a clinical study of stevens-johnson syndrome and toxic … · a clinical study of stevens-johnson...

J Korean Surg Soc 2010;78:133-139□ 원 저 □

DOI: 10.4174/jkss.2010.78.3.133

133

Correspondence to: Yong Suk Cho, Department of General Surgery,Hangang Sacred Heart Hospital, Hallym University Medical Center,94-200, Yeongdeungpo-dong 7-ga, Yeongdeungpo-gu, Seoul 150- 719, Korea. Tel: 02-2639-5442, Fax: 02-2678-4386, E-mail: [email protected]

Received October 5, 2009, Accepted December 18, 2009

A Clinical Study of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: Efficacy of Treatment in Burn Intensive Care Unit

Departments of Surgery and 1Plastic Surgery, Burn Center, Hangang Sacred Heart Hospital, College of Medicine, Hallym University, 2Department of Dermatology and Cutaneous Biology Research Institute,

Yonsei University College of Medicine, Seoul, Korea

Haejun Yim, M.D., Jin Mo Park, M.D.2, Yong Suk Cho, M.D., Dohern Kim, M.D.,

Jun Hur, M.D., Wook Chun, M.D., Jong Hyun Kim, M.D., Dong Kook Seo, M.D.1

Purpose: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), potentially life-threatening skin diseases with organ failures caused by drugs, require specialized intensive care. However, SJS and TEN have usually been managed in general wards and intensive care units by most doctors. This study describes the efficacy of treatment in the burn intensive care unit (BICU) compared to previous general treatments.Methods: To investigate the clinical features, outcomes and benefits of 11 patients with SJS and TEN treated in our burn intensive care unit. Data on 11 patients who were treated between January 2004 and December 2008 were collected via a retrospective chart review. Also, the data were reviewed with previous literatures on SJS and TEN treatments.Results: Patients were classified with overlap SJS/TEN (n=4, 36.36%) or TEN (n=7, 63.64%). Nonsteroidal anti-inflammatory drugs (NSAIDs) were the most common causative agents. Hepatitis was the most common organ involvement in both overlap SJS/TEN (n=1, 9.1%) and TEN (n=4, 36.36%). Renal dysfunction (n=4, 36.36%) and respiratory disorders (n=3, 27.27%) were seen in some cases. Mean time of total reepithelization was 9 days and mean hospital day was 14.66 days. Two patients with TEN died from sepsis with multi-organ failure, and the mortality rate was 18.18%.Conclusion: Adequate treatment of SJS and TEN in the BICU supports efficacy with a low mortality rate, short healing time, short hospitalization and fewer complications. (J Korean Surg Soc 2010;78:133-139)

Key Words: Burn intensive care unit, Stevens-Johnson syndrome, Toxic epidermal necrolysis

INTRODUCTION

Stevens-Johnson syndrome (SJS) and toxic epidermal ne-

crolysis (TEN) are characterized by widespread epidermal

necrosis and mucosal involvement secondary to keratino-

cyte apoptosis mostly by drugs with high mortality. Though

the pathophysiology has not yet been fully elucidated, both

disorders are considered to be within the same spectrum,

except the involved body areas.(1-4) Several treatments with

advanced dressing material and drug therapy were intro-

duced. Some authors not by dermatologist but by surgeons

suggested some advantages of burn intensive care unit

(BICU) treatment in SJS and TEN. There were some

reports of clinical studies of SJS and TEN in Korean

dermatologic literature, however, only limited number of

reports included treatment in the burn intensive care

unit.(5-7) However, the BICU supports the patients with

proper thermoregulations, intensive fluid replacement with

electrolyte balance, enteral nutrition, infection control and

wound management with specialized nursing. Those spe-

cialized treatments of BICU provide the efficacy with a low

mortality rate, short healing time, short hospitalization and

134 J Korean Surg Soc. Vol. 78, No. 3

fewer complications. Therefore, the aim of the present

study is to present the efficacy of the burn intensive care

unit treatment with necessity in SJS and TEN.

Herein, we report our interesting retrospective study in

treating SJS and TEN in the burn intensive care unit with

literature reviews.

METHODS

1) Patients

A retrospective review was performed on all 11 patients

who visited our hospital burn center for SJS/TEN from

January 2004 to December 2008. All of them were ad-

mitted to the burn intensive care unit.

