Dermatologic Diseases in Pregnancy

Lawrence Charles Parish, MD, MD (Hon)

Clinical Professor of Dermatology and Cutaneous Biology, Director of the Jefferson Center for
International Dermatology, Jefferson Medical College of Thomas Jefferson University, Philadelphia,
Pennsylvania; Visiting Professor of Dermatology, Tulane University School of Medicine, New Orleans,
Louisiana, USA
Jennifer L. Parish, MD
Assistant Clinical Professor of Dermatology and Cutaneous Biology, Jefferson Medical College of
Thomas Jefferson University, Philadelphia, Pennsylvania; Assistant Professor of Dermatology, Tulane
University School of Medicine, New Orleans, Louisiana, USA
 INTRODUCTION
 PHYSIOLOGIC CUTANEOUS CHANGES IN PREGNANCY

 PIGMENTARY CHANGES

 VASCULAR CHANGES

 STRUCTURAL CHANGES

 APPENDAGEAL CHANGES

 SPECIFIC DERMATOSES OF PREGNANCY

 OTHER DERMATOSES AND INFECTIONS AFFECTED IN PREGNANCY

 REFERENCES

INTRODUCTION
Pregnancy may result in a number of cutaneous changes, ranging from physiologic alterations in
pigmentation to serious dermatologic diseases. These can be divided into physiologic changes, which
include pigmentary, vascular, structural, and appendageal alterations and the specific dermatitides
that may develop only during pregnancy or the postpartum period. These entities include
polymorphic eruption of pregnancy, pemphigoid gestationis, impetigo herpetiformis, and cholestasis
of pregnancy, plus the less well understood prurigo of pregnancy, papular dermatitis of pregnancy,
and pruritic folliculitis of pregnancy.1, 2, 3, 4, 5

PHYSIOLOGIC CUTANEOUS CHANGES IN PREGNANCY

Pregnancy is characterized by significant hormonal, immunologic, and metabolic alterations. While
the details of these modifications are beyond the scope of this chapter, they play an obvious role in
the physiologic changes of pregnancy.6, 7

PIGMENTARY CHANGES
Hyperpigmentation occurs in at least 90% of pregnant women, being more obvious in lighter-
skinned women. Pregnant women generally observe a mild generalized hyperpigmentation of the
nipples, the areolae, and the vulva. The increase in the melanocyte-stimulating hormone, estrogen,
and progesterone, each play a role in these changes.8
Linea nigra

Linea alba, a line extending from the xiphoid to the pubic region, hyperpigments during pregnancy
to become the “linea nigra.” This darkening usually only diminishes slightly.

Melasma

"Mask of pregnancy," or chloasma, develops in 50–70% of pregnant women during the second
trimester. Macular pigmentation appears in a symmetrical pattern on the forehead, temples, cheeks,
upper lip, and even the chin (Fig. 1). Similar changes can be found in about 20% of women taking
oral progestational agents. While this condition may diminish within 1 year after delivery or after
discontinuation of oral contraceptives, about 30% of women are bothered by this discoloration for
some time. Ultraviolet (UV) exposure increases the problem of melasma. Treatment involves the use
of bleaching agents such as hydroquinone 4% cream, sometimes augmented by the addition of
topical tretinoin or mequinol and tretinoin solution. Such therapy needs to be continued for many
months and should be used in conjunction with sunscreens to prevent further
hyperpigmentation.8, 9 Tretinoin, like all retinoids, should not be prescribed during
pregnancy,10 although hydroquinone is acceptable for use during pregnancy. Lasers, such as the ruby
laser (694 nm) and the Q-switched alexandrite laser (755 nm), have shown unpredictable and limited
benefit in the treatment of epidermal-dermal pigmented lesions such as melasma. 11

Fig. 1. Melasma, or “mask of pregnancy.”

