Pediatric Dermatology Vol. 26 No.

4 458464, 2009

Oral Lichenoid Drug Eruption: A Report of a Pediatric Case and Review of the Literature
Victoria Woo, D.D.S.,* Julia Bonks, D.M.D., Lyubov Borukhova, D.M.D., and David Zegarelli, D.D.S.
*School of Dental Medicine, University of Nevada, Las Vegas, Nevada, Columbia University College of Dental Medicine, New York, New York

Abstract: Lichenoid drug eruptions are seen most frequently on the skin and seldomly affect the mucosal surfaces. Oral involvementknown as oral lichenoid drug eruptionis more common in the adult population and has been associated with numerous medications. Pediatric-onset oral lichenoid drug eruption is an exceptionally rare nding with only isolated cases published in the literature. The nonspecic appearance and latent presentation of pediatric oral lichenoid drug eruption can cause confusion in diagnosis and treatment. We report a case of oral lichenoid drug eruption occurring in a 15-year-old and explore challenges in the clinical and histologic recognition of this condition.

Drug eruptions represent a spectrum of cutaneous and mucosal changes related to oral, parenteral, or inhaled exposure to medications (1,2). The clinical presentation of drug eruptions is variable and may mimic the immune-mediated mucosal diseases including lichen planus, pemphigus vulgaris, mucous membrane pemphigoid, and lupus erythematosus (LE) (3). A wellrecognized form of chronic drug reaction is the lichenoid drug eruption (LDE), which may manifest on the skin, oral mucosa, or both sites (4); of the two, oral LDE (OLDE) is less common than cutaneous LDE (57) and may occur independently of skin lesions (4). The intraoral sites of predilection of OLDE include the posterior buccal mucosa, tongue, oor of mouth, palate, and alveolar ridges (810). There appears to be a preference for unilateral distribution (1113). Clinically, lesions of OLDE are morphologically identical to those of idiopathic oral lichen planus (OLP). They can exhibit a
Address correspondence to Victoria Woo, D.D.S., Columbia UniversityDivision of Oral Pathology, 630 W. 168th Street, PH15W-1562 New York, NY 10032, or e-mail: vlw2104@columbia. edu. DOI: 10.1111/j.1525-1470.2009.00953.x

classic reticular pattern or a predominantly erosive pattern, depending on the drug implicated (14). Furthermore, the histologic appearance and immunologic prole of drug-induced lichenoid lesions are nearly identical to their idiopathic counterpart (6,1517). Oral lichenoid drug eruptions have been reported in association with an extensive list of medications. The most commonly implicated drug classes include: penicillamine (5,18), antimalarials (19), gold salts (5,12), antihypertensives, including b-blockers (4,5,18,20,21) and angiotensin inhibitors (5,6,2123), nonsteroidal antiinammatory drugs (5,24,25), and HIV medications (5,26,27). The time from initial medication intake to lesion appearance is variable, ranging from weeks to months with an average delay in onset of 23 months (6). Demographically, OLDEs tend to be seen in adult patients and are rare ndings in the pediatric population (7), which the authors consider to be patients 15 years of

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2009 The Authors. Journal compilation 2009 Wiley Periodicals, Inc.