2) Diagnostic criteria

Diagnoses were made by dermatologists with histopa-

thological confirmation. The patients were divided into

three groups according to the following criteria of Bas-

tuji-Garin et al.(8,9). Bullous erythema multiforme (EM):

epidermal detachment involving ＜10% of the body sur-

face, coupled with localized typical targets or raised atypical

targets. SJS: epidermal detachment of ＜10% of the body

surface in association with widespread erythematous or

purpuric macules or flat atypical targets. SJS/TEN overlap:

epidermal detachment of 10% to 30% of the body surface

plus widespread purpuric macules or flat atypical targets.

TEN with spots: epidermal detachment of ＞30% of the

body surface coupled with wide spread purpuric macules

or flat atypical targets. TEN without spots: large sheets of

epidermal detachment involving ＞10% of the body surface

without purpuric macules or target lesions.

3) Evaluations

Data regarding demographics, causative agents, pattern

of involvement, underlying diseases, complications, mortali-

ty, and morbidity were obtained. As it is difficult to con-

firm which drugs are responsible for SJS/TEN, we checked

all drugs used within 3 weeks of onset.(5) Severity of illness

score for toxic epidermal necrolysis (SCORTEN) was eva-

luated during the first 24 hours of admission. From the

SCORTEN score, expected mortality and expected death

case were calculated. SCORTEN includes seven clinical

variables: 1) age above 40 years, 2) presence of malignancy,

3) tachycardia above 120/min, 4) involvement of ＞10%

of body surface area, 5) serum urea ＞28 mg/dl, 6) serum

glucose ＞252 mg/dl and 7) bicarbonate ＜20 mEq/L.(10)

4) Treatment

All patients received proper fluid and electrolyte resusci-

tation, pain management, nutritional support, wound care,

surgical debridement of dead tissue by intensive care unit

specialist. For the wound management, moisture retentive

dressings such as MedifoamⓇ (Hydrophilic polyurethane

foam dressing; Il Dong & Biopol, Korea), AQUACELⓇ

(ConvaTec, UK) or ActicoatTM (Smith & nephew, Canada)

were applied. Sulfonamide-containing topical agents were

avoided. Antibiotics were applied only to treat systemic

infections depending on the wound, urine, and blood

cultures, which were checked twice a week. Steroids were

prohibited and any steroid agents used prior to admission

were discontinued. Ten patients in the burn intensive care

unit were treated with intravenous immunoglobulin (IVIG)

at a dose of 1 g/kg/day for 3 to 7 days (mean 4.3 days).

RESULTS

1) Demographics

A total of 11 patients (9 males and 2 females, mean age

31.81 years, range 5∼83 years) were included in this study.

According to the criteria of Bastuji-Garin et al.,(8,9) four

patients were diagnosed with SJS/TEN (n=4, 36.36%) and

seven with TEN (n=7, 63.64%). Six (54.55%) of the pa-

tients had underlying diseases, including hypertension, con-

gestive heart failure, gout, nephritic syndrome, epilepsy,

and glaucoma (Table 1).

2) Medication history

The most common causative drugs were NSAIDs (6 of

11 patients, 54.55%) for upper respiratory infections. Two

patients (18.18%) took allopurinol for gout. Two others

had taken prednisolone for nephrotic syndrome. One (9.1%)

Haejun Yim, et al：A Clinical Study of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: Efficacy of Treatment in Burn Intensive Care Unit 135

Table 1. The clinical profiles related with medication of 11 patients with SJS/TEN overlap and TEN

Patient No. Criteria Age/SexOnset*(days)

TBSA†

(%)Underlying preexisting disease

Previousdrug allergy

Offending drugs

1 SJS/TEN 41/M 5 18 Upper respiratory infection − NSAIDs‡

2 SJS/TEN 6/F 5 27 Acute pharyngeal tonsillitis, mycoplasma pneumonia − NSAIDs 3 SJS/TEN 83/F 3 27 Upper respiratory infection − NSAIDs 4 SJS/TEN 5/M 3 27 Acute pharyngeal tonsillitis − NSAIDs 5 TEN 48/M 21 36 Hypertension, congestive heart failure, gout − Allopurinol 6 TEN 79/M 5 40 Hypertension, congestive heart failure, gout − Allopurinol 7 TEN 7/M 5 60 Upper respiratory infection − NSAIDs 8 TEN 8/M 9 60 Epilepsy − Carbamazepine 9 TEN 15/M 3 90 Nephrotic syndrome − Prednisolone10 TEN 45/M 5 95 Upper respiratory infection, glaucoma − NSAIDs11 TEN 13/M 35 100 Nephrotic syndrome − Prednisolone

