1 s2.0 S1521693415000371

Best Practice & Research Clinical Obstetrics and Gynaecology 29 (2015) 732e740
Contents lists available at ScienceDirect
Best Practice & Research Clinical

Obstetrics and Gynaecology
journal homepage: www.elsevier.com/locate/bpobgyn
12
Skin disease in pregnancy

Boutros Soutou, MD, Faculte de medecine a, b, *, 1,
lim Aractingi, MD, PhD, Faculte
Se de medecine c, d, 2
a
Facult
e de medecine, Universite saint-Joseph, 11-5076 Riad el Solh, Beirut, Lebanon
b
Centre Hospitalier du Nord, 100 Jdeidet Zgharta, Lebanon
c
Facult
e de m
edecine, Paris 5 descartes, Service de Dermatologie, Ho^pital Cochin Tarnier, 89, rue d'Assas,
75006 Paris, France
d
Equipe Cellules souches foetales, Inserm UMR S 938 & UPMC, CDR St Antoine, 27, rue de Chaligny,
75012 Paris, France
Skin manifestations during pregnancy are common and diversi-

Keywords:
ed. This review will focus on the most important entities to be
pregnancy
skin abnormality recognized by obstetricians. These are, on the one hand, physio-
polymorphic eruption of pregnancy logical changes, where unnecessary investigations should be
atopic eruption of pregnancy avoided, and on the other, the specic dermatoses of pregnancy.
pemphigoid gestationis These develop electively in pregnancy, and they are currently
impetigo herpetiformis grouped into three disorders: polymorphic eruption of pregnancy,
atopic eczema of pregnancy, and pemphigoid gestationis. Argu-
ments for recognition of these are presented including detection of
anti-BP180 antibodies. Follow-up and treatment depend on the
precise diagnosis. Risks in fetal prognosis may occur in rare
pemphigoid gestationis cases.
2015 Elsevier Ltd. All rights reserved.
Skin disease in pregnancy
Dermatological manifestations associated with pregnancy can be grouped into ve categories: (i)
physiological changes, (ii) pregnancy-specic dermatoses, (iii) cutaneous infections affecting fetal
outcome, (iv) various intercurrent dermatoses affected by or affecting pregnancy, and (v) side effects of
topical cutaneous treatments and fetal risk of such treatments. These manifestations, mainly
* Corresponding author. Universite Saint-Joseph, 11-5076 Riad el Solh, Beirut, Lebanon.

