CASE REPORT

Severe DRESS Syndrome Managed With Therapeutic

Plasma Exchange
AUTHORS: Thomas Alexander, MD, MPH,a Edward Iglesia
BA,b Yara Park, MD,c Daniel Duncan, MD,c David Peden, MD, abstract
MS,a,d Saira Sheikh, MD,a and Maria Ferris, MD, MPH, PhDa
Drug reaction with eosinophilia and systemic symptoms (DRESS) syn-
Departments of aPediatrics, cPathology and Laboratory Medicine,
drome is a rare but increasingly described phenomenon of immune
and dMicrobiology and Immunology, University of North Carolina
at Chapel Hill, Chapel Hill, North Carolina; and bRobert Wood activation and organ dysfunction in association with a wide variety of
Johnson Medical School, Piscataway Township, New Jersey medications. This reaction shows a broad spectrum of clinical pre-
KEY WORDS sentation and severity, ranging from mild to lethal. Treatment strat-
adverse drug reaction, plasma exchange, drug hypersensitivity, egies of immune suppression appear be helpful in some cases, but
lamotrigine, bupropion
treatment failures occur frequently with reported mortality rates of
ABBREVIATIONS
5% to 10%. We present a pediatric case of DRESS syndrome associ-
CMV—cytomegalovirus
DRESS—drug reaction with eosinophilia and systemic symptoms ated with either lamotrigine or bupropion, leading to multiorgan in-
EBV—Epstein-Barr virus volvement and life-threatening complications of respiratory failure
HHV—human herpes virus and cardiac arrest. After failing to improve with removal of these
IVIg—intravenous immunoglobulin
PLEX—plasma exchange medications and administration of systemic corticosteroids, our pa-
TNF—tumor necrosis factor tient showed dramatic, sustained clinical response to therapeutic
Dr Alexander wrote the description of the case and portions of plasma exchange. To our knowledge, this is the first reported case
the discussion; Mr Iglesia wrote portions of the discussion; Dr of therapeutic plasma exchange used for life-threatening DRESS syn-
Ferris developed the treatment plan and reviewed the case
drome in a pediatric patient. This case suggests needed research for
report and discussion; Dr Park consulted on the treatment plan
and contributed to the discussion; Dr Duncan wrote portions of this therapeutic option in life-threatening DRESS syndrome resistant
the discussion; Dr Peden consulted on the treatment plan and to high-dose steroids. Pediatrics 2013;131:e945–e949
reviewed the case report and discussion; and Dr Sheikh
contributed to the initial discussion and reviewed the discussion
write up.
www.pediatrics.org/cgi/doi/10.1542/peds.2012-2117
doi:10.1542/peds.2012-2117
Accepted for publication Nov 5, 2012
Address correspondence to Thomas Alexander, MD, MPH, 3516
Keats Place, Raleigh, NC 27609. E-mail: thomasbalexander@yahoo.
com
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).
Copyright © 2013 by the American Academy of Pediatrics
FINANCIAL DISCLOSURE: The authors have indicated they have
no financial relationships relevant to this article to disclose.
FUNDING: No external funding.

