Review
Milia: A review and classification

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Milia are frequently encountered as a primary or secondary patient concern in pediatric and adult clinics, and in general or surgical dermatology practice. Nevertheless, there are few studies on the origin of milia and, to our knowledge, there is no previous comprehensive review of the subject. We review the various forms of milia, highlighting rare variants including genodermatosis-associated milia, and present an updated classification.

Section snippets

Origin

Few studies have investigated the origin of milia.3, 4, 5, 6 In general, primary milia are thought to originate from the sebaceous collar of vellus hairs (lower infundibulum), whereas secondary milia are believed to derive from eccrine ducts more commonly than from overlying epidermis, hair follicles, or sebaceous ducts.

Epstein and Kligman3 performed serial sectioning of 4 types of milia: primary milia and secondary milia caused by epidermolysis bullosa (EB), dermabrasion, and experimental

Congenital milia

Congenital milia occur in 40% to 50% of newborns, favoring the face (especially the nose), scalp, upper aspect of trunk, and upper extremities, without significant racial or sex difference (Fig 2).7, 8, 9, 10, 11, 12, 13 Congenital milia present with a few or numerous lesions and tend to resolve spontaneously within weeks to several months. Milia may be less common and of delayed onset in premature newborns.12 The main differential diagnosis is sebaceous hyperplasia, which appears as follicular

Genodermatoses with milia

Milia may be a major or minor feature of many genodermatoses (Table II).

Secondary milia

Secondary milia represent a localized form of milia that may be disease associated, medication associated, or caused by trauma. Secondary milia may resolve spontaneously but tend to persist. Postbullous (particularly subepidermal) milia are the classic disease-associated type.147 EB and porphyria cutanea tarda are typical examples. Other diseases reported with secondary milia include bullous pemphigoid, herpes zoster,148 contact dermatitis,149 bullous lupus erythematosus,150 Sweet syndrome,151

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    Funding sources: None.

    Conflicts of interest: None declared.

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