A case of lichenoid drug eruption associated with sildenafil citratus

A 53-year-old man developed lichenoid lesions on the upper chest, posterior surfaces of the trunk, and abdominal region about three months before his first visit. Physical examination and laboratory findings were normal; histopathology showed vacuolar degeneration of basal keratinocytes in association with a dense lympho-histioid infiltrate arranged in a lichenoid pattern with a few melanophages and eosinophils. The fact that our patient had been irregularly taking sildenafil citratus (Viagra) led to the hypothesis of a lichenoid drug-induced eruption. Our hypothesis was confirmed by clinical resolution three weeks after discontinuation of sildenafil citratus; moreover, the patient avoided the drug for about four months, and the eruption didn't reappear. Subsequently, we performed a challenge test with the drug, and the patient developed similar lichenoid lesions. Lichenoid eruptions are rather common dermatoses that can be induced by a great number of environmental agents and are clinically but not pathogenetically well defined. We report the present case because, despite the great number of drugs that can be implicated in the development of lichenoid eruptions, the association of such dermatoses and sildenafil citratus had been described only once previously in the literature until now. Furthermore, we wish to remark on the significance of a detailed anamnestic history to make the correct differential diagnosis between lichenoid drug-induced eruptions and lichen planus. This has a great clinical importance because simple discontinuation or substitution of the drug causes lichenoid drug-induced eruption resolution.     

Oral Lichenoid Drug Eruption: A Report of a Pediatric Case and Review of the Literature

Abstract:   Lichenoid drug eruptions are seen most frequently on the skin and seldomly affect the mucosal surfaces. Oral involvement—known as oral lichenoid drug eruption—is more common in the adult population and has been associated with numerous medications. Pediatric-onset oral lichenoid drug eruption is an exceptionally rare finding with only isolated cases published in the literature. The nonspecific 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.     

Simvastatin-induced lichenoid drug eruption

Cutaneous drug eruptions have a variety of clinical features. Lichenoid drug eruptions are rare and may be difficult to diagnose. A case of a simvastatin-induced lichenoid eruption with skin and mucosal involvement is reported.     

Lichenoid Drug Eruption with Prominent Nail Changes Due to Leflunomide in a 12‐Year‐Old Child

We present the case of a 12‐year‐old‐girl who developed lichenoid dermatitis approximately 1 year after starting leflunomide for juvenile idiopathic arthritis. The eruption resolved promptly with discontinuation of the suspected culprit agent, supportive of a lichenoid drug eruption, but she subsequently developed markedly dystrophic nails with lichen planus–like features. A biopsy of her cutaneous findings at the time of initial presentation demonstrated lichenoid dermatitis, and a nail matrix biopsy was deferred given clinical correlation. Prominent nail changes in lichenoid drug eruptions, particularly in children, are rare but should be considered in children with new‐onset nail dystrophy.     

Lichenoid drug eruption induced by olanzapine

Lichenoid drug eruptions can mimic idiopathic lichen planus and other dermatoses. The list of drugs that can cause them is long and growing steadily. Although cutaneous side effects of antipsychotics are rare, various cutaneous manifestations have been reported in association with olanzapine. We present the case of a patient who developed an atypical lichenoid eruption due to olanzapine. A review of the literature in Medline from 1951 to 2007 and in the Índice Médico Español (Spanish Medical Index) revealed no previous cases of lichenoid eruptions associated with the use of this drug.     

A dissimilar biosimilar? Lichenoid drug eruption induced by an infliximab biosimilar

The advent of therapeutic antibodies, or biological medications, has transformed the treatment of many inflammatory diseases in dermatology. Recently, the development of biosimilars, biological drugs that are highly similar in quality, safety and efficacy to approved biologics, has changed this landscape. Although biosimilars are not identical to their reference product, they are required to have the same mechanism of action, route of administration, dosage form and strength as the reference product. This also leads to the possibility that subtle differences in the activity of these biosimilars can lead to differing clinical responses. We report the first case of a lichenoid eruption induced by a biosimilar to infliximab after switching from infliximab. Several days after initial infusion of the biosimilar, the patient developed a pruritic papulosquamous eruption that was biopsied to reveal a lichenoid drug eruption. Possible mechanisms for lichenoid drug eruptions as a result of tumour necrosis factor‐α inhibitor administration are discussed, along with reasons why such a reaction may occur with a biosimilar but not the original, reference product. This case report calls attention to the unique differences between biosimilars and biological medications that a clinician should consider prior to prescribing these medications.     

Lichenoid and subacute cutaneous lupus erythematosus-like dermatitis associated with antihistamine therapy

The authors report the occurrence of lichenoid and/or subacute lupus erythematosus-like eruptions in a group of patients receiving agents with antihistaminic properties. In 1 of the patients the eruption clinically resembled lichen planus, while in 5 patients the eruption resembled subacute cutaneous lupus erythematosus (SCLE). At a light microscopic level all cases showed a lichenoid dermatitis and in 4 cases the lesions were interpreted as representing subacute lupus-like eruptions by virtue of the presence of alternating cell poor and lichenoid interface dermatitis, suprabasilar lymphocytosis around degenerating keratinocytes, and dermal mucinosis. Despite the resemblance at a clinical and light microscopic level to SCLE, anti-Ro seropositivity could not be established in any of the cases. One case, however, did demonstrate antihistone antibodies in concert with a high antinuclear antibody titer. A causal association was implicated by virtue of lesional resolution following drug withdrawal. The association of cutaneous eruptions resembling SCLE with antihistamine intake is seemingly a novel one. The possible pathogenetic basis of the eruptions is discussed.     

