This condition is not considered to be a true idiopathic leukoplakia since the causative agent has been identified. It is one of the most common oral lesions associated with HIV infection, along with pseudomembraneous candidiasis. The appearance of the lesion often heralds the transition from HIV to acquired immunodeficiency syndrome (AIDS). Syphilitic leukoplakia
This term refers to a white lesion associated with syphilis, specifically in the tertiary stage of the infection. It is not considered to be a type of idiopathic leukoplakia, since the causative agent Treponema pallidum is known. It is now rare, but when syphilis was more common, this white patch usually appeared on the top surface of the tongue and carried a high risk of cancerous changes. It is unclear if this lesion was related to the condition itself or whether it was caused by the treatments for syphilis at the time. Esophagus
Leukoplakia of the esophagus is rare compared to oral leukoplakia. The relationship with esophageal cancer is unclear because the incidence of esophageal leukoplakia is so low. It usually appears as a small, nearly opaque white lesion that may resemble early esophageal squamous cell carcinoma. The histologic appearance is similar to oral leukoplakia, with hyperkeratosis and possible dysplasia. Bladder
In the context of lesions of the mucous membrane lining of the bladder, leukoplakia is a historic term for a visualized white patch which histologically represents keratinization in an area of squamous metaplasia.
Differential diagnosis
Staphylococcal scalded skin syndrome
Drug-induced linear immunoglobulin A dermatosis
Acute graft versus host disease
Acute generalized exanthematous pustulosis
Erythroderma
Drug reaction with eosinophilia and systemic symptoms aka DRESS
A generalized morbilliform eruption

Treatment
The primary treatment of TEN is discontinuation of the causative factor(s), usually an offending drug, early referral and management in burn units or intensive care units, supportive management, and nutritional support.Current literature does not convincingly support use of any adjuvant systemic therapy. Initial interest in Intravenous immunoglobulin (IVIG) came from research showing that IVIG could inhibit Fas-FasL mediated keratinocyte apoptosis in vitro. Unfortunately, research studies reveal conflicting support for use of IVIG in treatment of TEN. Ability to draw more generalized conclusions from research to date has been limited by lack of controlled trials, and inconsistency in study design in terms of disease severity, IVIG dose, and timing of IVIG administration. Larger, high quality trials are needed to assess the actual benefit of IVIG in TEN. Numerous other adjuvant therapies have been tried in TEN including, corticosteroids, ciclosporin, cyclophosphamide, plasmapheresis, pentoxifylline, acetylcysteine, ulinastatin, infliximab, and granulocyte colony-stimulating factors (if TEN associated-leukopenia exists). There is mixed evidence for use of corticosteroids and scant evidence for the other therapies. A meta-analysis from 2002 concluded that there is no reliable evidence for the treatment of TEN. Thalidomide did not show any benefit and was associated with increased mortality compared with placebo. Prognosis
The mortality for toxic epidermal necrolysis is 25–30%. People with SJS or TEN caused by a medication have a better prognosis the earlier the causative medication is withdrawn.