Managing subacute cutaneous lupus erythematosus

Managing a patient with subacute cutaneous lupus erythematosus subsequent to ultraviolet exposure is challenging to health care professionals. A discussion of the disease process, a case study, and practical strategies for patient care will be presented.     

Bullous subacute cutaneous lupus erythematosus

We describe a 59-year-old woman, with a history of autoimmune disease and disseminated uterine leiomyosarcoma, who developed a photoaggravated, blistering skin eruption. An initial rash, at the outset of treatment with chemo- and radiotherapy, resembled erythema multiforme. Review of the original skin biopsy showed it to be subacute cutaneous lupus erythematosus. There were no systemic symptoms or signs to suggest systemic lupus erythematosus. The much later photoaggravated rash consisted mainly of bullae and eventual epidermal denuding which resembled toxic epidermal necrolysis. We propose that the clinical and histological diagnosis is one of bullous subacute cutaneous lupus erythematosus in a patient with no other features of systemic lupus erythematosus.     

Terbinafine-induced subacute cutaneous lupus erythematosus

BACKGROUND: Recently, the induction of subacute cutaneous lupus erythematosus (SCLE) and exacerbation of systemic lupus erythematosus by terbinafine have been reported. OBJECTIVE: We describe 4 cases of SCLE, one associated with chilblain lupus, which occurred during therapy with oral terbinafine for onychomycosis. METHODS: Of 21 consecutive patients with SCLE attending the outpatient dermatology department at Muenster University clinic during a 1-year period, 4 patients with terbinafine-induced SCLE were seen. Patients were examined fully and photographed; histologic findings as well as serologic and follow-up data were evaluated. RESULTS: In addition to high titers of antinuclear antibodies (ANA) with a homogeneous pattern, anti-Ro(SS-A) antibodies were present; in 3 of 4 women, anti-La(SS-B) antibodies were also found. All patients had anti-histone antibodies as in drug-induced lupus and showed the characteristic genetic association of SCLE with the HLA-B8,DR3 haplotype; moreover, in 2 cases, HLA-DR2 was also present. After discontinuation of terbinafine, ANA titers decreased; anti-histone antibodies also became undetectable within 4(1/2) months in 3 patients concomitant with subsidence of the SCLE eruption in all patients. CONCLUSION: Terbinafine is a drug that appears to infrequently induce SCLE with high titers of ANAs and anti-histone antibodies in genetically susceptible persons.     

Bupropion-induced subacute cutaneous lupus erythematosus

Subacute cutaneous lupus erythematosus is a subset of cutaneous lupus erythematosus with unique immunological and clinical features. The first series of patients found to have drug-induced subacute cutaneous lupus erythemotosus were secondary to hydrochlorothiazide. Since that time, several other drugs have been implicated in the induction of subacute cutaneous lupus erythemotosus. A 44-year-old woman presented with a 9-week history of a mildly pruritic, photosensitive rash that started on her chest. One month prior to her skin outbreak she was started on bupropion for mild depression. She was noted to have multiple annular erythematous plaques on her anterior chest, shoulders, back, arms and face. The patient was advised to stop the bupropion and to start topical tacrolimus, and was encouraged to apply a broad-spectrum sunscreen. Her skin completely cleared within 1 month of initiating this treatment regimen. This case is a unique example of bupropion-induced subacute cutaneous lupus erythemotosus. Our patient exemplifies the necessity of a complete medical history, including current medications, especially when subacute cutaneous lupus erythemotosus is suspected.     

Terbinafine-induced subacute cutaneous lupus erythematosus

BACKGROUND: Nearly 10% of lupus erythematosus (LE) are drug induced. More than 60 different drugs are involved in iatrogenic LE. We report herein 3 cases of terbinafine-induced LE. OBSERVATIONS: Three patients receiving terbinafine for a suspected dermatophytic infection developed a subacute cutaneous LE, within 7 weeks following terbinafine introduction. The patients' medical history included sicca syndrome, lung carcinoma and Kikuchi disease, respectively. Clinical remission occurred within 15 weeks following terbinafine withdrawal. DISCUSSION: Sixteen cases of terbinafine-induced LE have been previously reported, including 13 women. The median age was 54 years. Prior autoimmunity was reported in 10 cases, including 5 pre-existing LE. The median delay between terbinafine introduction and LE onset was 5 weeks. The median time until clinical recovery following terbinafine withdrawal was 8 weeks. CONCLUSION: Terbinafine should be prescribed only in patients with proven dermatophytosis. We recommend cautious monitoring in patients with pre-existing autoimmunity. The diagnosis of terbinafine-induced LE should lead to the immediate and definitive withdrawal of the drug.     