VASCULAR CHANGES
The vascular changes seen in pregnancy are greatly influenced by
changes in maternal hormones such as human chorionic
gonadotropin (hCG), adrenocorticotrophic hormone (ACTH)-like
substance, thyrotropin-releasing hormone, and estrogen. These hormones may trigger increases in
cardiac output, vascular proliferation, congestion, and vasomotor instability (Table 1).7, 11, 12

Table 1. Vascular changes in pregnancy

Spider nevi
Palmar erythema
Hemangiomas
Granuloma gravidarum (pyogenic granuloma)
Varicosities
Purpura

Spider nevi

Spider nevi are bright red, blanchable, small arterioles with fine vessels radiating from the center.
They are typically observed at the end of the first trimester and gradually increase in size throughout
pregnancy. These are mainly seen on the skin drained by the superior vena cava, particularly around
the eyes (Fig. 2). Fair-skinned individuals have a higher incidence than African-Americans (67%
versus 11%, respectively). Most spider nevi regress postpartum, but a small percentage persists and
requires treatment with electrocautery or laser. 9

Fig. 2. Spider nevi on the face.

Palmar erythema

Palmar erythema is mottled erythema of the thenar and hypothenar eminences with sparing of the
digits. It is seen in two-thirds of pregnant women during the first trimester and resolves in the
postpartum period. Palmar erythema may also be seen in other conditions such as lupus
erythematosus, hepatic cirrhosis, and hyperthyroidism, indicating a possible role of increased
estrogen levels as a common cause.7

Varicosities

Increased distension in the superficial venous vasculature of legs (i.e. varicose veins), vagina,
vestibule (i.e. Jacquemier–Chadwick sign), and rectum (i.e. hemorrhoids) are common in pregnancy.
About 40% of pregnant women are affected. Hormonal factors and increased intra-abdominal
pressure play a role. Elevation of the legs and lying-in, as in the Trendelenburg position, helps to
decrease varicose veins. Varicose veins often regress in the postpartum period;
however, sclerotherapy may be necessary (Fig. 3).7, 9

Fig. 3. Varicosities of the lower extremity.

Granuloma gravidarum or pyogenic granuloma

Granuloma gravidarum is a benign, rapidly proliferating vascular lesion that commonly occurs at
sites of previous trauma on the face, neck, and fingers (Fig. 4). Pregnancy, irritation, and increased
estrogen levels are predisposing factors. Surgical removal can be readily accomplished. 13

Fig. 4. Granuloma gravidarum: rapidly growing friable

vascular lesion at a site of trauma.

Hemangioma

Hemangiomas occur spontaneously in 5% of pregnancies during the second or third trimesters with
a propensity for the hands and neck (Fig. 5).12Nonpalpable purpura, usually seen on the lower
extremities, is also a common finding during the second trimester of pregnancy. 14 Both hemangiomas
and purpura regress postpartum.

Fig. 5. Hemangioma: new growth adjacent to the areola.

STRUCTURAL CHANGES
Striae gravidarum

Striae gravidarum, or “stretch marks,” occur commonly on the abdomen, thighs, and buttocks of
pregnant women. These appear as atrophic, wrinkled, erythematous, purplish bands that fade only
slightly over time (Fig. 6). Striae occur in 90% of fair-skinned individuals, usually in the third
trimester of pregnancy. The pathogenesis of striae formation is unclear. Proposed hypotheses
include increased lateral stress on connective tissue and increased glucocorticoid levels due to
elevated adrenocortical activity.7, 15 Currently, there is no effective treatment for striae. Contrary to
popular belief, cocoa butter, massage, shea butter, and aloe vera preparations have no efficacy.

Fig. 6. Striae distensae: atrophic purplish bands on the medial

aspect of the thigh.

Molluscum fibrosum gravidarum

Molluscum fibrosum gravidarum are benign, small, pedunculated, tan-to-brown, fleshy papules
similar to acrochordons (skin tags) that are commonly seen on the neck, axillae, inner aspects of the
thighs, and inframammary folds. They frequently appear during the second half of pregnancy and
may even regress postpartum. Their etiology is unclear. Treatment options include shave excision,
electrocautery, cryosurgery, and scissors removal.

