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خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده: 1

Dermatoses of pregnancy

Dermatoses of pregnancy
Author:
Miriam Keltz Pomeranz, MD
Section Editors:
Charles J Lockwood, MD, MHCM
Robert P Dellavalle, MD, PhD, MSPH
Deputy Editor:
Rosamaria Corona, MD, DSc
Literature review current through: May 2025. | This topic last updated: May 29, 2025.

INTRODUCTION — 

The dermatoses of pregnancy are a heterogeneous group of pruritic inflammatory dermatoses that occur exclusively during pregnancy and/or in the immediate postpartum period [1]. These include the following conditions, which are discussed below:

Pemphigoid gestationis

Polymorphic eruption of pregnancy (PEP; pruritic urticarial papules and plaques of pregnancy)

Atopic eruption of pregnancy (AEP; eczema in pregnancy, prurigo of pregnancy, pruritic folliculitis of pregnancy)

Pustular psoriasis of pregnancy (PPP), although not classified as a specific dermatosis of pregnancy, is also discussed here.

Normal physiologic changes of the maternal skin and appendages during pregnancy and intrahepatic cholestasis of pregnancy are reviewed elsewhere.

(See "Maternal adaptations to pregnancy: Skin and related structures".)

(See "Intrahepatic cholestasis of pregnancy".)

EVALUATION OF THE PREGNANT INDIVIDUAL WITH A PRURITIC ERUPTION — 

Pruritus during pregnancy is a major symptom of specific dermatoses of pregnancy, although it may also be physiologic (idiopathic pruritus or pruritus gravidarum) or associated with common inflammatory skin diseases, infections, or infestations (eg, allergic contact dermatitis, pityriasis rosea, scabies) occurring coincidentally during pregnancy [1-3]. Severe generalized pruritus, especially if including the palms and soles, in the absence of primary skin lesions suggests intrahepatic cholestasis of pregnancy. (See "Intrahepatic cholestasis of pregnancy".)

Urgency of evaluation — A new pruritic skin eruption that occurs during pregnancy requires immediate evaluation and diagnosis. Consultation with a dermatologist is appropriate when the diagnosis is unclear because delayed diagnosis or misdiagnosis of specific dermatoses associated with pregnancy may pose a significant risk to the fetus (preterm delivery, small for gestational age) and the mother [4]. The initial assessment involves:

History – Obtaining a detailed medical history, including personal and family history of atopy, obstetric history (primigravida, multiple gestation pregnancy, similar illness in previous pregnancies), and time of onset of the current eruption (early or late pregnancy).

Skin examination – Total body skin examination for type and distribution of lesions.

Skin biopsy – Skin biopsy for histopathologic examination and direct immunofluorescence (DIF) staining if the diagnosis is uncertain and pemphigoid gestationis is suspected. A skin biopsy should also be performed to confirm a clinical diagnosis of pustular psoriasis of pregnancy (PPP).

Laboratory tests – Laboratory testing (eg, total serum bile acids, metabolic panel, circulating antibodies against the bullous pemphigoid antigen 180 [BP180]) is indicated based on the clinical findings (table 1) and if there is clinical suspicion of a condition associated with fetal and maternal risk, such as pemphigoid gestationis, intrahepatic cholestasis of pregnancy, and generalized pustular psoriasis.

When to suspect a specific dermatosis of pregnancy — In a pregnant individual presenting with rash and pruritus, a specific dermatosis of pregnancy can be suspected based on history and clinical features, including time of onset and type and distribution of lesions (table 1 and algorithm 1 and algorithm 2). In particular:

Eczematous lesions with a flexural distribution suggest atopic eruption of pregnancy (AEP) (picture 1A). (See 'Atopic eruption of pregnancy' below.)

Nodular lesions on the limbs suggest prurigo-type AEP (picture 2). (See 'Atopic eruption of pregnancy' below.)

Involvement of striae is common in polymorphic eruption of pregnancy (PEP) (picture 3). (See 'Polymorphic eruption of pregnancy' below.)

Urticarial lesions are most common with PEP or pemphigoid gestationis, which also can display vesicular lesions. (See 'Polymorphic eruption of pregnancy' below and 'Pemphigoid gestationis' below.)

