Indian J Dermatol 2009; 54(1) 1

Introduction
Erythroderma is an intense generalized redness of the
skin; it was frst described by Von Hebra in 1868. It is an
infammatory disorder characterized by an extreme state of
skin dysmetabolism that gives rise to extensive erythema
and scaling all over the body. This condition classically
involves greater than 90% of the body surface. The
erythrodermic state is of great concern because it poses
signifcant risk of morbidity and mortality, in addition to
the risks inherent to the underlying disease and its therapy.
Erythroderma can be fatal, even when properly managed,
primarily because of its metabolic burden and complications.
Hence it is mandatory to establish its etiopathology in
order to facilitate precise management. This disorder may
be the morphologic presentation of a variety of cutaneous
and systemic diseases, and a thorough workup is essential.
A detailed outline of the patients history to elicit possible
triggering events, including infections, drug ingestion,
topical application of medications, sun/ultraviolet exposure
and other factors, should be determined. Management
of the skin disorder continues to be a challenge due to
its multiple etiologies. The prognosis of erythroderma is
determined by its underlying cause.
There is a paucity of information on erythroderma in
Africa. The growing increase in use of herbal medicines,
[1]

the HIV epidemic,
[2]
hospital visits in advanced disease
stages and limited investigational resources in Third
World environments all exacerbate the life-threatening
nature of this condition. With increasing use of herbal
and nonherbal medicines, more individuals are at risk of
contracting erythroderma.
Two Illustrative Cases
Case 1
A 14-year-old African girl was referred to our Benin
City clinic in 2005 for generalized scaling and erythema
of 5 years duration. The pruritic patches were frst noted
on the face and trunk and later involved the entire body.
There was no preexisting dermatosis, nor prior medical
problems. There was no prior exposure to chemical
precipitants of dermatitis. Family history was negative
for similar conditions or skin disorders. The exfoliation
did not improve with herbal medicines (Yoruba Agbo
leaves). Physical examination showed extensive non-
uniform erythematous scaly patches involving the scalp,
face, trunk, arms, legs, palms and soles [Figure 1]. Scalp
lesions formed whitish yellow scales with hair loss. On
the soles, the exfoliative eruption led to severe sloughing
of the epidermis [Figure 2]. Laboratory investigations and
biopsy results were nonspecifc. The etiology could not be
determined due to limited resources in our clinic. She was
treated with intravenous and topical steroids and was lost
to follow-up.
Case 2
A 64-year-old man presented to our Benin City clinic in
2005 with an acute eruption of numerous erythematous
plaques that had appeared 2 weeks following oral intake
of an unknown amount of Aloe vera leaves taken to
enhance well-being. There was no history of preexisting
dermatologic or medical conditions. Physical examination
Review Article
ERYTHRODERMA: REVIEW OF A POTENTIALLY LIFE-THREATENING
DERMATOSIS
Cynthia Okoduwa, W C Lambert, R A Schwartz, E Kubeyinje, A Eitokpah,
Smeeta Sinha, W Chen
Abstract
Erythroderma, or generalized exfoliative dermatitis, is a disease characterized by erythema and scaling of greater than
90% of the bodys surface. The resultant dysmetabolism is potentially life threatening. A detailed history is to identify and
treat the underlying cause of this dermatitis. We present two cases of erythroderma in African patients and review this
important disease.
Key Words: Erythroderma, causes, African patients
Indian J Dermatol 2009:54(1):1-6 DOI: 10.4103/0019-5154.48976
From the Department of Dermatology and Pathology, New Jersey
Medical School, 185 South Orange Avenue, Newark, New Jersey
07103, USA. Address for correspondence: Dr. Cynthia Okoduwa,
Department of Dermatology and Pathology, New Jersey Medical
School, 185 South Orange Avenue, Newark, New Jersey 07103
USA. E-mail: roschwar@cal.berkeley.edu
Indian J Dermatol 2009; 54(1) 2
revealed scaling plaques with prominence on the scalp,
trunk and extremities [Figure 3, Figure 4]. Laboratory
investigations were consistent with dehydration and
infammatory changes. Topical and oral steroids achieved
rapid improvement of the lesions.