E-mail addresses: bsoutou@gmail.com (B. Soutou), selim.aractingi@gmail.com (S. Aractingi).
1
Tel.: 961 3 741478; Fax: 961 6 555290.
2
Tel.: 33 1 58 41 18 13; Fax: 33 1 58 41 17 65.
http://dx.doi.org/10.1016/j.bpobgyn.2015.03.005
1521-6934/ 2015 Elsevier Ltd. All rights reserved.
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B. Soutou, S. Aractingi / Best Practice & Research Clinical Obstetrics and Gynaecology 29 (2015) 732e740 733
physiologic changes and specic dermatoses, will be the focus of this review. They are important to
recognize as diagnostic studies and monitoring are mandatory in some disorders while workup is
unnecessary in others.
Cutaneous physiological changes during pregnancy
During pregnancy, the following three main precipitating factors induce the development of skin
changes: (i) the increase in the level of circulating hormones, (ii) the intravascular volume expansion,
and (iii) the compression from the enlarging uterus.
In the skin, almost all cell types such as keratinocytes, melanocytes, broblasts, inammatory cells,
and components such as pilosebaceous units, sweat glands, and blood vessels express receptors to the
various previously cited secreted molecules. The main subsequent modications result in an increase
in keratinocyte proliferation, angiogenesis, melanogenesis, collagen synthesis, and an increase in T
helper 2 (Th2) lymphocytes and regulatory T cells.
According to the cell type targeted, the modications of the skin are divided into pigmentary,
vascular, structural, and adnexal changes. These changes are called physiological due to the following
reasons: they correspond to the expected consequences of the new hormonal, metabolic, immune, and
vascular status of a pregnant woman; they affect the majority of these women; they commonly appear
early on in the period of pregnancy; and they tend to resolve spontaneously after delivery.
Pigmentary changes
Hyperpigmentation is the most frequent skin modication found in pregnancy. Estrogens and
progesterone synergistically stimulate melanogenesis. In addition, the increased levels of melanocyte-
stimulating hormone have a direct effect on the skin. Hyperpigmentation manifests early in the rst
trimester, mainly affecting women with darker complexion and body areas of normally darker
pigmentation. After delivery, it fades variably from one patient to another. The most commonly affected
sites are the areolae and/or nipples, the periumbilical area and the linea nigra, the anogenital region,
the axillae, and the thighs [1]. Naevi, freckles, and recent scars also may darken.
Facial hyperpigmentation, or melasma, most commonly manifests on the forehead, the cheeks, the
upper lip, and the chin, consisting of greyebrown plaques. Many risks factors are clearly associated
with melasma including dark skin type, Amerindian ancestry, chronic sun exposure, hormonal stimuli,
and antidepressant/anxiolytic use [2]. It begins after the third month; it usually regresses in the
postpartum period, but it can recur for years after with sun exposure, oral contraception, or future
pregnancies. Treatment of melasma is preferred after the end of lactation as some molecules used such
as hydroquinone and tretinoin can be teratogenic. Meanwhile, preventive measures including mainly
sun avoidance and sunscreen protection are the most effective [3].
Vascular changes
During pregnancy, there is activation of endothelium and decreased vascular smooth muscle tone
leading to reduced peripheral vascular resistance. At the same time, intravascular volume expansion
and compression from the enlarging gravid uterus cause venous congestion. All these factors explain
the different vascular changes of skin during pregnancy.
Spider telangiectasias (spider angiomas)

These lesions typically begin, at the end of the rst trimester, in the area of skin drained by the
superior vena cava (face, neck, arms, and hands). They present as a punctiform central redness (cor-
responding to a dilated afferent arteriole) with radiating capillaries and surrounding erythema. These
lesions increase in number through pregnancy especially in women with lighter complexions [4]. If the
number of spider angiomas increases abnormally, the liver status should be checked as estrogen
catabolism decreases in liver diseases. Spider telangiectasias often disappear within weeks after de-
livery. Persistent lesions can be effectively treated with ne-needle cautery, pulsed dye laser, or intense
pulse light system.
734 B. Soutou, S. Aractingi / Best Practice & Research Clinical Obstetrics and Gynaecology 29 (2015) 732e740
Palmar erythema
This sign also appears during the rst trimester, more frequently in white women, and fades within
1 week post partum. The following two patterns are distinguished: (a) diffuse mottled erythema of the
entire palms, and (b) erythema restricted to the thenar and hypothenar eminences, the meta-
carpophalangeal joints, and the nger pads. Palmar erythema is attributed to venous engorgement, but
hyperthyroidism, cirrhosis, lupus, and salbutamol intake are differential diagnoses that should be kept
in mind [5].
Vasomotor instability
During pregnancy, women frequently experience episodes of pallor, facial ushing, hot-and-cold
sensations, and cutis marmorata (reticulate bluish erythema of the lower legs when exposed to cold).
Venous congestion signs