Erythematous plaques with sterile pustules at the periphery starting at flexural areas suggest PPP (picture 4). (See 'Pustular psoriasis of pregnancy' below.)

When to refer to dermatology — Any patient with lesions suggesting pemphigoid gestationis (see 'Pemphigoid gestationis' below) or PPP (see 'Pustular psoriasis of pregnancy' below) should be referred to a dermatologist for evaluation and diagnosis. Consultation with dermatology is also appropriate for any patient in whom the clinical diagnosis is unclear.

SPECIFIC DERMATOSES OF PREGNANCY

Atopic eruption of pregnancy — Atopic eruption of pregnancy (AEP) is a pruritic disorder of pregnancy that presents as an eczematous or papular eruption in patients with an atopic background. It starts during early pregnancy, with most cases occurring before the third trimester, and it tends to recur in subsequent pregnancies.

Terminology — "Atopic eruption of pregnancy" is a unifying term that includes several entities that were previously considered distinct entities [5]:

Eczema in pregnancy.

Prurigo of pregnancy (also called prurigo gestationis of Besnier, Nurse's early-onset prurigo of pregnancy, Spangler's papular dermatitis of pregnancy, and linear immunoglobulin M [IgM] disease of pregnancy).

Pruritic folliculitis of pregnancy.

This classification scheme is based on the presence of shared clinical features, including a possible association with atopy. However, not all experts agree that pruritic folliculitis of pregnancy and prurigo of pregnancy are best "lumped" within a disorder of atopic diathesis [6].

None of the disorders classified within this group are associated with adverse effects on the fetus [7].

Epidemiology — AEP is the most common pregnancy dermatosis, accounting for over 50 percent of all cases [5]. Its precise incidence is unknown. AEP is associated with a personal or family history of atopy (seasonal rhinitis, asthma, and/or atopic dermatitis) and is the first manifestation of atopic skin changes in most cases [5,8].

Pathogenesis — AEP is thought to be triggered by immunologic changes associated with pregnancy. It is postulated that reduced production of T helper type 1 (Th1) cytokines and enhancement of T helper type 2 (Th2) cytokine production, which is known to occur during pregnancy, may contribute to the development of eczema [9]. A relationship with a history of atopy has been proposed but remains controversial [5,8,10].

Clinical manifestations

Onset – AEP often begins during the first or second trimester and is the first manifestation of atopic dermatitis in most cases. In patients with a history of atopic dermatitis, AEP may represent a recurrence of atopic dermatitis after years of remission or a flare in patients with ongoing atopic dermatitis before pregnancy [8,11].

Lesion characteristics and distribution

Eczema – Most patients with AEP present with a widespread, eczematous eruption (the E-type AEP) involving the face, neck, and flexural areas, similar to classic atopic dermatitis (picture 1A-B) [5]. However, any area of the skin may be affected. Lesions may be eczematous patches or intact or excoriated papules. Papules can be follicle based, grouped, or scattered. Skin dryness, which may be severe, is invariably present.

Prurigo of pregnancy – A less common presentation of AEP is prurigo of pregnancy (also called P-type AEP), which presents with erythematous, excoriated papules or nodules on the extensor surfaces of the limbs and trunk (picture 2) [8,10-12]. Lesions are grouped and may be crusted or appear eczematous. In one series, all 12 patients had abdominal involvement, with some also having the legs, wrists, and hands affected [8]. The eruption usually resolves in the immediate postpartum period [8], although it can persist for up to three months [13].

Pruritic folliculitis of pregnancy – In rare cases, AEP presents as a follicular, papulopustular eruption (formerly known as pruritic folliculitis of pregnancy). Scattered, follicle-based papules and pustules initially appear on the abdomen but may spread to the trunk and extremities and become generalized [6,8,14]. The appearance is similar to that of steroid-induced acne and is only mildly pruritic [6].

Clinical course — The eruption typically clears within two weeks of delivery [15,16]. However, persistent symptoms postpartum or resolution before delivery have been reported [8,14].

