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Milia

MedGen UID:
504701
Concept ID:
CN000991
Finding
 
HPO: HP:0001056

Definition

Presence of multiple small cysts containing keratin (skin protein) and presenting as tiny pearly-white bumps just under the surface of the skin. [from HPO]

Term Hierarchy

Conditions with this feature

Gorlin syndrome
MedGen UID:
2554
Concept ID:
C0004779
Neoplastic Process
Nevoid basal cell carcinoma syndrome (NBCCS) is characterized by the development of multiple jaw keratocysts, frequently beginning in the second decade of life, and/or basal cell carcinomas (BCCs) usually from the third decade onward. Approximately 60% of individuals have a recognizable appearance with macrocephaly, bossing of the forehead, coarse facial features, and facial milia. Most individuals have skeletal anomalies (e.g., bifid ribs, wedge-shaped vertebrae). Ectopic calcification, particularly in the falx, is present in more than 90% of affected individuals by age 20 years. Cardiac and ovarian fibromas occur in approximately 2% and 20% of individuals respectively. Approximately 5% of children with NBCCS develop medulloblastoma (primitive neuroectodermal tumor [PNET]), generally the desmoplastic subtype. Peak incidence is at age two years. Life expectancy in NBCCS is not significantly different from average.
Dystrophic epidermolysis bullosa
MedGen UID:
37179
Concept ID:
C0079294
Disease or Syndrome
Based on the most recent classification system, dystrophic epidermolysis bullosa (DEB) includes three subtypes: Recessive DEB, severe generalized (RDEB-sev gen) (formerly called Hallopeau-Siemens type (RDEB-HS). Recessive DEB, generalized other (RDEB-O) (formerly called non-Hallopeau-Siemens type (RDEB-non-HS). Dominant DEB (DDEB) . In RDEB-sev gen, blisters affecting the whole body may be present in the neonatal period. Oral involvement may lead to mouth blistering, fusion of the tongue to the floor of the mouth, and progressive diminution of the size of the oral cavity. Esophageal erosions can lead to webs and strictures that can cause severe dysphagia. Consequently, severe nutritional deficiency and secondary problems are common. Corneal erosions can lead to scarring and loss of vision. Blistering of the hands and feet followed by scarring fuses the digits into "mitten" hands and feet, a hallmark of this disorder. The lifetime risk of aggressive squamous cell carcinoma is over 90%. In contrast, the blistering in the less severe forms of RDEB-O may be localized to hands, feet, knees, and elbows with or without involvement of flexural areas and the trunk, and without the severe, mutilating scarring seen in RDEB-sev gen. In DDEB, blistering is often mild and limited to hands, feet, knees, and elbows, but nonetheless heals with scarring. Dystrophic nails, especially toenails, are common and may be the only manifestation of DDEB.
Epidermolysis bullosa herpetiformis, Dowling-Meara
MedGen UID:
38194
Concept ID:
C0079295
Disease or Syndrome
Epidermolysis bullosa simplex (EBS) is characterized by fragility of the skin (and mucosal epithelia in some cases) that results in nonscarring blisters caused by little or no trauma. The current classification of epidermolysis bullosa (EB) includes two major types and 12 minor subtypes of EBS; all share the common feature of blistering above the dermal-epidermal junction at the ultrastructural level. The four most common subtypes of EBS are the focus of this GeneReview: EBS, localized (EBS-loc; previously known as Weber-Cockayne type). EBS, Dowling-Meara type (EBS-DM). EBS, other generalized (EBS, gen-nonDM; previously known as Koebner type). EBS-with mottled pigmentation (EBS-MP) . The phenotypes for these subtypes range from relatively mild blistering of the hands and feet to more generalized blistering, which can be fatal. In EBS-loc, blisters are rarely present or minimal at birth and may occur on the knees and shins with crawling or on the feet at approximately age18 months; some individuals manifest the disease in adolescence or early adulthood. Blisters are usually confined to the hands and feet, but can occur anywhere if trauma is significant. In EBS, gen-non DM, blisters may be present at birth or develop within the first few months of life. Involvement is more widespread than in EBS-loc, but generally milder than in EBS-DM. In EBS-MP, skin fragility is evident at birth and clinically indistinguishable from EBS-DM; over time, progressive brown pigmentation interspersed with hypopigmented spots develops on the trunk and extremities, with the pigmentation disappearing in adult life. Focal palmar and plantar hyperkeratoses may occur. In EBS-DM, onset is usually at birth; severity varies greatly, both within and among families. Widespread and severe blistering and/or multiple grouped clumps of small blisters are typical and hemorrhagic blisters are common. Improvement occurs during mid- to late childhood. EBS-DM appears to improve with warmth in some individuals. Progressive hyperkeratosis of the palms and soles begins in childhood and may be the major complaint of affected individuals in adult life. Nail dystrophy and milia are common. Both hyper- and hypopigmentation can occur. Mucosal involvement in EBS-DM may interfere with feeding. Blistering can be severe enough to result in neonatal or infant death.
