Keywords: disseminated superficial actinic porokeratosis; dsap; mevalonate; porokeratosis; topical cholesterol; topical lovastatin.

Figure 1. A. White arrows indicate DSAP lesions on the left forearm before treatment. B. White circles highlight areas of lesion resolution on the left forearm after two months of treatment.

DSAP: disseminated superficial actinic porokeratosis.

Figure 2. A. White arrows indicate DSAP lesions on the right forearm before treatment. B. White circles highlight areas of lesion resolution on the right forearm after two months of treatment.

DSAP: disseminated superficial actinic porokeratosis.

Figure 3. Flowchart depicting cholesterol biosynthesis pathway. The site of action of lovastatin is depicted in red. Genes implicated in DSAP pathogenesis are italicized.

Acetyl-CoA: acetyl-coenzyme A; acetoacetyl-CoA: acetoacetyl-coenzyme A; HMG-CoA: β-hydroxy β-methylglutaryl-coenzyme A; MVK: mevalonate kinase; PVMK: phosphomevalonate kinase; MVD: mevalonate diphosphate decarboxylase; Geranyl-PP: geranyl pyrophosphate; DSAP: disseminated superficial actinic porokeratosis.