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11 Dermatological Changes During andAfter Pregnancy
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11.3.2 Pemphigoid Gestationis (PG)
• Synonyms: Herpes gestationis
Pearls and Pitfalls
PG is an autoimmune disease caused by antibodies
against collagen XVII.Its diagnosis is based on a
combination of clinical ndings, skin biopsy of
perilesional skin, and determination of serum antibodies. Treatment is based on topical corticosteroids, although the more severe cases may require
prednisone 0.5 mg/kg. Due to the maternofetal
antibodies’ transmission, up to 10% of newborns
might experience mild symptoms. Furthermore, it
is associated with an increased risk of premature
labor and with small-for- gestational-age newborns.
Recurrence is common in subsequent pregnancies.
This is a rare, blistering, bullous, pruritic, and
self-limiting rash that appears towards the end of
pregnancy (second or third trimester) or in the
immediate postpartum period, although it can
appear at any point during pregnancy [17]. It is an
autoimmune disease and is the only pregnancyspecic dermatosis that can also affect the skin of
the newborn, as occurs in up to 10% of the cases
of dermatosis of pregnancy due to the transfer of
antibodies through the placenta, although the
effect is generally mild [9]. Its estimated incidence is 1:20,000 to 1:50,000 pregnancies. On
rare occasions, it is associated with trophoblastic
tumors such as hydatidiform mole or choriocarcinoma [10].
11.3.2.1 Pathogenesis
It is caused by circulating IgG1 antibodies against
the bullous pemphigoid antigen of 180kDa, also
known as collagen XVII, a transmembrane glycoprotein of hemidesmosomes expressed in the
basal membrane of the skin. The primary site in
which autoimmunity originates seems to be the
placenta, because the autoantibodies attach not
only to the basal membrane of the epidermis, but
also to the membrane of the chorionic and amniotic epithelium (both of which have an ectodermal origin) [15, 17].
Currently, the stimulus that triggers the production of antibodies is unknown, but the focus
has been put on immunogenetics and a potential
cross-reactivity between the placental tissue and
the skin, because autoantibodies also attach to the
amniotic basal membrane. Some authors have
suggested that it is triggered by an anomalous
expression of anti-MHC class II DR3/DR4 antibodies (paternal haplotype) that start an allogeneic response to the placental basal membrane,
which, in turn, presents cross- reactivity with the
skin [9]. The incidence of anti- HLA antibodies is
almost 100% in patients with a history of
PG.Since the only source of different human leukocyte antigens is generally the placenta (which
usually comes from the father), the universal
nding of anti-HLA antibodies implies a high
frequency of immunity attacks during gestation.
Women with PG also exhibit an elevated expression of class II MHC antigens (DR, DP, DQ) in
their chorionic villi [9, 10].
11.3.2.2 Signs
PG is clinically characterized by a sudden onset
of skin lesions on the torso, particularly on the
abdomen and often inside the navel or in the surrounding area (Fig.11.3) [5]. Pruritus may precede the appearance of visible lesions. The rash
generally starts on the torso as urticarial plaques
or papules surrounding the navel. Vesicles may
also appear. It then rapidly evolves to a generalized pemphigoid-like rash with papules and urticarial pruritic plaques followed by clustered
herpetiform vesicles or tense blisters on erythematous plaques. This eruption may affect the entire
body including palms and soles (Fig.11.4) [15],
but the face and mucosal areas are only rarely
involved [17].
11.3.2.3 Diagnosis
Its diagnosis is based on a combination of clinical
ndings, the biopsy of perilesional skin, and the
determination of serum antibodies against the
NC16A domain of protein BP180 [19]. Levels of
autoantibodies are not related to the severity of
this condition and do not offer clues to its prognosis [16]. These levels may remain elevated up
to 1 year after pregnancy and persist in subsequent pregnancies without any other signs of
pemphigus [9].
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Fig. 11.3 Blistering urticarial papules and plaques in a
pregnant woman (image a), which are rapidly evolved to
a generalized rash with urticarial papules and plaques
(image b). Notice the navel involvement, which is an
unlikely nding in polymorphic eruption of pregnancy
11.3.2.4 Dierential Diagnosis
It is important to distinguish PG from polymorphic eruption of pregnancy, because both conditions may present urticarial lesions and
drug-induced eruptions or multiform erythema. It
is also important to appreciate how it differs from
dermatitis herpetiformis, which is associated
with gluten sensitivity, lesions that generally
appear on the elbows, the knees, the back of the
forearms, the back, the buttocks, and the scalp,
with granular IgA deposits visible under direct
immunouorescence [9].