Terbinafine-induced subacute cutaneous lupus erythematosus

Terbinafine is a synthetic oral allylamine that is used for systemic treatment of microscopy- or culture-proven dermatophyte infections of skin and nails. It is normally well-tolerated and side effects include transient gastrointestinal symptoms and skin reactions that can occur in up to 2.3% of treated patients. Subacute cutaneous lupus erythematosus (SCLE) is a skin reaction that has been reported secondary to use of a variety of drugs. The number of reports of SCLE with terbinafine is limited. We demonstrate 2 patients in one dermatology clinic who presented with a predisposing autoimmune diathesis within 3 months of each other.     

Terbinafine-induced subacute cutaneous lupus erythematosus

Oral terbinafine is licensed for use in onychomycosis after positive confirmation of infection. We describe five cases of subacute cutaneous lupus erythematosus associated with terbinafine therapy. All cases had positive antibodies to extractable nuclear antigens, predominantly anti-Ro, and several had a history of pre-existing autoimmune disease. Terbinafine should only be prescribed after confirmation of infection by microscopy or culture.     

Nitrendipine-induced subacute cutaneous lupus erythematosus

A 66-year-old man presented with widespread annular and bullous subacute cutaneous lupus erythematosus (SCLE), developed after starting treatment for hypertension with the calcium channel blocker nitrendipine. A few days after withdrawal of the drug, while cutaneous manifestations were improving, left hemiparesis occurred. Laboratory investigations showed, in addition to anti-Ro, anti-La and anti-histone antibodies, the presence of lupus anticoagulant, anticardiolipin antibodies, prolonged APTT and thrombocytopenia. On the basis of the spontaneous regression of the patient's skin lesions after discontinuation of the drug, a possible relationship between nitrendipine intake, the clinical events and the biological findings is discussed.     

Pathogenesis of subacute cutaneous lupus erythematosus

Subacute cutaneous lupus erythematosus (SCLE) is a photosensitive form of lupus‐specific skin lesion that is strongly associated with the presence of anti‐Ro/SSA autoantibody. The pathogenesis of SCLE includes genetic, environmental and immunologic factors. Recent studies provide strong evidence for the involvement of innate and cell‐mediated immunity, underlying the important role of plasmacytoid dendritic cells, interferon‐α and antibody‐dependent cell cytotoxicity. In addition, a variety of cytokines, chemokines and adhesion molecules have been found to participate in the expansion phase of the autoimmune effector mechanisms. This article summarizes the recent immunological findings and reviews the current mechanisms which are implied in the development of the disease.     

Sweet's syndrome in subacute cutaneous lupus erythematosus

A 67-year-old man being treated with prednisone, 15 mg/day, for subacute cutaneous lupus erythematosus developed widespread, tender, erythematous plaques, arthralgias, and fever. Clinically, the cutaneous lesions mimicked lupus erythematosus. The diagnosis of acute febrile neutrophilic dermatosis, or Sweet's syndrome, was confirmed by histologic examination of three biopsy specimens, which revealed prominent dermal edema, extensive infiltration with intact and karyorrhectic polymorphonuclear leukocytes, and perivascular and appendiceal lymphocytes in the absence of leukocytoclastic angitis.     

Thalidomide treatment of subacute cutaneous lupus erythematosus

Two patients with subacute cutaneous lupus erythematosus were treated with a low dosage of thalidomide. This resulted in rapid improvement of skin lesions in both patients and in the disappearance of severe fatigue in one patient.     

Papulonodular mucinosis with subacute cutaneous lupus erythematosus

A 30-year-old woman with subacute cutaneous lupus erythematosus presented with a facial eruption, painful and swollen ulcers of her digits, and asymptomatic lesions on her abdomen. The laboratory findings were consistent with subacute cutaneous lupus erythematosus with an anticardiolipin antibody. A biopsy specimen of the asymptomatic lesions on her abdomen showed mucin within the upper reticular dermis. Papulonodular mucinosis is a rare but well-documented finding associated with systemic and cutaneous forms of lupus erythematosus. The etiology and pathogenesis of this finding remain to be elucidated.