Skin Modifications During Pregnancy
Tuesday, March 07, 2006
Pregnancy-related skin modifications are diverse. They include
physiological consequences that are linked to the hormonal,
immunological, and vascular modifications induced by pregnancy, as
well as several others signs that may signify the presence of a
disease that requires diagnosis and treatment. Therefore, when
facing a pregnant woman asking for advice about skin signs or
symptoms, the successive questions you should ask are:
- Do these signs or symptoms correspond to physiological
modifications linked to pregnancy?
- If not, do they correspond to cutaneous disorders specifically
related to the pregnancy or are they related to a condition that is
independent from the pregnancy?
- Is treatment available or needed?
If treatment is needed, consideration of the fetus is warranted,
even for topical treatment.
Signs and Symptoms Corresponding to Physiological
Pigmentary disorders, affecting 85-95% of pregnant women, are the
most frequently encountered modifications linked to
pregnancy.1 As expected for other abnormalities of
pigmentation, these are more obvious in genetically pigmented
individuals. These changes are usually local and may begin early in
pregnancy. They are linked to several biological phenomena,
including the increased production of α-melanocyte-stimulating
hormone (α-MSH), estrogens and progesterone, and sun exposure.
Hyperpigmentation of the linea alba is the most commonly
observed pigmentation change (75% of cases), and it is called linea
nigra. It usually extends from the pubis to the umbilicus but
sometimes may reach the xyphoid appendix.2 This
pigmentation almost always clears after delivery, although some
minor changes may remain.
Chloasma is a symmetrical, non-homogeneous hyperpigmentation
involving the front and/or the malar and/or the mandibular areas of
the face. It usually begins after the first trimester and is
worsened by sun exposure. Its occurrence ranges from 5-75% of
pregnant women.3 The major problem is that it regresses
slowly and inconstantly. It may last up to 6-18 months after
delivery, and flares may still occur with sun exposure even long
after the pregnancy ends. There are three types of chloasma
according to the depth of the pigment deposition, the prognosis
being poorer when melanin deposition occurs in the dermis.
Treatment should be given only after delivery, and it should rely
on the combination of photoprotection and topical depigmenting
agents, primarily hydroquinone 2-5%. Oral contraception should be
handled with caution as it may trigger new flares.
Nipple pigmentation affects 40% of pregnant women, and it may
involve the areola alone or it may include the surrounding skin.
Axillary and/or inguinal pigmentation are rare. Finally, the vulva
may also become pigmented.
The pathogenesis of striae is not certain. It could result from
hormonal changes - including steroids - on extracellular matrix
production by dermal fibroblasts.4 Striae are easily
recognized by the patient. They may be narrow or wide, their width
sometimes reaching up to 2 cm. Initially inflammatory, the striae
ultimately become white and atrophic and develop in 60-90% of
pregnant women.1-3 The main sites are the abdomen and
thighs, followed by breasts and then the buttocks. Striae involve
preferentially young primagravada and begin during the third
trimester. No preventive technique has been validated up until now.
Restorative measures may be considered only after delivery; they
may rely on topical retinoids and/or the pulse dye laser.
Most of the following vascular abnormalities reflect the
biological activity of high levels of estrogens on endothelial
cells, leading to their proliferation.
The spider nevus is easy to recognize, having a central
erythematous "arteriole" and radiating thin-walled vessels.
Compression of the central vessel temporarily obliterates the
lesion with blanching of the spider "legs". When released, the
threadlike vessels quickly refill with blood from the central
arteriole. These lesions predominate on the upper half of the body
(eyebrows, face), but some may also occur on the hands. Most of
these (75%) regress after delivery.1,2
Unilateral nevoid telangiectasia consists of acquired patches of
superficial telangiectases in a unilateral linear distribution.
These are plain, sometimes with a blanching halo surrounding each
lesion, occurring primarily on the thorax and face. The diagnosis
is based on clinical findings and their evolution is toward
spontaneous regression after delivery.
Palmar erythema is another consequence of the vascular
proliferation that occurs with pregnancy, described in 30-60% of
pregnant women.1 Some authors have discriminated between
a diffuse form and a more restricted erythema involving only finger
pulps, thenar, and hypothenar protuberances.
Venous circulation is altered during pregnancy, frequently
leading to the development of multiple signs and symptoms. The
pathogenesis of venous insufficiency is multifactorial and relies
on hypervolemia that alters valvular continence. There is decreased
velocity of venous flow, resulting in increased venous pressure and
compression of iliac veins by a dilated uterus. Venous
insufficiency induces lower limb edema with pain, varicose veins,
rarely thrombophlebitis, and purpura. Pregnant women should be
informed of this risk.
This is a peculiar skin modification in this context: Indeed, it
is still "physiological" as it is the consequence of hormonal
estroprogestative changes in pregnancy, but it may be visible
enough to require a treatment. Acne is found in 23% of pregnancies
with a variable severity.2 The main issue for
pregnancy-associated acne is the choice of therapeutic options. In
summary, retinoids - including topical ones - and the cyclines are
contraindicated throughout pregnancy. In contrast, benzoyl peroxide
and oral and topical erythromycin or zinc are allowed.