*Time of onset clinical disease following the institution of a new drug regimen; †TBSA = total body surface area; ‡NSAIDs = nonsteroidal anti-inflammatory drugs.

patient had taken the antiepileptic drug carbamazepine for

epilepsy. The average period between taking the relevant

drug to the appearance of symptoms was 9 days. Both

overlap SJS/TEN (100%) and TEN (71.4%) showed symp-

toms within 2 weeks. The mean percentage total body

surface area (TBSA) of skin involvement was 24.75% (18∼

30%) in overlap SJS/TEN and 68.7% (31∼100%) in TEN

(Table 1).

3) Clinical courses

The time from appearance of the first skin lesions to

the initiation of therapy varied from 1 to 10 days (mean

4.27 days). The mean period of hospital care to complete

skin healing time was 9 days (8∼12 days). The mean

period of hospitalization was 14.66 days (7∼22 days). All

patients showed involvement of the mucous membranes,

including the buccal, conjunctival, and genital mucosae.

4) Complications

During admission, coagulase negative staphylococcus, P.

aeruginosa, A. baumannii, and methicillin-resistant staphylo-

coccus aureus were cultured. On laboratory examination,

neutropenia was found in three cases and normocytic

anemia in six cases. The most common complication was

hepatitis, which was seen in one case in the overlap

SJS/TEN group and four cases in the TEN group. Acute

renal failure occurred in four cases in the TEN group.

Continuous renal replacement therapy (CRRT) was applied

in two patients. Two patients developed sepsis and three

patients had disseminated intravascular coagulation (DIC).

Conjunctivitis developed in six patients.

5) Mortality and SCORTEN evaluation

Two of eleven patients died of septic complications with

DIC due to TEN, resulting in a mortality rate of 18.18%

(Table 2). In two patients, acute renal failure and pneu-

monia were accompanied with a SCORTEN score of 5.

The mean SCORTEN score were 2.5 in the overlap SJS/

TEN group and 3.85 in the TEN group. Three patients

had a score of 5. One patient had a score of 4. Four

patients had as score of 3 and three patients had a score

of 2 (Table 3). The number of expected deaths was 5.058,

but the actual number of deaths was 2 (Table 4).

DISCUSSION

Drugs cause adverse reactions to the skin which can

occasionally be life threatening, such as SJS and TEN.

Although most adverse reactions are transient, SJS and

TEN can be persistent and are often accompanied with

multi-organ failure.(10) Cases with skin surface involve-

ment of ＜10% TBSA are diagnosed as SJS, while those

showing involvement of ＞30% TBSA are called TEN.

Epidermal detachment between 10% and 30% is classified


as SJS/TEN overlap. SJS occurs predominantly in children

and adolescents, whereas TEN occurs in all ages regardless

of sex and race.(11) The incidence rates of SJS and TEN

are approximately 1∼7 cases and 0.4∼1.2 cases per 1

million people, respectively, per year.(11-15) The inciden-

ces of TEN and drug reactions are generally higher among

patients with HIV infection, SLE, and bone marrow trans-

plantation.(16) The most frequently implicated drugs are

sulfonamide antibiotics, aromatic anticonvulsants such as

phenytoin, phenobarbital, and carbamazepine, beta-lactam

antibiotics, nevirapine, abacavir, NSAIDs, allopurinol, la-

motrigine, tetracyclines, and quinolones.(17) Other causes

of SJS and TEN include herpes simplex virus, Mycoplasma

pneumoniae, Mycobacterium tuberculosis, group A streptococci,

hepatitis B virus, Epstein-Barr virus, Francisella tularensis,

Yersinia spp., enterovirus, Histoplasma spp., Coccidioides spp.,

and HIV.(18) In our series, NSAIDs (6 cases, 54.55%) were

the most common causative agents, followed by allopurinol,

prednisolone and carbamazepine. One girl was positive for

anti-mycoplasma antibodies, suggesting that the disease may

have been due to mycoplasma infection. Patients with over-

lap SJS/TEN and TEN showed prodromal symptoms with

fever, chills, myalgia, and sore throat for several days. The

mean period of incubation was 9 days. Careful attention

to medical history and clinical suspicion are essential to

distinguish prodromal symptoms from symptoms of other

diseases.(19)

