Kava-induced acute cutaneous toxicity: An increasingly recognized characteristic clinicohistologic pattern.

To the Editor: We read with great interest the case report by Brown-Joel et al, Inflammatory sebotropic reaction associated with kava kava ingestion. The authors discuss an unusual sebotropic eruption thought to be caused by kava ingestion. We wanted to reinforce these characteristic clinicohistologic features by describing a similar presentation at our hospital center.

A 26-year old man without a significant medical history presented to the emergency department with a progressive cutaneous eruption for 1 week. Physical examination found diffuse, erythematous, and edematous papules and plaques on the face, neck, upper trunk, and proximal upper extremities (Fig 1, Fig 2). Two weeks prior, he started drinking an herbal tea supplement, kava. Similar to the case reported by Brown-Joel et al, the patient had mild neutrophilia (8.9 k/μL) and transaminitis: alanine aminotransferase, 91 (10-40 U/L); and aspartate aminotransferase, 55 (10-30 U/L). Two punch biopsies of the right upper back and arm revealed changes of suppurative folliculitis with perifolliculitis (Fig 3, Fig 4). Similar to the Brown-Joel et al case, presence of neutrophils was also noted within the hair follicles, particularly concentrated within the sebaceous glands. Given the clinical presentation and histology, acute cutaneous kava toxicity was the most likely etiology. Of note, unlike the prior report in which the patient did not benefit from prednisone and was started on cyclosporine, our patient responded to a 4-day course of oral prednisone (30 mg) and topical hydrocortisone 2.5% lotion with complete resolution.

Fig 1

Diffuse, erythematous, and edematous papules and plaques on the face and neck with scattered orofacial pustules.

Fig 2

Diffuse, erythematous, and edematous papules and plaques on the upper trunk.

Fig 3

Low-power view shows folliculocentric inflammatory infiltrate.

Fig 4

High magnification view shows neutrophilic infiltrate within a hair follicle and within a sebaceous gland.

It is well-established that chronic use of kava can cause a reversible ichthyosiform pellagroid dermopathy2, 3; however, detailed individual reports of cutaneous reactions to kava in an acute setting are sparse in the literature. Among the reported cases, significant similarity in primary cutaneous lesion morphology and histopathology is described; specifically, edematous papules and plaques tend to affect the face, upper trunk, and proximal upper extremities, which may be accompanied by systemic symptoms.1, 4, 5 Furthermore, there is striking folliculocentric inflammatory infiltrate on histology.1, 6 Acute kava-induced toxicity has also been described to cause maculopapular eruptions in a sebotropic distribution,1, 6, 7 an urticarial reaction, and a dermatomyositis-like illness. Additionally, although not described case by case and thus insufficient to infer causality, a systematic review on kava safety reported 29 kava-induced skin disorders, including Stevens-Johnson syndrome (n = 1), angioedema (n = 1), dermatitis (n = 3), erythema (n = 2), psoriasis (n = 1), pruritus (n = 5), rash (n = 9), increasing sweating (n = 1), and urticaria (n = 5).

We highlight this case because we feel it is vital for dermatologists to be aware of kava-induced cutaneous toxicities and to regularly ask patients about the use of complementary and alternative medicines. This is especially relevant when certain supplements have more than one name—such as ‘awa, ‘ava, yaqona, sakau, and malogu—for kava, and because access to these remedies is becoming more accessible, such as through dedicated kava bars that serve kava tea in New York, California, Texas, North Carolina, and Hawaii. Lastly, kava consumption may cause adverse interactions with prescribed medications, such as coma with benzodiazepines or excessive drowsiness with selective serotonin reuptake inhibitors. Therefore, knowledge about kava consumption is critical for astute recognition and appropriate management of cutaneous as well as neurologic and hepatic toxicities.