Epidemiology
The true incidence of erythroderma is unknown. Gehgal
and Srivastava
[3]
performed a large prospective study in the
Indian subcontinent, where they determined the incidence
to be 35 per 100,000 dermatologic outpatients. Sigurdsson
[4]

recorded the annual incidence in the Netherlands to be 0.9
per 100,000 inhabitants. In general, studies have shown a
male predominance, with the male-to-female ratio ranging
from 2:1 to 4:1, and the mean age between 40 and 60
years.
[3]
Rym et al. conducted a retrospective study of 80
erythrodermic adults, looking at patients examined between
1981 and 2000.
[5]
Patient information included clinical,
laboratory, histopathological and therapeutic data. The
incidence of erythroderma from the study was 0.3%, the
average age being 53.78 18 years; and the male-to-female
ratio, 2.2:1. These numbers may, however, underestimate
the current statistics in Third World environments such as
those in Africa.
Etiology
A major challenge lies in establishing the underlying cause
of erythroderma. Most published series reveal that the
majority of patients are diagnosed with psoriasis, spongiotic
dermatitis, drug reactions or cutaneous T cell lymphoma
(CTCL).
[6,7]
A preexisting dermatosis is the single most common cause
of adult erythroderma.
[3,5,8-13]
A number of dermatoses can
progress to erythroderma, but the most common include
psoriasis and eczema.
[3,5,9,12]
Rym et al. reported 41 of
80 erythrodermic patients had psoriasis,
[5]
a fnding not
inconsistent with Spanish, Middle Eastern and Indian
Figure 1: Fifteen-years-old girl with diffuse erythema and scaling of lower
extremities
Figure 2: Sloughing of epidermis of the soles in the above patient
Figure 3: Sixty-four-years-old man with papulosquamous plaques on the
scalp, arms and trunk
Figure 4: Erythematous scaling plaques of the lower extremities
Okoduwa, et al.: Erythroderma
Indian J Dermatol 2009; 54(1) 3
studies.
[3,9,12]
Psoriatic erythroderma may occur in relation
to withdrawal of systemic or topical glucocorticoids, use
of systemic medications such as lithium and antimalarials,
phototherapy burns, infection and systemic illnesses.
[14]
The apparent increase in the incidence of exfoliative
dermatitis may have a bearing on the introduction of
many new drugs. It is therefore important to consider all
drug exposures.
[14,15]
Patients presenting with morbilliform,
lichenoid or urticarial drug eruptions may develop
generalized exfoliative dermatitis.
[16]
This association has
been inferred from descriptions of patients on antiepileptic
medications, antihypertensive agents, antibiotics, calcium channel
blockers and a variety of topical preparations.
[14,17]
Severe
exfoliative erythrodermic dermatitis has been reported with
use of proton pump inhibitors.
[18]
Morar
[19]
identifed adverse
drug reactions to antituberculosis medication as the most
common cause of erythroderma in HIV-seropositive South
African patients. Rym et al.
[5]
implicated carbamazepine,
phenobarbital, penicillin and paracetamol. The intake of
herbal medicines, being very popular, may also increase
risk among Africans.
Erythroderma may be a cutaneous manifestation of
malignancy. The incidence of internal malignancy is
approximately 1%.
[20]
Reticuloendothelial neoplasms, as
well as internal visceral/blood vessel malignancies, may
manifest as erythroderma.
[16,21]
Laryngeal, thyroid, lung,
esophageal, gallbladder, gastric, colon, fallopian tube
and prostate carcinomas and lymphomas have all been
implicated.
[22-29]
Other associations include cutaneous T
cell lymphomas, which comprise mycosis fungoides and
Szary syndrome.
[20,30-32]
Mycosis fungoides may progress
from, accompany, or follow T cell lymphomas, and their
presentation may be similar to benign erythroderma.
[16,30,33,34]
The ability to distinguish malignant from benign
erythroderma may require an immunophenotypic study
with the use of advanced antibody panels.