APPENDAGEAL CHANGES
Eccrine sweat glands

Eccrine glands, which are involved in the regulation of body temperature through sweating, show a
gradual increase in activity during pregnancy. This physiologic change, along with an increase in
thyroid activity, may result in hyperhidrosis and increased miliaria. 7

Apocrine glands

Apocrine glands are confined to the axillae and perineum. These glands become functional about the
time of puberty. Pregnancy results in a decrease in activity of the apocrine glands, with possible
improvement of such conditions as hidradenitis suppurativa, which can also be called acne inversa. 7

Sebaceous glands

Sebaceous glands are sebum-producing glands associated with hair follicles. These glands
demonstrate increased activity in pregnancy, resulting in new-onset or exacerbation of pre-existing
acne, although a minority of patients show improvement of acne during pregnancy. 9, 16 Treatment of
acne during pregnancy is difficult. Most oral and some topical agents used to treat this condition are
not recommended during pregnancy. Based upon the severity of the acne, agents commonly
prescribed include topical benzoyl peroxide with or without antimicrobials and topical
sulfur/sulfacetamide preparations. Use of a cleansing agent, such aqua glycolic astringent, and
elimination of moisturizers are most helpful.

Hair

Pregnancy is associated with a decrease in the percentage of hair follicles in the telogen (resting)
phase.17 Many women notice an increase in the thickness and body of the scalp hair. Hirsutism, with
increased hair growth on the face, arms, legs, and back, may also be seen. Telogen effluvium, which
is a delayed telogen response, results in hair loss within 1–2 months postpartum. Hair regrowth is
commonly reported at approximately 6 months postpartum. No medical intervention is necessary,
and treatment should consist of patient education and reassurance. 18

Nails

Nail changes, such as onycholysis, transverse grooving, brittleness, and subungual keratosis, have
been reported in pregnancy. The cause of these uncommon findings is unclear. 7

SPECIFIC DERMATOSES OF PREGNANCY

There has been great controversy and confusion in the literature when discussing the dermatoses
that are unique to pregnancy. Many different names have been used to define clinically similar
disorders. Various classifications have been proposed ever since the first contribution was written by
Besnier in 1904 (Table 2).19

Table 2. Dermatoses of pregnancy

Classification Synonyms

Herpes gestationis Pemphigoid gestationis

Pruritic urticarial papules and plaques of pregnancy Polymorphic eruption of pregnancy

Toxemic rash of pregnancy

Toxic erythema of pregnancy

Late onset prurigo of pregnancy

Cholestasis of pregnancy Intrahepatic cholestasis of pregnancy

Classification Synonyms

Obstetric cholestasis

Prurigo gravidarum

Jaundice of pregnancy

Impetigo herpetiformis

Prurigo of pregnancy Early onset prurigo of pregnancy

Papular dermatitis of pregnancy

Pruritic folliculitis of pregnancy

Polymorphic eruption of pregnancy

Polymorphic eruption of pregnancy (PEP) was first described by Lawley in 1979 20 as pruritic
urticarial papules and plaques of pregnancy (PUPPP). Both PEP and PUPPP are terms that are
interchangeably used, with PEP being preferred in the current literature. PEP is the most common of
the dermatoses unique to pregnancy, with an incidence of 1 in 160. Seventy-five to eighty-five per
cent of cases occur in primigravidas, who experience an abrupt pruritic onset in the third trimester of
pregnancy, most commonly in the 35th to 39th week of gestation or immediately postpartum. 21 The
eruption begins on the abdomen along the striae distensae, sparing the umbilical and immediate
periumbilical area (Figs. 7 and 8).22 This is in contrast to pemphigoid gestationis, in which the
majority of cases arise in the umbilical area. PEP may spread to the thighs, buttocks, and extremities,
but facial involvement is rare. As the name implies, the skin manifestations are quite variable. These
include vesicular, target-like, annular or polycyclic papules or plaques that become confluent over
time (Figs. 9 and 10). Three categories have been defined23: type I, urticarial papules and plaques;
type II, nonurticarial erythema, papules, or vesicles; and type III, a combination of types I and II.
The cause of PEP is unknown. One proposed theory is the rapid stretching of the skin late in
pregnancy; this hypothesis is supported by the initial presentation of the eruption along the striae
distensae. Increased maternal and newborn weight gain lends support to this theory; there is a
higher incidence of PEP in twin pregnancies.22, 24, 25

Fig. 7. Polymorphic eruption of pregnancy: erythematous

papules along the striae distensae.

Fig. 8. Polymorphic eruption of pregnancy. Close-up view of

Fig. 7 showing the erythematous papules along the striae
distensae.

Fig. 9. Polymorphic eruption of pregnancy morphology:

coalescing urticarial papules on the abdomen.

Fig. 10. Polymorphic eruption of pregnancy morphology:

urticarial plaques on the lateral surface of the upper thigh.

