Phytophotodermatitis due to chinese herbal medicine decoction.

A 24-year-old female presented to the clinic complaining of bizarre patterns and linear streaks of hyperpigmentation on her legs and bizarre alutaceous patches on the neck and upper breast of her son for 7 days. Physical examination showed sharply demarcated hyperpigmented streaks on the extensor aspects of legs and bizarre brown maculae and patches on the right neck and upper chest of her son. Considering the history of Chinese herbal medicine decoction had been splashed onto these sites, phytophotodermatitis was definitely diagnosed.

Introduction

Phytophotodermatitis connotes phototoxic reactions consisting of erythema (with or without blistering) and delayed hyperpigmentation.[1] It is entirely independent of the immune system; that is, phytophotodermatitis can occurs in any individual and does not require prior sensitization. The ingredients needed to produce phytophotodermatitis include temporal exposure to both a photosensitizing substance (such as furocoumarins) and the appropriate wavelength of ultraviolet radiation (UVR).[1] Herein, we first report two cases of phytophotodermatitis after contact with Chinese herbal medicine (CHM) decoction.

Case Reports

Case 1

On June 28th 2009, a Chinese 24-year-old female presented to the clinic with a 7-day history of linear hyperpigmentation on her legs. Physical examination showed sharply demarcated hyperpigmented lines and curves on the extensor aspects of thighs and legs [Figure 1], bizarre fuscescent patches on the dorsal aspects of laps [Figure 2]. The patient complained of mild burning erythema on these sizes before 4 days, without any treatment, the preceding inflammatory reaction disappeared and left behind these rebarbative brown lines. We explored the history of exposure to any plants. She remembered that, before the onset of the rash, she had prepared the decoction of CHM (including atractylodes macrocephala, Cicada Slough, Pheretima asiatica, liquorice root, Astragalus mongholicus, Chinese Angelica, Sinensis, Pricklyash peel, Common Selfheal Fruit-Spike) for her son (Case 2). During the process, inadvertent splash of CHM decoction onto the skin happened to her and her son. At that time, she was in a skirt; the decoction was sprayed onto the dorsal aspects of laps and trickled down the legs to the ankles. Subsequently, she had extensive sun exposure throughout the day. One day thereafter, she developed mild erythema with slight and transient burning sensation on the sites of contact with the CHM decoction. Ultimately, a final diagnosis of phytophotodermatitis was established. The patient was prescribed with topical complex arbutin cream twice daily and vitamin C by mouth. The hyperpigmentation over the affected areas was slightly lightened 2 months after the initial clinical presentation.

Figure 1

Sharply demarcated hyperpigmented lines and curves on the extensor aspects of thighs and legs

Figure 2

Bizarre fuscescent patches on the dorsal aspects of laps

Case 2

An 11-month-old boy, the son of case 1, was referred to for evaluation of alutaceous maculae and patches on his right neck and upper chest [Figure 3] for 7 days. The boy suffered from fever cough and was prescribed with the CHM decoction (above mentioned) peros. Frequently, the boy struggled and refused to drink this decoction because of its bitter in taste. The physic liquor was sporadically sprinkle on his perioral areas and run down onto neck and upper chest, even splashed onto his mother's legs in one time. The child was exposed to sunlight. During the subsequent 24 h, a burning erythema developed on these sites, disappeared within 3–4 days, and remained brown patches.

Figure 3

Alutaceous maculae and patches on right neck and upper chest of the boy

Physical examination showed bizarre hyperpigmented maculae and patches with blurry borders on his right neck and upper chest. The skin covered by his suit was spared. Without any treatment, the light tan maculae and patches resolved during the 2-month follow-up.

Discussion

Phytophotodermatitis is a common cutaneous phototoxic reaction. Contact with plant-derived phototoxic substances (frequently found in umbilliferae, moracea, rutaceae, and leguminous) followed by sunlight exposure produces the clinical lesions. Furocoumarins, which are frequently found in limes, lemons, oranges, celery, fig, parsnip, parsley, carrots, dill, and perfumes, are photosensitizing chemical components and consist of psoralens, 5-methoxypsoralens, 8-methoxypsoralens, angelicin, bergaptol, and xanthotal.[2-4] The wavelengths of ultraviolet light that most efficiently produce phytophotodermatitis lie within the UV-A range and have peak activity at 335 nm.

