Department of Internal Medicine C, Rambam Medical Center and 1 The Technion School of Medicine, Haifa, Israel
Correspondence to: O. Fruchter, Department of Internal Medicine C, Rambam Medical Center, 8 Haaliah Street, Bat-Galim, Haifa, Israel, 31096. E-mail: oren_md{at}inter.net.il
SIR, A case history is presented of use of an artificial tanning device that provoked skin and systemic manifestations including serological markers of active systemic lupus erythematosus (SLE) in a previously healthy female.
Ultraviolet (UV) radiation-emitting sunbeds for self-tanning purposes have been available for around two decades. Sunbeds predominantly emit UV-A radiation (long wavelength, 315400 nm); however, in recent years sunbeds have been manufactured that produce higher levels of UV-B (medium wavelength, 280315 nm) to mimic the solar spectrum and speed up the tanning process [1]. Whereas sunlight is known to provoke cutaneous and systemic manifestations in patients with previously diagnosed systemic lupus erythematosus (SLE) [2], the role of UV exposure in triggering the appearance of the disease in healthy subjects is not established.
A healthy 22-yr-old female presented with generalized rash and polyarthritis following visits to a tanning salon. The patient had no history of allergic reactions to drugs, was taking no medications and had no family history of autoimmune disease.
The patient began visiting a tanning salon in which she underwent three sessions in a special tanning chamber on three separate days. Each tanning session lasted between 5 and 15 minutes, so the total time of exposure in the tanning chamber was roughly 30 minutes. On the day of the last session she developed a tender, burning, elevated, erythematous eruption on her abdomen, back, upper chest and extremities. Over the following days she had systemic low-grade fever and arthralgia accompanied by swelling that began in the right ankle and spread to the left ankle, knees and small joints of the hands, with a feeling of increased local warmth. The patient experienced morning stiffness in the small joints of her hands that lasted for more than 3 h after awakening and had malaise, decreased appetite and weight loss of 5 kg over the following 3 months. On examination, apart from generalized erythematous eruption on her torso and extremities, there were signs of active arthritis in both knee joints and the metacarpophalangeal and proximal interphalangeal joints bilaterally. Complete blood count revealed mild anaemia (haemoglobin 11.7 g%), leucopenia (white blood cells 3700/mm3) and normal platelet count. Further investigations revealed erythrocyte sedimentation rate of 60 mm/h, high-titre antinuclear antibodies (1/1600), positive anti-double-stranded DNA antibodies [46 IU/ml (normal range 020)] and low C3 [55.8 mg/dl (normal range 72156)] and C4 [3.5 mg/dl (normal range 1337)]. Activated partial thromboplastin time was 30.8 s and anticardiolipin antibodies were positive at 54.7 IU/ml (normal range 015). Creatinine clearance was normal but daily urine protein excretion was 760 mg/24 h. A biopsy of a skin lesion on the patient's arm revealed findings consistent with urticarial vasculitis, a disorder that has been described to affect SLE patients [3]. A diagnosis of SLE was made with four of the American College of Rheumatology classification criteria met [4]. The patient improved clinically and serologically after parenteral steroid therapy and remains reasonably well on plaquenil, prednisone and methotrexate.
Both cutaneous and systemic flare of SLE can occur following UV radiation [5]. Whereas once it was thought that only UV-B radiation can induce skin lesions in SLE patients, recent evidence supports the notion that UV-A, that is the predominant radiation emitted in sunbeds, can produce similar skin lesions with clinical and histological features compatible with lupus erythematosus [6, 7].
Several effects of UV radiation at the molecular and cellular level have been proposed to explain sunlight exposure as a cause of acute SLE exacerbation [8]. UV radiation is thought to play a role in the pathogenesis of SLE as it induces apoptotic keratinocytes that display surface antigens. One of the best known antigens is phosphatidylserine that normally resides at the inside of the cell membrane and following UV exposure can flip to the outside becoming exposed. Autoantibodies can now bind to the antigen, this will enable FcgR-bearing cells to interact with antibody-opsonized apoptotic cells via the FcgR resulting in the release of pro-inflammatory cytokines that play a central role in the autoimmunity process [8].
A single case-report described artificial tanning device use and SLE exacerbation in a patient with well-established SLE [9]. There is only one report of sunlight exposure followed by acute confusion that subsequently proved to be the first manifestation of SLE in a healthy male [10].
The current reported case is the first description of use of an artificial tanning device that triggered the appearance of SLE in a previously healthy subject.
Since SLE tends to appear in young women who are the predominant part of the population visiting tanning salons, and as tanning bed usage continues to increase in the Western world (partly due to its unrecognized adverse effects), clinicians should be aware of artificial tanning as a potential precipitating factor for SLE presentation.
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The authors have declared no conflicts of interest.
References
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