Fig. 11. Polymorphic

eruption of pregnancy direct
immunofluorescence:
granular band of C3 along
the skin basement
membrane zone.

Dermatopathologic examination shows variable epidermal spongiosis with a perivascular

inflammatory infiltrate in the dermis composed of lymphocytes, histiocytes, and a variable number
of eosinophils. Direct immunofluorescence (DIF) is negative for a linear band of C3 or IgG along the
skin dermoepidermal junction (DEJ); however, there have been reports of deposition of IgM, C3, and
IgA along the DEJ and blood vessels on DIF (Fig. 11). 23, 26 Differential diagnosis of PEP includes
pemphigoid gestations (PG), contact dermatitis, drug eruption, and viral exanthems. DIF of skin is
necessary to differentiate PEP from PG. The clinical course of PEP is usually self-limiting, with a
mean duration of 6 weeks. Pruritus is most severe in the first week of onset, with spontaneous
remission occurring within days of parturition. Maternal and fetal mortalities are unaffected. PEP
rarely occurs in subsequent pregnancies; however, a few cases of reoccurrence are reported in the
literature.21 Treatment involves symptomatic relief of pruritus with topical corticosteroids of low- to
mid-potency (use of ultra-high-potency corticosteroids for an extensive period of time should be
avoided) and pregnancy category B antihistamines such as loratadine and cetirizine. Hydroxyzine
and diphenhydramine are pregnancy category C antihistamines that have been used to relieve
pruritus. In cases of severe pruritus unresponsive to conservative measures, systemic corticosteroid
administration or induced delivery is considered.

Pemphigoid gestationis

Initially described by Milton in 187222 as “herpes gestationis,” this condition was renamed
pemphigoid gestationis (PG) in 1982 due to its clinical and immunofluorescence similarities with
bullous pemphigoid.27 Both names continue to be used; pemphigoid gestationis is more common in
the United Kingdom.28, 29

Estimated incidence of PG is 1 in 50,000 cases. Pemphigoid gestationis most commonly occurs in the
second or third trimester of pregnancy; about 25% of cases may have an initial presentation
immediately postpartum. Clinical presentation is an abrupt onset of an intensely pruritic, urticarial
eruption on the trunk that forms tense vesicobullous lesions (Figs. 12 and 13). About 50% of cases
have an initial presentation on the abdomen. Umbilical involvement accounts for a significant
number of cases of PG. As in PEP, facial and mucosal membrane involvement i rare. 29
 Fig. 12. Pemphigoid gestationis: urticarial plaques in the
periumbilical area with tense blisters.

Fig. 13. Pemphigoid gestationis: close-up view of the tense

blister in Fig. 12.

Accurate diagnosis is crucial in light of the variable clinical course of this disorder. Spontaneous
resolution over weeks to months postpartum is a common finding. About 75% of cases of PG present
with flares immediately postpartum. Recurrence in subsequent pregnancies with an earlier onset and
more severe clinical course is a common feature. Disease-free pregnancies (i.e. “skip pregnancies”)
with no cutaneous involvement in patients with a history of PG have occurred. There have also been
reports of PG flares developing with menstruation and the use of oral contraceptives (25% of
cases).28, 29

PG is an autoimmune disorder caused by the aberrant expression of the MHC II class antigen on the
chorionic villi of the placenta, which triggers an allogenic response to the placental basement
membrane zone and subsequent cross-reaction with maternal skin through the maternal
decidua.30, 31There are reports of occurrence of PG in association with hydatidiform mole and
choriocarcinoma.32, 33 Association of PG with other autoimmune diseases such as Graves' disease has
also been reported.34 Studies also show an increased incidence in HLA DR3 and DR4. HLA DR3
occurs in the same percentage of white persons as in African American persons; however, the
percentage of DR4 is lower in African-Americans, and this may explain the rarity of PG in this
population.35