[35]
Defnitive
diagnosis of erythroderma due to internal malignancy
cannot be made based on clinical presentation alone, but a
concomitant history of insidious development, progressive
decompensation, refractoriness to standard therapeutics and
absence of prior skin pathology may be existent.
[28]
Erythroderma is also associated with disorders that are
not readily classifed. It has been reported in association
with dermatophytosis, hepatitis, renal failure, acquired
immunodefciency syndrome, congenital immunodefciency
syndrome (Omenn syndrome), graft-versus-host disease,
histoplasmosis, lupus, dermatomyositis, thyrotoxicosis and
sarcoidosis.
[36-47]
Pathogenesis
Currently, the mechanism of erythroderma is unclear.
Adhesion molecules and their ligands play a signifcant
role in endothelial-leukocyte interactions, which impact
the binding, transmigration and infltration of lymphocytes
and mononuclear cells during infammation, injury or
immunological stimulation.
[48]
The rise in adhesion
molecule expression (VCAM-1, ICAM-1, E-selectin and
P-selectin) seen in exfoliative dermatitis stimulates dermal
infammation, which may lead to epidermal proliferation
and increased production of infammatory mediators.
[48]

The complex interaction of cytokines and cellular adhesion
molecules such as interleukin-1, -2 and -8; intercellular
adhesion molecule-I (ICAM-I); and tumor necrosis
factor (TNF)
[49]
results in signifcantly elevated epidermal
turnover rate, leading to above-normal mitotic rate.
[50]
The
amount of germinative cells increases and the transit time
of keratinocytes through the epidermis decreases, causing
loss of more cellular material from the surface.
[14]
Sigurdsson et al. conducted an immunohistochemical study
and observed that the dermal infltrate in patients with Szary
syndrome mainly showed a T-helper 2 (Th2) cytokine profle,
in contrast to a T-helper 1 (Th1) cytokine profle in benign
reactive erythroderma, which suggests that a relatively
uniform clinical picture in erythroderma does not imply
similar pathomechanisms for various etiologies.
[48,51]
Clinical Features
The pattern observed is erythematous patches, which
increase in size and coalesce to form extensive areas of
erythema, and eventually spread to involve most of the
skin surface.
[50,52]
Some studies have shown sparing of the
nose and paranasal areas, and this has been described as
the nose sign.
[53,54]
The epidermis appears thin, giving a glossy appearance
to the skin. Once erythema has been established, white or
yellow scales develop that progress to give the skin a dry
appearance with a dull scarlet and gray hue.
[14]
Induration
and thickening of the skin from edema and lichenifcation
may provoke a sensation of severe skin tightness in the
patient.
[14]
The skin is bright red, dry, scaly and warm to
touch.
Some patients may experience involvement of their palms
and soles, with hair loss and nail shedding.
[55]
Involved
nails are thick, lusterless, dry, brittle, and show ridging
of the nail plate.
[50]
Subungual hyperkeratosis, distal
onycholysis, splinter hemorrhages occur; and sometimes,
the nails may shed.
[14]
Shelley
[56]
described alternating
bands of nail plate discontinuity and leukonychia in drug-
induced erythroderma.
Sometimes, the clinical presentation may be suggestive
of the underlying cause. Typical psoriasiform plaques
may be apparent in early erythrodermic psoriasis.
Pityriasis rubra pilaris shows islands of sparing, orange-
colored palmoplantar keratoderma and hyperkeratotic
follicular papules on juxta-articular extensor surfaces.
[14]

The violaceous papules and reticulated buccal mucosal
lesions of lichen planus may be evident. Joly et al.
[57]

described three African patients presenting with lichenoid
Okoduwa, et al.: Erythroderma
Indian J Dermatol 2009; 54(1) 4
erythroderma different from the classic form of lichen
planus pemphigoides. The presence of heavy crusts on
the palms and soles with subungual hyperkeratosis raises
the possibility of Norwegian scabies.
[14]
In patients with
pemphigus foliaceus, crusted patches and erosions may
appear on the face and upper trunk. A heliotrope rash,
poikiloderma, Gottrons papules, periungual telangiectases
and muscle weakness may be seen in erythrodermic
dermatomyositis.
