doi: 10.1111/j.1365-4632.2006.02715.

x
Review
Oxford, UK
International
IJD
Blackwell
1365-4632
45 Publishing,
Publishing
Journal Ltd,
of
Ltd.
Dermatology
2005

Polymorphic eruption of pregnancy

Pregnancy eruption
Petropoulou
REVIEW et al.

Haritini Petropoulou, MD, Sofia Georgala, MD, and Andreas D. Katsambas, MD

From the Department of Dermatology, Abstract

University of Athens School of Medicine,
Andreas Sygros Hospital for Skin and
Venereal Diseases, Athens, Greece
Correspondence
Professor Andreas D. Katsambas
Department of Dermatology and Venereology
‘Andreas Sygros’ Hospital
5 Dragoumi Street
Kesariani 161 21
Athens
Greece
E-mail: katsabas@internet.gr
chpetropoulou@hotmail.com
Polymorphic eruption of pregnancy (PEP) is a benign, self-limiting, pruritic disorder of
pregnancy, which usually affects the primigravida during the last trimester or immediately
postpartum. Its pathogenesis is unclear and its clinical manifestations are variable, leading
frequently to an incorrect diagnosis. In cases of PEP the histological findings are nonspecific
and the laboratory results, including direct immunofluorescence (DIF) and indirect
immunofluorescence (IIF), are negative. Polymorphic eruption of pregnancy is not associated
with any fetal risk and symptomatic treatment is all that is usually required.
In this review we present the clinical presentation of PEP and a differential diagnosis which
defines PEP as a separate entity. We will also review all current data of possible etiologic factors,
histologic and immunologic findings, prognosis and therapy.

incidence of approximately 1 in 160 deliveries9,10 (Table 1). It

Introduction
Polymorphic eruption of pregnancy (PEP) is the most common
of all the specific dermatoses of pregnancy. Several different
terminologies have been applied to this condition, which was
initially described by Bourne1 in 1962 as a “toxaemic rash of
pregnancy”; but as it was not found to be associated with pre-
eclampsia this term has been abandoned. Since then several
other designations have been used to describe this entity,
including “late onset prurigo of pregnancy,”2 “toxic erythema
of pregnancy”3 and “pruritic ulticarial papules and plaques of
pregnancy” (PUPPP).4 The term PUPPP was introduced by
Lawley et al. in 1979, reporting a specific eruption in seven
pregnant women. Later, Holmes and Black5,6 proposed the
term PEP to encompass all the clinical manifestations, which
include urticarial papules, plaques, polycyclic erythematous
wheals, vesicles, targetoid lesions and occasionally bullae. The
new term has the advantage of being both clinically accurate
and also free from any misleading connotations; but in some
quarters, disagreement persists about the presumed identity
of PUPPP and PEP. Some suggest that the former is more
narrowly defined by clinical findings than the latter.7,8 Although,
the term PUPPP is mostly used in the United States and PEP
in Europe, it is generally agreed that PEP and PUPPP are
identical dermatoses.5
Epidemiology
Polymorphic eruption of pregnancy is the most common of
642 the specific dermatoses of pregnancy, with an estimated
is observed predominantly in primiparous women and has
been correlated with multiple pregnancies and excessive
maternal and fetal weight gain. The male : female ratio in the
offspring of the affected women was found to be 2 : 1,11
although the relevance of this finding is not yet clear.12
Pathogenesis
The pathogenesis of PEP is under investigation. No correla-
tion has been established with pre-eclampsia or atopy.9 There
has been no evidence to suggest an autoimmune mechanism
involved with PEP,13 nor evidence of circulating immune
complexes.14 In exceptional cases, familial occurrence has been
reported.15 Polymorphic eruption of pregnancy has not been
associated with any human leukocyte antigens (HLAs).10,14
The localization of lesions to abdominal striae, the high
frequency of twins16 or multiple pregnancies,11 and the increase
in maternal weight gain and neonatal birthweight16 suggest
that abdominal distension or a reaction to this may trigger
PEP. It has been proposed that rapid excessive weight gain
during the late months of pregnancy leads to stretching of the
abdorminal skin with damage to the connective tissue of the
striae, triggering the inflammatory response of PEP.16,17 Other
authors18 have postulated that during the aging of the placenta
in the third trimester, a substance is released into the maternal
circulation which triggers fibroblast proliferation.
Futhermore, a recent study19 suggests that by expressing
progesterone receptor (PR), human keratinocytes act as targets
for progesterone action. Suprabasal keratinocytes from samples