Dermatopathologic examination of PG shows subepidermal vesicle formation with focal necrosis of

keratinocytes. The dermis shows papillary edema and a perivascular infiltrate consisting mainly of
eosinophils and a few lymphocytes. An occasional finding on histopathology is the alignment of
eosinophils along the dermoepidermal junction. DIF shows a characteristic linear band of C3 along
the skin basement membrane zone of patients with PG (Fig. 14). Linear C3 deposition on DIF is
diagnostic of PG in the correct clinical setting and is used to differentiate PEP from PG. 36 Using this
method, about 25% of cases also present with IgG deposits along the basement membrane zone.
Indirect immunofluorescence (IIF) demonstrates the “PG factor,” which consists of circulating IgG
complement-fixing anti-basement membrane zone antibodies in serum of patients with PG.
Complement-activated IIF using monoclonal antibodies directed against IgG 1 demonstrates this
factor in all PG patients.37 Clinically, titers of PG factor do not correlate with disease severity. The PG
factor is an IgG directed against a 180-kD hemidesmosomal (transmembrane) component of the
basement membrane zone.38Electron microscopy also demonstrates the C3 and IgG deposits in the
lamina lucida.39

Fig. 14. Pemphigoid gestationis by direct

immunofluorescence: linear band of C3 along basement
membrane zone of the skin.

In PG, 10% of the infants born to affected mothers have skin lesions that resemble PG; this is not the
case with PEP. DIF and IIF studies carried out on some of these infants are consistent with a
diagnosis of PG.29 There has been considerable controversy in assessing fetal morbidity and mortality
associated with PG.40 Recent consensus on infant morbidity indicates a slight increase in prematurity
and small size for gestational age.41, 42 The differential diagnosis of PG includes PEP, allergic contact
dermatitis, and drug eruption. A precise clinical history accompanied by diagnostic tests such as
histopathology and DIF helps to distinguish among these disorders. Treatment options include oral
steroids (0.5 mg/kg daily) with a possible increase in dose around the time of delivery to avoid
postpartum exacerbations. Other options include plasmapheresis, topical corticosteroids, and
antihistamines, all of which offer limited benefit. After delivery, depending upon breastfeeding
status, alternative treatments may include dapsone, methotrexate, and cyclosporine. 29

Impetigo herpetiformis

Impetigo herpetiformis is an acute eruption of pustular psoriasis during pregnancy (most often
presenting in the third trimester) in individuals with no prior history of psoriasis. The first case was
described by Von Hebra in 1872; since then, about 100 cases have been reported. 43 Clinical
presentation involves sterile pustules on an erythematous base that progressively become more
confluent.44 This eruption commonly begins on the flexural and inguinal skin and gradually spreads
to the trunk and involves the periumbilical skin (Figs. 15 and 16). Mucous membrane involvement of
the oropharynx and the esophagus is also seen. Impetigo herpetiformis is associated with
constitutional symptoms such as elevated temperature; gastrointestinal symptoms including nausea,
vomiting, and diarrhea; central nervous system symptoms such as delirium; and the musculoskeletal
manifestation of tetany due to hypocalcemia.8, 45 Recurrent eruptions in subsequent pregnancies
usually present with an earlier onset and more severe course. 45 There have also been reports of
exacerbation of this condition in affected patients associated with later use of oral contraceptives. 46

Fig. 15. Impetigo herpetiformis: diffuse erythematous

papulosquamous eruption on the trunk and extremities.

Fig. 16. Impetigo herpetiformis: coalescing erythematous

papules with silvery scale.

Early diagnosis and treatment is important. The few reported cases are associated with an increased
risk of fetal mortality due to placental insufficiency, increased stillbirths, and fetal
abnormalities.45 Laboratory findings include evidence of leukocytosis, elevated erythrocyte
sedimentation rate, hypoalbuminemia, and hypocalcemia.8 Histopathologic examination of skin
biopsy specimens is consistent with pustular psoriasis. The epidermis shows parakeratosis and
elongation of rete ridges with spongiform pustules of Kogoj. DIF, as in psoriasis, is negative. 45

Treatment involves oral corticosteroids (with limited benefit), correction of hypocalcemia,

supportive measures, and antimicrobials to prevent secondary infections. Termination of pregnancy
is usually curative.45, 46 Retinoids (isotretinoin) and light therapy are more effective means of
treatment that can be used postpartum.

