Thalidomide in dermatology. New indications for an old drug

Calderón, Perla; Anzilotti, Michele; Phelps, Robert

doi:10.1046/j.1365-4362.1997.00298.x

Cited by 49 publications

(33 citation statements)

References 59 publications

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“…Thalidomide has been proposed as a treatment of TEN because it is a potent inhibitor of TNF-α [102, 103.] However, in a double-blind, randomized, placebo-controlled study, a significant excess of mortality occurred in the thalidomide group (400 mg/day, orally for a 5-day course) [104].…”

Section: Ten Treatmentsmentioning

confidence: 99%

Novel Treatments for Drug-Induced Toxic Epidermal Necrolysis (Lyell’s Syndrome)

Paquet

Pierard

Quatresooz³

2005

Int Arch Allergy Immunol

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Drug-induced toxic epidermal necrolysis (TEN) is a life-threatening disease characterized by extensive destruction of the epidermis. It apparently results from the formation of specific toxic drug metabolites by the keratinocytes. The mortality rate which averages 25–30% is mainly due to secondary septicemia, and to ionic and metabolic disturbances following loss of epidermal integrity. Apoptosis is the likely mechanism leading to massive keratinocyte death in TEN. Dysregulations in the tumor necrosis factor-α (TNF-α) pathway, CD95 system (Fas ligand, CD95L; Fas receptor, CD95R) and calcium homeostasis in the epidermis are involved in this apoptotic process. An active role has also been ascribed to T lymphocytes, macrophages and factor XIIIa-positive dermal dendrocytes. Despite progress, treatment of TEN remains controversial. In the past, systemic glucocorticoids were used in order to target the inflammatory reaction in TEN. However, there was no evidence for improvement of the healing process, while corticosteroids worsened the prognosis by increasing the risk of septicemia. Only a few cases have been treated with other drugs including cyclophosphamide, pentoxyfilline, thalidomide, anti-TNF-α antibodies and cyclosporin A. In the recent past, some TEN patients were treated with intravenous human immunoglobulins (IVIG). The rationale for such a treatment was to block the CD95 system on keratinocytes. The early promising clinical results of IVIG treatment in TEN were subsequently challenged. This review compares the effectiveness and drawbacks of the major drugs presently used in TEN treatment. Some future prospects in TEN management are also discussed.

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Section: Ten Treatmentsmentioning

confidence: 99%

Novel Treatments for Drug-Induced Toxic Epidermal Necrolysis (Lyell’s Syndrome)

Paquet

Pierard

Quatresooz³

2005

Int Arch Allergy Immunol

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“…The unexpected clinical improvement observed in these patients prompted interest in the use of thalidomide as an immunomodulating agent. 21 The efficacy of this medication has been demonstrated in various dermatologic disorders, including discoid lupus erythematosus, chronic cutaneous lupus erythematosus, benign lymphocytic infiltrate of Jessner, adult Langerhans cell histiocytosis, cutaneous sarcoidosis, Behçet's disease, erosive lichen planus, and pyoderma gangrenosum. [22][23][24] As thalidomide has been beneficial in other neutrophilic dermatoses, including pyoderma gangrenosum and Behçet's disease, it stands to reason that it would improve Sweet's lesions as well.…”

Section: Discussionmentioning

confidence: 99%

Thalidomide in the treatment of recalcitrant Sweet's syndrome associated with myelodysplasia

Browning

Dixon

Malone

et al. 2005

Journal of the American Academy of Dermatology

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“…9-11 It appears particularly promising for the management of HIV-related complications, including aphthous and oesophageal ulcers, and wasting syndromes, [12][13][14] cutaneous lesions of systemic lupus erythematosus 15 and cutaneous and pulmonary sarcoidosis. 16 Interest in the drug has also been renewed by demonstration of its activity in chronic graft-versus-host disease, 17,18 although poor tolerance frequently limits its use.…”

Section: Thalidomide In the Treatment Of Erythema Nodosum Leprosum (Ementioning

confidence: 99%

“…36,37 By acting as a costimulator, thalidomide increases the response of T cells to T-cell receptor-mediated stimulation, yielding increased proliferation and greater production of interleukin-2 (IL-2), IL-10 and interferon gamma (IFN-g). 9,38,39 Thalidomide increases the number of natural killer cells, while these cells exhibit augmented cytotoxic activity against tumour cells. 40 In addition, it downregulates IL-5, IL-6, IL-8 and IL-12 production.…”

Section: Alternative Mechanisms Of Actionmentioning

confidence: 99%