Berlock dermatitis
A phototoxic dermatitis from perfume and sunlight.
Berlock dermatitis is a form of phytophotodermatitis, a phototoxic inflammatory skin reaction caused by contact with a light-sensitizing botanical agent followed by exposure to ultraviolet A (UV-A) light. It is notable for the pendant-like streaks of hyperpigmentation it produces on the neck, face, and arms, historically linked to the use of bergamot oil in perfumes.
Quick Facts
- Term coined by
- Rosenthal
- Year term coined
- 1925
- Associated photosensitizer
- bergapten
- Historical product involved
- Eau de Cologne
Facts from the source article.
Did You Know?
- The term "berloque" comes from the French word for trinket or charm.
- Berlock dermatitis is not an immunologic response; no prior exposure to the photosensitizing agent is required.
- Heat and moisture tend to exacerbate the reaction.
Signs and symptoms
A reaction typically begins within 24 hours of exposure and peaks at 48–72 hours. The skin initially reddens, itches, and burns. Large blisters (bullae) form within 48 hours and may leave black, brown, or purplish scars lasting years. Hyperpigmentation results from melanin production triggered by furanocoumarins. The condition can affect any age; in children it has been mistaken for child abuse.
Causes
Berlock dermatitis is caused by contact with a phototoxic substance, such as bergamot oil, followed by UV-A exposure. Bergamot oil contains bergapten, a linear furanocoumarin derived from psoralen. The photosensitizing plants belong mainly to four families: Apiaceae (carrot family), Rutaceae (citrus family), Moraceae (mulberry family), and Fabaceae (legume family). The carrot family accounts for about half of reported species. False bishop's weed (Ammi majus) is a major source of xanthotoxin. Cultivated foods like celery, parsnip, and parsley can cause occupational cases. Invasive phototoxic species include wild parsnip and tall hogweeds (Heracleum species). The citrus family Rutaceae is the second most common; lime is a well-known trigger.
Prevention
Avoid contact with phototoxic plants and citrus fruits. Do not incinerate such plants, as this disperses the substances. Wear long trousers, long sleeves, gloves, and protective eyewear when handling these plants. If protective clothing is unavailable, apply sunscreen to exposed areas. After outdoor activity, shower and wash clothing promptly. If contact occurs, wash the area with soap and cold water and avoid sunlight for at least 48 hours. Stay indoors and avoid light through windows. If going outside is necessary, cover the area with sun-protective clothing or apply sunscreen. The reaction is triggered by UVA (320–380 nm); use products labeled "Broad Spectrum" by FDA standards. UPF-labeled clothing may be unreliable.
History
The photosensitizing effects of plants were known in ancient Egypt around 2000 B.C., when Ammi majus juice was applied to vitiligo patches followed by sun exposure. In A.D. 50, Dioscorides noted pigment return from fig leaves. In 1815 Chaumton reported dermatitis from cow parsnip sap; in 1887 Sornevin reported Heracleum sphondylium dermatitis, but neither recognized the role of ultraviolet radiation. The term "berloque dermatitis" was coined by Rosenthal in 1925 for pendant-like pigmentation streaks. In 1916 Freund had correctly attributed these effects to sun exposure after using Eau de Cologne, which contains bergamot oil. Bergamot oil contains bergapten, named after the bergamot orange. In 1937 Miescher and Burckhardt suspected light sensitization from Heracleum mantegazzianum; Kuske later confirmed it. In 1942 Klaber introduced "phytophotodermatitis." Darrell Wilkinson described the clinical entity in the 1950s. By 1980 the photosensitizing effects of various plants were well known.
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