Vol. 23, No. 3, 2011
Corresponding author: Christina M. Ambros-Rudolph, M.D., Department
of Dermatology, Medical University of Graz, Auenbruggerplatz 8,
A-8036 Graz, Austria. Tel: 43-316-385-80542, Fax: 43-316-385-12466,
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Ann DermatolVol. 23, No. 3, 2011DOI: 10.5021/ad.2011.23.3.265
Dermatoses of Pregnancy - Clues to Diagnosis, Fetal
Risk and Therapy
Christina M. Ambros-Rudolph, M.D.
Department of Dermatology, Medical University of Graz, Graz, Austria
The specific dermatoses of pregnancy represent a hetero-
geneous group of pruritic skin diseases that have been
recently reclassified and include pemphigoid (herpes)
gestationis, polymorphic eruption of pregnancy (syn. pruritic
urticarial papules and plaques of pregnancy), intrahepatic
cholestasis of pregnancy, and atopic eruption of pregnancy.
They are associated with severe pruritus that should never be
neglected in pregnancy but always lead to an exact work-up
of the patient. Clinical characteristics, in particular timing of
onset, morphology and localization of skin lesions are
crucial for diagnosis which, in case of pemphigoid
gestationis and intrahepatic cholestasis of pregnancy, will be
confirmed by specific immunofluorescence and laboratory
findings. While polymorphic and atopic eruptions of
pregnancy are distressing only to the mother because of
pruritus, pemphigoid gestationis may be associated with
prematurity and small-for-date babies and intrahepatic
cholestasis of pregnancy poses an increased risk for fetal
distress, prematurity, and stillbirth. Corticosteroids and
antihistamines control pemphigoid gestationis, polymor-
phic and atopic eruptions of pregnancy; intrahepatic
cholestasis of pregnancy, in contrast, should be treated with
ursodeoxycholic acid. This review will focus on the new
classification of pregnancy dermatoses, discuss them in
detail, and present a practical algorithm to facilitate the
management of the pregnant patient with skin lesions. (Ann
Dermatol 23(3) 265∼∼275, 2011)
Atopic eruption of pregnancy, Dermatoses of pregnancy,
Intrahepatic cholestasis of pregnancy, Pemphigoid ges-
tationis, Polymorphic eruption of pregnancy, Pruritus
Complex endocrinologic, immunologic, metabolic and
vascular changes associated with pregnancy may influ-
ence the skin in various ways. Skin findings in pregnancy
can roughly be classified as physiologic skin changes,
alterations in pre-existing skin diseases, and the specific
dermatoses of pregnancy. Physiologic skin changes in
pregnancy include changes in pigmentation, alterations of
the connective tissue, vascular system, and endocrine
function as well as changes in hair and nails (Table 1)1.
Pregnancy is also known to influence the course of
pre-existing skin diseases in both positive and negative
ways2. A typical example is psoriasis, a classical Th1-
associated disease, which often improves in pregnancy,
only to worsen after delivery. A special case in this
context is impetigo herpetiformis, which today is regarded
as a variant of generalized pustular psoriasis presenting in
pregnancy, accompanied by systemic signs such as fever,
chills, vomiting, diarrhea and tetanic seizures due to
hypocalcemia. Diseases primarily associated with a
Th2-immune response, such as lupus erythematosus and
other autoimmune dermatoses, in contrast, character-
istically deteriorate during pregnancy and improve after
delivery. This is thought to be due to a temporary
imbalance that develops between the differential cytokine
secretion profiles and the preferential cellular or humoral
dominated Th1 and Th2 mediated immune responses in
order to prevent rejection of the fetus. Another disease
typically affected in its course by pregnancy is acne,
which most often improves, but can also be quite
Table 1. Physiologic skin changes in pregnancy1
Physiologic skin changes in pregnancy
Hyperpigmentation (diffuse with accentuation
of areolae mammae and linea nigra)
Increased hormone levels (estrogen, progesterone, MSH) lead to
hyperpigmentation (by up to 90% of pregnant women) and
Aggravating factors: dark skin, UV exposition. Melasma
Striae distensae Occur in up to 90% of patients, probably combined effects of genetic
predisposition, abdominal distension and hormonal factors.
Spider angiomas, teleangiectasia
Gingiva hyperemia and hyperplasia
Increased eccrine gland function (except palms)
Decreased apocrine gland function
Disturbed sebaceous gland function
(acne gravidarum, Montgomery glands)
Postpartal telogen effluvium
Postpartal androgenetic alopecia (rare; typically
Weight gain, redistribution of volume and hormonal factors lead
to edema and varicosities and to formation of new vessels.
Main manifestation in the third trimester, usually reversible after
Increased incidence of milaria, hyperhidrosis and dyshidrotic
eczema on the one hand and improvement of hidradenitis
suppurativa on the other. Data on sebaceous gland activity
Prolongation of anagen phase leads to hypertrichosis during
pregnancy, synchronized transition into the telogen phase later
to postpartal effluvium.
Normalization within 6∼12 months.
Entirely unspecific and reversible.
tenacious (“acne gravidarum”). Nevi tend to darken and
enlarge, especially on the abdomen and breasts. The
assumption that pregnancy has deleterious effects on the
course of melanoma has not been substantiated; however,
diagnostic and therapeutic decisions are often delayed in
pregnancy leading to a more advanced tumor stage and
hence worse prognosis.
The specific dermatoses of pregnancy represent a hetero-
geneous group of severely pruritic inflammatory derma-
toses associated exclusively with pregnancy and/or the
immediate postpartum period. The rarity of these diseases,
their variable clinical morphology, the lack of unequivocal
diagnostic tests (with the exception of immunofluore-
scence in pemphigoid gestationis) as well as limited
treatment options have led to confusing terminologies and
have made their management difficult over decades. This
article addresses the specific dermatoses of pregnancy in
particular as a new classification has been recently est-
ablished based on the results of a retrospective two-centre
study on more than 500 pregnant patients3.
The first specific dermatosis of pregnancy reported was
pemphigoid gestationis, which Milton described in 1872
under the name herpes gestationis4. The term “herpes”
referred to the characteristic “creeping” blister formation.
Only after the introduction of immunofluorescence micro-
scopy and the discovery of specific linear complement
deposition along the dermo-epidermal junction zone (DEJ)
in 1973 could this disease entity be differentiated from the
other dermatoses of pregnancy. In 1904 Besnier described
another pregnancy-related disease which he termed
prurigo gestationis5. The original description as well as
illustration resemble today’s picture of atopic dermatitis;
of interest, at that time, what we define today as atopic
dermatitis was known as prurigo. Costello (1941) employ-
ed this term and designated all pregnancy-related derma-
toses which were not herpes gestationis as prurigo
gestationis of Besnier and reported an incidence of 2%6.
In the further course of time the disease was also referred
to as early onset prurigo of pregnancy or prurigo of pre-
gnancy7. Bourne (1962) described a further pregnancy-
related dermatosis under the name toxemic rash of
Dermatoses of Pregnancy
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