Diagnosis

Clinical – The diagnosis is usually clinical, based upon the recognition of clinical features in a patient with a personal or family history of atopy. A skin biopsy is not generally helpful, as the findings are nonspecific. However, a biopsy should be performed if there is diagnostic uncertainty or suspicion of pemphigoid gestationis. (See 'Pemphigoid gestationis' below.)

Although laboratory testing is not generally indicated, up to 70 percent of patients may have elevated serum immunoglobulin E (IgE) levels [5]. In patients presenting with folliculitis, a pustule should be cultured to rule out bacterial or candidal folliculitis.

Histopathologic – Spongiosis and a perivascular mononuclear infiltrate are common features of eczematous eruptions [8]. Epidermal hyperkeratosis or parakeratosis may also be present. A dermal perivascular lymphocytic infiltrate without eosinophils can also be noted. The epidermis may show acanthosis, hyperkeratosis, and parakeratosis.

A follicle-centered lymphohistiocytic infiltrate containing neutrophils, eosinophils, and plasma cells and neutrophilic pustules with histopathologic features of sterile folliculitis can be seen in folliculitis-type AEP [8,14,16].

Direct immunofluorescence (DIF) and indirect immunofluorescence (IIF) studies are negative.

Differential diagnosis — The differential diagnosis of AEP includes (algorithm 1):

Dermatitides not specifically associated with pregnancy, including:

Allergic contact dermatitis (see "Allergic contact dermatitis: Clinical features and diagnosis")

Pityriasis rosea (see "Pityriasis rosea")

Maculopapular drug eruption (see "Exanthematous (maculopapular) drug eruption")

Scabies. (See "Scabies: Epidemiology, clinical features, and diagnosis".)

Polymorphic eruption of pregnancy (PEP) or early pemphigoid gestationis – The clinical differentiation of prurigo-type AEP from PEP or early pemphigoid gestationis may be difficult. In these cases, a skin biopsy may be helpful for the correct diagnosis. Although prurigo-type AEP and PEP share several histopathologic features, the finding of lymphocytic vasculitis, eosinophils in the interstitial dermis, edema, and mucin deposition in the dermis suggest PEP rather than AEP [7]. (See 'Diagnosis' below.)

Scratch lesions secondary to pruritus from intrahepatic cholestasis of pregnancy. (See "Intrahepatic cholestasis of pregnancy".)

Treatment — The goal of treatment is relief of symptoms. Like nonpregnant patients with eczema, patients with AEP should be encouraged to maintain adequate skin hydration through the frequent use of emollients. (See "Treatment of atopic dermatitis (eczema)", section on 'Maintaining skin hydration'.)

Topical corticosteroids – Low- to mid-potency topical corticosteroids (groups 4 to 6 (table 2)) are sufficient for controlling symptoms in most cases and can be safely used during pregnancy [17-19]. Topical corticosteroids are applied once or twice daily until improvement. Vehicles for topical corticosteroids and doses are illustrated in the tables (table 3A-B). (See "Treatment of atopic dermatitis (eczema)", section on 'Topical corticosteroids'.)

Narrowband ultraviolet B (NBUVB) – NBUVB therapy, if available and feasible to the patient, is a treatment option for AEP uncontrolled with topical corticosteroids and is considered safe during pregnancy [20,21]. NBUVB can be administered two to three times per week. (See "UVB phototherapy (broadband and narrowband)", section on 'Dosimetry and treatment protocols'.)

DupilumabDupilumab, a monoclonal antibody that blocks the interleukin (IL) 4 receptor alpha subunit to inhibit both IL-4 and IL-13 pathways, has been used in patients with antepartum atopic dermatitis to maintain disease control during pregnancy [22]. However, data on its safety during pregnancy are limited.

A propensity score-matched cohort study using data from the United States Collaborative Network of TriNetX assessed the risk of adverse pregnancy outcomes (eg, preterm labor, spontaneous abortions, edema, proteinuria, hypertensive disorders, infections) among 293 individuals exposed to dupilumab during pregnancy and an equal number of controls without dupilumab exposure, matched by age, ethnicity, and risk factors for adverse pregnancy outcomes [23]. The rates of adverse pregnancy outcomes were similar in the two groups. Of note, the risk for preterm labor was lower in the dupilumab-exposed group than in the control group (3.8 versus 7.24 percent; hazard ratio [HR] 0.11, 95% CI 0.03-0.45).

