LAUSR

Kava is prepared from the plant Piper methysticum. It has been used for centuries in South Pacific communities, and dried kava root is exported internationally. We report a case of an acute inflammatory sebotropic eruption and urticaria in a patient following kava consumption. A 23-year-old white woman presented with a 5-day history of a widespread, pruritic, erythematous rash, which had started on her right forearm. The patient’s medical history included anxiety. She used no regular medication, and denied the use of any herbal medications or supplements. On physical examination, urticated, erythematous plaques were seen, which were most prominent on the trunk and proximal arms (Fig. 1a–d). Scattered pustules were present on the upper back and face, with some facial swelling and scaling. The patient was febrile (temperature 38.0 °C) with palpable cervical lymphadenopathy. Other vital signs were normal. The differential diagnosis included early pustular psoriasis, pityriasis rubra pilaris, acute generalized eruptive pustulosis and viral exanthem. An incisional biopsy was taken from the right arm, and histological examination revealed folliculocentric inflammation, rich in neutrophils (Fig. 2a–c). Fungal yeast forms were detected deep in the follicle (Fig. 2d), mimicking a fungal folliculitis. Laboratory investigations showed a significantly raised alanine aminotransferase level (297 U/L; normal range 7–35 U/L), with normal bilirubin and alkaline phosphatase levels. Mild lymphopenia (0.6 9 10/ L; 1.0–3.0 9 10/L) was present, but white blood cell, neutrophil and eosinophil counts were normal. Blood cultures and a throat swab for respiratory viruses were negative. The initial treatment plan was topical steroids and oral histamine. One week later the patient presented with acute facial swelling and a history of transient, urticated plaques on the limbs. On this occasion the patient reported that she had been using a kava supplement, which she had purchased online as an anxiolytic. Oral prednisolone was given for 5 days, and the patient was advised to stop taking kava. Liver function tests normalized and at the 3-month follow-up, there had been no subsequent episodes. Kava has been used for centuries in South Pacific communities for medicinal, social and cultural purposes. Prepared from the roots of P. methysticum, its active ingredients (kavalactones) have anxiolytic and euphoric effects. Kava became more widely available in Western countries in the 1990s, and by the early 2000s, sales were worth approximately US$200 million a year. However, kava was soon implicated in several cases of acute liver failure, and it was banned afterwards in many countries, including the UK in 2003. This toxicity was unexpected from its use in the Pacific Islands, and debate exists whether this represents medical undersurveillance in the Pacific Islands or differences in use in Western countries. In 2007, a World Health Organization (WHO) report concluded that kava-induced hepatotoxicity was rare. In our case, the RUCAM (Roussel Uclaf Causality Assessment Method) score was 6, suggesting probable causality for the supplement. The WHO report suggested that chemicals other than kavalactones may have been responsible for hepatotoxicity. Potential causes include use of substandard kava due to high demand (including aerial parts of the plant, which contain toxic alkaloids), adulteration of kava products *Correspondence: Dr Lloyd Steele, Department of Dermatology, St Mary’s Hospital, Milton Road, Portsmouth, PO3 6DW, UK E-mail: [email protected]