Varicosities appear in 40% of pregnant women starting from the second month [4]. Additional
precipitating factors are genetic predisposition and prolonged standing. Leg raising and elastic
stockings are effective methods of prevention.
- Those localized on the legs, the pelvis, and the perineum may have a small risk of thrombosis [5].
They usually regress post partum. Lesions persisting 3 months post partum may be treated with
sclerosing agents and laser.
- Hemorrhoids with pain and bleeding occur in 40% of patients, mainly associated with constipation,
high birth weight of the newborn, and prolonged straining during delivery. Hemorrhoids are
common during the last trimester of pregnancy and the rst month post partum [6]. Preventing
constipation with laxatives and bers has a benecial effect [7].
- The Jacquemier sign (varicosities of the vestibule and vagina) and the Chadwick sign (bluish tint of
the mucosa) are two early diagnostic signs of pregnancy [8].
Nonpitting edema of the legs but also possibly of the face and the eyelids is due to uid leakage in
the extracellular milieu when the venous hydrostatic pressure increases. It is very frequent in the
morning during the last few months of pregnancy [4,9]. It should be noted that persistent edema of the
face and the hands may be indicative of preeclampsia.
Purpura of the legs is also possible in the second half of pregnancy due to excessive fragility of skin
capillaries induced by venous hypertension in lower limbs. Purpura should always warrant a check of
the platelet count, as it is an unusual physiological sign of pregnancy.
Vascular proliferation signs