International Journal of Dermatology 2006, 45, 642–648 © 2006 The International Society of Dermatology
Petropoulou et al.
Table 1 Classification of specific dermatoses of pregnancy and
their incidence
Specific dermatoses of pregnancy Incidence
Polymorphic eruption of pregnancy 1 : 160
Prurigo of pregnancy 1 : 300
Pruritic folliculitis of pregnancy Probably rare
Pemphigoid gestationis 1 : 40 000 –60 000
of PEP stained positively for PR and lesional epidermis of PEP
showed positive PR immunoreactivity, while nonlesional
epidermis did not. Multiple gestation is associated with higher
estrogen and progesterone levels.20 In a prospective study,11
sex hormone levels were compared between 44 patients
with PEP and healthy control pregnant women in the same
trimester. There was no significant difference for serum
β-hCG, oestradiol or androgens, except for serum cortisol,
which was significantly reduced (P = 0.03) in PEP compared
with controls, suggesting a hormonal influence.
Fetal factors may contribute to the pathogenesis of PEP.
The presence of fetal cells in the peripheral blood of pregnant
women has been well established.21,22 It has also been
reported21 that as early as 6 weeks after the last menstrual
period, 30% of women have circulating fetal DNA increasing
to greater than 90% in the third trimester. A recent study23
has implicated the presence of male fetal progenitor cells in
maternal circulation for up to 27 years post partum, and a
case of recurrent PEP-like lesions in a nonpregnant woman
28 years after the last pregnancy has been also reported.22
This “circulating fetal microchimerism” has been recently
demonstrated in women with PEP.24 As pregnancy is associ-
ated with peripheral chimerism, particularly during the
third trimester, it is supported that fetal cells may migrate to
maternal skin and lead to an inflammatory reaction.25
Male DNA was also found in the dermis and epidermis
from skin lesions of women with PEP who were carrying male
fetuses, but in none of the controls.22,24
Consideration of factors such as parity, multiple pregnancy
and paternity has opened a new area of investigation into the
pathogenesis of PEP.
Clinical Presentation
Polymorphic eruption of pregnancy occurs commonly in pri-
migravidae during the last few weeks of pregnancy (between
36 and 39 weeks’ gestation), but skin lesions can also be
developed in the second trimester or in the immediate post-
partum period. Occurences at other stages of pregnancy have
also been observed. Recurrence in subsequent pregnancies
with menses or oral contraceptives is uncommon.7,10 There is
no particular maternal age that PEP is likely to be developed.14
© 2006 The International Society of Dermatology
Pregnancy eruption Review 643
Figure 1 Prominent pruritic ulticarial lesions are present in
striae distensae on the abdomen
The mean duration of the eruption is 6 weeks, although it
is rarely severe for more than 1 week,10 and resolves a few
days after delivery.26 The most common symptom is pruritus,
often leading to disturbed sleep patterns and in some cases
pain. The eruption usually begins with urticarial papules and
plaques, in association with striae distensae (Fig. 1); however,
it can be polymorphous throughout its duration10,11 (Table 2).
In 70% of cases the eruption resembles toxic erythema-like
lesions; some 40% of patients develop vesicles on top of
the papules overlying striae.10,12 Targetoid lesions are present
in 20% of cases,10,12 and annular or polycyclic wheals in
18%.10,12,27,28 In exceptional cases, small bullous lesions as a
result of coalescing vesicles have been reported;29 a white halo
around the papules30 and sterile pustules have also been
observed.31 During the resolution of the eruption, most of the
patients develop fine scaling and crusting on the lesions which
may appear eczematous.10
Lesions usually start in the abdominal striae with periumbil-
ical sparing,4,28 but in some cases the eruption can develop on
the abdomen without striae.12 The rash may spread over the
thighs, buttocks, back, arms and legs. The palms, soles and
scalp are commonly spared.10 Facial involvement is rarely
reported, 32 while hair and nails are not involved. 33 Oral
or genital mucosal lesions have not been described and
dyshidrosis-like lesions on the extremities are unusual.34 Poly-
morphic eruption of pregnancy frequently shows a koebner
or isomorphic phenomenon.10 No systemic associations have
been found.33
In a recent study,28 the authors tried to characterize the
clinical findings in PEP based on the long-term clinical
International Journal of Dermatology 2006, 45, 642–648
644 Review Pregnancy eruption
Table 2 Summary of polymorphic eruption of pregnancy
Clinical data Clinical signs
Onset in the third Pruritic polymorphous lesions