Although many treatment options for TEN have been

proposed, no satisfactory treatment guidelines have yet

been developed. The mortality rate associated with TEN is

known as ranging from 20% to 75%.(7-10) In the present

series, 11 patients had an extensive mean body surface area

involvement of 52.73% (18∼100%) with mortality rate of

18.18%.

Since the first report of clinical studies of SJS and TEN

by Kim et al.(7) in 1991, there were few more reports by

some authors in Korean dermatologic literature.(5,6)

However, as shown in articles, those studies did not in-

clude the burn intensive care unit but in the general ward.

Compared to those previous studies, the burn intensive

care unit treatment presents some positive points (Table 5).

Tabl

e 2.

The

clin

ical

cou

rse

and

outc

ome

of 1

1 pa

tient

s

Patie

nt N

o.C

rite

ria

Tim

e to

trea

t* (

days

)T

ime

tohe

al†

(da

ys)

Leng

th o

fho

spita

lst

ay (

days

)

Muc

osal

invo

lvem

ent

Org

anism

grow

th‡

Seps

is/

DIC

§O

ther

org

an i

nvol

vem

ent

Res

idua

lco

mpl

icat

ion

Out

com

e

1

2

3

4

5

6

7

8

9

10

11

M

ean

SJS/

TEN

SJS/

TEN

SJS/

TEN

SJS/

TEN

TEN

TEN

TEN

TEN

TEN

TEN

TEN

　

2 2 7 1 2 3 4 2 10 7 7 4.2

7

8 11 14 8 13 − 11 14 8 − 12 9

10 11 20 10 13 12 11 20 15 7 22 14.6

6

＋＋＋＋＋＋＋＋＋＋＋

No

grow

thN

o gr

owth

CN

S∥

No

grow

thC

NS

MR

SA¶ ,

CN

SM

RSA

P. a

erug

inos

a, A

.bau

man

nii

P. a

erug

inos

a, A

.bau

man

nii

A.

baum

anni

iP.

aer

ugin

osa,

A.b

aum

anni

i

−/−

−/−

−/−

−/−

−/−

＋/＋ −/−

−/＋

−/−

＋/＋ −/−

−Pn

eum

onia

− −H

epat

ic f

ailu

re,

acut

e re

nal

failu

reA

cute

ren

al f

ailu

re,

pneu

mon

ia−

Hep

atic

fai

lure

, ac

ute

rena

l fa

ilure

−A

cute

ren

al f

ailu

re,

pneu

mon

ia,

pleu

ral

effu

sion

−

−C

onju

nctiv

itis

−C

onju

nctiv

itis

Con

junc

tiviti

sC

onju

nctiv

itis

−C

onju

nctiv

itis

−C

onju

nctiv

itis

−

Rec

over

edR

ecov

ered

Rec

over

edR

ecov

ered

Rec

over

edD

ead

Rec

over

edR

ecov

ered

Rec

over

ed

Dea

dR

ecov

ered

*Tim

e fr

om a

ppea

ranc

e of

fir

st s

kin

lesi

ons

to t

he i

nitia

tion

of t

hera

py;

†T

ime

from

sta

rt o

f ho

spita

l tr

eatm

ent

to c

ompl

ete

skin

hea

ling

or r

eepi

thel

izatio

n; ‡

Org

anism

cul

ture

d fr

ombl

ood

duri

ng t

reat

men

t; § D

IC =

diss

emin

ated

int

rava

scul

ar c

oagu

latio

n; ∥

CN

S =

coag

ulas

e ne

gativ

e St

aphy

loco

ccus

; ¶ M

RSA

= m

ethi

cilli

n-re

sista

nt S

taph

yloco

ccus

aur

esus

.