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age or younger. The disparity in prevalence is likely due to the more frequent use of medications and to the multiplicity of medications used in older individuals in our older population. Moreover, the majority of medications associated with OLDE are used for the treatment of predominantly adult-onset conditions (7). In this article, we present a pediatric patient with OLDE who demonstrated dramatic improvement on discontinuation of his systemic medications. CASE REPORT A 15-year-old male was referred for evaluation of bilateral buccal mucosal and tongue lesions of more than 1-year duration. The patient reported that his lesions were painful, particularly when exposed to certain foods and liquids. A past medical history revealed that he was under treatment by a psychiatrist for insomnia and mood swings. His medications included risperidone (Risperdal) and carbamazepine (Tegretol), which he had been taking for 2 years. Further questioning revealed no other medical conditions, no family history of lichen planus (LP), no history of hepatitis B vaccination, and no signicant exposure to cinnamon-containing products or foodstus. On intraoral examination, erosive lesions with white striated peripheral borders were observed involving the right and left buccal mucosa (Fig. 1A) and lateral tongue borders (Fig. 1B). The ulcers corresponded to the occlusal planes, suggestive of a Koebner phenomenon. A predominantly reticular lesion was also evident upon the lower labial mucosa. There were no adjacent dental restorations and no cutaneous involvement was noted. The clinical dierential diagnosis included OLP versus an oral mucosal lichenoid reaction. A biopsy was performed of the left buccal mucosa and revealed hyperparakeratosis with an underlying lichenoid inltrate containing scattered neutrophils. Interface mucositis, characterized by intraepithelial lymphocytic exocytosis and colloid bodies, was also evident (Fig. 2). A histopathologic diagnosis of hyperkeratosis and lichenoid mucositis was made. The patient was provided with a topical steroid mouthrinse (dexamethasone suspension 0.5 mg 5mL). On follow-up 2 weeks later the lesions were unchanged. An OLDE related to the patients medications was strongly suspected. Upon consultation with the patients psychiatrist, both medications were stopped. On follow-up 1 month later, the patient reported 100% subjective improvement in his symptoms. Clinically, there was almost complete resolution of the ulcerations although residual white striations were noted involving the right and left posterior buccal mucosa (Fig. 3A). The bilateral tongue borders were clinically normal (Fig. 3B). A drug re-challenge was oered but refused by his parents due to discomfort

Figure 1. (A) Oral lichenoid eruption: Erosions associated with white striations of left buccal mucosa. (B) Oral lichenoid eruption: Large erosion with white, striated periphery of left lateral tongue border.

Figure 2. Photomicrograph of oral biopsy demonstrating a lichenoid inltrate with intraepithelial lymphocytes and colloid bodies (hematoxylin and eosin, magnication 100).

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DISCUSSION Pediatric LDE is infrequent due to the relative uncommon use of systemic medications in this age group. A review of the current literature revealed several cases of cutaneous LDE in children (28,29). However, reports of OLDE are extremely rare and may be related to lack of recognition or misdiagnosis as other clinical entities, including idiopathic LP. We performed a Medline and PubMed search for pediatric OLDE cases published in the English-language literature and found only two cases, presented in Table 1 (29,30). The patients listed in this table fullled the criteria for OLDE, including a history of systemic medication intake, clinical and histologic evidence of lichenoid mucositis, and resolution of lesions with drug cessation. It is noteworthy that formal analysis of documented cases was often dicult due to a wide variation in reporting techniques and diagnostic criteria. A complete listing of OLDE-causing medications used in the pediatric population is beyond the scope of this paper. However, an abbreviated list is provided in

TABLE 2. OLDE-Associated Systemic Medications Used in the Pediatric Population

Antianxiety psychotropic agents (clonazepam, diazepam, lorazepam, temazepam, tricyclic antidepressants) Antibiotics (tetracycline) Anticonvulsants (carbamazepine, lorazepam, oxcarbazepine, phenytoin, valproate sodium) Antidiabetics (insulin) Antidiarrheals (bismuth) Antinammatory agents (aspirin, fenclofenac, ibuprofen, naproxen, rofecoxib) Antifungals (amphotericin B, ketoconazole) Antimalarials (chloroquine, hydroxychloroquine, pyrimethamine, quinidine, quinine) Antituberculosis antimycobacterial agents (isoniazid, streptomycin, rifampin) Antiulcer agents (cimetidine, ranitidine, omeprazole) Bipolar agents (lithium) Chemotherapeutic agents (dactinomycin) Thyroid replacement agents (thyroxine) OLDE, oral lichenoid drug eruption.

Figure 3. (A) Appearance of oral mucosa 1 month following drug withdrawal: Residual white striations of left buccal mucosa. (B) Appearance of oral mucosa 1 month following drug withdrawal: Left lateral tongue border with no clinical evidence of disease.

associated with his initial lesions. At 1-year follow-up, there were persistent reticular lesions of the bilateral buccal mucosa but no evidence of ulceration. The patient has been placed on annual oral pathology recall and continues to be followed closely by his psychiatrist.