Lichenoid eruption following hepatitis B vaccination: first North American case report

Lichen planus is often found in association with a variety of underlying conditions. In particular, liver diseases such as primary biliary cirrhosis, primary sclerosing cholangitis, hepatitis C, and hepatitis B have been implicated in cutaneous lichen planus. Of interest, there is mounting evidence that lichen planus-like eruptions can occur following administration of the hepatitis B vaccine, which has recently become a routine immunization in many parts of the world. We present what we believe to be the first North American case of lichenoid drug eruption associated with the hepatitis B vaccine and provide a brief review of other reported cases of lichenoid eruption seen following hepatitis B vaccination.     

Two patients with isoniazid-induced photosensitive lichenoid eruptions confirmed by photopatch test

Causative agents of drug eruptions are frequently unknown, and skin tests with candidate drugs would be useful before systemic challenge. It remains to be clarified how phostosentive lichenoid drug eruptions are induced, but allergy, including delayed type allergy, has been suggested. Two patients who had taken anti-tuberculous drugs developed a lichenoid drug eruption, primarily on sun-exposed skin. Patch and photopatch tests were performed with each of the ingested drugs (10% in petrolatum). Photopatch tests to isoniazid (INH) were positive. These were confirmed by oral challenge followed by irradiation with UVA. In conclusion, photopatch tests facilitated identification of the causative drug in two patients with photosensitive lichenoid eruptions to INH.     

Pembrolizumab-induced pseudoepitheliomatous eruption consistent with hypertrophic lichen planus

Pembrolizumab, an anti-programmed cell death-1 (PD-1) antibody preparation, has been shown to induce various dermatologic adverse events which may present with delayed onset or even after discontinuation of therapy. We report a 78-year-old female patient with a stage II lung adenocarcinoma treated with pembrolizumab, who developed lichenoid eruptions and multiple cutaneous plaque/nodular eruptions as pseudoepitheliomatous hyperplasia, during and up to 2 months after discontinuation of pembrolizumab therapy. Multiple skin biopsies revealed epidermal hyperplasia with hyperkeratosis, hypergranulosis, diffuse to patchy lichenoid lymphocyte infiltrate with scattered eosinophils and neutrophils, confluent to scant dyskeratosis of the lower epidermis, minimal to overt invagination, and cystic proliferation of squamous epithelium to papillomatosis with hypergranulosis and keratosis. Overall, multiple patterns were present with similarities to lichenoid drug eruption, lichen planus, early invasive squamous cell carcinoma, early keratoacanthoma, and verruca. However, the findings ultimately supported a diagnosis of hypertrophic lichen planus. All the lesions resolved with oral prednisone, hydroxychloroquine, and topical triamcinolone acetonide ointment 0.1%. In summary, our case shows that pembrolizumab can induce lichenoid eruption with pseudoepitheliomatous hyperplasia, and these lesions can clinically and pathologically mimic early invasive squamous cell carcinomas or keratoacanthomas.     

Lichenoid eruption produced by captopril

Captopril, an oral active dipeptidylcarboxypeptidase inhibitor with antihypertensive properties, has been reported to have the following cutaneous side effects: macular and papular skin eruptions, urticaria, angioedema, mouth ulcers, pemphigus, and pityriasis rosea-like eruptions. Here, to the best of our knowledge, is the first case in which a pityriasis rosea-like eruption evolved into a lichenoid drug eruption. Also discussed is the remarkable similarity in the side effects of captopril, gold compounds, d-penicillamine, and organic mercurials.     

Carbamazepine-induced lichenoid eruption

Carbamazepine-induced skin eruptions are common but lichenoid skin rashes associated with this drug are not well documented. We report here a patient with a lichenoid drug eruption secondary to carbamazepine.     

Guanfacine‐Induced Lichenoid Drug Eruption in a Child with Autism and Attention Deficit Hyperactivity Disorder

Lichenoid drug eruptions (LDEs) have a variety of medication causes. We report a case of a 5‐year‐old boy with autism and attention deficit hyperactivity disorder treated with guanfacine who developed pruritic lesions consistent with LDEs. Rechallenge was not attempted. There are several clinical and histopathologic clues that may distinguish LDEs from lichen planus.     

Tiopronin-induced lichenoid eruption in a patient with liver disease and positive patch test reaction to drugs with sulfhydryl group

A 62-year-old woman suffering from liver cirrhosis developed lichenoid eruptions after 2 years of treatment with tiopronin. The lesions healed spontaneously within a month after withdrawal of the drug. In patch testing, the patient reacted positively, not only to tiopronin, but also to captopril and D-penicillamine, neither of which she had ever taken before. The provocation test was positive only to tiopronin, and its histological findings revealed lichenoid reaction. It is suggested that the sulfhydryl group may play a role in the etiology of tiopronin-induced lichenoid drug eruption.     