[26,42]
Papuloerythroderma of Ofuji presents
in elderly men as fat-topped red papules that become
generalized erythrodermic plaques without the involvement
of abdominal skin folds (deck chair sign).
[58-60]
Postoperative erythroderma, a type of graft-versus-host
disease following surgery along with blood transfusion,
is marked by erythroderma, fever, pancytopenia, hepatic
insuffciency and diarrhea and may be fatal.
[50]
Exfoliative
dermatitis may also develop in HIV-infected patients with
forid manifestations.
[38]
The presence of lymphadenopathy and hepatosplenomegaly,
particularly in association with liver dysfunction and
fever, may suggest a drug hypersensitivity syndrome
or malignancy.
[14]
Gynecomastia has been reported in
some patients, possibly refecting a hyperestrogenic state,
although the signifcance of this fnding is unclear.
[13]
Laboratory Findings
Laboratory fndings in the erythrodermic patient are usually
nonspecifc.
[16]
Common abnormalities are mild anemia,
leukocytosis with eosinophillia, elevated sedimentation
rate, decreased serum albumin, increased uric acid,
abnormal serum protein electrophoresis with polyelevation
in the gamma globulin region and elevated IgE levels.
[49,61]

Eosinophilia is generally a nonspecifc fnding, although
a highly elevated count raises the possibility of a
lymphoma.
[52]
Circulating Szary cells may be present;
but whereas less than 10% is considered nonspecifc in
the setting of erythroderma, the presence of 20% or more
raises the suspicion for Szary syndrome.
[13,62]
Histopathology
Biopsy specimens tend to have many nonspecifc
features.
[16]
Hyperkeratosis, parakeratosis, acanthosis and
a chronic perivascular infammatory infltrate, with or
without eosinophils, are examples.
[6]
The clinicopathologic
correlation is diffcult because nonspecifc features of
erythroderma may mask the specifc features of an
underlying dermatosis. Direct immunofuorescence studies
may be of diagnostic utility in cases of erythroderma
secondary to pemphigus foliaceus, bullous pemphigoid,
graft-versus-host disease and connective tissue disorders.
[52]
Management
The initial management of erythroderma is the same
regardless of etiology. This should include replacement of
nutritional, fuid and electrolyte losses.
[6]
Local skin-care
measures should be employed, such as oatmeal baths as
well as wet dressings to weeping or crusted sites followed
by the application of bland emollients and low-potency
corticosteroids.
[63]
Known precipitants and irritants are to be
avoided; and underlying cause, with its complications, is to be
treated.
[6,16,50]
Secondary infections are treated with antibiotics.
Edema in dependent areas, such as in periorbital and pedal
areas, may require diuretics.
[63]
Hemodynamic or metabolic
instability should be addressed adequately. Serum protein,
electrolyte and blood urea levels should be monitored. This
condition may resist therapy until the underlying cause is
treated; hence it is important to determine underlying etiology
early in its management.
[63,64]
In Africa and other Third World
environments, however, this may not be possible.
Course
The disease course is greatly infuenced by etiology. It is
progressive when due to drug allergy, lymphoma, leukemia,
contact allergens or staphylococcal scalded skin syndrome.
[3,6,13,50]
A slower course is observed if from a primary
skin disease such as psoriasis or atopic dermatitis.
[3,6,13,50]

Drug-induced erythroderma patients recover completely
with prompt diagnosis and treatment.
[6,50]
The outcome is
unpredictable in idiopathic erythroderma, and its course is
marked by multiple exacerbations; prolonged corticosteroid
use is often required.
[16,50,62]
Prognosis
Conficting reports have been published regarding the
prognosis of patients with erythroderma in developed
nations. The most common causes of death in patients
with erythroderma are pneumonia, septicemia and heart
failure.
[16,63]
Elderly patients who develop complications
such as infection, fuid/electrolyte imbalances and cardiac
failure are at higher risk of mortality.
[16,50]
Initial studies
record death rate in the range of 4.6% to 64%,
[5,9,16,49,50,61]

but this has since been reduced due to advancement in
diagnosis and therapy.
[50]
In Third World countries, such
as parts of Africa, the former prognosis may be more
accurate.