Hyperplasia of the interdental papillae of the gingival mucosa is frequently observed during the
third trimester of pregnancy [8]. It can be mild and asymptomatic or severe with intense pain and
bleeding. Poor dental hygiene, periodontal disease, local irritants, and nutritional deciencies are
triggering factors. Healing is progressive in the postpartum period.
Epulis gravidarum, misnamed pyogenic granulomas, represents asymptomatic erythematous
fragile nodules of the gingival mucosa corresponding to hyperplasia of mucosal capillaries and bro-
blasts or of the skin itself. Triggers are physical trauma and irritation (plaque deposits and gingivitis).
Epulis regresses within months after delivery and recurs in later pregnancies. Considerable bleeding
allows surgical excision.
Structural changes
Striae distensae
In the third trimester, striae begin as linear red to purple bands. They develop on the abdomen, the
breasts, the thighs, the inguinal folds, and the arms. They fade gradually and leave white atrophic
bands. Risk factors in primiparous women are young maternal age, elevated maternal body mass index
(BMI), excessive maternal weight gain, macrosomia, and personal and familial history of striae. Causes
seem multiple including mechanical stretching of the skin and hormonal reduction of elastic bers
through steroids, estrogens, and relaxin. A recent genome-wide association study (GWAS) suggested an
association with mutations of genes encoding for elastic microbrils [10]. All preventive measures have
been failures [11,12]. The appearance of recent purplish striae may improve with pulsed dye laser or
0.1% tretinoin cream, two treatments reserved for at least 3 months post partum [13,14].
Acrochordons
Skin tags grow during the second half of pregnancy. They correspond to small pedunculate lightly
pigmented polyps on the neck, the axillary, the inframammary, and the inguinal folds. They have no
malignant potential. They often shrink after delivery. Otherwise, removal is simple with snipping,
cryotherapy, or cautery.
Adnexal changes
Hair
During pregnancy, fewer anagen (growing) hair follicles enter the telogen (shedding) phase. Scalp
and body hair will increase in number, thickness, and brightness, especially on the face, the arms, and
the legs. This pattern reverses within 6 months post partum [5].
Two to four weeks after delivery, the scalp hair enters a prolonged telogen phase and sheds pro-
fusely (telogen efuvium) during 3e4 months. Later on, hair completely grows within 6e15 months
[15]. However, anemia, iron deciency, and thyroid dysfunction should be evaluated if any doubt is
present.
Nails
Nails grow faster and become brittle. Other manifestations are uncommon and reversible (sub-
ungual thickening, longitudinal melanonychia (brown pigmentation arranged lengthwise along the
nail unit), transversal grooves (linear narrow depressions of the nail), and distal onycholysis) [5].
Sebaceous glands
As an early sign of pregnancy, sebaceous glands enlarge on the areola and appear as multiple brown
papules (Montgomery's glands), starting from the sixth week of gestation. They regress spontaneously
after delivery [5,15].
Facial skin may become greasy in the third trimester due to increased sebaceous glands activity.
Acne frequently develops during pregnancy. The diagnosis is easy but the treatment should exclude
cyclins and retinoids. Erythromycin and benzoyl peroxide can be prescribed.
Sudoral glands
Eccrine sweat gland activity increases through pregnancy with subsequent hyperhidrosis and
miliaria (pruriginous inammation of the glands) [15]. Apocrine gland activity seems to decrease.
Specic dermatoses of pregnancy
The specic dermatoses of pregnancy strictly occur during or immediately after pregnancy. The
pathophysiology of dermatoses of pregnancy remains poorly understood. Furthermore, their previous
classication has led to a confusing set of names and acronyms. Currently, the three specic derma-
toses of pregnancy are as follows: polymorphic eruption of pregnancy (PEP), atopic eczema of preg-
nancy (AEP), and pemphigoid gestationis (PG). Intrahepatic cholestasis of pregnancy and impetigo
herpetiformis (IH) are not, strictly speaking, specic dermatoses of pregnancy. However, their
knowledge is essential when considering fetal and maternal risks.
Polymorphic eruption of pregnancy
PEP is a pruritic disorder that predominantly affects women in the third trimester of their rst
pregnancy [16e18]. Earlier or postpartum onsets are possible. Incidence may vary between 0.06% and
0.8% of pregnancies [16,17,19]. Intensely pruritic urticarial papules and plaques appear rst on the
lower abdomen, particularly on the striae distensae and typically sparing the periumbilical area. The
eruption may spread to the rest of the trunk and extremities (Fig. 1). However, the face, palms, and soles
are rarely affected [19]. In approximately 50% of cases, eczematous, vesicular, or target-like lesions can
also be seen [20].
Histology is not specic. It variably shows dermal edema and polymorphous mononuclear inltrate
with eosinophils found in half of cases. Spongiosis, acanthosis, and parakeratosis are the main
epidermal changes [20]. Direct immunouorescence is constantly negative.
Pathogenic mechanisms are still unclear. However, many interesting ndings can be mentioned:
- There are no hormonal abnormalities, no human leukocyte antigen (HLA) associations, and no
proles of autoimmunity.
- Twin or triplet pregnancy with further abdominal skin distension, and probably higher maternal
weight gain and newborn birth weight, could have some role in the development of PEP over striae
distensae [21]. However, the hypothesis of skin inammation secondary to mechanical distension
cannot be considered as a unique valid explanation as PEP may affect other cutaneous areas not
subject to such distension.
- The presence of fetal keratinocytes in skin lesions probably corresponds to a secondary repair
phenomenon more than a primary source of inammation [22,23].
Signicant associations were found with higher rates of male fetuses, cesarean delivery, and mul-
tiple pregnancies [18,24]. However, PEP does not inuence the outcome of pregnancy. Spontaneous
remission occurs within 3e6 weeks after delivery. The recurrence rate in later pregnancies is low.
Treatment with a once-daily application of potent or ultrapotent topical steroids relieves symptoms.
Emollients and antihistamines may add some favorable effect when pruritus is very intense. If PEP is
widespread, systemic steroids, for example, prednisolone 20e30 mg, will usually suppress cutaneous
inammation.
Atopic eczema of pregnancy
AEP appears to be the most frequent of specic dermatoses in pregnancy [18]. Unlike PEP, the
eruption starts in 76% of patients during the rst and second trimesters. Diagnostic criteria are not very
specic. Indeed, these correspond to pruritic dermatosis with a background of personal or familial
atopy. High immunoglobulin E (IgE) serum levels and previously known dry skin are not mandatory.
Lesions are featured as pruritic eruption of eczema-like lesions ares in the same sites of atopic
eczema, mainly the inside of the knees and elbows (Fig. 2). However, in almost a third of cases,
elementary lesions consist of papular and nodular prurigo of the extremities.
Histology has no distinguishing features. Direct immunouorescence is negative. High serum levels
of IgE are present in 20e70% of cases [25].
Fig. 1. Polymorphic eruption of pregnancy. Urticarial papules on the skin of the abdomen of a patient in the third trimester of her
rst pregnancy.
Fig. 2. Atopic eczema of pregnancy. Papulovesicular plaque with pruritus on the elbow fold during a are in a pregnant patient.
Immunity mechanisms change during pregnancy with a switch toward a dominant humoral im-
mune response and an increased release of Th2 cytokines (interleukin (IL)-4 and IL-10). This may partly
explain de novo ares and acute exacerbations of pre-existing atopic dermatitis [26,27]. The role of a
genetic background for atopy and the implication of laggrin gene mutations require more
investigation.
Maternal outcome is favorable even in severe and extended ares of AEP. Recurrences can occur in
later pregnancies. Fetal prognosis is not altered, but the offspring of affected pregnancies are at a risk of
developing atopic eczema during childhood [27].
As in atopic dermatitis, Treatment consists of topical steroids to cure ares and emollients applied
on a regular basis in order to improve skin dryness. Ultraviolet B (UVB) phototherapy that appears to be
safe in pregnancy can control severe and steroid-resistant eruptions.
Pemphigoid gestationis
PG is an autoimmune skin disease, immunologically similar to bullous pemphigoid, but epidemi-

