Erythrodermic and Pustular Psoriasis

Bioethics and Psoriasis

“…The TNFα, IL 17 and IL 12/23 are all well-known cytokines involved in the pathogenesis of psoriatic lesions. Inhibition of the above cytokines, results in ultimate clearing of the psoriatic lesions [8] TLR2 targets the biofilms via receptor sites within the biofilm itself [9]. We have shown its presence surrounding the biofilms in the eccrine sweat ducts in eczema and associated with the plaques in the brains of Alzheimer's disease patients [10,11].…”

Erythrodermic Psoriasis: Current and Future Role of Biologicals

“…Recent evidence suggests that biological agents, including both anti-tumor necrosis factor (TNF)-a agents and ustekinumab, may be more useful in the management of EP [2,8,12,20]. Unfortunately, subjects with EP are usually excluded from all pivotal trials involving biological agents, and this evidence is currently dispersed in small case series and single case reports.…”

“…In the second form, more common in arthropathic psoriasis, the characteristics of the disease are often lost (typically, an extensive erythema is observed, with or without scaling and no recognizable psoriatic plaque), the disease is generally unstable, the patient may be febrile and ill, and there is an appreciable mortality; in contrast to the previous form, itching is often severe [18]. The course of EP may vary from prolonged and chronic (more common for the first clinical subtype) to acute and rapid progressive (more typical of the second clinical subtypes); sometimes, EP may follow a relapsing-remitting pattern, with classic plaques of psoriasis vulgaris during remitting phases [1,4,7,8].…”

“…Various severe and sometimes fatal complications have been reported in association with EP, including sepsis from skin pathogens (especially Staphylococcus aureus), shock and acute renal failure due to skin fluid loss, acute respiratory distress syndrome, hydroelectrolytic abnormalities, severe anemia, impaired thermoregulation causing hypothermia, severe protein loss, and high-output congestive heart failure due to derangements in the distribution of blood [1,3,4,8].…”

“…The reason that EP appears is not understood, but several factors are recognized as possible triggers, including systemic illness (e.g., HIV infection), emotional stress, ultraviolet (UV) burns, topical tar, alcoholism, and abrupt withdrawal of anti-psoriatic drugs (rebound phenomenon) such as oral and potent topical steroids, methotrexate, and efalizumab [4,[7][8][9][10]. Interestingly, rebound after efalizumab discontinuation has been reported mainly in patients who have not had a satisfactory clinical response [10].…”