11.3.2.5 Treatment
The objectives of the treatment are to sooth the
itchy skin and prevent the appearance of blisters.
In mild cases, powerful topical corticoids associ-
Fig. 11.4 The lesions may affect palms and soles, but
rarely involve face or mucosal areas
The classic histological nding of a subepidermal vesicle is present in a minority of patients,
and it is more common to nd unspecic mixed
cellular inltrate with a variable amount of eosinophils at the dermoepidermal junction [15]. The
presence of eosinophils is the most constant histological nding in PG [18]. Direct immunouorescence makes it possible to observe a linear
deposition of C3 throughout the area of the basal
membrane [9].
ated with emollients and systemic antihistamines
may sufce [5]. In more severe cases, or cases
that do not respond to topical drugs, prednisone
0.5mg/kg may be used, although the dose must
be progressively reduced as soon as blisters stop
appearing [15]. Flare-ups associated with childbirth require a temporary increase in the dose
[10]. Women with severe and persistent PG after
childbirth may require higher doses of oral corticoids (up to 2g/kg/day), or even other immunosuppressant agents such as cyclosporin or
rituximab [9].
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11.3.2.6 Prognosis
Although its presentation and clinical evolution
may vary considerably, spontaneous improvement is common in the nal stages of pregnancy.
It is associated with an increased risk of premature labor and with the newborn being small for
its gestational age, the risk being related to the
severity of the disease [18]. There is no increased
risk of abortion [9]. Recurrence is common in
subsequent pregnancies (up to 75%), although
recurrence and/or are-ups are also associated
with menstruation and oral contraceptives.
Women with a history of PG may have an
increased risk of developing Graves’ disease [10].
PG may resolve before labor, but it ares up
after childbirth in 75% of patients and reappears
in at least 2% of patients as a result of contraceptive use or during menstruation. In most cases, it
resolves spontaneously within the rst weeks/
months after labor. It generally reappears in subsequent pregnancies, at greater intensity, although
it may also skip pregnancies [15, 18].
11.3.3 Polymorphic Eruption
ofPregnancy (PEP)
• Synonyms: Pruritic urticarial papules and
plaques of pregnancy (PUPPP), Bourne’s tox-
emic rash of pregnancy, late-onset prurigo of
pregnancy, toxemic rash of pregnancy
Pearls and Pitfalls
PEP is a common gestational dermatosis characterized by papules and urticarial plaques that usually start inside pregnancy stretch marks during
the last stages of the third trimester. Unlike PG, it
does not affect the periumbilical region.
Diagnosis is clinical, and most patients respond
to topical corticoid therapy and oral antihistamines. There is no risk to the mother or fetus.
Recurrences are rare.
immunouorescence or ELISA.It is more common in primigravida women in the nal weeks
of their pregnancy and/or in the immediate postpartum period. Its etiopathogenesis is unknown.
The risk factors for its development include
multiple pregnancies and weight gain by the
mother [17].
11.3.3.1 Signs
Signs include papules and urticarial plaques that
usually start inside pregnancy stretch marks during the last stages of the third trimester or in the
immediate postpartum period, and which generally do not affect the periumbilical region
(Fig.11.5). Its onset is more frequent in the last
stage of the third trimester (85%) or in the immediate postpartum period (15%) [15, 17]. The
eruption generally spreads over several days,
although it does not usually affect the face, palms,
or soles. As the disease progresses, polymorphic
lesions appear (vesicles, erythema, targets, and
eczematous lesions) (Fig.11.6) [5, 10].
11.3.3.2 Diagnosis
Its diagnosis is clinical, based on the history of
the patients and the ndings of a physical examination. Its histological characteristics are unspecic (supercial and deep perivascular inltrate,
interstitial lymphocytic inltrate that may be
accompanied by eosinophils), with negative
immunouorescence [9]. The ordinary analytical
assessment is normal.
The differential diagnosis must take into
account erythema multiforme, viral exanthem,
and scabies [9].
11.3.3.3 Treatment
Most of the patients improve with topical corticoid therapy and oral antihistamines. The
most severe cases and/or cases with intense
itching may require the use of systemic corticoids [5, 15].