trimester in the striae, around the umbilicus,
thighs, arms, buttocks
Primigravidas
Association with May have small vesicles
multiple gestation
Resolves with delivery
observations. The clinical features were categorized from
57 patients with PEP into three types:
• Type I: mainly urticarial papules and plaques;
• Type II: nonurticarial erythema, papules, or vesicles and;
• Type III: combinations of the two forms.
Type I differed from types II and III regarding the clinical
appearance and distribution (absence of face, palm and sole
lesions) only. Trimester onset, parity and immunofluorescence
findings were not significantly different among these three
groups.
The number of twin or multiple pregnancies in PEP seems
to be significantly increased.11 The frequent occurrence of
twin pregnancies in series of PEP cases has been noted, with
reported incidences of twins of 9%,35 10%,16 11%8 and
16%.14 In a recent study11 of 44 women presenting with
PEP, there were six sets of twins and one set of triplets. The
occurrence of PEP in triplet pregnancies was first described
in 1991.17 The authors suggested that increased abdominal
distension may be a trigger eliciting the occurrence of PEP
in these pregnancies. Futhermore, another recent study36
reported a prevalence of 7.89 PEP cases out of 200 multiple
gestation pregnancies, compared with one PEP case out of
200 singleton pregnancies (0.5%).6 The findings of this study
suggest that multiple pregnancies are at a high risk of devel-
oping PEP with 2.9% of twin and 14% of triplet pregnancies
affected. In a recent meta-analysis,7 a higher prevalence of
multiple gestation pregnancy (11.7%) among patients with
PEP was observed and interestingly the majority were twin
pregnancies (9.92%). Therefore, patients with a multiple
pregnancy may be more susceptible to the development of
PEP and not to the other dermatoses of pregnancy.37
Pathology
Skin biopsy reveals nonspecific findings (Table 2). Spongiosis,
acanthosis, parakeratosis or hyperkeratosis of the epidermis
and papillary dermal edema leading to subepidermal vesicle
formation may be present.38 A superficial and mid-dermal,
perivascular, inflammatory cell infiltrate is presented with a
variable number of eosinophils, lymphocytes and histiocytes.
International Journal of Dermatology 2006, 45, 642–648
Petropoulou et al.
Pathology Treatment
Biopsy:upper dermal edema, Topical corticosteroids,
perivascular lymphohistiocytic antihistamines and rarely short
infiltrate with eosinophils cource of oral corticosteroids
Immunofluorescence: negative
A recent study39 reports scattered eosinophils which infiltrate
the upper dermis with extracellular deposition of eosinophil
granule proteins in a granular pattern between collagen
bundles and patchy diffuse staining of the bundles themselves;
eosinophil involvement in PEP is more consistent than
neutrophil and mast cell involvement. The eosinophils are
increased not only in skin biopsy, but also in the hematocrit
of patients with PEP.
Immunohistochemical studies40 show an infiltrate composed
primarily of T-helper lymphocytes. These studies reveal
activated T cells (HLA-DR+, CD25+, LFA-1+) in the dermis
associated with increased numbers of CD1a+, CD54+ (ICAD+
– 1+) dendritic cells and CD1a+ epidermal Langerhans cells
in lesional skin compared with perilesional unaffected skin.
These findings may imply a delayed hypersensitivity reaction
to an unknown antigen.
Direct immunofluorescence (DIF) of perilesional skin is
usually negative in the majority of PEP cases. However, some
equivocal DIF findings have been reported in PEP, such as
minimal C3 deposition along the epidermal basement mem-
brane zone (BMZ),4,11 perivascular C3, fibrin in dermis,14,27,28
and antiepidermal cell-surface antibodies.41 Direct immuno-
fluorescence can rarely show a speckled or linear band of
immunoglobulin IgM deposition along the BMZ.11 Although
indirect immunofluorescence (IIF) is negative,11 one study42
described circulating antibasement membrane IgM in five
patients with PEP and negative DIF. Finally, hematological
and biochemical tests do not reveal any abnormality.26
Differential Diagnosis
The most frequent considerations in the differential diagnosis
are shown in Table 3. The variable morphology of the eruption
may lead to incorrect diagnoses such as drug reaction,
scabies, mild gestational pemphigoid (PG) or other disorders.
A detailed history, physical examination and information
about recent drug intake will help to inform the correct dia-
gnosis. Polymorphic eruption of pregnancy is distinguished
from pruritic folliculitis of pregnancy on the basis of the
follicular nature of the lesions and histopathologic features.43
© 2006 The International Society of Dermatology
Petropoulou et al. Pregnancy eruption Review 645