Epidermolysis bullosa simplex, Koebner type
MedGen UID:
86897
Concept ID:
C0079299
Congenital Abnormality
Epidermolysis bullosa simplex (EBS) is characterized by fragility of the skin (and mucosal epithelia in some cases) that results in nonscarring blisters caused by little or no trauma. The current classification of epidermolysis bullosa (EB) includes two major types and 12 minor subtypes of EBS; all share the common feature of blistering above the dermal-epidermal junction at the ultrastructural level. The four most common subtypes of EBS are the focus of this GeneReview: EBS, localized (EBS-loc; previously known as Weber-Cockayne type). EBS, Dowling-Meara type (EBS-DM). EBS, other generalized (EBS, gen-nonDM; previously known as Koebner type). EBS-with mottled pigmentation (EBS-MP) . The phenotypes for these subtypes range from relatively mild blistering of the hands and feet to more generalized blistering, which can be fatal. In EBS-loc, blisters are rarely present or minimal at birth and may occur on the knees and shins with crawling or on the feet at approximately age18 months; some individuals manifest the disease in adolescence or early adulthood. Blisters are usually confined to the hands and feet, but can occur anywhere if trauma is significant. In EBS, gen-non DM, blisters may be present at birth or develop within the first few months of life. Involvement is more widespread than in EBS-loc, but generally milder than in EBS-DM. In EBS-MP, skin fragility is evident at birth and clinically indistinguishable from EBS-DM; over time, progressive brown pigmentation interspersed with hypopigmented spots develops on the trunk and extremities, with the pigmentation disappearing in adult life. Focal palmar and plantar hyperkeratoses may occur. In EBS-DM, onset is usually at birth; severity varies greatly, both within and among families. Widespread and severe blistering and/or multiple grouped clumps of small blisters are typical and hemorrhagic blisters are common. Improvement occurs during mid- to late childhood. EBS-DM appears to improve with warmth in some individuals. Progressive hyperkeratosis of the palms and soles begins in childhood and may be the major complaint of affected individuals in adult life. Nail dystrophy and milia are common. Both hyper- and hypopigmentation can occur. Mucosal involvement in EBS-DM may interfere with feeding. Blistering can be severe enough to result in neonatal or infant death.
Recessive dystrophic epidermolysis bullosa
MedGen UID:
36311
Concept ID:
C0079474
Disease or Syndrome
Based on the most recent classification system, dystrophic epidermolysis bullosa (DEB) includes three subtypes: Recessive DEB, severe generalized (RDEB-sev gen) (formerly called Hallopeau-Siemens type (RDEB-HS). Recessive DEB, generalized other (RDEB-O) (formerly called non-Hallopeau-Siemens type (RDEB-non-HS). Dominant DEB (DDEB) . In RDEB-sev gen, blisters affecting the whole body may be present in the neonatal period. Oral involvement may lead to mouth blistering, fusion of the tongue to the floor of the mouth, and progressive diminution of the size of the oral cavity. Esophageal erosions can lead to webs and strictures that can cause severe dysphagia. Consequently, severe nutritional deficiency and secondary problems are common. Corneal erosions can lead to scarring and loss of vision. Blistering of the hands and feet followed by scarring fuses the digits into "mitten" hands and feet, a hallmark of this disorder. The lifetime risk of aggressive squamous cell carcinoma is over 90%. In contrast, the blistering in the less severe forms of RDEB-O may be localized to hands, feet, knees, and elbows with or without involvement of flexural areas and the trunk, and without the severe, mutilating scarring seen in RDEB-sev gen. In DDEB, blistering is often mild and limited to hands, feet, knees, and elbows, but nonetheless heals with scarring. Dystrophic nails, especially toenails, are common and may be the only manifestation of DDEB.
Junctional epidermolysis bullosa gravis of Herlitz
MedGen UID:
36328
Concept ID:
C0079683
Disease or Syndrome
Junctional epidermolysis bullosa (JEB) is characterized by fragility of the skin and mucous membranes, manifest by blistering with little or no trauma. Blistering may be severe and granulation tissue can form on the skin around the oral and nasal cavities, fingers and toes, and internally around the upper airway. Blisters generally heal with no significant scarring. Broad classification of JEB includes Herlitz JEB (aka lethal) and non-Herlitz JEB (aka non-lethal). In Herlitz JEB, the classic severe form of JEB, blisters are present at birth or become apparent in the neonatal period. Congenital malformations of the urinary tract and bladder may also occur. In non-Herlitz JEB, the phenotype may be mild with blistering localized to hands, feet, knees, and elbows with or without renal or ureteral involvement. Some individuals never blister after the newborn period. Additional features shared by JEB and the other major forms of epidermolysis bullosa (EB) include congenital localized absence of skin (aplasia cutis congenita), milia, nail dystrophy, scarring alopecia, hypotrichosis, pseudosyndactyly, and other contractures.
