Topical cholesterol/lovastatin for the treatment of porokeratosis: A pathogenesis-directed therapy.


Journal

Journal of the American Academy of Dermatology
ISSN: 1097-6787
Titre abrégé: J Am Acad Dermatol
Pays: United States
ID NLM: 7907132

Informations de publication

Date de publication:
Jan 2020
Historique:
received: 10 06 2019
revised: 13 08 2019
accepted: 20 08 2019
pubmed: 27 8 2019
medline: 1 7 2020
entrez: 27 8 2019
Statut: ppublish

Résumé

Porokeratosis is associated with mevalonate pathway gene mutations. Therapeutic options are few and often limited in efficacy. We hypothesized that topical therapy that aims to replenish cholesterol, an essential mevalonate pathway end-product, and block the accumulation of mevalonate pathway toxic metabolites could alleviate porokeratosis. To study the efficacy of topical cholesterol/lovastatin in different variants of porokeratosis. We enrolled a series of 5 porokeratosis patients,1 with disseminated superficial actinic porokeratosis, 2 with porokeratosis palmaris et plantaris disseminata, and 2 with linear porokeratosis. Patients were genotyped before initiation of therapy. Patients then applied topical cholesterol/lovastatin twice daily to a unilaterally defined treatment area for up to 3 months. The response was evaluated and patients photographed at every visit. Three patients had MVD mutations, and 2 patients had PMVK mutations. Treatment with topical cholesterol/lovastatin (but not cholesterol alone) resulted in near complete clearance of disseminated superficial actinic porokeratosis lesions after 4 weeks of therapy and moderate improvement of porokeratosis palmaris et plantaris disseminata lesions and linear porokeratosis lesions. There were no adverse events. Case series design with a small number of patients. Topical cholesterol/lovastatin is an effective and well-tolerated therapy for porokeratosis that underscores the utility of a pathogenesis-based therapy that replaces deficient end products and prevents accumulation of potentially toxic precursors.

Sections du résumé

BACKGROUND BACKGROUND
Porokeratosis is associated with mevalonate pathway gene mutations. Therapeutic options are few and often limited in efficacy. We hypothesized that topical therapy that aims to replenish cholesterol, an essential mevalonate pathway end-product, and block the accumulation of mevalonate pathway toxic metabolites could alleviate porokeratosis.
OBJECTIVE OBJECTIVE
To study the efficacy of topical cholesterol/lovastatin in different variants of porokeratosis.
METHODS METHODS
We enrolled a series of 5 porokeratosis patients,1 with disseminated superficial actinic porokeratosis, 2 with porokeratosis palmaris et plantaris disseminata, and 2 with linear porokeratosis. Patients were genotyped before initiation of therapy. Patients then applied topical cholesterol/lovastatin twice daily to a unilaterally defined treatment area for up to 3 months. The response was evaluated and patients photographed at every visit.
RESULTS RESULTS
Three patients had MVD mutations, and 2 patients had PMVK mutations. Treatment with topical cholesterol/lovastatin (but not cholesterol alone) resulted in near complete clearance of disseminated superficial actinic porokeratosis lesions after 4 weeks of therapy and moderate improvement of porokeratosis palmaris et plantaris disseminata lesions and linear porokeratosis lesions. There were no adverse events.
LIMITATIONS CONCLUSIONS
Case series design with a small number of patients.
CONCLUSION CONCLUSIONS
Topical cholesterol/lovastatin is an effective and well-tolerated therapy for porokeratosis that underscores the utility of a pathogenesis-based therapy that replaces deficient end products and prevents accumulation of potentially toxic precursors.

Identifiants

pubmed: 31449901
pii: S0190-9622(19)32648-9
doi: 10.1016/j.jaad.2019.08.043
pmc: PMC7039698
mid: NIHMS1558770
pii:
doi:

Substances chimiques

Anticholesteremic Agents 0
Drug Combinations 0
Ointments 0
Cholesterol 97C5T2UQ7J
Lovastatin 9LHU78OQFD
Phosphotransferases (Phosphate Group Acceptor) EC 2.7.4.-
phosphomevalonate kinase EC 2.7.4.2
Carboxy-Lyases EC 4.1.1.-
pyrophosphomevalonate decarboxylase EC 4.1.1.33

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

123-131

Subventions

Organisme : NIAMS NIH HHS
ID : R01 AR071491
Pays : United States
Organisme : NIAMS NIH HHS
ID : T32 AR007016
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007205
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2019. Published by Elsevier Inc.

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Auteurs

Lihi Atzmony (L)

Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut; Department of Genetics, Yale University School of Medicine, New Haven, Connecticut; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Young H Lim (YH)

Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut; Department of Genetics, Yale University School of Medicine, New Haven, Connecticut; Department of Pathology, Yale University School of Medicine, New Haven, Connecticut.

Claire Hamilton (C)

Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut.

Jonathan S Leventhal (JS)

Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut.

Annette Wagner (A)

Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Amy S Paller (AS)

Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Keith A Choate (KA)

Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut; Department of Genetics, Yale University School of Medicine, New Haven, Connecticut; Department of Pathology, Yale University School of Medicine, New Haven, Connecticut. Electronic address: keith.choate@yale.edu.

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Classifications MeSH