TABLE 1. Reported Cases of Pediatric Oral Lichenoid Drug Eruption

Author Ridola et al (29) Kanwar et al (30) Present case No. cases 1 1 1 Age sex 20 mos M 4 yrs M 15 yrs M Drug implicated Dactinomycin Dactinomycin Risperidone, carbamazepine Site Lips, face trunk, limbs Oral NS, axillae, groin pubic region, chest BM, tongue Clinical features Reticular, papular NS Erosive Time onset* time resolve 12 d 1 mo 7 d 1 mo ?mo 1 mo Comments Topical steroids given; resolution despite continued vincristine

*Time of lesional onset after drug administration, Time of lesional resolution after drug withdrawal. M, male; NS, not specied; BM, buccal mucosa.

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Table 2 (8,3134). Of note, several of these medications have been implicated in both oral and cutaneous lichenoid eruptions. The diagnosis of OLDE may be challenging due to its nonspecic clinical ndings and rarity in the pediatric population. A clear temporal relationship between lesion onset and drug intake is not always obvious due to variable latent periods, which ranges from an average of 12 months (29) to reportedly 2 years in duration (6,24,35,36). Therefore, extended latency from initial drug exposure does not preclude the diagnosis of OLDE. Furthermore, oral lesions have presented after medication withdrawal in exceptional cases (37). In this setting, a high index of clinical suspicion is required to prompt evaluation of a drug-induced etiology. Lastly, identifying the causal agent can also become problematic in patients taking multiple medications, although the most recently administered drug should be suspected rst. Further complicating the diagnosis of OLDE is the wide array of oral conditions that can present with lichenoid-appearing lesions. The dierential diagnosis for OLDE in a child should include OLP, lichenoid amalgam reaction, and cinnamon stomatitis; less likely considerations include lesions of LE, oral manifestations of chronic graft-versus-host disease, and erythema multiforme. The latter ve conditions can be excluded by evaluating the following: direct contact with amalgam restorations, exposure to cinnamon containing products; systemic involvement and positive serologic tests for LE; history of bone marrow transplant; and characteristic clinical ndings such as hemorrhagic crusted lips and target skin lesions (Table 3) (8,12). Hepatitis B vaccination (3840) and liver disorders, such as chronic active hepatitis (41), have also been associated with oral lichenoid lesions but can be appropriately eliminated
TABLE 3. Dierential Diagnosis of OLDE
Condition Oral lichen planus Lichenoid amalgam reaction Systemic lupus erythematosus Graft-versus-host disease Erythema multiforme Age sex Middle-aged; elderly F Any M = F Avg. 30 yrs F Any M = F 2030 yrs M = F Sites

during history taking. Therefore, the main diagnostic dilemma involves dierentiating OLDE from OLP, the latter being a rare but documented condition in children (4246). Clinical, microscopic, and immunologic similarities make distinction between OLDE and OLP dicult if not impossible in certain cases. This is compounded by the lack of clearly dened and standardized criteria in the diagnosis of OLDE. Attempts at identifying histologic features specic to OLDE have been met with variable success. Purported histologic features favoring the diagnosis of OLDE include a deep and diuse subepithelial inltrate composed of lymphocytes, plasma cells, neutrophils with or without eosinophils; perivascular inammation; and intraepithelial colloid bodies (4,12,13,15,4749). However, most authors agree that these ndings are not exclusive to OLDE and can also be seen in OLP as well as other mucocutaneous conditions (e.g., discoid LE) (15,47,50). In contrast to traditional histology, immunouorescence analysis may be of help in distinguishing OLDE from OLP. While both conditions show similar ndings on direct immunouorescence studiesnamely, a shaggy deposition of brinogen along the basement membrane zone and immunoglobulin M-positive colloid bodies (5,8,51)detection of circulating basal cell cytoplasmic autoantibodies (BCCA) by indirect immunouorescence may favor a diagnosis of OLDE (11). A positive BCCA test, characterized by a distinct string of pearls pattern on serum analysis, has been documented in OLDE by many authors (11,52,53) and may be a useful ancillary test to support a drug-induced etiology. Furthermore, immunouorescence testing also serves to rule out other immune-mediated vesiculobullous diseases, such as LE, pemphigus vulgaris, and mucous membrane pemphigoid.