PEP is a common gestational dermatosis,
with an incidence of 1:200 pregnancies [9],
characterized by a typical clinical presentation,
with normal results in the analysis and negative
11.3.3.4 Prognosis
There is no risk to the mother or fetus, and recurrence is rare. Its evolution is self-limiting, and it
disappears 2weeks after labor [10].
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Fig. 11.5 PEP rash usually begins in the stretch marks of
the abdomen, without affecting periumbilical area
(images a and b). The urticarial papules may grow
together forming larger wheal-like plaques on the
abdomen or thighs (images c and d)
Fig. 11.6 PEP lesions are polymorphous and sometimes may adopt a vesicle-like appearance (a). The intense pruritus
may also induce the apparition of excoriations (b)
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11.3.4 Intrahepatic Cholestasis
ofPregnancy (ICP)
• Synonyms: Cholestasis of pregnancy, obstet-
ric cholestasis, cholestatic jaundice of preg-
nancy, prurigo gestationis
Pearls and Pitfalls
ICP is a hormone-dependent cholestasis that
appears in the last stages of pregnancy. Usually, it
presents as pruritus followed by scratching lesions.
Diagnosis is made upon nding an elevated total
serum concentration. The total serum concentration of bile acid can predict adverse fetal effects,
and it is associated with an increase of fetal death
when it exceeds 100μmol/L.Treatment is based
on oral ursodeoxycholic acid and usually requires
close monitoring.
Warning Box
Although the prognosis for the mother is good,
there are increased risks of premature birth, intrapartum fetal distress, and fetal death. Therefore,
maintaining a high level of suspicion might allow
early diagnosis and treatment, which in turn may
prevent fetal damage.
It is a rare form of cholestasis that is reversible, hormone dependent, and associated with
genetics. It generally appears in the last stages of
pregnancy (mainly in the third trimester) as pruritus without primary skin lesions [5]. Thus, the
usual presentation of this condition is the absence
of clinically evident lesions. Secondary skin
changes are correlated with the duration of the
disease, and they range from tiny excoriations to
severe nodular prurigo [10]. Its incidence is
greater in multiple pregnancies [9, 10]. It is the
most common hepatic condition that appears
exclusively during pregnancy [15].
11.3.4.1 Signs
Prurigo generally starts on the palms and soles.
The most commonly affected areas are the extensor regions of extremities, buttocks, and abdomen [15]. Jaundice is only present in 10% of
patients and is usually a complication in the most
severe and prolonged cases (in these cases, it may
be associated with steatorrhea, with the subsequent vitamin K deciency and the increased risk
of intra- and postpartum hemorrhage) [9, 10].
The prurigo is maintained until delivery and then
spontaneously resolves within days [20].
Prolonged evolution is rare, and this makes it
necessary to rule out other pathologies (mainly
primary biliary cirrhosis) [9, 17].
11.3.4.2 Pathogenesis
A decrease in the bile acid excretion rate causes
an increase in serum concentration, which leads
to intense pruritus for the mother and harmful
effects for the fetus (the bile acid that enters the
placenta may cause acute fetal anoxia) [9]. Some
of the known predisposing factors include mutations in the genes encoding the bile transport proteins. Therefore, a mild dysfunction that is
asymptomatic in nonpregnant women may
become symptomatic when the capacity of the
transporters to segregate substrates is exceeded
[14, 18].
11.3.4.3 Diagnosis
An elevated total serum concentration of bile
acid is a diagnostic factor (>11μmol/L in pregnant women; normal range in nonpregnant
women: 0–6 μmol/L) [15, 20]. Levels of transaminases may be elevated. In women with jaundice, the level of conjugated (direct) bilirubin is
elevated and prothrombin time may be high [20].
The liver ultrasound is generally normal, although
in women with jaundice, calculi may be observed.
Its histology is unspecic, and immunouorescence is negative [10].
The total serum concentration of bile acid can
predict adverse fetal effects. When it exceeds
100 μmol/L, it is associated with an increased
risk of fetal death [20].
11.3.4.4 Treatment
The treatment is based on oral ursodeoxycholic
acid [20].