References
1. Busia K. Medical provision in Africa. Phyother Res 2005;19:
919-23.
2. Ferrante P, Delbue, S., Mancuso, R. The manifestation of
AIDS in Africa: An epidemiological overview. J Neurovirol
2005;11:50-7.
3. Sehgal VN, Srivastava G. Exfoliative dermatitis: A prospective
study of 80 patients. Dermatologica 1986;173:278-84.
4. Sigurdsson V, Steegmans PH, van Vloten WA. The incidence
of erythroderma: A survey among all dermatologists in The
Netherlands. J Am Acad Dermatol 2001;45:675-8.
5. Rym BM, Mourad M, Bechir Z Dalenda E, Faika C, Iadh AM,
et al. Erythroderma in adults: A report of 80 cases. Int J
Dermatol 2005;44:731-5.
Okoduwa, et al.: Erythroderma
Indian J Dermatol 2009; 54(1) 5
6. Rothe MJ, Bialy TL, Grant-Kels JM. Erythroderma. Dermatol
Clin 2000;18:405-15.
7. Balasubramaniam P, Berth-Jones J. Erythroderma:90% skin
failure. Hosp Med 2004;65:100-2.
8. Akhyani M, Ghodsi ZS, Toosi S, Dabbaghian H. Erythroderma:
A clinical study of 97 cases. BMC Dermatol 2005;5:5.
9. Botella-Estrada R, Sanmartin O, Oliver V, Febrer I, Aliaga A.
Erythroderma: A clinicopathological study of 56 cases. Arch
Dermatol 1994;130:1503-7.
10. Hasan T, Jansen CT. Erythroderma: A follow-up of ffty cases. J
Am Acad Dermatol 1983;8:836-40.
11. Leenutaphong V, Kulthanan K, Pohboon C, Suthipinittharn P,
Sivayathorn A, Sunthonpalin P. Erythroderma in Thai patients. J
Med Assoc Thailand 1999;82:743-8.
12. Pal S, Haroon TS. Erythroderma: A clinico-etiologic study of 90
cases. Int J Dermatol 1998;37:104-7.
13. Sigurdsson V, Toonstra J, Hezemans-Boer M, van Vloten WA.
Erythroderma: A clinical and follow-up study of 102 patients,
with special emphasis on survival. J Am Acad Dermatol
1996;35:53-7.
14. Rubins AY, Hartmane IV, Lielbriedis YM, Schwartz RA.
Therapeutic options for erythroderma. Cutis 1992;49:424-6.
15. Breathnach SM. Management of drug eruptions: Part II,
Diagnosis and treatment. Australas J Dermatol 1995;36:187-91.
16. Karakayli G, Beckham G, Orengo I, Rosen T. Exfoliative
dermatitis. Am Fam Physician 1999;59:625-30.
17. Guin JD, Phillips D. Erythroderma from systemic contact
dermatitis: A complication of systemic gentamicin in a patient
with contact allergy to neomycin. Cutis 1989;43:564-7.
18. Cockayne S, Gawkrodger D, McDonagh A. Severe erythrodermic
reactions to the proton pump inhibitors omperazole and
lansoprazole. Br J Dermatol 1999;141:173-4.
19. Morar N, Dlova N, Gupta AK, Naidoo DK, Aboobaker J,
Ramdial PK. Erythroderma: A comparison between HIV positive
and negative patients. Int J Dermatol 1999;38:895-900.
20. Chakraborty. Lymphoma as a cause of exfoliative dermatitis.
Indian J Dermatol 1983;28:121-3.
21. Nishijima S. Papuloerythroderma associated with hepatocellular
carcinoma. Br J Dermatol 1998;139:1115-6.
22. Axelrod JH, Herbold DR, Freel JH, Palmer SM. Exfoliative
dermatitis: Presenting sign of fallopian tube carcinoma. Obstet
Gynecol 1988;71:1045-7.
23. Deffer TA, Overton-Keary PP, Goette DK. Erythroderma
secondary to esophageal carcinoma. J Am Acad Dermatol
1985;13:311-3.