PEDIATRICS Volume 131, Number 3, March 2013 e945

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DRESS syndrome is a type of drug hy-
persensitivity defined by a constellation
of findings associated with hyperin-
flammation related to a medication
exposure. The syndrome or a variation
has been described in the literature
since the 1950s under the names
drug-induced pseudolymphoma, an-
ticonvulsant hypersensitivity syndrome,
drug-induced delayed multiorgan hy-
persensitivity syndrome, and drug-
induced hypersensitivity syndrome.1–5
Kardaun et al describe the following
general features of hypersensitivity
syndrome/DRESS syndrome1: drug-
induced immunologic background, later
onset than other drug reactions, longer
duration than common “drug rashes,”
multiorgan involvement, lymphocyte acti-
vation, eosinophilia, and frequent virus
reactivation.
Although it was initially reported in
association with anticonvulsant medi-
cations,2 it has since been associated
with most medication classes.6 Bocquet
et al first presented the name DRESS
during a review of what was previously
termed hypersensitivity syndrome.3 As
initially defined by Bocquet et al, DRESS
diagnostic criteria required cutaneous
drug eruption, hematologic abnormal-
ities, and systemic involvement.3 The
nomenclature DRESS may cause con-
fusion because eosinophilia is not re-
quired to make the diagnosis. The
diagnosis is particularly challenging
because of delayed symptom onset, the
wide spectrum of clinical presentation
and organ involvement, and the variety
of nomenclature for the syndrome.7,8
CASE DESCRIPTION
A 14-year-old African American girl with
no significant medical history was ad-
mitted to an inpatient psychiatric unit
for suicidal ideation, diagnosed with
bipolar disorder, and treated with
lamotrigine and bupropion.
Seventeen days after initiation of these 2
medications, she developed a generalized
e946 ALEXANDER et al
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erythematous skin rash, high-grade
fevers, and lymphadenopathy. She
presented to an emergency depart-
ment, where she was prescribed
clindamycin for acute lymphadenitis.
Two weeks later, she was admitted
to the hospital with fever, rash, diffuse
tender lymphadenopathy, painful ex-
udative pharyngitis, and glossitis.
Laboratory investigation revealed trans-
aminitis, eosinophilia, and atypical lym-
phocytes, leading to concern for an
adverse drug reaction. Lamotrigine
and bupropion were stopped, and the
patient improved with supportive care.
She was discharged, only to return
twice with generalized pain, fever, severe
painful exudative pharyngitis, and glos-
sitis. Workup was negative for antinu-
clear antibody; double-stranded DNA;
HIV; Epstein-Barr virus (EBV); cytomeg-
alovirus (CMV); hepatitis A, B, and C;
streptococcal pharyngitis; urinary tract
infection; bacteremia; human herpes
virus type 6 titer; and mononucleosis.
She was transferred to a tertiary care
center for management of acute kidney
injury 46 days after the initiation of
lamotrigine and bupropion. Around
the time of transfer, she had improve-
ment in her skin rash and hepatitis
but suffered from volume overload,
anemia, pancreatitis, kidney injury, and
thyroiditis. A percutaneous ultrasound-
assisted renal biopsy revealed severe
acute and subacute tubulointerstitial
nephritis with granulomatous inflam-
mation. Systemic steroids (intravenous
methylprednisolone 250 mg daily) were
started on day 49, and her renal func-
tion began to improve. However, on day
50, she developed respiratory distress,
necessitating intensive care. Two days
later, on day 52, she was intubated for
hypoxic respiratory failure. Much later
in the same day, she had a 6-minute
cardiac arrest secondary to torsades de
pointes. She received 1 dose of epineph-
rine and 1 episode of cardioversion
with subsequent return of spontaneous
circulation. At the time of cardiac arrest,
magnesium level was 1.9 mg/dL, and
potassium level was 5.0 mmol/L. Her QTc
was prolonged to 521 ms hours before
the cardiac arrest. Her QT interval was
normal on admission to the tertiary care
center and normal on follow-up as an
outpatient. The etiology of her QT pro-
longation, torsades de pointes electrical
rhythm, and cardiac arrest is not clear
but could have been secondary to sys-
temic inflammation or myocarditis or
possibly medication effect. She did not
receive any known QT prolonging med-
ication on the day of the arrest.
In light of her rapidly progressive
clinical deterioration in the setting of
DRESS syndrome and incomplete re-
sponse to IV corticosteroids, we elected
to proceed promptly with plasma ex-
change (PLEX), although we also con-
sidered intravenous immunoglobulin
(IVIg), immunomodulators, and the con-
tinuation of high-dose steroids. PLEX was
performed every other day for a total of
4 procedures. One plasma volume was
exchanged with each procedure, and 5%
albumin was used as replacement. She
tolerated all the procedures well. Within
12 hours of the first PLEX session, her
course improved dramatically. She fi-
nally became afebrile, her pancreatic
enzymes decreased by 50% from 6059 to
3051 U/L. C-reactive protein fell rapidly,
and she was extubated without compli-
cation 4 days after initiation of PLEX. Her
endomyocardial biopsy performed 4
days after initiation of PLEX did not show
signs of inflammation or eosinophilia.
Her liver function, renal function, and
eosinophilia continued to trend posi-
tively and she was discharged on day 68
with a slow prednisone taper over 2
months in attempt to continue to sup-
press inflammation. In follow-up 3 weeks
after discharge, she showed continued
clinical and laboratory improvement. At
3 months, she was asymptomatic, with
normal laboratory values except for
treated hypothyroidism (Figure 1).