Two distinct photochemical reactions have been described in phytophotodermatitis. A type I reaction occurs in the absence of oxygen, whereas a type II reaction occurs in the presence of oxygen. These photochemical reactions damage cell membranes and DNA and result in DNA interstrand cross-linking between the psoralen furan ring and the thymines or the cytosines of DNA. This results in activation of arachidonic acid metabolic pathways and in cell death (sunburn cells and apoptotic keratinocytes).[5] Clinically, erythema, blistering, epidermal necrosis, and eventual epidermal desquamation occur.

A postinflammatory pigment alteration may follow the acute phase of this phototoxic reaction. This alteration occurs primarily by two mechanisms. First, melanin, which is normally found in the epidermis, “falls” into the dermis and is ingested by melanophages. Second, an increased number of functional melanocytes and melanosomes are distributed in the epidermis following phytophotodermatitis and also account for the hyperpigmentation. This hyperpigmentation may serve as a protective mechanism against further UV injury. Clinically, this corresponds with irregular hyperpigmentation seen as the end stage of the phototoxic reaction.

Phytophotodermatitis most commonly occurs in the spring and the summer when furocoumarins are at their highest concentration in plants and when UV exposure is greatest for patients. It is frequently found in people who spend a lot of time participating in outdoor activities,[6] beach-goers, and children playing outdoors. Therefore, phytophotodermatitis is most commonly found on skin sites exposed to plants and sunlight, such as arm and leg, but it may occur anywhere. Its acute phase manifests as erythema, and end stage as postinflammatory hyperpigmentation. Lesions may or appear as hyperpigmented patches without a preceding erythematous phase, as happened in Case 1. Bizarre inflammatory patterns and linear streaks of hyperpigmentation are key clues to diagnosing phytophotodermatitis. These patterns often result from brushing against a plant's stems or leaves while outdoors or from the liquid spread of lime juice over the hand or down the forearm.

Jorge et al.[7] reproduce phytophotodermatitis in animal models by spraying peel juice of Tahiti lemon onto the skin of epilated albino rats and observe its serial pathological changes. After 24 h spongiosis, vacuolization and keratinocyte necrosis are observed, clinically there are no changes. After 48 h, erythema appears with intra- and subepidermal blistering. Almeida et al.[8] examined the epidermis in induced phytophotodermatitis using transmission electron microscopy in order to detect histological changes even before lesions are visible by light microscopy, they found vacuolization in keratinocytes immediately after induction. After 1 h, desmosomal changes were also observed in addition to vacuolization. Keratin filaments were not attached to the desmosomal plaque. Free desmosomes and membrane ruptures were also seen. At 2 h after induction, similar changes were found, and granular degeneration of keratin was also observed.

Phytophotodermatitis is a clinical diagnosis. The sunburn like reactions with unusual configurations should suggest the diagnosis. A history of contact with one of the offending plants and subsequent sunlight exposure should be sought.

There is no specific treatment for phytophotodermatitis.[9] Most commonly, it is a localized cutaneous phenomenon resulting initially in a burning sensation. In severe cases, analgesics, antihistamines for itching, and wet compresses may be used. Blistered areas should be kept clean to prevent secondary infection. Eventually, the affected sites may desquamate and develop permanent hyperpigmentation or hypopigmentation. However, scarring is rare.

Comparing with previous description about phytophotodermatitis, our report has the following characteristics. First, our patients’ lesions were caused by inadvertent splash of CHM decoction onto the skin, did not result from exposure to fresh fluid of plants. The boiled CHM included eight kinds of plant in which Chinese angelica and Pricklyash peel containing furocoumarins that can induce phytophotodermatitis. Second, the lesions in case 1 mainly presented bizarre hyperpigmented lines and curves depending on how the decoction drip over the skin surface without obviously acute inflammatory reaction such as erythema and blister.