Other Signs and Symptoms
Many other modifications may occur during pregnancy:
- Gingivae hyperplasia and occasional bleeding may occur.
- Nail growth may be accelerated, leading to shiny, delicate
nails. Distal onycholysis is possible.
- Modifications of the hair follicle cycle may occur, with a
slower shift from anagen to telogen hair, allowing the impression
of more hair. In the same way, hypertrichosis alone - without
hirsutism - is possible. Following pregnancy, rapid hair loss,
termed telogen effluvium, may occur.
- An increase in acrochordons - skin tags - during pregnancy is
classically reported in textbooks. However, original series have
not reported this hallmark.
Signs and Symptoms Related to Specific Dermatoses of
A peculiar characteristic of pregnancy is the fact that there
are skin conditions that are chronologically linked to this period.
This means that these diseases appear only during pregnancy and
that they resolve after delivery.
The frequency of intra-hepatic cholestasis of pregnancy
(IHCP) varies, ranging from 0.02% of pregnancies series up
to 2.4% of pregnancies in specific countries, such as Chile or
China. Its pathogenesis is unknown, but most authors speculate that
it could result from abnormalities in bile secretion, related to
estrogens. This condition is usually limited to isolated pruritus
without skin lesions. However, itching may lead to excoriations or
linear crusts, and those are present in up to one-third of patients
with IHCP.5,6 Many patients have elevated levels of
serum biliary acids, with subsequent increases in transaminases.
Obtaining an early diagnosis is mandatory as prolonged cholestasis
may induce fetal consequences that are linked to the accumulation
of biliary salts in the child's brain. Pregnant women with IHCP are
therefore followed closely to prevent fetal distress. In addition,
treatments such as cholestyramine or ursodesoxycholic acid may be
Pemphigoid gestationis (PG), formerly herpes
gestationis, is a fascinating model of autoimmunity restricted to
pregnancy. Previously, PG was considered to be very rare, occurring
in only 1 out of 50,000 pregnancies. This figure results from
series published when PG was considered only if a blistering
eruption was present. However, this appears to be wrong. Indeed,
more recent studies - in which direct immunofluorescence was done
on skin blisters, as well as papular eruptions - finally revealed
that PG affected 1 in 1,600 pregnancies.6,7
This discrepancy demonstrates that PG was commonly
non-blistering. The disease begins in the third trimester, usually
on the abdomen, in the periumbilical area, then disseminates.
Itching is intense and lesions may indeed be blisters, but, as
stated above, may also include arciform plaques and papules.
Diagnosis requires a skin biopsy. Histology is not specific,
showing dermal edema, mononuclear infiltrate together with
eosinophils and usually dermo-epidermal detachment. However, direct
immunofluorescence discloses the linear deposits of
immunoreactants, C3 more frequently than Ig, at the
dermal-epidermal junction. Serum analysis shows the presence of
antibodies that react against the 180kd BPAG 2 antigen. In the
future, the routine use of the BP180 Elisa may allow sparing of
skin biopsy. Classical analyses of the anti-epidermal complement
binding antibody has been abandoned.
PG may flare after delivery or may occur for the first time
after delivery. An important point is that PG displays usual
recurrences during subsequent pregnancies (50-70%).2
Such recurrences may also occur in patients with a history of PG
after treatment with oral contraceptives in 20-50% of
cases.8 Pathogenesis is linked to the development of
autoantibodies targeting the 180kd antigen of the dermal epidermal
junction. Affected women have susceptibility genes for autoimmune
diseases: 43-45% of PG females are HLA DR3/DR4 versus 3% in control
population, and 90% of PG females have a C4 null
allele.9 Another point is that placentas of women with
PG disclose the abnormal expression of classical HLA class I
antigens, these antigens being usually absent at this
site.10 There is reactivity of the woman's sera with the
Therefore, the speculative statement of pathogenesis is as
follows: HLA class I paternal antigens are aberrantly expressed on
the placenta; women prone to autoimmunity mount an immune humoral
reaction against some of these; some these anti-paternal HLA I
antibodies cross-react with the cutaneous 180 kd antigen; and
pemphigoid develops. The fact that the disease does not usually
relapse when the father differs for subsequent pregnancies supports
this hypothesis. PG is associated with some risks in pregnancy:
there are higher rates of prematurity and of caesarean section. The
reasons for these remain unknown, although transient blisters may
be found in babies. Treatment relies usually on oral steroids (0.5
mg/kg), although limited forms - close to bullous pemphigoid -
could be treated with topical steroids.
Polymorphic eruptions of pregnancy (PEP) have
been individualized in the 1980s to include many entities that did
not deserve to be separated.12 Therefore, PEP appeared
as a disease beginning in the third trimester of pregnancy that can
affect primigravida. The lesions begin as in PG on the abdomen,
then usually disseminate. The immediate periumbilical skin is
usually spared, and the eruption predominates in the striae. This
pruritic eruption consists of papules, urticarial plaques, and more
In the absence of treatment, spontaneous healing occurs weeks
after delivery and flares are rarely noted in subsequent
pregnancies (5%).6 Contraception given after delivery
does not induce relapses. Biopsies have non-specific features, with
a mononuclear infiltrate, sometimes eosinophils, and epidermal
spongiosis. Direct immunofluorescence is mandatory: indeed, PG may
present as a third trimester eruption of plaques without blisters.