DISCUSSION
Using the RegiSCAR scoring system
proposed by Kardaun et al, our patient
had a “definite” case of DRESS.1 Addi-
tionally, our patient met the criteria
for the diagnosis of DRESS or “atypical
drug-induced hypersensitivity syn-
drome” under the criteria set forth by
Bocquet et al and the Japanese con-
sensus group, respectively.3,9 Despite
FIGURE 1
Timeline of events (symptoms, laboratory markers of organ dysfunction, presentation to medical care,
transfer to tertiary care center, and therapeutic interventions). **Exposure to lamotrigine and
bupropion.
PEDIATRICS Volume 131, Number 3, March 2013
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meeting diagnostic criteria, our patient’s
asynchronous timing of clinical mani-
festations made the diagnosis difficult.
Her skin rash and hepatitis were im-
proving when she first showed signs of
acute kidney injury. The exact onset of
thyroid and pancreatic involvement is
unclear. Her pulmonary and cardiac
symptoms did not present clinically
until her rash had resolved and hepa-
titis was improving. The exact etiology
CASE REPORT
of her cardiac arrest remains unclear
because her endomyocardial biopsy
and cardiac enzyme levels were nor-
mal. Notably, our patient had evidence
of inflammation in 6 organ systems in
addition to the hematologic and skin
abnormalities.
The pathogenesis of DRESS remains
incompletely understood. At least 44
drugs have been reported to be asso-
ciated with DRESS, including, most
frequently, aromatic anticonvulsants.6
Lamotrigine is a well-described medi-
cation leading to DRESS syndrome.10–12
Bupropion has not been shown to
cause DRESS but has been associated
with mild serum sickness reactions.13
Clindamycin has not been associated
with DRESS and is temporally unlikely
to be the culprit medication in our case.
Suggested mechanisms for DRESS and
other hypersensitivity syndromes in-
clude reactive metabolites leading to
stimulation of CD4+ and CD8+ T cells
through a variety of mechanisms,14–17
and interleukin-5 and tumor necrosis
factor (TNF)-a release from CD4+ and
CD8+ cells, resulting in activation of
eosinophils and inflammation.18,19 In
DRESS syndrome specifically, studies
have shown an oligoclonal prolifer-
ation of activated virus-specific and
nonspecific T cells resulting from se-
quential reactivation of the herpes vi-
ruses HHV-6, HHV-7, EBV, and CMV,15,20–23
especially in the setting of drug-induced
hypogammaglobulinemia permitting
viral reactivation.24,25 Parvovirus B19
and mycoplasma can lead to findings
similar to DRESS syndrome.26–28 Our
patient had negative EBV, CMV, and
HHV-6 titers. We did not assess for
HHV-7 reactivation, mycoplasma infec-
tion, or parvovirus B19 infection.
The management of DRESS calls for
early recognition and withdrawal of
offending medications. Current treat-
ment is variable, and reports are
conflicting. It is unclear if other
drug reactions have similar enough
e947
pathogenesis that therapeutic trials of
Stevens-Johnson syndrome or toxic
epidermal necrolysis should directly
inform treatment of DRESS. Systemic
corticosteroids are the current cor-
nerstone of treatment of DRESS.29,30
Options that have been successfully
used in the face of clinical deterioration
include pulsed methylprednisolone,31
other immunosuppressive agents such
as cyclosporine and cyclophospha-
mide,32–34 and IVIg.35–37 Acute pancre-
atitis dampened enthusiasm for using
pulse corticosteroids in this patient.
Although adverse effects may accom-
pany PLEX and IVIg administration,
we favored these interventions be-
cause of their rapid onset of action.
We chose PLEX over IVIg because a re-
cent description of 6 patients with
DRESS treated with IVIg suggested
that risk outweighed benefits.38 Fur-
thermore, we were concerned about
volume overload with IVIg infusion. We
were finally concerned that the cardiac
arrest may have been due to myocar-
ditis, and a recent reported case of
DRESS with myocarditis responded to
PLEX plus rituximab.39
REFERENCES
1. Kardaun SH, Sidoroff A, Valeyrie-Allanore L,
et al. Variability in the clinical pattern of
cutaneous side-effects of drugs with sys-
temic symptoms: does a DRESS syndrome
really exist? Br J Dermatol. 2007;156(3):
609–611
2. Saltzstein SL, Ackerman LV. Lymphadenop-
athy induced by anticonvulsant drugs and
mimicking clinically pathologically malig-
nant lymphomas. Cancer. 1959;12(1):164–