Table 4. Mortality assessed by SCORTEN data in SJS/TEN overlapand TEN patients

SCORTEN*score

No. ofpatients

Expectedmortalityrate (%)

No. ofexpected

death case

No. of actual

death case

0∼1 0 3.2 0 02 3 12.1 0.363 03 4 35.3 1.412 04 1 58.3 0.583 0＞5 3 90 2.700 2Total 12 − 5.058 2

*SCORTEN = score for toxic epidermal necrolysis.

Table 3. SCORTEN* data in SJS/TEN overlap and TEN patients

Patient No. CriteriaAge

(＞40 yr)Malignancy

BSA†

(＞10%)

Serumbicarbonate

(＜20 mEq/L)

Serum glucose(＞252 mg/dl)

BUN‡

(＞28 mg/dl)Heart rate

(＞120/min)Score

1 SJS/TEN ＋ − ＋ − − − ＋ 3 2 SJS/TEN − − ＋ − − − ＋ 2 3 SJS/TEN ＋ − ＋ − − − ＋ 3 4 SJS/TEN − − ＋ − − − ＋ 2 5 TEN ＋ − ＋＋ − ＋＋ 5 6 TEN ＋ − ＋＋ − ＋＋ 5 7 TEN − − ＋ − − − ＋ 2 8 TEN − − ＋＋ − ＋＋ 4 9 TEN − − ＋ − − ＋＋ 310 TEN ＋ − ＋＋ − ＋＋ 511 TEN − − ＋ − − ＋＋ 3Mean 3.7

*SCORTEN = score for toxic epidermal necrolysis; †BSA = body surface area; ‡BUN = blood urea nitrogen.

First, the burn intensive care unit treatment shortened the

time of complete reepithelization. By Kim et al.(5), they

studied 5 patients of SJS and 10 patients of TEN, mean

time to total reepithelization time was 14.1 days. However,

our study showed 9 days for total reepithelization. Second,

the burn intensive care unit treatment shortened the length

of hospital days. In our study the mean length of hos-

pitalization was 14.66 days, but in other studies it was

much longer as 16.9 days by Kim et al.(6), 19.7 days by

Kim et al.(7) and 20.6 days by Kim et al.(5). Third, the

patients received treatment in the burn intensive care unit

showed relatively well controlled vital signs without fluc-

tuation hemodynamic changes also reduced the chance of

eye complications (54.54%) and respiratory distress (27.27

%). The mortality rate (n=2, 18.18%) in our study is

relatively lower than other studies.(7-10) In 2002 reported

by Kim et al.,(11) 10 patients of TEN received IVIG and

4 of them died of sepsis and complications. In case of

mortality, both of them died of sepsis and those patients

had poor underlying conditions which easily enable to

develop into sepsis. One patient was 79 years-old man with

past history of hypertension, congestive heart failure and

gout involving 40% of TBSA and the other patient was

45 years-old man with involving 95% of TBSA.

There are a few suggestive reasons for strong points of

the burn intensive care unit treatments. First, similar to

other burn centers, treatment at our burn unit focused on

providing thermoregulation, fluids and electrolyte therapy,

enteral nutrition (if possible), wound management, and

infection control. Such supportive treatments could short-

en both the reepithelization and hospitalization period.

Also with proper antibiotics, respiratory distress including

pneumonia was reduced. Second, we did not administer

steroids to any patients. Instead of using steroids, in-

travenous immunoglobulin (IVIG, 1 g/kg/day) was ad-

ministered in 10 cases for a mean of 4.3 days. The

therapeutic effects of immunoglobulin are likely to involve

inhibition of Fas-mediated keratinocyte death by naturally

occurring Fas-blocking antibodies contained within human

immunoglobulin preparations acting directly on the Fas-Fas

ligand system at the keratinocyte surface.(20,21) Using oral


steroids in SJS and TEN is still in debate. Kim et al.(22)