Cholestasis of pregnancy

Cholestasis of pregnancy was initially described by Svanborg 47 and Thorling48 in 1954. Cholestasis of
pregnancy has been referred to by many other names, including prurigo gravidarum, intrahepatic
cholestasis of pregnancy, jaundice of pregnancy, and obstetric cholestasis. The etiology is believed to
be multifactorial, and the condition occurs in 0.02–2.4% of pregnancies. Studies show an increased
incidence among certain ethnic groups, such as some South American Indians. There is also a
seasonal variation in the prevalence of this condition, with a higher incidence in the winter months.
Fifty per cent of cases are believed to be familial, and a higher association has been seen in twin
pregnancies.49, 50 Another possible factor that contributes to the pathogenesis of this condition is the
effect of estrogen and other female hormones on the metabolism and secretion of hepatic bile. 8, 49

Cholestasis of pregnancy, as the name implies, occurs only in pregnancy (most commonly during the
third trimester) and resolves after delivery, with a 40–60% rate of recurrence in subsequent
pregnancies. Clinical presentation includes severe generalized pruritus with no primary skin lesions.
Secondary excoriations due to scratching may be the only skin findings. The extent and severity of
pruritus fluctuates until the time of delivery.49, 51Most severe pruritus occurs at night. 18 About 20% of
patients present with mild jaundice. This condition is the second most common cause of gestational
jaundice; viral hepatitis is the most common cause. 29 Laboratory values demonstrate elevated levels
of bile salts, serum aminotransferases, alkaline phosphatase, and γ-glutamyl
transpeptidase.49, 51 Because there are no primary skin lesions, skin biopsy results for histology and
DIF are normal.

Pruritus greatly improves after delivery, and complete resolution is achieved within a few days. In
cases in which symptoms continue to persist, other causes of cholestasis should be addressed. 49 There
have been reports of recurrence of symptoms with use of oral contraceptives. 51 The differential
diagnosis of pruritus in pregnancy should include parasitic infections, allergic skin reactions, and
other metabolic disorders.

Fetal and maternal prognosis shows an increase in premature labor and low birth weight. The fetus
and the mother are at an increased risk of intracranial and postpartum hemorrhage, respectively,
due to deficiency in vitamin K, which results in cases of prolonged fat malabsorption. 29, 51Treatment
options range from bed rest, a low-fat diet, and topical emollients in mild cases to the use of agents
such as cholestyramine, ursodeoxycholic acid (UDCA), and S-adenosyl-L-methionine in more severe
cases. Studies have shown better outcomes for both mother and infant with administration of UDCA
compared with placebo. In severe cases, fetal monitoring and cesarean section may be required. 51

Prurigo of pregnancy

Prurigo of pregnancy was initially described by Besnier in 1904 20 as prurigo gestationis. It commonly
occurs in the second to third trimester of pregnancy as discrete erythematous excoriated papules on
the trunk and the extensor aspect of the lower extremities (Fig. 17). The incidence is roughly 1 in 300
pregnancies. The pathogenesis of this eruption is believed to be the presence of atopy in the pregnant
woman. Histolologic examination of skin biopsy specimens shows parakeratosis and mild acanthosis
with a mixed inflammatory infiltrate of neutrophils and eosinophils in the perivascular area. DIF
results and laboratory values are normal. There is no increased fetal or maternal risk, and treatment
involves symptomatic relief with topical corticosteroids and antihistamines. 8, 29

Fig. 17. Prurigo of pregnancy: discrete erythematous

excoriated papules on the extensor surface of the arm.

Papular dermatitis of pregnancy

Papular dermatitis of pregnancy was initially described by Spangler in 1962 52 as a generalized papular
erythematous and pruritic eruption with central crust. The distribution is on the abdomen with
spread to the extremities. An increased level of urine hCG and a decrease in the urinary estriol level,
in combination with a significant increase in fetal morbidity and mortality, was initially described.
Many believe that papular dermatitis of pregnancy and prurigo of pregnancy are similar entities.
Histopathology and DIF findings are similar. The high fetal risk initially reported by Spangler 52 has
not been reproducible in other studies.53

Pruritic folliculitis of pregnancy

Pruritic folliculitis of pregnancy was first described by Zoberman and Farmer in 1981. 54 Onset of
eruption most commonly occurs in the second or third trimester of pregnancy as small erythematous
papules around follicles. The eruption is typically monomorphic with distribution on the trunk and
extremities (Fig. 18). Histopathologic examination shows folliculitis, and the DIF is negative.
Differential diagnosis involves papular dermatitis or steroid-induced acne. The fetus is unaffected,
and the treatment includes topical benzoyl peroxide. 8, 54

Fig. 18. Pruritic folliculitis of pregnancy: erythematous

papules centered around hair follicles on the back.