Epidermolysis bullosa simplex, Cockayne-Touraine type
MedGen UID:
87016
Concept ID:
C0080333
Disease or Syndrome
Epidermolysis bullosa simplex (EBS) is characterized by fragility of the skin (and mucosal epithelia in some cases) that results in nonscarring blisters caused by little or no trauma. The current classification of epidermolysis bullosa (EB) includes two major types and 12 minor subtypes of EBS; all share the common feature of blistering above the dermal-epidermal junction at the ultrastructural level. The four most common subtypes of EBS are the focus of this GeneReview: EBS, localized (EBS-loc; previously known as Weber-Cockayne type). EBS, Dowling-Meara type (EBS-DM). EBS, other generalized (EBS, gen-nonDM; previously known as Koebner type). EBS-with mottled pigmentation (EBS-MP) . The phenotypes for these subtypes range from relatively mild blistering of the hands and feet to more generalized blistering, which can be fatal. In EBS-loc, blisters are rarely present or minimal at birth and may occur on the knees and shins with crawling or on the feet at approximately age18 months; some individuals manifest the disease in adolescence or early adulthood. Blisters are usually confined to the hands and feet, but can occur anywhere if trauma is significant. In EBS, gen-non DM, blisters may be present at birth or develop within the first few months of life. Involvement is more widespread than in EBS-loc, but generally milder than in EBS-DM. In EBS-MP, skin fragility is evident at birth and clinically indistinguishable from EBS-DM; over time, progressive brown pigmentation interspersed with hypopigmented spots develops on the trunk and extremities, with the pigmentation disappearing in adult life. Focal palmar and plantar hyperkeratoses may occur. In EBS-DM, onset is usually at birth; severity varies greatly, both within and among families. Widespread and severe blistering and/or multiple grouped clumps of small blisters are typical and hemorrhagic blisters are common. Improvement occurs during mid- to late childhood. EBS-DM appears to improve with warmth in some individuals. Progressive hyperkeratosis of the palms and soles begins in childhood and may be the major complaint of affected individuals in adult life. Nail dystrophy and milia are common. Both hyper- and hypopigmentation can occur. Mucosal involvement in EBS-DM may interfere with feeding. Blistering can be severe enough to result in neonatal or infant death.
Multiple eruptive milia
MedGen UID:
83356
Concept ID:
C0343079
Neoplastic Process
Follicular atrophoderma and basal cell epitheliomata
MedGen UID:
87539
Concept ID:
C0346104
Neoplastic Process
Bazex syndrome is an X-linked dominant disorder characterized by a triad of congenital hypotrichosis, follicular atrophoderma affecting the dorsa of the hands and feet, the face, and extensor surfaces of the elbows or knees, and the development of basal cell neoplasms, including basal cell nevi and basal cell carcinomas from the second decade onward (Yung and Newton-Bishop, 2005). Rombo syndrome (180730) has similar features, but shows autosomal dominant inheritance.
Basan syndrome
MedGen UID:
140808
Concept ID:
C0406707
Congenital Abnormality
Complete congenital absence of dermatoglyphs is a rare syndrome characterized by autosomal dominant inheritance of the lack of ridges on palms and soles, neonatal acral blisters and facial milia, adult traumatic blistering and fissuring, absent or reduced sweating of palms and soles, and contracture of digits. Additional features may include single palmar transverse crease, palmoplantar keratoderma, and nail grooving (summary by Limova et al., 1993).
Dominant dystrophic epidermolysis bullosa, albopapular type
MedGen UID:
140935
Concept ID:
C0432322
Congenital Abnormality
Orofaciodigital syndrome 9
MedGen UID:
162908
Concept ID:
C0796102
Disease or Syndrome