In a systematic review that included 13 reports (68 patients with pre-existent atopic dermatitis, 69 pregnancies), dupilumab was administered continuously (22 percent of patients) or intermittently (78 percent of patients) during pregnancy [24]. Spontaneous abortion was reported in 11 cases, with a rate (26 percent) similar to that in the general population.

In another systematic review of 15 observational studies with 115 pregnant females exposed to dupilumab for an average of 28 weeks during pregnancy, the weighted prevalence of spontaneous abortion was 18.9 percent (95% CI 5.3-38.2), similar to the rates estimated in the general population (11 to 22 percent) [25]. No congenital malformations were reported.

Oral antihistamines – First-generation sedating oral antihistamines, such as chlorpheniramine, or second-generation loratadine and cetirizine may be helpful for controlling pruritus. (See "Recognition and management of allergic disease during pregnancy", section on 'Oral antihistamines'.)

Prognosis — AEP has not been associated with adverse effects on the fetus [8]. AEP may recur with subsequent pregnancies [10,11].

Polymorphic eruption of pregnancy — PEP, also called pruritic urticarial papules and plaques of pregnancy, is a benign self-limiting pruritic inflammatory disorder that usually affects primiparous individuals in the last few weeks of pregnancy or immediately postpartum [26].

Epidemiology — PEP is relatively common, occurring in approximately 1 in 160 to 300 pregnancies [11,15]. Three-quarters of patients with the classic type of PEP are nulliparous [27].

Pathogenesis — The etiology and pathogenesis of PEP are poorly understood [11,27].

One hypothesis is that stretching of the abdominal skin results in damage to the connective tissue with exposure of dermal antigens that trigger an inflammatory response [28,29]. This hypothesis is supported by the observation that PEP occurs more frequently in multiple gestations, where the degree of skin stretching is much increased [15,28,30,31].

Another hypothesis is that PEP represents an immunologic response to circulating fetal antigens. One study demonstrated male fetal deoxyribonucleic acid (DNA) in maternal skin lesions, a possible result of blood chimerism (fetal cells detected in maternal blood throughout pregnancy) [32]. However, this hypothesis has not been confirmed, although several studies have reported a preponderance of male fetuses in individuals with PEP [8,33,34].

Clinical manifestations

Onset – PEP usually occurs in nulliparous individuals late in the third trimester (mean onset 35 weeks) but may develop postpartum [27,33,35]. There are also rare case reports of first and second trimester disease [27].

Lesion characteristics and distribution – PEP typically presents with extremely pruritic, erythematous papules within striae (picture 3). Abdominal striae are the most common initial site, with characteristic periumbilical sparing, and may be the only involved site [33].

In most cases, the lesions spread to the extremities, chest, and back and coalesce to form urticarial plaques (picture 5A-B) [36]. White halos often surround the erythematous papules in patients with lightly pigmented skin (picture 6). The face, palms, and soles are usually spared.

Over the course of the disease, approximately one-half of the patients develop more polymorphic lesions, including target-like lesions exhibiting three distinct rings/color changes, or erythematous patches and vesicles [10,26,27,36].

Clinical course — The eruption generally lasts four to six weeks and resolves within two weeks postpartum. However, it may last longer or resolve prior to delivery [10].

Diagnosis

Clinical – The diagnosis of PEP is usually clinical, based on history and physical examination (algorithm 2 and table 1). A skin biopsy is generally not necessary for diagnosis but may be performed in cases of diagnostic uncertainty. There are no laboratory abnormalities related to PEP [33].

Histopathologic

Routine histopathology – Histopathologic examination of a skin biopsy shows a perivascular (superficial and deep) and interstitial lymphocytic infiltrate containing eosinophils [7]. Features of lymphocytic vasculitis may be seen in some cases. Epidermal changes, including mild epidermal hyperplasia, spongiosis, and parakeratosis, are seen in approximately 30 to 50 percent of cases [7,36]. Additional findings include dermal edema and focal deposition of mucin.

