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Year : 1996  |  Volume : 62  |  Issue : 4  |  Page : 270-271

Systemic corticosteroids in toxic epidermal necrolysis

Correspondence Address:
Sandipan Dhar

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Source of Support: None, Conflict of Interest: None

PMID: 20948085

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How to cite this article:
Dhar S. Systemic corticosteroids in toxic epidermal necrolysis. Indian J Dermatol Venereol Leprol 1996;62:270-1

How to cite this URL:
Dhar S. Systemic corticosteroids in toxic epidermal necrolysis. Indian J Dermatol Venereol Leprol [serial online] 1996 [cited 2019 Oct 19];62:270-1. Available from: http://www.ijdvl.com/text.asp?1996/62/4/270/4422

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The role of systemic corticosteroids in the management of toxic epidermal necrolysis (TEN) is a subject of controvesy. Some workers believe that the patients who receive corticosteroids experience a poorer outcome than those who do not,[1] whereas others feel that steroids reduce the morbidity and mortality when given early enough and in sufficiently high dosage (prednisolone 2-8mg/kg/day).[2] In a study of 30 patients with drug-induced TEN (DTEN), it was observed that overall prognosis was much better in those patients who were put on high dose systemic steroids within 7 days of its development.[3] Our recent experience of treating TEN in children and adolescents with systemic steroids was also quite encouraging.[4]

In an appraisal, Pasricha highlighted the usefulness of high dose corticosteroid started very early in the management of TEN.[5] A rapid tapering followed by withdrawal within 2 weeks was recommended.

It is not difficult to understand why early institution of steroid would reduce mortality in TEN. Majority of TEN cases are due to antibody dependent cell mediated cytotoxicity (ADCC) type of hypersensitivity phenomenon which is very sensitive to corticosteroids.[6] Thus, steroid instituted in high doses and early in the diseases halts ADCC reaction preventing further tissue damage by the ongoing process of TEN. Once tissue damage (maximum within first 7 days) has occurred, human body systems have to face its consequences and steroids have very little role to play. Once steroids have counteracted ADCC phenomenon and further tissue damage, and the offending drug has been omitted, no more steroids are required and these should be tapered rapidly and stopped.[5] Unnecessary prolongation of steriod therapy may increase the mortality by increasing the incidence of secondary infection and sepsis.[1]

There are occasional reports of patients with TEN not responding to even very high dose(s) of corticosteroid(s) instituted from the beginning. In these patients, a mixed lymphocyte reaction with the production of killer lymphocytes, resembling acute graft versus host diseases (GVHD) is the probable underlying process.[6]

It is, therefore, felt that if the corticosteroids are used in low dosage, later in the disease and there is lengthy tapering (3 Ls), their usefulness is questioned. It is the lack of knowledge and expertise about how to use it rather than the lack of its efficacy which has made the role of corticosteroid(s) a matter of debate.

  References Top

1.Revuz J, Roujeaue JC, Guillaume JC, et al. Treatment of toxic epidermal necrolysis:Creteil's experience. Arch Dermatol 1987;123:1156-8.  Back to cited text no. 1    
2.Stables GI, Lever RS. Toxic epidermal necrolysis and systemic corticosteroids. Br J Dermatol 1993;128:357.  Back to cited text no. 2    
3.Kaur S, Nanda A, Sharma VK. Elucidation and management of 30 patients of drug induced toxic epidermal necrolysis (DTEN). Ind J Dermatol Venereol Leprol 1990;56:196-9.  Back to cited text no. 3    
4.Sharma VK, Dhar S. Clinical pattern of cutaneous drug eruption among children and adolescents in north India. Pediatric Dermatol 1995;12:178-83.  Back to cited text no. 4    
5.Pasricha JS. Management of toxic epidermal necrolysis. Ind J Dermatol Venereol Leprol 1990;56:458-9.  Back to cited text no. 5    
6.Heng MYC, Drug-induced toxic epidermal necrolysis. Br J Dermatol 1985;113:597-600.  Back to cited text no. 6    


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