Konstantinos Bassioukas, Christina Stergiopoulou, J. Hatzis
Contact Dermatitis · 2004
Read the original publication at the publisher’s page
Abstract
A 40-year-old Italian man and his wife presented with extensive skin lesions. On examination, generalized dusky erythema, oedema, vesicles and bullae, especially on the thighs and the trunk of the man and the face and the trunk of the woman, were seen. Their 9-year-old boy was only partially and less severely affected. All 3 were fair skinned, type III according to Fitzpatrick's classification (1), and they had come to Greece in July for a holiday. They had severe pain rather than pruritus. 2 days earlier, they had prepared themselves an aqueous extract using boiled tap water and fresh-ground fig leaves, which they had collected from the surrounding countryside. The concoction was of unknown concentration. Soon after, they applied this homemade artificial suntan promoter all over their skin and exposed themselves to the burning midday sun to acquire a quick tan, except for their son who came in contact accidentally with both the mixture and the sun. Few hours later, as they were soaked in perspiration, they felt increasing burning and pain, but they thought this was mild sunburn. By the time, the initial erythema developed into erythroderma, and in some areas evolved into vesicles and bullae, the pain became severe. Personal and family history was negative. Full blood count revealed only leucocytosis (20 300 and 13 500/µl, respectively, for the man and the woman). Routine haematological and biochemical tests were otherwise normal, as well as urine analysis and chest X-ray. They were admitted to a dark room and treated with wet compresses, baths, emollients, topical corticosteroids 2 times daily and oral methylprednisolone 0.5 mg/kg daily and acetylsalicylic acid 325 mg daily. 2 weeks later, they left in remission but with residual partial hyperpigmentation, tapering the corticosteroids and with the suggestion to avoid the sun, shield with clothing and apply sunscreens every 2 hr. Phytophotodermatitis describes the reaction to sunlight of skin previously in contact with certain species of plants and is a phototoxic reaction. Furocoumarins are a chemical component common to the plant families Compositae (e.g. milfoil, yarrow), Umbelliferae (e.g. parsley, celery, parsnip, carrot), Leguminosae (bavchi, scurf pea), Rutaceae (e.g. lime, bitter orange) and Moraceae (fig), which all are capable of inducing photodermatitis (2, 3). The Moraceae comprises 53 genera with around 1400 species, approximately 800 of which are in the genus Ficus (4). Studies (5, 6) have detected furocoumarins in all parts of Ficus carica (fig) including the milky sap. The leaf and shoot saps contain 2 photoactive furocoumarin compounds, psoralen and bergapten. These are more plentiful in the leaf and are also present in the leaf extract. Tests revealed that psoralens and bergapten were present throughout the growing season and that psoralens were always the more plentiful. The phototoxic response is due to the presence of these compounds and primarily to the presence of psoralen, as the concentration of this compound is significantly greater and it is at least 4 times more photoactive on human skin than bergapten (6, 7). Contact with the leaf sap or shoot sap followed by sun exposure may therefore lead to such a phototoxic reaction. The increased incidence of fig phytophotodermatitis during spring and summer can be attributed to the higher concentrations of furocoumarins during these 2 seasons, in addition to other factors such as heat, humidity and increased exposure during the fruiting season (5, 6). In our cases, we believe that the aqueous extract of fig leaves, rich in psoralens in this season, was the culprit of the phototoxic reaction, enhanced by the heat and humidity of perspiration and the susceptibility of their fair skin, as they did not mentioned contact with any other phototoxic agent. The use of boiled ground fig leaves in these cases shows that, even after boiling temperatures, furocoumarins are still capable of eliciting phytophotodermatitis and, to our knowledge, this has not been reported before. The clinical appearance (dusky erythema, oedema, linear streaks, vesicles and bullae) on sun-exposed areas and the severe pain were both characteristic of phytophototoxic contact dermatitis. There have been reported anaphylactic reactions after ingestion of fresh fig (8) and to Ficus benjamina (9), which seems to share some common allergens. Our patients did not show any manifestations of such a reaction. Leucocytosis in both the man and the woman, in our opinion, was attributable to the extensive skin inflammation (10). Treatment of the acute reaction is symptomatic. Severely affected individuals may need hospital admission, wet compresses and paraffin gauze dressings, together with potent analgesia. Corticosteroids may be helpful if the eruption is oedematous. Hyperpigmentation may persist for several months and is best left untreated. Areas affected by phototoxic reactions may remain hypersensitive to UV light for several months or years and subsequent sun protection is advisable (11).