24. Harper TG, Latuska RF, Sperling HV. An unusual association
between erythroderma and an occult gastric carcinoma. Am J
Gastroenterol 1984;79:921-3.
25. Kameyama H, Shirai Y, Date K, Kuwabara A, Kurosaki R,
Hatakeyama K. Gallbladder carcinoma presenting as exfoliative
dermatitis (erythroderma). Int J Gastrointest Cancer 2005;35:153-5.
26. Nousari HC, Kimyai-Asadi A, Spegman DJ. Paraneoplastic
dermatomyositis presenting as erythroderma. J Am Acad
Dermatol 1998;39:653-4.
27. Patrizi A, Pileri S, Rivano MT, Di Lernia V. Malignant
histiocytosis presenting as erythroderma. Int J Dermatol
1990;29:214-6.
28. Rosen T, Chappell R, Drucker C. Exfoliative dermatitis:
Presenting sign of internal malignancy. Southern Med J
1979;72:652-3.
29. Bittencourt AL, Barbosa H, Brites C, Ferraz N.
Clinicopathological aspects of HTLV-1 positive and negative
T-cell lymphoma. Eur J Dermatol 1997;7:283-9.
30. vonderheid EC, Bernengo MG, Burg G. Update on erythroderma
cutaneous T-cell lymphoma-Report of International Society for
Cutaneous Lymphoma. J Am Acad Dermatol 2002;46:95-106.
31. Burns MK, Cooper KD. Cutaneous T-cell lymphoma associated
with HIV infection. J Am Acad Dermatol 1993;29:394-9.
32. Higgins EM, du Vivier AW. Cutaneous manifestations of
malignant disease. Br J Hosp Med 1992;48:552-4.
33. Vonderheid EC. On the diagnosis of erythrodermic cutaneous
T-cell lymphoma. J Cutan Pathol 2006;33:27-42.
34. Vonderheid EC, Bernengo MG. The Sezary syndrome:hematologic
criteria. Hematol Oncol Clin North Am 2003;17:1367-89.
35. Abel EA, Lindae ML, Hoppe RT, Wood GS. Benign and
malignant forms of erythroderma: Cutaneous immunophenotypic
characteristics. J Am Acad Dermatol 1988;19:1089-95.
36. Fujiwara E, Tado O, Sasaki H, Hayashi Y. An autopsy case
of postoperative erythroderma after nephroureterectomy
possibly induced by graft-versus-host reaction following blood
transfusion. Nippon Hinyokika Gakkai Zasshi - Jpn J Urol
1992;83:348-51.
37. Gupta R, Khera V. Erythroderma due to dermatophyte. Acta
Dermatol Venereol 2000.
38. Janniger CK, Gascon P, Schwartz RA, Hennessey NP, Lambert
WC. Erythroderma as the initial presentation of the acquired
immunodefciency syndrome. Dermatologica 1991;183:143-5.
39. Mutasim DF. Severe subacute cutaneous lupus erythematosus
presenting with generalized erythroderma and bullae. J Am Acad
Dermatol 2003;48:947-9.
40. Nazzari G, Crovato F, Nigro A. Papuloerythroderma (Ofuji):
Two additional cases and review of the literature. J Am Acad
Dermatol 1992;26:499-501.
41. Otsuka S, Kunieda K, Hirose M, Takeuchi H, Mizutani Y,
Nagaya M, et al. Fatal erythroderma (suspected graft-versus-
host disease) after cholecystectomy: Retrospective analysis.
Transfusion 1989;29:544-8.
42. Pierson JC, Taylor JS. Erythrodermic dermatomyositis. J Am
Acad Dermatol 1993;28:136.
43. Schwartz RA, Leevy CM, Cohen PJ, Lambert WC. Erythroderma
with fulminant hepatitis: A possible association. Cutis
1986;37:56-8.
44. Takedai T, Yamamoto I, Tokeshi J. Acute generalized pustular
psoriasis presenting with erythroderma associated with shock and
acute renal failure. Hawaii Med J 2003;62:278-81.
45. Yungmann MP, Ford MJ. Histoplasmosis presenting as
erythroderma in a patient with the acquired immunodefciency
syndrome. Int J Dermatol 2003;42:636-9.
