Xeroderma pigmentosum | |
---|---|
Other names | DeSanctis-Cacchione syndrome[1][2]
XP1 / XP2 / XP3 / XP4 / XP5 / XP6 / XP7[3] Xeroderma pigmentosum I/II/III/IV/V/VI/VII[3] Xeroderma pigmentosum complementation group A/B/C/D/E/F/G[3] xeroderma pigmentosum group A/B/C/D/E/F/G[3] |
An eight-year-old girl from Guatemala with xeroderma pigmentosum[4] | |
Specialty | Medical genetics |
Symptoms | Severe sunburn after only a few minutes in the sun, freckling in sun-exposed areas, dry skin, changes in skin pigmentation[1] |
Complications | Skin cancer, brain cancer, cataracts[1] |
Usual onset | Becomes visible ~6 months of age[2] |
Duration | Lifelong |
Causes | Genetic disorder (autosomal recessive)[1] |
Diagnostic method | Based on symptoms and confirmed by genetic testing[5] |
Differential diagnosis | Trichothiodystrophy, Cockayne syndrome, cerebrooculofacioskeletal syndrome, erythropoietic protoporphyria[6] |
Prevention | No cure available |
Treatment | Completely avoiding sun or UV rays, retinoid creams, vitamin D[5][6] |
Prognosis | Life expectancy is shortened by about 30 years.[7] |
Frequency | • 1 in 100,000 (worldwide)[3]
• 1 in 370 (India) [citation needed] • 1 in 22,000 (Japan)[3] • 1 in 250,000 (US)[8] • 1 in 430,000 (Europe) • 1 in 1,000,000 (UK)[3] |
Xeroderma pigmentosum (XP) is a genetic disorder in which there is a decreased ability to repair DNA damage such as that caused by ultraviolet (UV) light.[1] Symptoms may include a severe sunburn after only a few minutes in the sun, freckling in sun-exposed areas, dry skin and changes in skin pigmentation.[1] Nervous system problems, such as hearing loss, poor coordination, loss of intellectual function and seizures, may also occur.[1] Complications include a high risk of skin cancer, with about half having skin cancer by age 10 without preventative efforts, and cataracts.[1] There may be a higher risk of other cancers such as brain cancers.[1]
XP is autosomal recessive, with mutations in at least nine specific genes able to result in the condition.[1][6] Normally, the damage to DNA which occurs in skin cells from exposure to UV light is repaired by nucleotide excision repair.[1] In people with xeroderma pigmentosum, this damage is not repaired.[1] As more abnormalities form in DNA, cells malfunction and eventually become cancerous or die.[1] Diagnosis is typically suspected based on symptoms and confirmed by genetic testing.[5]
There is no cure for XP.[6] Treatment involves completely avoiding the sun.[6] This includes protective clothing, sunscreen and dark sunglasses when out in the sun.[6] Retinoid creams may help decrease the risk of skin cancer.[6] Vitamin D supplementation is generally required.[5] If skin cancer occurs, it is treated in the usual way.[6] The life expectancy of those with the condition is about 30 years less than normal.[7]
The disease affects about 1 in 100,000 worldwide.[3] By region, it affects about 1 in 370 in India, 1 in 20,000 in Japan, 1 in 250,000 people in the United States and 1 in 430,000 in Europe.[8] It occurs equally commonly in males and females.[9] Xeroderma pigmentosum was first described in the 1870s by Moritz Kaposi.[5][9] In 1882, Kaposi coined the term xeroderma pigmentosum for the condition, referring to its characteristic dry, pigmented skin.[9] Individuals with the disease have been referred to as "children of the night" or "moon children".[10]
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was invoked but never defined (see the help page).