Management of Nonstaphylococcal Toxic Epidermal Necrolysis: Follow-Up Study of 16 Case Histories

Tegelberg-Stassen, M. J. A. M.; Vloten, W. A. van; Faille, H. Baart de la

doi:10.1159/000248010

Cited by 32 publications

(8 citation statements)

References 7 publications

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“…Phenytoin should be discontinued immediately. In most of the cases, a significant recovery is observed in the dermal lesions and symptoms with the application of high-dose steroids, although others have reported no benefit from steroids [14]. Furthermore, corticosteroids may also be a contributing factor, increasing the risk of TEN [15].…”

Section: Discussionmentioning

confidence: 99%

Toxic Epidermal Necrolysis after Cranial Radiotherapy and Phenytoin Treatment

Dinçbaş¹,

Yörük

Demirkesen

et al. 2004

Oncol Res Treat

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Background: There are few reports about Stevens-Johnson syndrome, a bullous form of erythema multiforme, that can develop in patients treated with cranial irradiation and antiepileptic drugs, especially with phenytoin. We present a patient who developed toxic epidermal necrolysis, a rare and severe form of Stevens-Johnson syndrome, during cranial radiotherapy and phenytoin treatment. Case Report: A 65-year-old male patient with stage IIIB non-small cell lung carcinoma developed a brain metastasis. The patient was treated with phenytoin and dexamethasone. Palliative total cranial irradiation was performed. On the 23rd day of phenytoin administration, erythema and edema in the radiotherapy area and lips, as well as widespread maculopapular eruptions and rashes in the upper thoracic area were observed. The dermal lesions progressed to bullae and subsequently toxic epidermal necrolysis covering 70% of the whole body surface developed. The patient died within 15 days of appearance of the lesions due to secondary infections, despite supportive and symptomatic treatment. Conclusion: Although toxic epidermal necrolysis is a rare toxicity it must always be considered during cranial irradiation and antiepileptic prophylaxis.

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Section: Discussionmentioning

confidence: 99%

Toxic Epidermal Necrolysis after Cranial Radiotherapy and Phenytoin Treatment

Dinçbaş¹,

Yörük

Demirkesen

et al. 2004

Oncol Res Treat

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“…Daily doses as high as 1 g of hydrocorticosone were recommended to prevent the extension of epidermal loss and to minimize the systemic manifestations of the disease. Several recent open studies also reported benefits following the use of systemic glucocorticoids including parenteral dexamethasone (4 mg twice daily) [62], oral prednisolone (60 mg/day) [63] and oral/intravenous prednisone (200–400 mg/day) [64]. Of 32 patients treated in these studies, only 1 died and the others fully recovered.…”

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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“…However, the comparison with Bactrim® (table III) suggests alternative explanations, including genetic diversity of users with resulting altered drug metabolism (Gilles & Clyde 1974;Sarikabhuti et al 1988), environmental factors such as sunlight (Ortel et al 1989;Ott 1987), or coinfections and comedications. While most toxic epidermolysis cases are drug related (Roujeau et al 1990;Tegelberg-Stassen 1990), infections contribute to EM/SJS, particularly in children (Maleville et al 1983). Agents implicated include herpes simplex virus (Britz & Sibulkin 1975;Hutchison & Kelly 1978), human immunodeficiency virus (HIV) [Bull & Staughton 1990;Schoefer et al 1989;Sugarman et al 1990] and Mycoplasma pneumoniae (B6ttiger et al 1975;Larregue et al 1982;Rodriguez Marcos & Jimenez 1983).…”

Section: Discussionmentioning

confidence: 99%

How Frequent are Notified Severe Cutaneous Adverse Reactions to Fansidar®?

1993

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An attempt was made to estimate the risk of severe cutaneous adverse reactions (SCARs) to Fansidar (sulfadoxine plus pyrimethamine). Cases were identified through a spontaneous reporting system. Persons exposed were estimated using sales data of 27 countries reporting one SCAR case for either Fansidar or a related product, Bactrim (cotrimoxazole; sulfamethoxazole plus trimethoprim). Between 1974 and 1989, 126 cases were notified for Fansidar: 87 cases of erythema multiforme or Stevens-Johnson syndrome, and 39 cases of toxic epidermic necrolysis. 86% of cases were reported in Europe or North America. In 116 cases with use known, prophylaxis was the reason in 103, and treatment in 13. Toxic epidermolysis and erythema multiforme/Stevens-Johnson syndrome had case fatalities of 36 (95% confidence intervals 21 to 53%) and 9% (4 to 18%), respectively. Fansidar users were estimated at 117 million, and the overall SCAR risk to be 1.1 (0.9 to 1.3) per million. For developing countries with mainly single dose use, the risk was estimated to 0.1 (0.0 to 0.1) per million. For Europe and North America with mainly prophylactic use, the risk was 10 (8 to 12) and 36 (23 to 48) per million, respectively. Prophylactic use had a 40 times higher risk than single dose therapeutic use. The aggregated risk peaked in 1984-1985, with global and North American SCAR frequencies of 3.4 (2.4 to 4.3) and 72 (41 to 102) per million, respectively. After 1985, North America reported only one further case despite continued use by an estimated 0.3 million persons.(ABSTRACT TRUNCATED AT 250 WORDS)

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Management of Nonstaphylococcal Toxic Epidermal Necrolysis: Follow-Up Study of 16 Case Histories

Cited by 32 publications

References 7 publications

Toxic Epidermal Necrolysis after Cranial Radiotherapy and Phenytoin Treatment

Toxic Epidermal Necrolysis after Cranial Radiotherapy and Phenytoin Treatment

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

How Frequent are Notified Severe Cutaneous Adverse Reactions to Fansidar®?

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