Oral-facial-digital syndrome is actually a group of related conditions that affect the development of the oral cavity (the mouth and teeth), facial features, and digits (fingers and toes). Researchers have identified at least 13 potential forms of oral-facial-digital syndrome. The different types are classified by their patterns of signs and symptoms. However, the features of the various types overlap significantly, and some types are not well defined. The classification system for oral-facial-digital syndrome continues to evolve as researchers find more affected individuals and learn more about this disorder. The signs and symptoms of oral-facial-digital syndrome vary widely. However, most forms of this disorder involve problems with development of the oral cavity, facial features, and digits. Most forms are also associated with brain abnormalities and some degree of intellectual disability. Abnormalities of the oral cavity that occur in many types of oral-facial-digital syndrome include a split (cleft) in the tongue, a tongue with an unusual lobed shape, and the growth of noncancerous tumors or nodules on the tongue. Affected individuals may also have extra, missing, or defective teeth. Another common feature is an opening in the roof of the mouth (a cleft palate). Some people with oral-facial-digital syndrome have bands of extra tissue (called hyperplastic frenula) that abnormally attach the lip to the gums. Distinctive facial features often associated with oral-facial-digital syndrome include a split in the lip (a cleft lip); a wide nose with a broad, flat nasal bridge; and widely spaced eyes (hypertelorism). Abnormalities of the digits can affect both the fingers and the toes in people with oral-facial-digital syndrome. These abnormalities include fusion of certain fingers or toes (syndactyly), digits that are shorter than usual (brachydactyly), or digits that are unusually curved (clinodactyly). The presence of extra digits (polydactyly) is also seen in most forms of oral-facial-digital syndrome. Other features occur in only one or a few types of oral-facial digital syndrome. These features help distinguish the different forms of the disorder. For example, the most common form of oral-facial-digital syndrome, type I, is associated with polycystic kidney disease. This kidney disease is characterized by the growth of fluid-filled sacs (cysts) that interfere with the kidneys' ability to filter waste products from the blood. Other forms of oral-facial-digital syndrome are characterized by neurological problems, particular changes in the structure of the brain, bone abnormalities, vision loss, and heart defects.
Oculodentodigital dysplasia
MedGen UID:
167236
Concept ID:
C0812437
Disease or Syndrome
Oculodentodigital syndrome is characterized by a typical facial appearance and variable involvement of the eyes, dentition, and fingers. Characteristic facial features include a narrow, pinched nose with hypoplastic alae nasi, prominent columella and thin anteverted nares together with a narrow nasal bridge, and prominent epicanthic folds giving the impression of hypertelorism. The teeth are usually small and carious. Typical eye findings include microphthalmia and microcornea. The characteristic digital malformation is complete syndactyly of the fourth and fifth fingers (syndactyly type III) but the third finger may be involved and associated camptodactyly is a common finding (summary by Judisch et al., 1979). Neurologic abnormalities are sometimes associated (Gutmann et al., 1991), and lymphedema has been reported in some patients with ODDD (Brice et al., 2013). Genetic Heterogeneity of Oculodentodigital Syndrome An autosomal recessive form of ODDD (257850) is also caused by mutation in the GJA1 gene, but the majority of cases are autosomal dominant.
Epidermolysis bullosa pruriginosa
MedGen UID:
266151
Concept ID:
C1275114
Disease or Syndrome
Dystrophic epidermolysis bullosa is an inherited skin fragility disorder associated with anchoring fibril abnormalities and sublamina densa blistering. EB pruriginosa is a rare distinct clinical subtype of dystrophic EB in which skin fragility, blistering, and scar formation are associated with intense pruritus, nodular prurigo-like lichenified lesions, nail dystrophy, and variable presence of albopapuloid lesions (McGrath et al., 1994; Cambiaghi et al., 1997). The onset of these clinical features may be evident in early childhood, but in some cases is delayed until the second or third decade of life. Autosomal dominant, autosomal recessive, and sporadic inheritance patterns have all been described in this disorder.
Oral-facial-digital syndrome
MedGen UID:
307142
Concept ID:
C1510460
Disease or Syndrome
Oral-facial-digital syndrome type I (OFD1) is associated with dysfunction of primary cilia and is characterized by the following abnormalities: Oral (lobed tongue, hamartomas or lipomas of the tongue, cleft of the hard or soft palate, accessory gingival frenulae, hypodontia, and other dental abnormalities). Facial (widely spaced eyes or telecanthus, hypoplasia of the alae nasi, median cleft or pseudocleft upper lip, micrognathia) . Digital (brachydactyly, syndactyly of varying degrees, and clinodactyly of the fifth finger; duplicated hallux [great toe]; preaxial or postaxial polydactyly of the hands). Brain (intracerebral cysts, corpus callosum agenesis, cerebellar agenesis with or without Dandy-Walker malformation) . Kidney (polycystic kidney disease). As many as 50% of individuals with OFD1 have some degree of intellectual disability, which is usually mild. Almost all affected individuals are female. However, males with OFD1 have been described, mostly as malformed fetuses delivered by women with OFD1.
EPIDERMOLYSIS BULLOSA SIMPLEX, KOEBNER TYPE
MedGen UID:
377058
Concept ID:
C1851569
Disease or Syndrome
EPIDERMOLYSIS BULLOSA HERPETIFORMIS, DOWLING-MEARA TYPE
MedGen UID:
342037
Concept ID:
C1851571
Disease or Syndrome
Transient bullous dermolysis of the newborn
MedGen UID:
343607
Concept ID:
C1851573
Disease or Syndrome
Based on the most recent classification system, dystrophic epidermolysis bullosa (DEB) includes three subtypes: Recessive DEB, severe generalized (RDEB-sev gen) (formerly called Hallopeau-Siemens type (RDEB-HS). Recessive DEB, generalized other (RDEB-O) (formerly called non-Hallopeau-Siemens type (RDEB-non-HS). Dominant DEB (DDEB) . In RDEB-sev gen, blisters affecting the whole body may be present in the neonatal period. Oral involvement may lead to mouth blistering, fusion of the tongue to the floor of the mouth, and progressive diminution of the size of the oral cavity. Esophageal erosions can lead to webs and strictures that can cause severe dysphagia. Consequently, severe nutritional deficiency and secondary problems are common. Corneal erosions can lead to scarring and loss of vision. Blistering of the hands and feet followed by scarring fuses the digits into "mitten" hands and feet, a hallmark of this disorder. The lifetime risk of aggressive squamous cell carcinoma is over 90%. In contrast, the blistering in the less severe forms of RDEB-O may be localized to hands, feet, knees, and elbows with or without involvement of flexural areas and the trunk, and without the severe, mutilating scarring seen in RDEB-sev gen. In DDEB, blistering is often mild and limited to hands, feet, knees, and elbows, but nonetheless heals with scarring. Dystrophic nails, especially toenails, are common and may be the only manifestation of DDEB.
Epidermolysis bullosa with pyloric atresia
MedGen UID:
384018
Concept ID:
C1856934
Disease or Syndrome
Epidermolysis bullosa with pyloric atresia (EB-PA) is characterized by fragility of the skin and mucous membranes, manifested by blistering with little or no trauma; congenital pyloric atresia; and ureteral and renal anomalies (dysplastic/multicystic kidney, hydronephrosis/hydroureter, ureterocele, duplicated renal collecting system, absent bladder). The course of EB-PA is usually severe and often lethal in the neonatal period. Most affected children succumb as neonates; those who survive may have severe blistering with formation of granulation tissue on the skin around the mouth, nose, fingers, and toes, and internally around the trachea. However, some affected individuals have little or no blistering later in life. Additional features shared by EB-PA and the other major forms of EB include congenital localized absence of skin (aplasia cutis congenita) affecting the extremities and/or head, milia, nail dystrophy, scarring alopecia, hypotrichosis, contractures, and dilated cardiomyopathy.
Epidermolysa bullosa simplex and limb girdle muscular dystrophy
MedGen UID:
347335
Concept ID:
C1856936
Disease or Syndrome
Epidermolysis bullosa simplex with muscular dystrophy is an autosomal recessive disorder characterized by early childhood onset of progressive muscular dystrophy and blistering skin changes (Fine et al., 1989). Fine et al. (1991) reported a revised classification of the subtypes of inherited epidermolysis bullosa. In reports of 2 consensus meetings on EB, Fine et al. (2000, 2008) referred to EB with muscular dystrophy due to PLEC1 mutations as a form of basal simplex EB. Fine et al. (2000, 2008) also eliminated the term 'hemidesmosomal,' which had previously been proposed for this entity (Uitto et al., 1997) because ultrastructural analysis can demonstrate tissue abnormalities of the hemidesmosomes.
Spiegler-Brooke syndrome
MedGen UID:
346703
Concept ID:
C1857941
Disease or Syndrome
Brooke-Spiegler syndrome is an autosomal dominant disorder classically characterized by the appearance of multiple skin appendage tumors such as cylindroma, trichoepithelioma, and spiradenoma. These tumors are typically located in the head and neck region, appear in early adulthood, and gradually increase in size and number throughout life (Scheinfeld et al., 2003). Because BRSS, familial cylindromatosis, and MFT1 are allelic, and because different manifestations of each have been described within a single family, many consider these disorders to represent a phenotypic spectrum of a single disease entity (Gerretsen et al., 1995; Lee et al., 2005; Bowen et al., 2005; Young et al., 2006; Saggar et al., 2008). Blake and Toro (2009) provided a review of Brooke-Spiegler syndrome and pathogenic mutations in the CYLD gene.
Epidermolysis bullosa dystrophica, autosomal recessive, localisata variant
MedGen UID:
382144
Concept ID:
C2673611
Disease or Syndrome
Epidermolysis bullosa dystrophica inversa, autosomal recessive
MedGen UID:
435963
Concept ID:
C2673612
Disease or Syndrome
Epidermolysis Bullosa Dystrophica With Subcorneal Cleavage
MedGen UID:
436495
Concept ID:
C2675683
Disease or Syndrome
Epidermolysa bullosa simplex and limb girdle muscular dystrophy
MedGen UID:
418981
Concept ID:
C2931072
Disease or Syndrome