11.3.4.5 Prognosis
Although the prognosis for the mother is good,
there are increased risks of premature birth (20–
60%), intrapartum fetal distress (20–30%), and
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fetal death (1–2%) [9, 20]. Fetal risk is associated
with the serum concentration of bile acid, particularly when it is over 40 μmol/L [10, 20].
Therefore, this is the most important gestational
pruritic disorder, and it must be diagnosed and
treated from an early stage in order to prevent
fetal damage. Recurrence is observed in 45–70%
of subsequent pregnancies [20].
11.3.5 Pustular Psoriasis
ofPregnancy (PPP)
• Synonyms: Impetigo herpetiformis
Pearls and Pitfalls
PPP is a rare variant of psoriasis that usually
appears in the third trimester. While not a pregnancy-specic dermatosis per se, given the relevance of its rapid recognition and treatment, it is
still included in this category. The most severe
cases may require hospitalization and close monitoring of both mother and fetus. Systemic corticoids are often the rst-line therapy with low-dose
cyclosporine as an alternative. PPP is associated
with placental insufciency, miscarriage, fetal
growth restriction, and stillbirth. It has a high risk
of recurrence in subsequent pregnancies.
PPP is a very rare variant of generalized pustular psoriasis that appears during pregnancy or is
triggered by it. This condition generally appears in
the third trimester, but it may appear before that
stage or in the immediate postpartum period [21].
In the past, it was known as impetigo herpetiformis, but it is not associated with bacterial colonization or with the herpes virus. There is controversy
regarding its inclusion in the list of specic dermatoses of pregnancy, since it is not a type of dermatosis as such, but rather a variant of psoriasis.
However, given the relevance of its rapid recognition and treatment, it is still included in this category [9, 10]. Hypoparathyroidism, hypocalcemia,
stress, and infections have been suggested as
potential triggers of pustular psoriasis [21].
11.3.5.1 Signs
Symmetrical erythematous plaques with peripheral sterile pustules in a circinate pattern [21].
The plaques evolve and expand across the
peripheral area, whereas the center erodes and
crusts over. The eruption starts in the exural
areas and spreads centrifugally [9]. The torso
and extremities are usually affected, while the
hands, feet, and face are not. There may be oral
and esophageal lesions as well as nail involvement. In severe cases, the rash may develop into
erythroderma. There is generally no itching,
although the general condition is affected (malaise, fever, anorexia, nausea, vomiting, diarrhea,
tetany) [10, 21].
11.3.5.2 Complementary Tests
The diagnosis can be clinical, although a biopsy
is usually recommended for histological conrmation, given the potentially severe consequences of the disease and its treatment on the
fetus [21]. Leukocytosis and increased ESR are
common [9]. Hypocalcemia leading to tetany
may also occur.
The differential diagnosis distinguishes PPP
from infections, such as candidiasis, impetigo,
and tinea corporis, which may be ruled out
through the examination of cultures and reactions
to drugs [9, 10].
11.3.5.3 Treatment
Treatment includes hospitalization and close
monitoring of mother and fetus, correction of
hypocalcemia if it is present, and maintenance of
hydroelectrolytic balance [21].
Systemic corticoids are the initial therapy
(moderate cases, approximately 30 mg/day;
severe cases, up to 60–80 mg/day for several
days, with progressive reduction when the symptoms improve, and close monitoring in case of
are-ups) [21]. Low doses of cyclosporin
(2–3 mg/kg/day) may be an alternative to systemic corticoids during pregnancy. It is classied
as category C, with low teratogenic effects,
although there is a risk of preterm labor and of
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the newborn being small for its gestational age
[21]. Other treatments, such as anti-TNFα (iniximab), have been used satisfactorily in isolated
cases [9]. Phototherapy with narrowband UVB is
safe during pregnancy, and PUVA is recommended during breastfeeding. Some experts recommend a combination with antibiotics
(cephalosporin), even though the pustules are
sterile [9].
In severe and recalcitrant cases and in cases
that do not respond to treatment, labor may be
induced as an alternative, because the eruption
generally resolves after birth [9].
11.3.5.4 Prognosis
PPP generally resolves in the postpartum period,
but there is a high risk of recurrence in subsequent pregnancies. It may be associated with placental insufciency, miscarriage, fetal growth
restriction, or stillbirth [21].