Table 3 Differential diagnosis of polymorphic eruption of
pregnancy
Contact dermatitis
Drug eruptions
Viral exanthems
Insect bites
Pityriasis rosea
Erythema multiforme
Pruritic folliculitis of pregnancy
Prurigo of pregnancy
Gestational pemphigoid
Prurigo of pregnancy begins earlier, lacks urticarial lesions,
persists throughout pregnancy and may rarely recur with
subsequent pregnancies.2
Pre-bullous PG resembles PEP and it is important to distin-
guish between these two entities, as the prognosis is different
(Table 4). Gestational pemphigoid tends to recur in subsequent
pregnancies, unlike PEP. There is also an increased risk of
prematurity and possibly small-for-gestational age births in
PG.44 Developing lesions in PG consist of pruritic urticarial
papules and polycyclic wheals, resulting later in target lesions
and finally large tense bullae. Although vesicles can be found in
PEP, they are unlikely to be larger than 2–3 mm in diameter.10
There is also a significant difference in the involvement of the
umbilicus; PG frequently involves the umbilicus, while the
eruption usually dominates in periumbilical striae distensae
in PEP.26 Striae are seldom prominent in PG.10
Histologically, PEP and HG may be difficult to be distin-
guished at certain stages because both diseases may show
dermal edema and a perivascular lymphohistiocytic infiltrate
with eosinophils. In a recent study,39 the number of eosinophils
was usually far fewer in PEP than in PG. Comparatively, tissue
eosinophil infiltration and extracellular protein deposition
is more extensive in PG than in PEP. In the same study,
neutrophils were more prominent in PG specimens than in PEP
specimens; extracellular neutrophil elastase was minimally
present and similar in both diseases.
The combined presence of the DR3 and DR4 haplotypes
has been associated with an increased relative risk for PG,45
while their frequency in PEP is normal.3
Finally, it is important to perform a DIF for all cases of PEP
to avoid any diagnostic confusion with PG, which can overlap
clinically.46 The lack of deposits of immunoglobulins and
complement at the dermoepidermal junction is considered to
be the major criterion for the differential diagnosis between
PEP and PG.47 Linear deposits of C3 in BMZ are the immuno-
pathological hallmarks of patients with PG48 – most immuno-
pathologists require this finding before they accept the diagnosis
of this rare dermatosis of pregnancy.46,49 Relatively speaking,
most immunopathologists suggest that the presence of circul-
ating IgG anti-BMZ autoantibodies in patients with PG
exceeds 20%48 (esp., when 1 m NaCl split skin is used as a test
substrate).26
Prognosis
Polymorphic eruption of pregnancy resolves spontaneously
and rapidly postpartum. Apart from the discomfort brought
by the pruritus, the maternal prognosis is excellent and
generally the incidence of fetal morbidity and mortality
appears to be similar to normal pregnancies.44
Association of PEP with increased maternal or fetal weight
gain has been debated. Cohen et al.16 first reported an increased
maternal weight gain in twin pregnancies with PEP. They
compared the pregnancy weight gain of 30 patients suffering
from PEP with a group of age- and parity-matched controls
and noted a significantly greater weight gain in the PEP group.
Increased maternal weight gain was also noted in some