ologically related to pregnancy, postpartum, and rarely hydatidiform moles. The incidence ranges at
approximately one in 7000 [17,25,28]. PG usually affects multiparous women in their second or third
trimester. Onset in postpartum or the rst trimester is also reported. Intense pruritus precedes skin
eruption. Later on, urticarial pruritic papules, sometimes displaying an annular pattern, appear typi-
cally on the periumbilical skin. Then, they spread to the trunk and the extremities sparing the face and
the mucosa (Fig. 3). Later on, bullae can rise either on edematous plaques or on normal unaffected skin.
However, the presence of bullae remains rare. Most of the PG cases are non-bullous, showing pruritic
urticarial papules and eczema-like plaques, of variable progression, without mucosal involvement,
clinically similar to PEP's manifestations.
Histology shows spongiotic epidermis, subepidermal vesicles, dermal edema with a mild peri-
vascular inltrate of lymphocytes, histiocytes, and many eosinophils. These features are not very
specic and can also be seen in PEP. Diagnosis relies on direct immunouorescence. It shows a linear
Fig. 3. Pemphigoid gestationis. Annular urticarial plaques involving the periumbilical skin of a patient in the second trimester of her
second pregnancy.
deposit of C3 (IgG) along the basement membrane zone. In 69-90% of patients, indirect immuno-
uorescence detects IgG1 autoantibodies (herpes gestationis factor) targeting the hemidesmosomes of
the basal membrane. Western blotting shows circulating autoantibodies against either BPAg2 (180kD)
antigen alone or more rarely BPAg1 (230kD) and BPAg2 together. Lately, two tests have been suggested
to replace direct immunouorescence to diagnose PG:
- Autoantibodies of PG have a common antigenic site with the noncollagenic domain NC16a of BPAg2.
A specic and sensitive ELISA can depict anti-BPAg1-NC16a antibodies [29].
- Routine immunochemistry for anti-C4d in formalin-xed parafn-embedded tissue shows very
specically in PG linear C4d immunoreactant deposition along the basement membrane zone [30].
Serum titers of circulating IgG antibodies detected by conventional indirect immunouorescence