182
3. Bocquet H, Bagot M, Roujeau JC. Drug-
induced pseudolymphoma and drug hy-
persensitivity syndrome (drug rash with
eosinophilia and systemic symptoms: DRESS).
Semin Cutan Med Surg. 1996;15(4):250–257
4. Sontheimer RD, Houpt KR. DIDMOHS: a pro-
posed consensus nomenclature for the drug-
induced delayed multiorgan hypersensitivity
syndrome. Arch Dermatol. 1998;134(7):874–
876
5. Shiohara T, Iijima M, Ikezawa Z, Hashimoto
K. The diagnosis of a DRESS syndrome has
e948 ALEXANDER et al
Downloaded from pediatrics.aappublications.org at Indonesia:AAP Sponsored on January 11, 2015
Increased circulating cytokines likely
contribute to the pathogenesis of DRESS,
and we reasoned that reduction of
circulating cytokine levels would result
in prompt clinical improvement. PLEX
reduces systemic cytokines in other
settings of acute systemic inflamma-
tory disease. In a study of patients with
life-threatening meningococcal infec-
tions, PLEX accelerated the decline in
TNF-a as well as TNF soluble recep-
tors.40 Similarly, PLEX has lowered cir-
culating concentrations of TNF-a and
interleukin-6 in patients with acute
liver failure.41 Finally, a prospective trial
comparing PLEX to standard of care
for patients with sepsis and multiorgan
system failure demonstrated a sig-
nificant increase in survival of septic
patients receiving PLEX.42 The reported
action of PLEX to rapidly remove circu-
lating cytokines in a nonspecific fashion
and improve survival of septic patients
was the basis for our decision to use PLEX
in our patient.
In summary, our patient showed un-
questionable clinical deterioration
despite lamotrigine and bupropion
been sufficiently established on the basis
of typical clinical features and viral reac-
tivations. Br J Dermatol. 2007;156(5):1083–
1084
6. Cacoub P, Musette P, Descamps V, et al. The
DRESS syndrome: a literature review. Am J
Med. 2011;124(7):588–597
7. Peyrière H, Dereure O, Breton H, et al;
Network of the French Pharmacovigilance
Centers. Variability in the clinical pattern of
cutaneous side-effects of drugs with sys-
temic symptoms: does a DRESS syndrome
really exist? Br J Dermatol. 2006;155(2):
422–428
8. Kano Y, Shiohara T. The variable clinical
picture of drug-induced hypersensitivity
syndrome/drug rash with eosinophilia and
systemic symptoms in relation to the elic-
iting drug. Immunol Allergy Clin North Am.
2009;29(3):481–501
9. Tohyama M, Hashimoto K. New aspects of
drug-induced hypersensitivity syndrome. J
Dermatol. 2011;38(3):222–228
withdrawal for .2 weeks and 250 mg
of methylprednisolone IV for 4 days.
She was intubated, had a 6-minute
cardiac arrest, and remained persis-
tently febrile with continued signs of
multiorgan dysfunction. We therefore
proceeded with PLEX based on the
above thought process and a previ-
ous report of using PLEX in the set-
ting of DRESS and myocarditis.39 Our
patient showed marked improvement
of systemic inflammation and clinical
condition coincident with our use of
PLEX.
We feel that this outcome supports the
hypothesis that PLEX can effectively and
rapidly reduce morbidity and mortality
in patients with inflammation like that
encountered with DRESS that are re-
sistant to corticosteroids. Further-
more, PLEX has fewer toxicities than are
encountered with many other immu-
nosuppressives. Given the paucity of
evidence regarding treatment of acute
systemic drug reactions, we advocate
for a multicenter prospective random-
ized study of the efficacy of PLEX in
DRESS and similar diseases.
10. Mylonakis E, Vittorio CC, Hollik DA,
Rounds S. Lamotrigine overdose pre-
senting as anticonvulsant hypersensitiv-
ity syndrome. Ann Pharmacother. 1999;33
(5):557–559
11. Amante MF, Filippini AV, Cejas N, Lendoire J,
Imventarza O, Parisi C. Dress syndrome and
fulminant hepatic failure induced by
lamotrigine. Ann Hepatol. 2009;8(1):75–77
12. Roquin G, Peres M, Lerolle N, et al. First
report of lamotrigine-induced drug rash
with eosinophilia and systemic symptoms
syndrome with pancreatitis. Ann Phar-
macother. 2010;44(12):1998–2000
13. Beyens MN, Guy C, Mounier G, Laporte S,
Ollagnier M. Serious adverse reactions of
bupropion for smoking cessation: analysis
of the French Pharmacovigilance Database
from 2001 to 2004. Drug Saf. 2008;31(11):
1017–1026
14. Shear NH, Spielberg SP, Grant DM, Tang BK,
Kalow W. Differences in metabolism of
sulfonamides predisposing to idiosyncratic