Post-maternity changes in skin
Hyperpigmentation Vascular changes Striae Hair loss
Treatment
– Topical solution with
4% hydroquinone
– Supercial
dermabrasion
– Laser therapies
– May resolve
spontaneously
postpartum
– Intralesional corticoid
injection
– Surgical excision
– Laser therapies
11.4 Skin Changes During
andAfter Pregnancy
Pearls and Pitfalls
• Hyperpigmentation is the most common skin
alteration during pregnancy and generally
affects previously pigmented areas such as the
areola, the axilla, or the genitals. It usually
improves during puerperium.
• Melasma is more common among patients
with darker phototypes (IV to VI) in whom it
tends to persist after puerperium.
• Epulis is the most common vascular tumoral
lesion during pregnancy and usually resolves
spontaneously during puerperium.
• Diffuse hair loss during puerperium (postpar-
tum telogen efuvium) has a high prevalence.
It generally starts 3–6months after labor, with
an average duration of 2–5months.
– Retinoid creams
– Non-ablative
fractional laser
– Topical 2%
minoxidil
solution
11.4.1 Pigmentation
11.4.1.1 Hyperpigmentation
Between 85 and 90% of all pregnant women
present some degree of skin hyperpigmentation,
which is the most common skin alteration [4, 22].
Hyperpigmentation may be mild or moderate and
generally affects previously pigmented areas
such as the areola, the axilla, or the genitals [4].
Pigmentation of the linea alba, giving rise to what
is known as the linea nigra, and of scars is also
relatively common [3].
Changes in pigmentation are usually considered to be conditioned by the increase in melanin
production induced by the elevation of MSH,
estrogen, and progesterone levels [22].
11.4.1.2 Melasma
Melasma is the appearance of dark macules and
patches, mainly on the neck and face. The most
frequently affected anatomical regions are the
nose and the cheeks (Fig.11.7) [23]. It appears in
50–70% of pregnant women [4], generally starting during the rst trimester. It is more common
among patients with darker phototypes (III to VI)
[24, 25], in whom it tends to persist after puerperium [3]. Its pathogenesis involves hormonal factors and the action of UVA radiation [24], making
it particularly important for patients to use sunscreen with UV lters [24].
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Fig. 11.7 Blotchy at brown patches on both cheeks and
above the upper lip in a puerperal woman. Melasma is
more common in people with darker phototypes (specially
III and IV)
A. Mª. González-Pérez et al.
11.4.1.3 Nevi andMelanoma
Warning Box
Although nevi tend to become hyperpigmented
and increase their size symmetrically during pregnancy, there is no evidence of an increased risk of
malignancy development. Despite this fact, no
clinical or histopathological atypical condition of
the skin may be attributed to pregnancy.
Although nevi tend to become hyperpigmented
and to increase their size symmetrically during
pregnancy, they generally do so in areas that are particularly prone to expansion, such as the torso, and
they usually return to their normal state during puerperium [4, 26]. There is no evidence of an increased
risk of malignancy of the nevi during pregnancy
[27]. No clinical or histopathological atypical condition of the skin may be attributed to pregnancy
(Fig.11.8) [3, 27]. In addition, in the case of melanomas, some studies have reported that even though
melanomas that appear during pregnancy are generally thicker, on average, this does not mean that the
melanomas themselves are associated with a worse
prognosis [28, 29]. Therefore, it is important to
remain alert to any suspicious clinical or dermatoscopic changes, and biopsies of suspicious lesions
are indicated, just as in any other patient [26, 27].
a b
Fig. 11.8 Dysplastic nevi on the back. Notice the illdened borders and variable pigmentation. No clinical
atypia may be attributed to pregnancy. Thus, biopsies of
suspicious lesions are indicated just as in any other patient
(image a). Dermoscopy. Homogeneous pattern with
patchy distribution of hyperpigmented areas (image b)
ab
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11.4.2 Vascular Changes
Hormonal changes during pregnancy increase the
production of angiogenic factors such as vascular
endothelial growth factor (VEGF) or broblast
growth factor (FGF) [27], which cause an
increase in vascular distension, instability, and
proliferation [4]. In this regard, spider nevi and
varices are a common occurrence (Fig.11.9), as
well as the appearance of cutis marmorata, palmar erythema, and gingival hyperplasia [5].
On the other hand, the increase in venous
hydrostatic pressure may promote the appearance
of edema, generally on the lower limbs [16],
although it has also been described on the face
and hands [22]. Varices may also occur on the
lower limbs and the perianal region (hemorrhoids) [4, 30]. Varices tend to improve during
puerperium, but they do not achieve complete
remission [8].