correlate neither with disease activity nor with pregnancy outcome [18,31]. PG is in part related to a
genetic background; approximately 45% of women with PG (vs. 3% of the controls) display the HLA-DR3
allele. Moreover, 90% of PG women have a null C4 allele [32,33]. Furthermore, an abnormal expression
of HLA class II antigens has been shown in the trophoblasts of PG-affected women [34]. Therefore, the
proposed hypothesis is that a response of the maternal immune system against paternal HLA antigens
abnormally expressed on placenta will also target the collagen XVII present in the basal membrane
zone of the skin by cross-reaction. Such a hypothesis can explain PG being specic to one partner and
not another [35].
Maternal and fetal prognoses are good in PG despite some known overrisks of cesarean section,
prematurity, and low birth weight [28,36,37]. Obstetricians should be aware of the risk of intrauterine
growth retardation in PG. This risk is low, but it increases if PG appears early in the second trimester
and when bullous lesions are numerous. Ultrasound measurements should then be performed regu-
larly. Neonatal vesicles may appear in newborns of affected mother, but such eruption is infrequent,
usually mild, self-limited, and related to the transient passage of maternal antibodies. PG usually re-
gresses after delivery. A postpartum are is however reported in 75e85% of cases. Very rarely, some
cases may have an autonomous course for several years after pregnancy. Recurrences in later preg-
nancies are frequent (50e70%), with earlier onset and more severe form. Cases were also reported with
subsequent use of oral contraceptives.
There is no absolute consensus for the treatment of PG. However, similar to bullous pemphigoid, we
consider that rst-line treatment in PG is actually ultrapotent topical steroids [38e40]. In resistant
cases, systemic steroids at a daily dose of 0.5 mg/kg are necessary to control the disease.
Intrahepatic cholestasis of pregnancy (ICP) (refer to chapter on liver disease in pregnancy)
ICP is not strictly a skin disease as there are no primary skin lesions. ICP manifests by isolated
nocturnal itching mainly during the third trimester. Usually, skin appears normal. Excoriations and
prurigo secondary to scratching are the only possible skin manifestations.
Impetigo herpetiformis
IH is a very rare skin disorder sometimes reported outside pregnancy. Misnamed, IH is neither a
bacterial nor a herpesvirus infection. Onset occurs in primigravidae in their third trimester.
Erythematous plaques, secondarily bordered with sterile pustules, appear in the folds and extend
centrifugally. Fever, nausea, vomiting, and diarrhea are common. Hypoalbuminemia, secondary hy-
pocalcemia, or low serum levels of vitamin D should be systematically sought. True hypocalcemia
remains rare, and it is usually the reection of the hypoalbuminemia. Some authors consider IH as a
are of generalized pustular psoriasis triggered by pregnancy. This remains controversial as a personal
history of psoriasis is reported in only a third of patients. Maternal risk is linked to poor management
and/or to hypercalcemia-induced convulsions. Fetal death is possible due to placental ischemia.
Recurrence in successive pregnancies may start earlier. Oral contraceptives can also trigger a are.
Topical or systemic steroids and cyclosporine in resistant cases are the mainstay of treatment [41].
Practice points
Two recommendations are essential when dealing with skin disorders during pregnancy.
First, we should be able to recognize the dermatoses of pregnancy, and if there is any un-
certainty of the diagnosis, or if the pattern is suggestive of PG, then a skin biopsy is indicated.
Otherwise, excessive, unnecessary biopsies will be performed.
Second, all the dermatoses of pregnancy will improve with either topical or systemic ste-
roids. Steroid treatment is safe throughout pregnancy.
Research agenda
Cutaneous biology and interactions between skin components and hormones secreted
during pregnancy
An investigation into the role of fetal stem cells in the maternal circulation on tissue repair
and tumor development.
Conicts of interest
None.
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Best Practice & Research Clinical Obstetrics and Gynaecology 29 (2015) 732e740

Contents lists available at ScienceDirect

Best Practice & Research Clinical

Skin disease in pregnancy

Skin manifestations during pregnancy are common and diversi-

Skin disease in pregnancy

* Corresponding author. Universite Saint-Joseph, 11-5076 Riad el Solh, Beirut, Lebanon.

Cutaneous physiological changes during pregnancy

Spider telangiectasias (spider angiomas)

Venous congestion signs

Vascular proliferation signs

Specic dermatoses of pregnancy

Polymorphic eruption of pregnancy

Atopic eczema of pregnancy

PG is an autoimmune skin disease, immunologically similar to bullous pemphigoid, but epidemi-

Serum titers of circulating IgG antibodies detected by conventional indirect immunouorescence

Intrahepatic cholestasis of pregnancy (ICP) (refer to chapter on liver disease in pregnancy)

[1] Esteve E, Saudeau L, Pierre F, et al. Signes cutane

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