Table 4 Differences between polymorphic eruption of pregnancy and gestational pemphigoid

Feature PEP PG

Prominent striae Yes No

Involvement of the umbilicus No Yes
Large tense bullae No Yes
Multiple pregnancy Yes No
Risk of prematurity No Yes
Fetal prognosis Normal Small-for-gestational-age infants
Reccurence in subsequent pregnancies No Yes
Histopathology Upper dermal edema, perivascular infiltrate Subepidermal bullae containing
with few eosinophils numerous eosinophils
DIF Negative Linear C3 (100%)
IgG (25%) along BMZ
IIF Negative Low titer IgG against
BMZ
HLA associations No DR3, DR4

© 2006 The International Society of Dermatology International Journal of Dermatology 2006, 45, 642–648
646 Review Pregnancy eruption
studies,14,17 but not in others.35,50 It has also been supported16
that patients with PEP have an increased neonatal birth weight
compared with controls. The average newborn birth weight
was 3.6 ± 0.09 kg in the PEP group compared with 3.3 ±
0.08 kg in the control group. In contrast, two other studies35,50
have not reported any significantly increased newborn birth
weight in patients with PEP; the mean newborn birth weight
was 3.37 kg (excluding twins) for the PEP group and 3.45 kg
for the control group in the first study,35 and 3.56 kg and
3.30 kg in the second study,50 respectively.
In another study,51 resolution of the eruption in PEP was
unrelated to delivery of the infant. Early delivery in refractory
cases30 has not gained support. Only one case of transient
neonatal PEP involvement has been described.52
Finally, PEP usually does not recur in subsequent pregnan-
cies; when this happens the condition is much less severe and
the eruption is often developed during the first or second
trimester and is resolved prepartum.10 Therefore, the first
episode of PEP is the most severe and recurrence occurs in
very few cases, in contrast to PG.
Management
An important aspect in the management of PEP is the expla-
nation to the patient that this is a well-recognized entity,
associated with pregnancy, which will subside spontaneously
within a few weeks and does not involve any increased risk to
the mother or the fetus.
Considering the self-limited nature of PEP and the lack of
serious complications, only symptomatic treatment is usually
required. The majority of patients benefit from antipruritic
topical medications, emollients, moderately potent topical
corticosteroid creams or small doses of antihistamines
(chlorpheniramine maleate) (Table 2).26 However, the new
nonsedating antistamines are not recommended in pregnancy.
More severe cases of PEP, with intractable pruritus, can be
safely managed with a short course of oral prednisolone (20–
30 mg /day). Maternal steroid therapy during lactation is
also safe for the neonate (up to the equivalent of 40 mg pred-
nisolone daily). Severe cases of PEP have also been reported,
which were unresponsive to therapy, but improved dramati-
cally within a few hours or days of delivery by cesarean
section.30 Futhermore, a report of successful UVB treatment
in several patients with PEP has been reported.26 As resolution
occurs within 7–10 days of delivery, a conservative approach