Oral lesions Bilateral, symmetric; reticular > erosive; exacerbations White or atrophic striations; persistent Reticular; atrophic; nonspecic erosions Reticular; papular; atrophic nonspecic erosions Hemorrhagic crusting of lips; nonspecic ulcers; rapid onset

Diagnosis Clinical; histology; DIF Clinical; histology; ?mercury patch test Clinical; histology; DIF; serology for ANA, dsDNA History of bone marrow transplant; clinical; histology Clinical; histology to rule out other ulcerative processes

Skin: exor surfaces Oral: BM, tongue, gingival BM, lateral ventral tongue; contact with amalgam Multisystem: skin, kidney, cardiac Oral: BM, palate, gingiva Multisystem: skin, GI, liver Oral: BM, tongue, Lips Skin: hands, feet, genital Ocular: conjunctiva Oral: Lips, BM, tongue, FOM, soft palate

F, female; M, male; BM, buccal mucosa; FOM, oor of mouth; DIF, direct immunouorescence; ANA, antinuclear antibodies; dsDNA, double-stranded DNA antibodies; OLDE, oral lichenoid drug eruption.

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Although there are no universally accepted criteria for the diagnosis of OLDE, recent eorts by McCartan et al (17) have provided a more structured system for reporting cases. These authors suggest that reports should include: (1) an accurate clinical description of lesions with a dened temporal relationship with drug exposure, (2) evidence of histologic verication, and (3) documented lesion resolution on drug withdrawal. Moreover, lesion recurrence on drug re-challenge (provocation testing) and supportive immunouorescence testing will also help to conrm a medication-related cause (5,54). Lastly, some authors have used patch testing as an auxiliary tool in diagnosis (55), while others contend that a negative patch test cannot reliably rule out OLDE (56). The ideal treatment for OLDE consists of drug withdrawal or substitution with an alternate medication following consultation with the patients physician (18). Lesion resolution is typically observed within weeks to months after drug cessation although delayed responses may result in lesion persistence (57). Furthermore, faint residual striations or milder forms of erosive lesions are commonly observed following elimination of the medication (12), as seen in our patient. In many instances however, the severity of the medical condition for which the patient is being treated precludes drug discontinuation. In such cases, topical steroid therapy has been used but with variable to little success (24). Reportedly, select adult patients have beneted from systemic corticosteroid therapy (18), topical tacrolimus (58), and topical acetretin (59), although such treatments should be used with appropriate caution in children. Palliative remedies such as temporary mucosal protectants (e.g., milk of magnesia) may provide symptomatic relief (18). In addition, good oral hygiene practices are to be encouraged to prevent superimposed bacterial and fungal infections (18). In this report, the patient was taking risperidone and carbamazepine as prescribed by his psychiatrist. Risperidone is an antipsychotic agent used to manage schizophrenia and bipolar disorder. This medication is most often associated with central nervous system side eects such as agitation, somnolence, and dizziness (60). Carbamazepine is an anticonvulsant primarily indicated for treatment of epilepsy with similar neurologic sideeects as risperidone. To our knowledge, risperidone has been associated with lichenoid dermatitis (60) but is not a documented cause of OLDE. In contrast, carbamazepine has been implicated in OLDEs (8,11,31,61), cutaneous LDEs (61,62), lupus erythematosus-like drug eruptions (8,63,64) and xed drug eruptions (8,65). Although it cannot be stated with certainty which agent caused the OLDE in our patient, carbamazepine is

favored due to its more extensive history of drug reactions. In summary, the presentation of lichenoid lesions in the pediatric population should prompt evaluation for OLP and other conditions with intraoral lichenoid manifestations. A thorough history of systemic drug intake over the previous 12 months should be documented as a means to eliminate or support a diagnosis of OLDE (5). Due to the increasing recognition and pharmacologic management of childhood-onset illnesses, including attention decit hyperactivity disorder (66), it is possible that drug-related side-eects and oral complications may become more prevalent in the younger population. Therefore, it is important for clinicians to recognize the spectrum of medication-induced conditions, including OLDE, in order to avoid delays in diagnosis and treatment. REFERENCES
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