July 2012 Clinical Advisor

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lichen planus, primary HIV infection, and drug eruption. Lesions on the hands and feet may be confused with psoriasis, eczema, and discoid lupus erythematosus. Finally, tertiary syphilis may resemble sarcoidosis, tumors, lupus vulgaris, mycosis fungoides, and fungal infections. Penicillin G is still the treatment of choice for all stages of syphilis. The dose varies depending on the stage of the disease. Thus far, penicillin resistance to T. pallidum has not been detected. If a person is allergic to penicillin, a tetracycline may be used. Follow-up examinations are recommended at months 1, 3, 6, and 12 following antibiotic treatment of early syphilis, then every six months for two years. Patients with late syphilis should be followed for three years. Due to the sexually transmitted nature of this disease, many countries require documentation and notification of previous sexual partners.4 Given that this patient also had concurrent HIV infection, he was treated with benzathine (Bicillin) penicillin 2.4 million units intramuscular weekly for three doses. The rash resolved, and repeat serologic examination one month following antibiotic treatment was within normal limits. The patient will be followed for at least two years.

CASE #2

Discoid lupus erythematosus

Lupus erythematosus is a multisystem disorder that prominently involves the skin. In some, the cutaneous lesions also may serve as an indicator of underlying systemic disease. There are three major forms of cutaneous lupus. The first is acute cutaneous lupus erythematosus (ACLE), which is characterized by the classic malar erythema, or butterfly rash. ACLE is most commonly associated with underlying SLE. The second variant is subacute cutaneous lupus erythematosus (SCLE), which is a photosensitive eruption that is longerlasting than classic ACLE. Discoid lupus erythematosus (DLE) falls under the category of chronic cutaneous lupus, and these lesions are often long-lasting and scarring. Cazenave was the fi rst to describe and name lupus erythematosus in the mid-1800s.5 It was not until 1964 that Dubois categorized the disorder into a spectrum of disease ranging from cutaneous lesions to life-threatening internal

disease. In 1981 and 1982, Weston and Sontheimer found that anti-Ro antibodies were associated with neonatal lupus and SCLE, respectively.6,7 Lupus erythematosus is an autoimmune disorder that is believed to have a genetic predisposition with an environmental activator.8 Some propose that in the appropriate context, an immune response to a foreign antigen may lead to a limited and then broader autoimmune response. Ultimately, this ends with tissue injury. Certain autoantibodies are associated with certain skin diseases. For example, antibodies to double-stranded DNA (dsDNA) are seen in those with ACLE and antibodies to Ro are seen in those with SCLE. DLE is the most common type of cutaneous lupus and may involve the epidermis, upper dermis, and lower dermis. There is a much lower female-to-male ratio with discoid lupus (2:1) than with to systemic lupus (8:1). Lesions are most commonly found on the face, scalp, and ears, but may also be seen in a widespread distribution. It is unusual for DLE to be present below the neck without lesions also being present above the neck.9 Unlike other forms of lupus, there is no clear association between sun exposure and the development of DLE. Lesions may present with erythema, scaling, atrophy, dyspigmentation, and scarring. Active lesions may feel indurated due to the intense inflammatory infi ltrate in both the superficial and deep dermis. Follicular plugging and alopecia are other common features. The dyspigmentation is most often characterized by hyperpigmentation of the periphery with central hypopigmentation. Lesions on the palms and soles may be ulcerative or keratotic. Discoid lesions have potential for scarring and given enough time, most patients will develop disfiguring scars, which may impact their quality of life. The majority (90%-95%) of patients with DLE do not develop SLE. Those with widespread lesions may be at greater risk of systemic involvement. There are different histologic patterns that correspond to the various forms of cutaneous lupus. This write-up will discuss only the histopathologic findings seen in DLE. There is often marked hyperkeratosis and follicular plugging of the epidermis. The dermal-epidermal basement membrane zone is visibly thickened and obscured due to liquefaction degeneration. The thickening may be more apparent on periodic acid Schiff-stained sections. A lymphohistiocytic infi ltrate is seen in the superficial and deep dermis in both a perivascular and periadnexal distribution. The differential diagnosis of early lesions of DLE may be confused with syphilis, Jessner’s lymphocytis infiltrate, polymorphous light eruption, lymphocytoma cutis, lymphoma

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