is usually justified.
Conclusion
Polymorphic eruption of pregnancy is the commonest gesta-
tional dermatosis and is associated with multiple pregnancies.
Onset is usually in the third trimester and in a primigravida.
It has a variable clinical morphology and the lesions are
International Journal of Dermatology 2006, 45, 642–648
Petropoulou et al.
commonly confined to striae distensae. The eruption is self-
limited and lasts about 1–6 weeks. The histology of PEP is not
specific, the serologic investigations are normal, and the DIF
and IIF are both negative. The prognosis is favorable for the
mother and the child and symptomatic treatment is usually
sufficient.
It is important to recognize this entity because of the clinical
overlap mainly with PG, which is related to an increased risk
of prematurity and small-for-gestational age births. Direct
immunofluorescence is the key to differentiation with PG and
is relevant in helping the patient plan for future pregnancies.
Although PEP is now a well-recognized entity, substantial
work must be carried out to improve our understanding of
the molecular biologic and immunogenetic properties of this
disease.
Acknowledgments
We would like to thank Professor Martin M. Black (Depart-
ment of Dermatological Immunopathology, St John’s Institute
of Dermatology, Guy’s King’s and St Thomas’ School of Medi-
cine, St Thomas’ Hospital, London, UK) for providing the
clinical picture and his kind assistance in manuscript revision.
References
1 Bourne G. Toxaemic rash of pregnancy. Proc R Soc Med
1962; 55: 462–464.
2 Nurse DS. Prurigo of pregnancy. Australas J Dermatol 1968;
9: 258–267.
3 Holmes RC, Black MM, Dann J, et al. A comparative study
of toxic erythema of pregnancy and herpes gestationis.
Br J Dermatol 1982; 106: 499–510.
4 Lawley TJ, Hertz KC, Wade TR, et al. Pruritic urticarial
papules and plaques of pregnancy. JAMA 1979;
241: 1696–1699.
5 Holmes RC, Black MM. The specific dermatoses of
pregnancy: a reappraisal with special emphasis on a
proposed simplified clinical classification. Clin Exp
Dermatol 1982; 7: 65–73.
6 Holmes RC, Black MM. The specific dermatoses of
pregnancy. J Am Acad Dermatol 1983; 8: 405–412.
7 Kroumpouzos G, Cohen LM. Specific dermatoses of
pregnancy: an evidence-based systematic review. Am J
Obstet Gynecol 2003; 188: 1083–1092.
8 Powell FC, Dervan P, Wayte J, et al. Pruritic urticarial
papules and plaques of pregnancy (PUPPP): a
clinicopathological review of 35 patients. JEADV 1996; 6:
105–111.
9 Black MM. Dermatoses of pregnancy: new developments. J
Dermatol 2001; 28: 635–637.
10 Charles-Holmes R. Polymorphic eruption of pregnancy.
Semin Dermatol 1989; 8: 18–22.
11 Vaughan Jones SA, Hern S, Nelson-Piercy C, et al. A
prospective study of 200 women with dermatoses of
© 2006 The International Society of Dermatology
Petropoulou et al.
pregnancy correlating clinical findings with hormonal and
immunopathological profiles. Br J Dermatol 1999; 141: 71–
81.
12 Black MM. Polymorphic eruption of pregnancy. In: Black
MM, McKay M, Braude P, eds. Obstretric and Gynecologic
Dermatology. London: Mosby-Wolfe, 2002: 39–44.
13 Alcalay J, Ingber A, Kafri B, et al. Hormonal evaluation and