Immunohistochemistry – Immunohistochemical studies reveal a predominantly T helper lymphocytic infiltrate with an increased number of CD1a+, CD54+ (ICAM-1+) dendritic cells and CD1a+ epidermal Langerhans cells in lesional skin.

DIF – DIF is usually negative or may demonstrate a nonspecific deposition of complement component 3 (C3) and IgM or immunoglobulin A (IgA) deposits at the dermoepidermal junction or around blood vessels in a minority of cases [27]. These deposits are granular, not linear, as in pemphigoid gestationis. IIF is always negative.

Differential diagnosis

Early stage (urticarial) of pemphigoid gestationis – PEP can mimic the early urticarial phase of pemphigoid gestationis, although in contrast with pemphigoid gestationis, PEP typically spares the umbilical region (algorithm 2 and table 1). In uncertain cases, the two disorders can be distinguished by DIF of a biopsy specimen. (See 'Pemphigoid gestationis' below.)

Erythema multiforme – The target-like lesions of PEP may appear similar to erythema multiforme.

Other – Drug reactions, viral exanthems, and infestations (scabies) may also present with erythematous papules similar to PEP [11,27]. The clinical history, routine histology, and serology help in differentiating among these entities. (See "Drug eruptions" and "Scabies: Epidemiology, clinical features, and diagnosis".)

Treatment — The goal of treatment is relief of symptoms. Early delivery to end symptoms is rarely, if ever, necessary [37].

Topical corticosteroids – We suggest mid- to high-potency topical corticosteroids (groups 2 to 4 (table 2)) as initial therapy for PEP. Topical corticosteroids can be applied once or twice daily until improvement occurs. The cumulative amounts of topical corticosteroids used for the treatment of specific body areas in adults are shown in the table (table 3A). (See "Topical corticosteroids: Use and adverse effects", section on 'Use during pregnancy or lactation'.)

The safety of topical corticosteroid use during pregnancy is supported by several observational studies and meta-analyses [17,38]. However, the use of potent or superpotent topical corticosteroids exceeding 300 g during the whole pregnancy may be associated with an increased risk of low birth weight [39].

Systemic corticosteroids – In severe cases, a short course of systemic corticosteroids, such as prednisone or prednisolone 0.5 mg/kg per day for one week tapered over one to two weeks, may be given for rapid resolution of symptoms [26]. (See "Safety of rheumatic disease medication use during pregnancy and lactation", section on 'Glucocorticoids'.)

Oral antihistaminesChlorpheniramine, a first-generation oral antihistamine, or second-generation nonsedating oral antihistamines, such as loratadine and cetirizine, may be helpful to control pruritus. (See "Recognition and management of allergic disease during pregnancy", section on 'Oral antihistamines'.)

Prognosis — PEP poses no increased risk of fetal or maternal morbidity (other than maternal pruritus) [11,33]. Recurrence is rare [27,33].

Pemphigoid gestationis — Pemphigoid gestationis (formerly called herpes gestationis) is a rare autoimmune bullous disease that occurs during the second or third trimester of pregnancy and may be associated with increased fetal risk [40].

Epidemiology — Pemphigoid gestationis is rare. Its incidence has been estimated at 1 in 20,000 to 50,000 pregnancies. It only occurs during pregnancy, in the immediate postpartum period in a minority of cases, or as a paraneoplastic manifestation in females with gestational trophoblastic neoplasia [10,41,42].

Pathogenesis — Pemphigoid gestationis is an autoimmune subepidermal blistering disease [3].

Antigenic targets – Pemphigoid gestationis is caused by circulating immunoglobulin G1 (IgG1) autoantibodies directed against BP180 (collagen XVII), a transmembrane hemidesmosomal glycoprotein expressed in the basement membrane zone of the skin. The majority of patient sera bind to the extracellular NC16A epitope, but some bind to other epitopes on BP180, both intracellular and extracellular [43].

The primary site of autoimmunity seems to be the placenta, as antibodies bind not only to the basement membrane zone of the epidermis but also to that of chorionic and amniotic epithelia, both of ectodermal origin. It has been theorized that paternal major histocompatability complex (MHC) class II antigens found on the chorionic villi induce maternal antibodies to the amniotic basement membrane. These antibodies can then cross-react with skin and cause maternal (and sometimes newborn) disease [44].

