International Journal of Trichology

CASE REPORT
Year
: 2018  |  Volume : 10  |  Issue : 5  |  Page : 237--239

Development of pityriasis amiantacea after valproic acid therapy


Julio A Diaz-Perez1, Joel C Joyce2, Thomas L Cibull3, Thomas A Victor3,  
1 Department of Pathology, Northshore University Health System, University of Chicago, Chicago, IL; Department of Pathology, Jackson Health System, University of Miami, Miami, FL, USA
2 Division of Dermatology, Northshore University Health System, University of Chicago, Chicago, IL, USA
3 Department of Pathology, Northshore University Health System, University of Chicago, Chicago, IL, USA

Correspondence Address:
Julio A Diaz-Perez
Department of Pathology, Jackson Health System, University of Miami, Miami, FL
USA

Abstract

Here, we present the case of a 16-year-old male who developed pityriasis amiantacea (PA) after the use of valproic acid. We propose that the keratinocyte proliferative activity of valproic acid mediated through the inhibition of glycogen synthase kinase-3β, and subsequent activation of the Wnt/β-catenin pathway could play a role in the development of PA. We additionally review the most relevant characteristics of this disease.



How to cite this article:
Diaz-Perez JA, Joyce JC, Cibull TL, Victor TA. Development of pityriasis amiantacea after valproic acid therapy.Int J Trichol 2018;10:237-239


How to cite this URL:
Diaz-Perez JA, Joyce JC, Cibull TL, Victor TA. Development of pityriasis amiantacea after valproic acid therapy. Int J Trichol [serial online] 2018 [cited 2019 Aug 19 ];10:237-239
Available from: http://www.ijtrichology.com/text.asp?2018/10/5/237/246803


Full Text



 Introduction



Pityriasis amiantacea (PA) is a distinct inflammatory scaling reaction of the scalp that is characterized by the generation of firmly adherent, thick, waxy scales, which surround and attach to the hair bundles and take a silvery or yellowish coloration.[1],[2] The pathogenesis of PA remains almost completely unknown; its low frequency and diverse presentations have made PA a controversial disorder. Currently, evidence appears to indicate that PA is a prominent autoinflammatory response with possible participation of genetic and environmental factors.[1],[3] We describe an extraordinary case of PA on a patient with seborrheic dermatitis (SD) who manifested after the onset of valproic acid.

 Case Report



Our patient is a 16-year-old male with history of SD controlled by ketoconazole shampoo, who had episodes of impetigo caused by methicillin-sensitive Staphylococcus aureus effectively treated by cephalexin and mupirocin ointment. In addition, he had history of epilepsy. After starting valproic acid, he developed pruriginous, erythematous and yellowish scaly plaques on scalp, axillae, and pubic areas [Figure 1]. No pustules or erosions were identified. A biopsy was performed demonstrating psoriasiform hyperplasia, spongiosis involving epidermis and hair follicles, mounts of parakeratosis, serum crust, and follicular plugging. In the dermis was a superficial perivascular lymphohistiocytic infiltrate. In addition, deep and vellus hairs are observed in anagen and catagen, findings which are consistent with nonscarring alopecia. PAS stain is negative for fungal organisms [Figure 2]. A PA developing over SD was diagnosed, secondary to the possible effect of valproic acid. The patient was managed with a combination of clobetasol, salicylic acid, and ketoconazole shampoos. Furthermore, his antiepileptic therapy was switched to zonisamide. Two weeks later, a significant improvement of the patient presented with cutaneous lesions is documented.{Figure 1}{Figure 2}

 Discussion



Jean-Louis-Marc Alibert in 1832 first described PA as “la porrigine amiantace'e” because its scales reminded him of the mica-like substance observed in young birds. Since then, several names including tinea amintacea, asbestos scalp, tinea asbestina, or keratosis follicularis amiantacea have been used to describe PA.[1] PA has been described more commonly in the context of SD (one-third of cases); however, in addition, there are some reports in the setting of psoriasis vulgaris (other third of cases), followed by lichen planus, lichen simplex chronicus, atopic dermatitis, Darier's disease, tinea capitis, and pyogenic infections.[2],[4],[5] Several factors have been implicated in PA development such as drugs, anxiety, and abrupt changes in the environmental conditions.[6],[7],[8] Some descriptive data support a probable participation of tumor necrosis factor-alpha (TNF-α) and interferon-α in the pathogenesis of PA.[6],[7] In patients with Crohn's disease treated with TNF-α inhibitors, a stimulation of alternative pro-inflammatory pathways, including up-regulation of the IL-1 family, potential generation of autoreactive T cells, and keratinocyte proliferation, is observed.[6],[9]

Other medications associated with the development of PA include the inhibitor of the mutated BRAF gene (vemurafenib) for melanoma.[10] A careful understanding of these drug reactions could provide insights to prevent the development of PA lesions and also to allow an early diagnosis and management. However, one must keep in mind that cutaneous adverse effects can appear with variable time lapse. In our case, we observed that the disease was triggered after the use of valproic acid, a glycogen synthase kinase-3β (GSK-3β) inhibitor that stabilizes cytoplasmic β-catenin and facilitates the activation of the Wnt/β-catenin pathway.[11],[12] In our patient, valproic acid was started to manage a chronic epileptic disorder. Valproic acid GSK-3β inhibition promotes keratinocyte growth, especially in hair follicles, where its participation is critical for enhancing the proliferative activity of the dermal papilla and promoting the elongation of the hair shaft.[13] This proliferative capacity has made valproic acid a candidate for the treatment of alopecia.[11] Indirectly, valproic acid is also able to induce alkaline phosphatase similar to minoxidil.[12] In addition, valproic acid also induces growth factors such as insulin-like growth factor-1, fibroblast growth factor-10, and the follicular stem cell markers keratin-15 and CD34.[11],[14] However, because of the rarity of PA, no cases of the association of PA with VA have been published.

PA may occur at any age including children but is usually observed during teenage years. It is observed in both genders, with female predominance (60%–70%).[1] Clinically, all cases present with dry, scaly lesions that may be circumscribed or diffuse, with associated pruritus, erythema, and nonscarring alopecia.[9],[15] Histopathology demonstrates extensive spongiosis, acanthosis, hyperkeratosis, parakeratosis, follicular keratosis, and mixed inflammatory cell infiltrate.[16]

Microorganisms' role in PA development has been debated. Staphylococci are isolated as colonizers in up to 97% of the PA patients, more commonly S. aureus, followed by coagulase-negative staphylococci and micrococci.[1],[9] In addition, diverse species of fungus, including Microsporum canis, Trichophyton violaceum, Trichophyton rubrum, Trichophyton schoenleinii, and Trichophyton verrucosum, have been demonstrated in some reports.[17] These microorganisms could be also implicated in the maintenance of the disease, producing epidermal cell differentiation inhibitors, leading to perpetuate the disease.[3] Thus, the use of antibiotics plays a fundamental role in the treatment and/or prevention of PA recurrences.[17] The most commonly used antibiotic is ketoconazole 2% shampoo and oral griseofulvin (10 mg/kg). These medications have been associated with removal of scales after 2–3 months of treatment.[3]

In addition to the antimicrobial therapy, patients with PA require topical oil-based products to facilitate removal of the thick scales and crusts. Salicylic acid 5%–10% ointment is the most commonly employed. In severe cases, high-potency topical corticosteroids are beneficial (betamethasone dipropionate 0.1% solution).[2] In extensive and persistent disease, topical and oral retinoids are usually necessary taking precautions because of their teratogenicity.[1],[4]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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