Coarse facial features or coarse facies describes a constellation of facial features that are present in many inborn errors of metabolism. Features include:
large, bulging head
prominent scalp veins
"saddle-like, flat bridged nose with broad, fleshy tip"
large lips and tongue
small, widely spaced and/or malformed teeth
hypertrophic alveolar ridges and/or gumsHeads tend to be longer than normal from front to back, with a bulging forehead. This is because of the earlier than normal or premature fusion of skull bones in an affected individual. Causes
Several conditions are associated with coarse facial features. Acromegaly
Alpha-mannosidosis type II
Aspartylglycosaminuria
Battaglia Neri syndrome
Borjeson Syndrome
Chromosome 6q deletion syndrome
Coarse face - hypotonia - constipation
Congenital hypothyroidism
Dandy-Walker malformation (with mental retardation basal ganglia disease and seizures)
Dyggve-Melchior-Clausen Syndrome
Fucosidosis type 1
Fucosidosis type II
Gangliosidosis generalized GM1 (type 1)
Gangliosidosis GM1 (type 3)
GM1 gangliosidosis
Goldberg syndrome
Hyde-Forster-Mccarthy-Berry syndrome
Hyper IgE
Hypomelanosis of Ito
I cell disease
Immunodeficiency due to defect in MAPBP-interacting protein
Infantile sialic acid storage disorder
Job syndrome
Mannosidosis (alpha B lysosomal)
McCune-Albright Syndrome
Mental retardation (X-linked - epilepsy - progressive joint contractures - typical face)
Mental retardation (X-linked Raynaud type)
Mieschers syndrome
Morquio syndrome
Morquio syndrome type A
Morquio syndrome type B
MPS 3 C
MPS 3 D
Mucolipidosis III
Mucopolysaccharidosis type 2 Hunter syndrome- mild form
Mucopolysaccharidosis type 2 Hunter syndrome- severe form
Mucopolysaccharidosis type 3
Mucopolysaccharidosis type 6
Mucopolysaccharidosis type 7 Sly syndrome
Mucopolysaccharidosis type I Hurler syndrome
Mucopolysaccharidosis type I Hurler/Scheie syndrome
Mucopolysaccharidosis type I Scheie syndrome
Multiple endocrine abnormalities - adenylyl cyclase dysfunction
Multiple endocrine neoplasia type 2b
Neuraminidase deficiency (type II juvenile form)
Nodulosis-arthropathy-osteolysis syndrome
Nonkeratan-sulfate-excreting Morquio syndrome
Pituitary tumors (adult)
Sialidosis type II (congenital)
Sialidosis type II (infantile)
Sialuria syndrome
Simpson-Golabi-Behmel syndrome
Simpson-Golabi-Behmel syndrome - type 1 (SGBS1)
Skeletal dysplasia - coarse facies - mental retardation
Spondyloepimetaphyseal dysplasia (genevieve type)
Sulfatidosis juvenile (Austin type)
Winchester syndrome

See also
Facies (medical)

References
External links
https://web.archive.org/web/20090106211640/http://www.mps1disease.com/patient/about/mps_pt_symptom_coarse_facial_features.asp
Actinic prurigo is a  rare sunlight-induced, pruritic, papular or nodular skin eruption. Some medical experts use the term actinic prurigo to denote a rare photodermatosis that develops in childhood and is chronic and persistent; this rare photodermatosis, associated with the human leukocyte antigen HLA-DR4, is often called "Familial polymorphous light eruption of American Indians" or "Hereditary polymorphous light eruption of American Indians" but some experts consider it to be a variant of the syndrome known as polymorphous light eruption (PMLE). Some experts use the term actinic prurigo for Hutchinsons summer prurigo (aka hydroa aestivale) and several other photodermatoses that might, or might not, be distinct clinical entities. Symptoms
AP is characterized by itchy, inflamed papules, nodules, and plaques on the skin. Lesions typically appear hours or days after exposure of the skin to UV light, and follow a general pattern of sun-exposed areas. The face, neck, arms, hands, and legs are often affected, although lesions sometimes appear on skin that is covered by clothing and thus not exposed to UV light, thus making AP somewhat difficult to diagnose. AP is a chronic disease, and symptoms usually worsen in the spring and summer as the day lengthens and exposure to sunlight increases. Causes
The cause for actinic prurigo is unknown, however researchers believe that protein in our bodies may be a cause to the condition also:
•UV-A and UV-B light seem to be the main provoking agents.