46. Zemtsov A, Elks M, Shehata B. Thyrotoxicosis presenting as
generalized pruritic exfoliative dermatitis and fever. Dermatology
1992;184:157.
47. Yoon C, Lee C. Clinicopathological cases. Clin Exp Dermatol
2003;28:575-6.
48. Sigurdsson V, de Vries IJ, Toonstra J, Bihari IC, Thepen T,
Bruijnzeel-Koomen CA, et al. Expression of VCAM-1, ICAM-1,
E-selectin, and P-selectin on endothelium in situ in patients with
erythroderma, mycosis fungoides and atopic dermatitis. J Cutan
Pathol 2000;27:436-40.
Okoduwa, et al.: Erythroderma
Indian J Dermatol 2009; 54(1) 6
49. Wilson DC, Jester JD, King LE, Jr. Erythroderma and exfoliative
dermatitis. Clin Dermatol 1993;11:67-72.
50. Sehgal VN, Srivastava G, Sardana K. Erythroderma/exfoliative
dermatitis: A synopsis. Int J Dermatol 2004;43:39-47.
51. Sigurdsson V, Toonstra J, Bihari IC. Interleukin-4 and interferon-
gamma expression of the dermal infltrate in patients with
erythroderm and mycosis fungoides- an immunohistochemical
study. J Cutan Pathol 2000;27:436-40.
52. Freedberg IM. Exfoliative Dermatitis. In:Fitzpatricks
dermatology in general medicine. 6th ed. New York: McGraw
Hill; 2003. p. 1-17.
53. Kanwar AJ, Dhar S, Ghosh S. Nose sign in dermatology.
Dermatology 1993;187:278.
54. Agarwal S, Khullar R, Kalla G, Malhotra YK. Nose sign of
exfoliative dermatitis: A possible mechanism. Arch Dermatol
1992;128:704.
55. Jaffer AN, Brodell RT. Exfoliative dermatitis: Erythroderma can
be a sign of a signifcant underlying disorder. Postgrad Med
2005;117:49-51.
56. Shelley WB, Shelley ED. Shoreline nails: Sign of drug-induced
erythroderma. Cutis 1985;35:220-2.
57. Joly P, Tanasescu S, Wolkenstein P, Bocquet H, Gilbert D.
Lichenoid erythrodermic bullous pemphigoid of the African
patient. J Am Acad Dermatol 1998;39:691-7.
58. Harris DW, Spencer MJ, Tidman MJ. Papuloerythroderma-
-clinical and ultrastructural features. Clin Exp Dermatol
1990;15:105-6.
59. Ofuji S. Papuloerythroderma. J Am Acad Dermatol 1990;22:697.
60. Lacour JP, Perrin C, Ortonne JP. Ofuji papuloerythroderma: A
new European case. Dermatology 1993;186:190-2.
61. Nicolis GD, Helwig EB. Exfoliative dermatitis: A
clinicopathologic study of 135 cases. Arch Dermatol
1973;108:788-97.
62. Sigurdsson V, Toonstra J, van Vloten WA. Idiopathic
erythroderma: A follow-up study of 28 patients. Dermatology
1997;194:98-101.
63. Rothe MJ, Bernstein ML, Grant-Kels JM. Life-threatening
erythroderma: Diagnosing and treating the red man. Clin
Dermatol 2005;23:206-17.
64. Mutluer S, Yerebakan O, Alpsoy E, Ciftcioglu MA, Yilmaz E.
Treatment of papuloerythroderma of Ofuji with Re-PUVA:
A case report and review of the therapy. J Eur Acad Dermatol
Venereol 2004;18:480-3.
Received: July 2008. Accepted: August 2008.
Source of Support: Nil, Confict of Interest: Nil.
Okoduwa, et al.: Erythroderma
Author Institution Mapping (AIM)
Please note that not all the institutions may get mapped due to non-availability of the requisite information in the Google Map. For AIM of other
issues, please check the Archives/Back Issues page on the journals website.
Reproducedwith permission of thecopyright owner. Further reproductionprohibited without permission.