and Halebian et al.(23) reported 60% and 30% higher

mortality rates, respectively, in patients treated with me-

dium-to high-dose steroids. Also we did not apply any

topical antimicrobial agents such as sulfa-containing pro-

ducts, as they might be causative agents and have the risk

of systemic sensitization.(17) Third, we used aseptic and

highly qualified materials. As TEN occurs at the der-

mal-epidermal junction, wounds are essentially the same as

superficial partial-thickness burn wounds. Therefore, if

these wounds can be kept clean without any complications,

they can heal within 10 to 14 days. Based on this principle,

after cleaning with normal saline and removing all loose

skin and blisters, the wounds were dressed with mois-

ture-retentive dressing, such as MedifoamⓇ, AQUACELⓇ

or ActicoatTM. These moisture retentive dressings are ef-

fective in the management of partial-thickness burns be-

cause they provide an environment suitable for wound

healing, minimize evaporative water loss, and reduce pain.

Since these products also require relatively few changes,

they are convenient for nursing care, including hydro-

therapy, and reduction of overall cost.(23,24)

In conclusion, no specific treatment regimen has been

unequivocally shown to be effective in treating SJS and

TEN, and palliative care remains the cornerstone of TEN

treatments. Therefore, burn units are considered ideal for

the management of TEN patients because of their wide

experience in managing burn wounds and their ability to

provide infection control and basic life support. We expect

the collaborate therapy with a burn intensive care unit in

treating severe TEN and SJS patients will reduce the mor-

bidity and mortality rates.

REFERENCES

1) Lee JY, Oh MJ, Lee BJ, Choi DC. Comparison of clinical characteristics according to infection in Stevens-Johnson syn-

drome and toxic epidermal necrolysis. J Asthma Allergy Clin Immunol 2006;26:277-81.

2) Revuz J, Penso D, Roujeau JC, Guillaume JC, Payne CR, Wechsler J, et al. Toxic epidermal necrolysis. Clinical findings and prognosis factors in 87 patients. Arch Dermatol 1987;

Tabl

e 5.

A c

ompa

riso

n of

the

pre

viou

s st

udie

s on

SJS

and

TEN

tre

atm

ent

in g

ener

al w

ards

to

BIC

U t

reat

men

t

Rep

ort　

No.

of

patie

nts

　In

volv

emen

t of

ski

nar

ea (

TB

SA*,

%)

SCO

RT

EN†

(mea

n)

Re-

epith

eliz

atio

n tim

e (d

ays)

　Le

ngth

of

hosp

ital

stay

s (d

ays)

Mor

talit

y ra

te (

%)

SJS

Ove

rlap

TEN

　SJ

SO

verla

pT

ENSJ

SO

verl

apT

ENM

ean

　SJ

SO

verla

pT

ENM

ean

SJS

Ove

rlap

TEN

Mea

n

Kim

et

al.(5

) 5

8 2

　−

−−

3.5

10∼

1411

∼18

14∼

30 1

4.1

　12

∼21

20∼

3014

∼30

20.6

00

50

6.

7K

im e

t al

.(6)

153

149.

119

.867

.3−

−−

−−

3∼

38

3∼38

3

∼38

16

.90

0 1

4.3

6.

25K

im e

t al

.(7)

80

12−

−−

−−

−−

−

7∼30

0 3

∼90

19

.70

0 4

225

Our

cas

e 0

4 7

　0

24.

7568

.73.

70

8∼

14 8

∼14

9　

010

∼20

7∼

22 1

4.66

00

29

18.1

8

*TB

SA =

tot

al b

ody

surf

ace

area

; †

SCO

RT

EN =

sco

re f

or t

oxic

epi

derm

al n

ecro

lysis

.


123:1160-5.3) McGee T, Munster A. Toxic epidermal necrolysis syndrome:

mortality rate reduced with early referral to regional burn center. Plast Reconstr Surg 1998;102:1018-22.

4) Ruiz-Maldonado R. Acute disseminated epidermal necrosis types 1, 2, and 3: study of sixty cases. J Am Acad Dermatol 1985;13:623-35.

5) Kim JW, Kim ST, Song DH. A clinical observation of the patients with Stevens-Johnson syndrome and toxic epidermal necrolysis in Jeju island. Korean J Dermatol 2004;42:579-91.