autoimmune background in pruritic urticarial papules and
plaques of pregnancy. Am J Obstet Gynecol 1988; 158:
417–420.
14 Yancey KB, Hall RP, Lawley TJ. Pruritic urticarial papules
and plaques of pregnancy. Clinical experience in twenty-five
patients. J Am Acad Dermatol 1984; 10: 473–480.
15 Weiss R, Hull P. Familial occurrence of pruritic urticarial
papules and plaques of pregnancy. J Am Acad Dermatol
1992; 26 (5 Part 1): 715–717.
16 Cohen LM, Capeless EL, Krusinski PA, et al. Pruritic
urticarial papules and plaques of pregnancy and its
relationship to maternal-fetal weight gain and twin
pregnancy. Arch Dermatol 1989; 125: 1534–1536.
17 Beckett MA, Goldberg NS. Pruritic urticarial plaques and
papules of pregnancy and skin distention. Arch Dermatol
1991; 127: 125–126.
18 Ingber A, Alcalay J, Sandbank M. Multiple dermal
fibroblasts in patients with pruritic urticarial papules and
plaques of pregnancy. A clue to the etiology? Med
Hypotheses 1988; 26: 11–12.
19 Im S, Lee ES, Kim W, et al. Expression of progesterone
receptor in human keratinocytes. J Korean Med Sci 2000;
15: 647–654.
20 Campbell DM. Maternal adaptation in twin pregnancy.
Semin Perinatol 1986; 10: 14–18.
21 Ganshirt D, Garritsen HS, Holzgreve W. Fetal cells in
maternal blood. Curr Opin Obstet Gynecol 1995; 7: 103–
108.
22 Saraswat A, Rai R, Kumar B. Lesions resembling
polymorphic eruption of pregnancy several years after
pregnancy. Dermatology 2001; 202: 82.
23 Bianchi DW, Zickwolf GK, Weil GJ, et al. Male fetal
progenitor cells persist in maternal blood for as long as
27 years postpartum. Proc Natl Acad Sci USA 1996; 93:
705–708.
24 Aractingi S, Berkane N, Bertheau P, et al. Fetal DNA in skin
of polymorphic eruptions of pregnancy. Lancet 1998; 352:
1898–1901.
25 Nelson JL, Furst DE, Maloney S, et al. Microchimerism and
HLA-compatible relationships of pregnancy in scleroderma.
Lancet 1998; 351: 559–562.
26 Kroumpouzos G, Cohen LM. Dermatoses of pregnancy. J
Am Acad Dermatol 2001; 45: 1–19.
27 Alcalay J, Ingber A, David M, et al. Pruritic urticarial
papules and plaques of pregnancy. A review of 21 cases. J
Reprod Med 1987; 32: 315–316.
28 Aronson IK, Bond S, Fiedler VC, et al. Pruritic urticarial
papules and plaques of pregnancy: clinical and
immunopathologic observations in 57 patients. J Am Acad
Dermatol 1998; 39: 933–939.
© 2006 The International Society of Dermatology
Pregnancy eruption Review 647
29 Holmes RC, McGibbon DH, Black MM. Polymorphic
eruption of pregnancy with subepidermal vesicles. J R Soc
Med 1984; 77 (Suppl. 4): 22–23.
30 Beltrani VP, Beltrani VS. Pruritic urticarial papules and
plaques of pregnancy: a severe case requiring early
delivery for relief of symptoms. J Am Acad Dermatol 1992;
26 (2 Part 1): 266–267.
31 Ford MJ, Gammon WR, Kilpatrick TM. Pustular
eruption of the striae in a primigravida. Cutis 1992;
50: 225–228.
32 Esteve E, Saniez D, Serpier H, et al. Facial involvement in
papulous, prurient and urticarial skin disease in pregnancy.
Ann Dermatol Venereol 1996; 123: 122–123.
33 Ahmed AR, Kaplan R. Pruritic urticarial papules and
plaques of pregnancy. J Am Acad Dermatol 1981;
4: 679–681.
34 Normand F, Armingaud P, Esteve E. Dyshidrosis and