Gingival pyogenic granuloma, or epulis, is the
most common vascular tumoral lesion during
pregnancy (Fig. 11.10) [27], and it usually
resolves spontaneously during puerperium,
although in some cases, particularly those accompanied by intense hemorrhaging, surgical treatment may be required [27, 30].
11.4.3 Striae Gravidarum
Stretch marks are linear lesions that initially have
an erythematous or purplish color and that evolve
to become atrophic whitish scar-like lesions [31].
They are often symptomatic and accompanied by
itching and a burning sensation and may have a
profound emotional impact on patients [31, 32].
They are the second most common skin change
during pregnancy, with a prevalence that ranges
from 70 to 90%, depending on the series [3, 4],
and they are the most common alteration of the
connective tissue. They generally appear on the
breasts, abdomen, hips, buttocks, and thighs
(Fig.11.11) [22, 31].
Their origin is unknown, although some
authors have suggested that they may be triggered by the combination of several elements,
including genetic factors, weight gain and/or
periods of rapid growth, or hormonal changes
[31, 33]. The risk factors for the appearance of
stretch marks include age (higher risk at younger
ages), a maternal history of stretch marks, and
being overweight before pregnancy and before
delivery [32].
The most effective treatments include creams
with retinoids (e.g., tretinoin 0.05%) and non-
Fig. 11.9 Multiple spider angiomas in a pregnant woman’s chest (image a). The spider angioma, also known as
spider nevus or spider telangiectasia, is a vascular lesion
characterized by the dilatation of the skin vasculature. It
usually appears as a bright red dot surrounded by reddish
extensions with a weblike appearance (image b). They
may appear as solitary or multiple lesions
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Fig. 11.10 Ulcerated vascular lesion on the maxillary
gingiva and interdental papilla of a pregnant patient. The
patient also had a venous lake on the upper lip
Fig. 11.11 Whitish swollen lines following the skin tension lines of both breasts
ablative fractional laser [32]. For prevention,
creams with extract of Centella asiatica and daily
massages are the most strongly evidence-based
therapeutic approaches, although further research
into this topic is required [32].
11.4.4 Glands
The activity of eccrine and sebaceous glands
increases, whereas the activity of apocrine glands
decreases during puerperium [4]. The increased
activity of sebaceous glands promotes the growth
of Montgomery tubercles, which are papules
located on the areolas that revert to their pregestational state after labor [22, 23]. The effects of
the sebaceous activity on the potential worsening
of acne during pregnancy and puerperium are not
A. Mª. González-Pérez et al.
denitively established [22]. On the other hand,
the activity of eccrine sweat glands increases during pregnancy, with the possible appearance of
hyperhidrosis and miliaria [16].
11.4.5 Hair
11.4.5.1 Postpartum Telogen
Euvium
Diffuse hair loss during puerperium is a wellknown condition because of its prevalence and
the psychological impact it has on patients.
During pregnancy, the anagen phase becomes
longer, causing a degree of hirsutism and hypertrichosis [34, 35] that is affected by the increase
in levels of estrogens and progesterone
(Fig.11.12) [36, 37]. After childbirth, the levels
of both hormones decrease, and the alterations in
the hair cycle revert to their original state [38].
Therefore, the hair rapidly switches to the telogen phase, which, in turn, manifests itself as diffuse hair loss (>150 hairs per day) [36, 39]. The
latency period from childbirth to the onset of hair
loss varies among patients. It generally starts
3–6months after labor, with an average duration
of 2–5months [1, 34], although in some cases it
may last over a year [35].
11.4.5.2 Androgenetic Alopecia
Just as the rapid shedding of hairs under the inuence of estrogens to the telogen phase leads to the
appearance of telogen efuvium, it may also
reveal androgenetic alopecia, which leads to the
superimposition of the two conditions [36, 38]. In
most cases, this scenario follows the female pattern proposed by Ludwig, although in others it
may exhibit Hamilton’s male pattern (Fig.11.13)
[36]. Since it generally appears during puerperium, topical minoxidil may be used as treatment
without the risk of secondary effects for the newborn [36].
11.4.6 Nails
Although there are no known pathognomonic
changes that affect the nails during pregnancy
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