toxicity. Ann Intern Med. 1986;105(2):179–
184
15. Picard D, Janela B, Descamps V, et al. Drug
reaction with eosinophilia and systemic
symptoms (DRESS): a multiorgan antiviral
T cell response. Sci Transl Med. 2010;2(46):
46ra62
16. Pichler WJ, Naisbitt DJ, Park BK. Immune
pathomechanism of drug hypersensitivity
reactions. J Allergy Clin Immunol. 2011;127
(suppl 3):S74–S81
17. Williams DP, Kitteringham NR, Naisbitt DJ,
Pirmohamed M, Smith DA, Park BK. Are
chemically reactive metabolites responsi-
ble for adverse reactions to drugs? Curr
Drug Metab. 2002;3(4):351–366
18. Boet S, Noblet C, Haas-Hubscher C, Picard
D, Musette P, Dureuil B. Severe vancomycin-
induced drug rash with eosinophilia and
systemic symptoms syndrome imitating
septic shock. Eur J Anaesthesiol. 2009;26
(9):791–793
19. Choquet-Kastylevsky G, Intrator L, Chenal C,
Bocquet H, Revuz J, Roujeau JC. Increased
levels of interleukin 5 are associated with
the generation of eosinophilia in drug-
induced hypersensitivity syndrome. Br J
Dermatol. 1998;139(6):1026–1032
20. Descamps V, Valance A, Edlinger C, et al.
Association of human herpesvirus 6 in-
fection with drug reaction with eosino-
philia and systemic symptoms. Arch
Dermatol. 2001;137(3):301–304
21. Kano Y, Hiraharas K, Sakuma K, Shiohara T.
Several herpesviruses can reactivate in
a severe drug-induced multiorgan reaction
in the same sequential order as in graft-
versus-host disease. Br J Dermatol. 2006;
155(2):301–306
22. Shiohara T, Inaoka M, Kano Y. Drug-induced
hypersensitivity syndrome (DIHS): a reaction
induced by a complex interplay among her-
pesviruses and antiviral and antidrug im-
mune responses. Allergol Int. 2006;55(1):1–8
23. Pritchett JC, Nanau RM, Neuman MG. The
link between hypersensitivity syndrome
reaction development and human herpes
virus-6 reactivation. Int J Hepatol. 2012;
2012:723062
24. Aihara Y, Ito SI, Kobayashi Y, Yamakawa Y,
Aihara M, Yokota S. Carbamazepine-induced
PEDIATRICS Volume 131, Number 3, March 2013
Downloaded from pediatrics.aappublications.org at Indonesia:AAP Sponsored on January 11, 2015
hypersensitivity syndrome associated with
transient hypogammaglobulinaemia and
reactivation of human herpesvirus 6 infec-
tion demonstrated by real-time quantitative
polymerase chain reaction. Br J Dermatol.
2003;149(1):165–169
25. Kano Y, Shiohara T. Sequential reactivation
of herpesvirus in drug-induced hypersen-
sitivity syndrome. Acta Derm Venereol.
2004;84(6):484–485
26. Kosseian-Bal I, Bocquet H, Beneton N, et al.
Hypersensitivity syndrome during Myco-
plasma pneumoniae infection [in French].
Ann Dermatol Venereol. 1998;125(5):328–
330
27. Barash J, Dushnitzky D, Sthoeger D,
Bardenstein R, Barak Y. Human parvovi-
rus B19 infection in children: uncommon
clinical presentations. Isr Med Assoc J. 2002;
4(10):763–765
28. Regnier S, Descamps V, Boui M, et al. Par-
vovirus B19 infection mimicking drug-
induced hypersensitivity syndrome [in
French]. Ann Dermatol Venereol. 2000;127
(5):505–506
29. Eshki M, Allanore L, Musette P, et al. Twelve-
year analysis of severe cases of drug re-
action with eosinophilia and systemic
symptoms: a cause of unpredictable mul-
tiorgan failure. Arch Dermatol. 2009;145(1):
67–72
30. Uhara H, Saiki M, Kawachi S, Ashida A,
Oguchi S, Okuyama R. Clinical course of
drug-induced hypersensitivity syndrome
treated without systemic corticosteroids
[published online ahead of print April 28,
2012]. J Eur Acad Dermatol Venereol. Pub-
Meddoi:10.1111/j.1468-3083.2012.04547.x
31. Natkunarajah J, Goolamali S, Craythorne E,
et al. Ten cases of drug reaction with eo-
sinophilia and systemic symptoms (DRESS)
treated with pulsed intravenous methyl-