Therefore, determining that a cutaneous eruption developing during
pregnancy is a PEP requires the absence of an immunoreactant
deposition to be checked by immunofluorescence.
The pathogenesis of PEP remains unknown. Authors have proposed a
role for skin distension, suggesting that cutaneous tissue would be
inflamed because of mechanical distension. This hypothesis has not
been confirmed.14 There is no autoimmunity in PEP.
Vaughan Jones et al. have recently found a higher level of cortisol
level in women with PEP.15
Our group has found abnormal trafficking of fetal cells in this
disease, but these fetal cells could either trigger the disease (as
in a fetal anti-maternal reaction) or, in contrast, migrate into
the skin to repair established damage.16 This last
hypothesis is in line with other findings in which fetal cells
appear to differentiate into various phenotypes in peripheral
tissues in order to participate in lesion repair. Whatever the
cause, PEP has no deleterious consequences for the mother or the
baby and treatment relies on topical steroids and
Many other items could be added to this relatively short list.
Some are pre-existing skin conditions that may worsen during
pregnancy, such as lupus erythematosus or dermatomyositis. In
contrast, others (such as psoriasis) may improve during pregnancy.
Skin infections such as syphilis, rubella, parvovirus B19,
toxoplasmosis, varicella, and others could induce embryonic and/or
fetal diseases and should be recognized early. This highlights the
essential role of dermatologists in this context: to allow an early
The prognosis of melanoma is similar to that of non-pregnant
women, but a delay in diagnosis seems to happen, possibly due to
co-founding factors. Of note, there are no mole modifications
during pregnancy and quantitative measurements of nevi have not
shown any "physiological" growth of nevi.17 Therefore,
every modification of melanocytic lesions during pregnancy should
be interpreted with caution and not considered to be a
physiological growth of moles.
Finally, prescribing treatments, including topical ones, is
always delicate and it is important to always check recent
information of drug agencies before administration as
recommendations change frequently, even for some old molecules.
- Winton GB, Lewis CW. Dermatoses of pregnancy. J Am Acad
- Estève E, Saudeau l, Pierre F, et al. Signes cutanés
physiologiques au cours de la grossesse normale: étude de 60 femmes
enceintes. Ann Dermatol Venereol. 1994;121:227-31.
- Wade T, Wade SL, Jones HE. Skin changes and diseases associated
with pregnancy. Obstet Gynecol. 1978;52(2):233-42.
- Henry F, Pierard Franchimont C, Pans A, et al. Striae
distensae of pregnancy. An in vivo biomechanical evaluation.
Int J Dermatol. 1997;36(7):506-8.
- McDonald JA. Cholestasis of pregnancy. J Gastrol
- Roger D, Vaillant L, Fignon A, et al. Specific
pruritic diseases of pregnancy. A prospective study of 3192
pregnant women. Arch Dermatol. 1994;130(6):734-9.
- 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(5):474-8.
- Schornick JK, Black MM. Secondary autoimmune diseases in herpes
gestationis (pemphigoid gestationis). J Am Acad Dermatol.
- Schornick JK, Artlett CM, Jenkins RE, et al.
Complement polymorphism in herpes gestationis: association with C4
null allele. J Am Acad Dermatol. 1993;29(4):545-9.
- Bortwhick GM, Holmes RC, Stirrat GM. Placenta abnormal
expression of class II MHC antigens in placentae from patients with
pemphigoid gestationis: analysis of class II MHC subregion product
expression. Placenta. 1988;9(1):81-94.
- Ortonne JP, Hsi BL, Verrando P, et al. Herpes
gestationis factor reacts with the amniotic epithelial basement
membrane. Br J Dermatol. 1987;117(2):147-54.
- Holmes RC, Black MM. The specific dermatoses of pregnancy.
J Am Acad Dermatol. 1983;8(3):405-12.
- Aronson IK, Bond S, Fielder VC, et al. Pruritic
urticarial papules and plaques of pregnancy: clinical and
immunopathologic observations in 57 patients. J Am Acad
- Roger D, Vaillant L, Lorette G. Pruritic papules and plaques of
pregnancy are not related to maternal or fetal weight gain.
Arch Dermatol. 1990;126(11):1517.
- Vaughan Jones SA, Hern S, Nelson-Piercy C, et al. A
prospective study of 200 women with dermatoses of pregnancy
correlating clinical findings with hormonal and immunopathological
profiles. Br J Dermatol. 1999;141(1):71-81.
- Aractingi S, Berkane N, Bertheau P, et al. Fetal DNA
in skin of polymorphic eruption of pregnancy. Lancet.
- Pennoyer JW, Grin CM, Driscoll MS, et al. Changes in
size of melanocytic nevi during pregnancy. J Am Acad
Dermatol. 1997;36(3 Pt 1):378-82.