acral purpura during polymorphic dermatitis in
pregnancy: 2 cases. Ann Dermatol Venereol 2001;
128: 531–533.
35 Roger D, Vaillant L, Lorette G. Pruritic urticarial papules
and plaques of pregnancy are not related to maternal or fetal
weight gain. Arch Dermatol 1990; 126: 1517.
36 Elling SV, McKenna P, Powell FC. Pruritic urticarial papules
and plaques of pregnancy in twin and triplet pregnancies. J
Eur Acad Dermatol Venereol 2000; 14: 378–381.
37 Powell FC. Pruritic urticarial papules and plaques of
pregnancy and multiple pregnancies. J Am Acad Dermatol
2000; 43: 730–731.
38 Holmes RC, Jurecka W, Black MM. A comparative
histopathological study of polymorphic eruption of
pregnancy and herpes gestationis. Clin Exp Dermatol
1983; 8: 523–529.
39 Borrego L, Peterson EA, Diez LI, et al. Polymorphic eruption
of pregnancy and herpes gestationis: comparison of
granulated cell proteins in tissue and serum. Clin Exp
Dermatol 1999; 24: 213–225.
40 Carli P, Tarocchi S, Mello G, et al. Skin immune system
activation in pruritic urticarial papules and plaques of
pregnancy. Int J Dermatol 1994; 33: 884–885.
41 Trattner A, Ingber A, Sandbank M. Antiepidermal cell
surface antibodies in a patient with pruritic urticarial
papules and plaques of pregnancy. J Am Acad Dermatol
1991; 24 (2 Part 1): 306–308.
42 Zurn A, Celebi CR, Bernard P, et al. A prospective
immunofluorescence study of 111 cases of pruritic
dermatoses of pregnancy: IgM anti-basement membrane
zone antibodies as a novel finding. Br J Dermatol 1992;
126: 474–478.
43 Zoberman E, Farmer ER. Pruritic folliculitis of pregnancy.
Arch Dermatol 1981; 117: 20–22.
44 Sherard GB, III, Atkinson SM, Jr. Focus on primary care:
pruritic dermatological conditions in pregnancy. Obstet
Gynecol Surv 2001; 56: 427–432.
45 Shornick JK, Stastny P, Gilliam JN. High frequency of
histocompatibility antigens HLA-DR3 and DR4 in herpes
gestationis. J Clin Invest 1981; 68: 553–555.
International Journal of Dermatology 2006, 45, 642–648
648 Review Pregnancy eruption
46 Saurat JH. Immunofluorescence biopsy for pruritic
urticarial papules and plaques of pregnancy. J Am Acad
Dermatol 1989; 20: 711.
47 Goodall J. Routine immunofluorescence for pruritic
urticarial papules and plaques of pregnancy. J Am Acad
Dermatol 1988; 18 (5 Part 1): 1146.
48 Fabbri P, Caproni M, Berti S, et al. The role of T
lymphocytes and cytokines in the pathogenesis of
pemphigoid gestationis. Br J Dermatol 2003; 148: 1141–
1148.
49 Roger D, Vaillant L, Fignon A, et al. Specific pruritic
International Journal of Dermatology 2006, 45, 642–648
Petropoulou et al.
dermatoses of pregnancy: a prospective study of
3192 women. Arch Dermatol 1994; 130: 734–739.
50 Pauwels FC, Bucaille-Fleury L, Recanati G. Pruritic
urticarial papules and plaques of pregnancy: relationship to
maternal weight gain and twin or triplet pregnancies. Arch
Dermatol 1994; 130: 801–802.
51 Carruthers A. Pruritic urticarial papules and plaques of
pregnancy. J Am Acad Dermatol 1993; 29: 125.
52 Uhlin SR. Pruritic urticarial papules and plaques of
pregnancy. Involvement in mother and infant. Arch
Dermatol 1981; 117: 238–239.
© 2006 The International Society of Dermatology