OTHER DERMATOSES AND INFECTIONS AFFECTED IN

PREGNANCY
In addition to the dermatoses that are specific to pregnancy, many common dermatoses and
infections are affected by the hormonal and immunologic changes seen in pregnancy. These include
conditions such as atopic dermatitis, seborrheic dermatitis, psoriasis, condyloma acuminata, and
genital herpesvirus infection.

Atopic dermatitis

Atopic dermatitis (atopic eczema) is a chronic inflammatory skin condition with itching. There are
no primary lesions, but secondarily, there is erythema, scaling, lichenification, and sometimes
papules. With excoriations, there can be oozing, weeping, and secondary bacterial infection. While
atopic dermatitis may be associated with hay fever and/or asthma, either in the patient or in a
member of the family, there are no allergens to remove in atopic dermatitis. Atopic dermatitis may
improve during pregnancy. Treatment involves the use of topical steroids. Soap should be limited to
the critical areas: hands, face, axillae, and groin.

Seborrheic dermatitis

Seborrheic dermatitis is characterized by redness and scaling on the scalp, as well as the para-nasal,
submental, post-auricular, sternal, inframmamary, axillary, umbilical, and inguinal areas. The cause
remains elusive, although there is evidence that yeast of the Malassezia sp is involved, along with
interference with the skin barrier. Treatment includes the use of topical corticosteroids, ketoconazole
cream, and selenium sulfide foam. Occlusive agents, such as moisturizers and petrolatum, can set off
the dermatitis.

Psoriasis
Psoriasis is a chronic inflammatory and proliferating skin condition that presents as sharply
demarcated erythematous plaques with silvery scale. The effects of pregnancy on psoriasis are
variable. Retrospective studies usually show improvement or no change in this skin condition with
pregnancy.55, 56Treatment options include topical corticosteroids, calcipotriol, and tar. Oral agents
such as methotrexate, hydroxyurea, and retinoids are contraindicated during pregnancy. The new
biologics should also be avoided during the pregnant state, although some experts have found the
use of the biologics to outweigh the possible risks.

Human papillomavirus infection

The human papillomavirus (HPV) is a large virus, of which over 40 types are pathologic in humans.
Warts can occur in any part of the body and may be referred to as verrucae vulgaris. In the
anogenital area, these are commonly called condylomata acuminata, which often present as flesh-
colored, exophytic, cauliflower-like masses. The amount of viral DNA is also greatly increased during
pregnancy. Recognition of HPV infection is important because certain strains can be transmitted to
the fetus through an infected birth canal, with subsequent association with juvenile respiratory
papillomatosis in infants born to infected mothers. Respiratory papillomatosis in infants is rare
compared with the extent of condylomas in childbearing women; thus, performance of cesarean
section in this situation is controversial due to the inherent risks of the procedure itself. Treatment
options during pregnancy include trichloroacetic acid or salicyclic acid topical preparations,
cryotherapy, cautery, or laser ablation. Other topical agents such as podophyllin are contraindicated
during pregnancy. No treatment is more than 70% effective, because the virus remains within the
body for a lifetime.57

Herpes simplex virus infection

Herpes simplex virus (HSV) is a common cause of viral infections worldwide. HSV-1 and HSV-2
cause both primary and recurrent infections; primary infections are more severe. Infection clinically
presents as grouped vesicles on an erythematous base that may erode and form ulcerations. Lesions
frequently occur around the month, where they are referred to as cold sores, fever blister, or more
properly herpes simplex labialis. Asymptomatic shedding of the herpesvirus has also been shown in
the absence of any skin findings. Genital herpes infection (herpes progenitalis) at the time of delivery
is associated with a high risk of neonatal infection. Even in the absence of skin lesions in infected
newborns, neurologic and visceral organ damage can be severe. Recognition and treatment of herpes
infection during pregnancy is very important. Patients considered high risk for HSV infection should
be tested weekly with viral cultures, and if there is evidence of active infection or viral shedding,
cesarean delivery should be performed.20 Acyclovir is a pregnancy category C antiviral agent that is
used for primary or symptomatic infections. Valacyclovir (pregnancy category B) is also used in the
treatment of HSV during pregnancy.

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