prednisolone. Eur J Dermatol. 2011;21(3):
385–391
32. Harman KE, Morris SD, Higgins EM. Per-
sistent anticonvulsant hypersensitivity syn-
drome responding to ciclosporin. Clin Exp
Dermatol. 2003;28(4):364–365
33. Zuliani E, Zwahlen H, Gilliet F, Marone C.
Vancomycin-induced hypersensitivity re-
action with acute renal failure: resolution
CASE REPORT
following cyclosporine treatment. Clin
Nephrol. 2005;64(2):155–158
34. Laban E, Hainaut-Wierzbicka E, Pourreau F,
et al. Cyclophosphamide therapy for corti-
coresistant drug reaction with eosinophilia
and systemic symptoms (DRESS) syndrome
in a patient with severe kidney and eye
involvement and Epstein-Barr virus reac-
tivation. Am J Kidney Dis. 2010;55(3):e11–
e14
35. Fields KS, Petersen MJ, Chiao E, Tristani-
Firouzi P. Case reports: treatment of
nevirapine-associated dress syndrome with
intravenous immune globulin (IVIG). J Drugs
Dermatol. 2005;4(4):510–513
36. Santos RP, Ramilo O, Barton T. Nevirapine-
associated rash with eosinophilia and
systemic symptoms in a child with human
immunodeficiency virus infection. Pediatr
Infect Dis J. 2007;26(11):1053–1056
37. Kito Y, Ito T, Tokura Y, Hashizume H. High-
dose intravenous immunoglobulin mono-
therapy for drug-induced hypersensitivity
syndrome. Acta Derm Venereol. 2012;92(1):
100–101
38. Joly P, Janela B, Tetart F, et al. Poor benefit/
risk balance of intravenous immunoglobu-
lins in DRESS. Arch Dermatol. 2012;148(4):
543–544
39. Shaughnessy KK, Bouchard SM, Mohr MR,
Herre JM, Salkey KS. Minocycline-induced
drug reaction with eosinophilia and sys-
temic symptoms (DRESS) syndrome with
persistent myocarditis. J Am Acad Derma-
tol. 2010;62(2):315–318
40. van Deuren M, Frieling JT, van der Ven-
Jongekrijg J, et al. Plasma patterns of
tumor necrosis factor-alpha (TNF) and TNF
soluble receptors during acute meningo-
coccal infections and the effect of plasma
exchange. Clin Infect Dis. 1998;26(4):918–
923
41. Iwai H, Nagaki M, Naito T, et al. Removal of
endotoxin and cytokines by plasma ex-
change in patients with acute hepatic fail-
ure. Crit Care Med. 1998;26(5):873–876
42. Busund R, Koukline V, Utrobin U, Nedashkovsky
E. Plasmapheresis in severe sepsis and
septic shock: a prospective, randomised,
controlled trial. Intensive Care Med. 2002;
28(10):1434–1439
e949
 Severe DRESS Syndrome Managed With Therapeutic Plasma Exchange
Thomas Alexander, Edward Iglesia BA, Yara Park, Daniel Duncan, David Peden,
Saira Sheikh and Maria Ferris
Pediatrics 2013;131;e945; originally published online February 18, 2013;
DOI: 10.1542/peds.2012-2117
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PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

publication, it has been published continuously since 1948. PEDIATRICS is owned, published,
and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk
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 Severe DRESS Syndrome Managed With Therapeutic Plasma Exchange
Thomas Alexander, Edward Iglesia BA, Yara Park, Daniel Duncan, David Peden,
Saira Sheikh and Maria Ferris
Pediatrics 2013;131;e945; originally published online February 18, 2013;
DOI: 10.1542/peds.2012-2117

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pediatrics.aappublications.org/content/131/3/e945.full.html

PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

publication, it has been published continuously since 1948. PEDIATRICS is owned,
published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point
Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2013 by the American Academy
of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.

Downloaded from pediatrics.aappublications.org at Indonesia:AAP Sponsored on January 11, 2015