Recent clinical studies

Etiology

Milia DJ, Dua A, Paul JS, Tolat P, Brasel KJ
J Trauma Acute Care Surg 2013 Dec;75(6):1002-5; discussion 1005. doi: 10.1097/TA.0b013e3182a68756. PMID: 24256673
Fett N, Nevas J
Cutis 2013 Apr;91(4):191-2. PMID: 23763079
Di Milia L, Vandelanotte C, Duncan MJ
Sleep Med 2013 Apr;14(4):319-23. Epub 2013 Feb 16 doi: 10.1016/j.sleep.2012.12.007. [Epub ahead of print] PMID: 23419528
Milia M, Lefatzis N, Papakosta V, Theodossiadis P, Papathanassiou M
Clin Exp Optom 2013 May;96(3):346-8. Epub 2012 Sep 9 doi: 10.1111/j.1444-0938.2012.00798.x. [Epub ahead of print] PMID: 22957835
Luna PC, Larralde M
Pediatr Dermatol 2012 Jul-Aug;29(4):527-9. Epub 2011 Sep 9 doi: 10.1111/j.1525-1470.2011.01473.x. [Epub ahead of print] PMID: 21906143

Diagnosis

Milia DJ, Dua A, Paul JS, Tolat P, Brasel KJ
J Trauma Acute Care Surg 2013 Dec;75(6):1002-5; discussion 1005. doi: 10.1097/TA.0b013e3182a68756. PMID: 24256673
Fett N, Nevas J
Cutis 2013 Apr;91(4):191-2. PMID: 23763079
Milia M, Lefatzis N, Papakosta V, Theodossiadis P, Papathanassiou M
Clin Exp Optom 2013 May;96(3):346-8. Epub 2012 Sep 9 doi: 10.1111/j.1444-0938.2012.00798.x. [Epub ahead of print] PMID: 22957835
Fox GN, Mehregan DA, Jablonowski MN
Pediatr Dermatol 2013 Mar-Apr;30(2):263-4. Epub 2012 Jan 26 doi: 10.1111/j.1525-1470.2011.01673.x. [Epub ahead of print] PMID: 22276686
Lindenbaum L, Milia DJ
Surg Clin North Am 2012 Dec;92(6):1621-36. doi: 10.1016/j.suc.2012.08.013. PMID: 23153886

