Milia are very common, benign, keratin-filled cysts (see the image below).
View Image | Milia in a week-old infant. |
Primary milia are typically seen in infants but also may occur in children and adults. Secondary milia develop after trauma to the skin, such as after burns (eg, sunburns), dermabrasion, or in blistering disorders. Milia en plaque is a rare inflammatory condition characterized by plaques of milia in the periauricular area. Multiple eruptive milia is a condition characterized by the sudden development of crops of milia over the course of weeks to months.
Milia are tiny epidermoid cysts. The cysts may be derived from the pilosebaceous follicle. Primary milia arise on facial skin bearing vellus hair follicles. Secondary milia result from damage to the pilosebaceous unit.
Primary milia in newborns are so common that they can be considered normal (occurring in approximately half of all infants). Multiple eruptive milia and milia en plaque are rare entities.
No racial predilection is recognized for milia.
Sexual prevalence is equal for primary and secondary milia. Eruptive milia and milia en plaque occur more frequently in women.
Milia occur in persons of all ages but are typically found in infants.
Milia seen in infancy tend to spontaneously disappear within the first few weeks of life. Milia in older children and adults tend to persist.
Secondary milia arising from blisters rarely resolve.
Patients or their parents can be taught how to treat milia with a needle (see Treatment).
Milia are asymptomatic. In children and adults, they usually arise around the eye. Eruptive milia, as the name suggests, have a rapid onset, often within a few weeks.
Milia are superficial, uniform, pearly white to yellowish, domed lesions measuring 1-2 mm in diameter.
In milia en plaque, multiple milia arise on an erythematous plaque.[1]
Primary milia, in term infants, occur on the face, especially the nose. They also may be found on the mucosa (Epstein pearls) and palate (Bohn nodules). Primary milia in older children and adults develop on the face, particularly around the eyes.[2] Milia have been observed to occur in a transverse, linear distribution along the nasal groove in some children and around the areolae.[3, 4]
Secondary milia are found anywhere on the body at the sites affected by the predisposing condition.
Eruptive milia occur on the head, neck, and upper body.[5]
Milia en plaque manifests as distinct plaques on the head and neck. Plaques have been described in the postauricular area, unilaterally or bilaterally, the cheeks, the submandibular plaques, and on the pinna.[6, 7] A linear distribution has been described.[8]
Primary milia are believed to arise in sebaceous glands that are not fully developed, explaining the high prevalence in newborn infants. New evidence suggests that milia may originate from the outermost layers of the hair bulge of the outer root sheath.[9]
Secondary lesions arise following blistering or trauma due to disruption of the sweat ducts. Milia have been described in association with many disorders, including bullous pemphigoid, inherited and acquired epidermolysis bullosa, bullous lichen planus, porphyria cutanea tarda, and burns. Skin trauma from dermabrasion or radiotherapy can result in milia formation. Eruptive milia have arisen during vemurafenib treatment[10] and dovitinib treatment.[11]
Secondary milia have arisen after contact dermatitis. They have also arisen following a tattoo,[12] treatment of cutaneous leishmaniasis,[13] and after topical nitrogen mustard ointment for plaque stage mycosis fungoides.[14]
Secondary milia have been described following potent topical corticosteroid use.[15]
Milia are a feature of a number of very rare genodermatoses (eg, Bazex-Dupré-Christol syndrome).[16] Both primary milia and multiple eruptive milia have been reported as familial disorders with autosomal dominant inheritance.[17, 18]
The etiology of milia en plaque is unknown. One case has been induced by sorafenib, a multitargeted kinase inhibitor.[19]
No investigations are needed for simple milia. The clinical appearance is diagnostic. Investigation of the underlying disease is necessary in persons with secondary milia.
Performing a skin biopsy is necessary only if the diagnosis is in doubt. If milia en plaque is suspected, performing a biopsy is prudent to exclude follicular mucinosis and multiple trichoepitheliomata. In an elderly person with sun-damaged skin, Favre-Racouchot syndrome (nodular elastosis of the skin) needs to be excluded.
The histological features are identical to those of epidermoid cysts, but the cysts are much smaller. The milium is usually located in the superficial dermis and has a complete epithelial lining (with a granular cell layer). It contains a variable amount of lamellated keratin. The common primary milia in infants and children are found in the undifferentiated sebaceous hair collar surrounding vellus hair follicles. Milia secondary to blistering are often found in eccrine sweat ducts.
No topical or systemic medications are effective on primary and secondary milia. Single case reports have demonstrated the success of topical tretinoin[20] and oral etretinate,[21] and minocycline in treating patients with milia en plaque.
Milia can be safely left alone, but if the patient requests treatment, then incision with a cutting-edge needle and manual expression of the contents are effective.[22] This can be performed without local anesthetic. A paper clip has been successfully used to express the contents of the cyst.[23]
Milia en plaque has been treated effectively with electrodesiccation, carbon dioxide laser,[24] erbium:YAG laser,[25] dermabrasion,[26] and cryosurgery.[27]