Lupus erythematosus (SLE simply stated) is a chronic autoimmune disease where the immune system attacks the connective tissues of the body.
Without history of SLE, it appears that both explanations have been advanced. Characterized by erythematous patches of variable size, clearly defined and scaly which tend to resolve with atrophy, scarring, hyperpigmentation. The occurrence of lesions may be precipitated by trauma, stress, sunburn and exposure to cold. The visceral involvement is absent but very rare cases of occurrence of systemic lupus erythematosus have been reported in the suites. Haematological and serological changes detected in about half of patients suggest an autoimmune etiology.
Key Points:
It is clinically characterized by its erythematous, edematous or more or less scaly or papular. In the localized form, it is located mainly on the cheeks and nose, malar or ". On the backs of hands, especially lupus manifestations reach areas interarticular that, conversely, are observed in dermatomyositis. In the forms of bullous lupus hyperacute exist large separations, occurring always in lupus erythematous areas.
Oral lesions of lupus are acute erosion, localized preferentially on the gums, palate, cheeks or lips, sometimes well supported, sometimes very painful, embarrassing food. Achieving genital is much rarer, usually associated with damage oral. All these lesions heal quickly without scarring, apart from a possible hyperpigmentation sequelae in subjects with pigmented skin.
The differential diagnosis is mainly with rosacea that includes telangiectasia and pustules, with seborrheic dermatitis localized mainly in the nasolabial folds, with a predominant dermatomyositis face on the upper eyelids and purplish areas on the hands articular . Disseminated forms sometimes refer to eczema, rash or viral toxidermique. Hyperacute forms can discuss toxic epidermal necrolysis. Oral erosions of acute lupus are generally less extensive than those of Stevens-Johnson syndrome. Achieving genital lupus is rare, and generally more limited.
Clinically, SLE is manifested initially by lesions or erythematous macular papular or moving to an annular shape or form to a psoriasiform. In the annular lesions have edged contours polycyclic erythematous scaly or vesicular and crusted with a central hypo-pigmented greyish, sometimes covered with telangiectasia (Figure 3). Rarely, they can take an aspect of erythema multiforme (Rowell's syndrome). In the form psoriasiform lesions are papulosquamous, psoriasiform or pityriasiform, can coalesce to produce a profuse form, or an exfoliative. Both forms can be combined in the same patient. Whatever the form, the surface is reached, no visible follicular keratosis or squamous adherent. The lesions suggestive topography due to predominant distribution of photo-exposed areas with an attack roughly symmetrical face, neck, chest, shoulders, extensor surface of the arm, back of hands. The extension is possible on the trunk, with a common respect for the inside of the upper limbs, armpits and sides. The lower limb is rare. Regression of lesions is more or less rapid atrophy without scarring, but with pigmentation disorders (hypo-or hyperpigmentation) and telangiectasia sequelae.
The diagnosis may be reluctant with tinea, eczema ring, erythema multiforme, psoriasis, pityriasis rosea, a drug eruption. Pathological examination with direct immunofluorescence in lesional area eliminates the majority of these diagnoses, except in cases of erythema multiforme Rowell's syndrome or a drug eruption if diffuse lesions. In these cases, the clinical context that guides to the diagnosis of SLE.
Lupus erythematosus
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