Therapy

Milia P, Caserio M, Bani D, Rastelli TF, Sonaglia F, Bigazzi B, Bigazzi M
Ital J Anat Embryol 2013;118(1 Suppl):92-7. PMID: 24640583
Fett N, Nevas J
Cutis 2013 Apr;91(4):191-2. PMID: 23763079
Di Milia L, Vandelanotte C, Duncan MJ
Sleep Med 2013 Apr;14(4):319-23. Epub 2013 Feb 16 doi: 10.1016/j.sleep.2012.12.007. [Epub ahead of print] PMID: 23419528
Di Milia L, Waage S, Pallesen S, Bjorvatn B
PLoS One 2013;8(1):e55306. Epub 2013 Jan 25 doi: 10.1371/journal.pone.0055306. PMID: 23372847Free PMC Article
Pozo Jd, Castiñeiras I, Fernández-Jorge B
J Cosmet Laser Ther 2010 Aug;12(4):191-4. doi: 10.3109/14764172.2010.502455. PMID: 20590368

Prognosis

Milia DJ, Dua A, Paul JS, Tolat P, Brasel KJ
J Trauma Acute Care Surg 2013 Dec;75(6):1002-5; discussion 1005. doi: 10.1097/TA.0b013e3182a68756. PMID: 24256673
Di Milia L, Adan A, Natale V, Randler C
Chronobiol Int 2013 Dec;30(10):1261-71. Epub 2013 Sep 3 doi: 10.3109/07420528.2013.817415. [Epub ahead of print] PMID: 24001393
Fett N, Nevas J
Cutis 2013 Apr;91(4):191-2. PMID: 23763079
Di Milia L, Rogers NL, Åkerstedt T
PLoS One 2012;7(9):e45856. Epub 2012 Sep 21 doi: 10.1371/journal.pone.0045856. PMID: 23029278Free PMC Article
La Milia V
J Nephrol 2010 Nov-Dec;23(6):633-47. PMID: 20540028

Clinical prediction guides

Milia DJ, Dua A, Paul JS, Tolat P, Brasel KJ
J Trauma Acute Care Surg 2013 Dec;75(6):1002-5; discussion 1005. doi: 10.1097/TA.0b013e3182a68756. PMID: 24256673
Milia AF, Ruffo M, Manetti M, Rosa I, Conte D, Fazi M, Messerini L, Ibba-Manneschi L
J Cell Mol Med 2013 Dec;17(12):1525-36. Epub 2013 Nov 19 doi: 10.1111/jcmm.12177. [Epub ahead of print] PMID: 24251911
Di Milia L, Adan A, Natale V, Randler C
Chronobiol Int 2013 Dec;30(10):1261-71. Epub 2013 Sep 3 doi: 10.3109/07420528.2013.817415. [Epub ahead of print] PMID: 24001393
Milia E, Castelli G, Bortone A, Sotgiu G, Manunta A, Pinna R, Gallina G
Acta Odontol Scand 2013 May-Jul;71(3-4):599-609. Epub 2012 Aug 15 doi: 10.3109/00016357.2012.700063. [Epub ahead of print] PMID: 22891890
Waller B, Haber RM
Arch Dermatol 2012 Sep;148(9):1037-9. doi: 10.1001/archdermatol.2012.1625. PMID: 22986855

Recent systematic reviews

Mulekar SV, Isedeh P
Br J Dermatol 2013 Oct;169 Suppl 3:57-66. doi: 10.1111/bjd.12532. PMID: 24098901
Di Milia L, Adan A, Natale V, Randler C
Chronobiol Int 2013 Dec;30(10):1261-71. Epub 2013 Sep 3 doi: 10.3109/07420528.2013.817415. [Epub ahead of print] PMID: 24001393
Cagetti MG, Mastroberardino S, Milia E, Cocco F, Lingström P, Campus G
Nutrients 2013 Jul 5;5(7):2530-50. doi: 10.3390/nu5072530. PMID: 23857225Free PMC Article
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