6) Kim EJ, Lee JB, Kwon YH, Yun SJ, Kim SJ, Lee SC, et al. A clinical study of Stevens-Johnson syndrome and toxic epidermal necrolysis over the last five-year period in the Gwangju-Chon-

nam area. Korean J Dermatol 2006;44:574-8.7) Kim YG, Cho KH, Chung JH. A comparative clinical study of

toxic epidermal necrolysis and Stevens-Johnson syndrome. Kor-ean J Dermatol 1991;29:602-9.

8) Halebian P, Corder V, Herndon D, Shires GT. Clinical ma-

nagement: a burn center experience with toxic epidermal ne-

crolysis. J Burn Care Rehabil 1983;4:176-83.9) Bastuji-Garin S, Rzany B, Stern RS, Shear NH, Naldi L,

Roujeau JC. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multi-forme. Arch Dermatol 1993;129:92-6.

10) Pereira FA, Mudgil AV, Rosmarin DM. Toxic epidermal ne-

crolysis. J Am Acad Dermatol 2007;56:181-200.11) Kim KJ, Jee MS, Han MH, Choi JH, Sung KJ, Moon KC, et

al. The effect of high-dose intravenous immunoglobulin for the treatment of toxic epidermal necrolysis. Korean J Dermatol 2002;40:766-71.

12) Wolkenstein P, Latarjet J, Roujeau JC, Duguet JC, Boudeau S, Vaillant L, et al. Randomised comparison of thalidomide versus placebo in toxic epidermal necrolysis. Lancet 1998;352:1586-9.

13) Lohmeier K, Megahed M, Schulte KW, Stannigel H, Mayatepek E, Schroten H. Toxic epidermal necrolysis in a premature infant of 27 weeks’ gestational age. Br J Dermatol 2005;152:150-1.

14) Chan HL, Stern RS, Arndt KA, Langlois J, Jick SS, Jick H, et al. The incidence of erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis. A population-based study with particular reference to reactions caused by drugs

among outpatients. Arch Dermatol 1990;126:43-7.15) Roujeau JC, Guillaume JC, Fabre JP, Penso D, Flechet ML,

Girre JP. Toxic epidermal necrolysis (Lyell syndrome). Incidence and drug etiology in France, 1981-1985. Arch Dermatol 1990; 126:37-42.

16) Strom BL, Carson JL, Halpern AC, Schinnar R, Snyder ES, Shaw M, et al. A population-based study of Stevens-Johnson syndrome. Incidence and antecedent drug exposures. Arch Dermatol 1991;127:831-8.

17) McKenna JK, Leiferman KM. Dermatologic drug reactions. Immunol Allergy Clin North Am 2004;24:399-423, vi.

18) Roujeau JC, Kelly JP, Naldi L, Rzany B, Stern RS, Anderson T, et al. Medication use and the risk of Stevens-Johnson syndrome or toxic epidermal necrolysis. N Engl J Med 1995; 333:1600-7.

19) Fritsch PO, Ruiz-Maldonado R. Erythema multiforme, Stevens- Johnson syndrome and toxic epidermal necrolysis. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick’s Dermatology in General Medicine. 6th ed. New York: McGraw-Hill; 2003:543-57.

20) Schopf E, Stuhmer A, Rzany B, Victor N, Zentgraf R, Kapp JF. Toxic epidermal necrolysis and Stevens-Johnson syndrome. An epidemiologic study from West Germany. Arch Dermatol 1991; 127:839-42.

21) Viard I, Wehrli P, Bullani R, Schneider P, Holler N, Salomon D, et al. Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin. Science 1998;282:490-3.

22) Kim PS, Goldfarb IW, Gaisford JC, Slater H. Burn rounds: Stevens-Johnson syndrome and toxic epidermal necrolysis: a pathophysiologic review with recommendations for a treatment protocol. J Burn Care Rehabil 1983;4:91-100.

23) Halebian PH, Corder VJ, Madden MR, Finklestein JL, Shires GT. Improved burn center survival of patients with toxic epi-dermal necrolysis managed without corticosteroids. Ann Surg 1986;204:503-12.

24) Choi SW, Suh MS, Park SJ, Lim YK. Burn care of toxic epidermal necrolysis using allevynⓇ: a report of two cases. J Korean Burn Soc 2006;9:74-8.

a clinical study of stevens-johnson syndrome and toxic … · a clinical study of stevens-johnson...

Documents