Isonicotinic acid hydrazide induced anagen effluvium and associated lichenoid eruption.

A 32 year-old woman developed generalised lichenoid eruptions on her body followed by diffuse loss of scalp hair of the anagen effluvium type. She was receiving several anti-tubercular drugs, including rifampicin, isonicotinic acid hydrazide (INH), pyrazinamide, and ethambutol, for abdominal tuberculosis. INH, which is a leading cause of drug eruptions in the above group of drugs was withdrawn. However, the other antitubercular drugs were continued along with 40 mg of prednisolone in a single daily morning dose. The latter was discontinued slowly over a period of 10 weeks. There was complete recovery of hair loss and the regrowth started after 12 weeks of alopecia. Such anagen effluvium with lichenoid eruption following INH therapy has not been observed previously. The complete recovery from anagen effluvium is difficult to explain, but it could have been because of the early initiation of corticosteroid.     

Letter: Lichenoid eruption induced by etanercept

Lichenoid drug eruption is an uncommon, but previously reported, side effect of anti-tumor necrosis factor therapy. The majority of these adverse events relate to infliximab. We report a patient who developed a lichenoid eruption on the back of her hands during etanercept therapy. She improved with topical treatment and discontinuation of the drug was not necessary. The physiopathological link between anti-TNF treatment and lichenoid eruptions remains unclear. It is important to realize that a lichenoid reaction pattern may occur during anti-TNF agent treatment.     

Lichenoid eruptions in children

Lichenoid eruptions are quite common in children and can result from many different origins. In most instances the precise mechanism of disease is not known, although it is usually believed to be immunologic in nature. Certain disorders are common in children, whereas others more often affect the adult population. Lichen striatus, lichen nitidus, Gianotti-Crosti syndrome, and lichen spinulosus are examples of lichenoid lesions that are more common in children than adults. Distinguishing these diseases is necessary for prediction of the course of the eruption and for optimal management. In most cases, certain clinical characteristics enable the clinician to reach a diagnosis, whereas in other cases biopsy is required for a definitive answer. Many of these lesions are self-limited and only require symptomatic treatment, although corticosteroids can hasten resolution in certain disorders. Discontinuation of the medication is often sufficient for resolution of lichenoid drug eruptions.     

Purpura of the ears: a distinctive vasculopathy with circulating autoantibodies complicating long-term treatment with levamisole in children

The cutaneous side-effects of levamisole include non-specific and lichenoid eruptions, fixed drug eruption and, very rarely, cutaneous vasculitis. We describe a distinctive clinical and histological vasculopathy with immunological abnormalities in children with paediatric nephrotic syndrome receiving long-term levamisole treatment. Four boys and one girl were identified. Their average age was 10 years. Levamisole had been used for an average of 24 months. Purpura of the ears was the most common finding corresponding histologically to a vasculopathic reaction pattern ranging from a leucocytoclastic and thrombotic vasculitis to a vascular occlusive disease without true vasculitis but with associated antinuclear, antiphospholipid and anticytoplasmic antibodies. The eruption resolved in all patients 2-3 weeks after the discontinuation of levamisole, but serum autoantibodies persisted for 2-14 months.     

Lichenoid drug reaction due to sildenafil

Lichenoid drug eruptions are difficult to distinguish from lichen planus. Determining the offending agent is complicated by the proliferation of lifestyle medications that the patient may not consider a medication. A case of lichenoid drug eruption due to sildenafil, which was taken for sexual enhancement, is presented.     

Fixed Drug Eruptions

Drug eruptions often have nonspecific clinical findings, and the evaluation of the probability of an eruption being a drug-induced event is difficult. A few types of drug eruption do not present such problems, and the fixed drug eruption is one of those whose clinical findings are specific enough to allow a diagnosis. The fixed drug eruption is a commonly reported type of drug eruption. The incidence of fixed drug eruptions has tended to increase, although the overall number of drug eruption cases has decreased. This is one of the reasons why fixed drug eruptions are familiar to dermatologists. The most characteristic findings of a fixed drug eruption are recurrence of similar lesions at the same sites and healing with residual hyperpigmentation. The residual hyperpigmentation serves as an indicator of site recognition. Diagnosis is not always easy; for example, as is the case for nonpigmenting fixed drug eruptions, which do not have any residual hyperpigmentation. The development of molecular biology may help to clarify the pathogenesis of fixed drug eruptions, but the reason for their recurrence on the same sites is still unknown. Identification of the causative drug or drugs is essential for the management of fixed drug eruptions, as it is for other drug eruptions. The causative drug or drugs and cross-reactants should be avoided to prevent recurrence. To date, rechallenge is the most reliable method of identifying causative drugs, but increasingly the use of skin tests has gained the attention of investigators. The validity and the problems of skin tests are discussed, and an approach to the clinical management of fixed drug eruptions is presented.