Blister formation – As in bullous pemphigoid, the binding of antibodies to antigens within the basement membrane zone stimulates an inflammatory cascade that results in separation of the epidermis from the dermis. (See "Epidemiology and pathogenesis of bullous pemphigoid and mucous membrane pemphigoid".)

Genetic predisposition – The hypothesis of a genetic predisposition is supported by the observation of an association between pemphigoid gestationis and class II human leukocyte antigen (HLA) phenotype HLA-DR3/HLA-DR4 [45,46].

Clinical manifestations

Onset – Pemphigoid gestationis most often occurs in the second or third trimester of pregnancy. Intense pruritus may precede the onset of visible skin lesions. In approximately 10 percent of cases, it occurs in the immediate postpartum period [47].

Lesion characteristics and distribution – The rash typically begins on the abdomen as urticarial plaques or papules surrounding the umbilicus (picture 7 and picture 8A-C and table 1) [10,11,48]. Vesicles may also be present (picture 9). Lesions may be seen on the palms and soles but rarely on the face or mucous membranes. The eruption spreads rapidly and forms tense blisters (picture 10A-C). The entire body surface may be involved, but the mucous membranes are usually spared.

Clinical course – Most cases spontaneously resolve in the weeks to months following delivery. Occasionally, it may remit prior to delivery. However, most patients have a flare postpartum, and some subsequently have a flare with the use of oral contraceptive pills or during menses. The disease usually recurs with subsequent pregnancies and is often worse [11] but may also skip pregnancies [49].

Diagnosis — The diagnosis of pemphigoid gestationis is based on the combination of clinical findings (algorithm 2 and table 1), examination of a lesional skin biopsy for routine histopathology and a perilesional skin biopsy for DIF, and measurement of serum levels of anti-BP180 antibodies by enzyme-linked immunosorbent assay (ELISA).

Pathology – Biopsy of a vesiculating lesion (using routine histologic processing) reveals a subepidermal vesicle with a perivascular lymphocytic and eosinophilic infiltrate. Eosinophils may appear at the dermoepidermal junction and fill the vesicle. Basal cell necrosis and edema of the dermal papillae are usually noted.

DIF – Using a snap-frozen perilesional skin biopsy, DIF reveals a homogeneous, linear deposit of complement C3 at the basement membrane zone (picture 11). The presence of C3 is pathognomonic for pemphigoid gestationis in a pregnant patient. Immunoglobulin G (IgG) deposits are also present in 30 to 40 percent of patients but are not a criterion for diagnosis.

Laboratory tests – Antibodies against the noncollagenous extracellular domain of BP180 known as NC16A (the primary site for antibody binding in bullous pemphigoid) can be detected in the serum by a commercially available ELISA assay (BP180 NC16A ELISA). This test is sensitive and specific for the diagnosis of pemphigoid gestationis, and its positivity can be considered diagnostic in patients with typical clinical features [50,51]. The sensitivity and specificity of the BP180 NC16A ELISA test range from 96 to 100 percent [50-52].

The levels of circulating anti-BP180 antibodies correlate with disease severity and are useful to monitor the response to treatment. The anti-BP180 levels tend to remain elevated up to one year after pregnancy and may persist during subsequent pregnancies even in the absence of a new episode of pemphigoid gestationis [53].

Differential diagnosis — The differential diagnosis of pemphigoid gestationis primarily includes the following (algorithm 2):

PEP – The early urticarial plaques of pemphigoid gestationis are clinically and histologically indistinguishable from PEP. (See 'Polymorphic eruption of pregnancy' above.)

Clinical criteria – A clinical clue to help differentiate the two disorders is that PEP often begins in the striae, while pemphigoid gestationis is truly periumbilical (table 1). A tool called the Pregnancy Dermatoses Clinical Scoring System (PDCSS) has been proposed to differentiate pemphigoid gestationis from PEP in settings with limited access to DIF or testing for specific circulating antibodies [54]. Elements of clinical history (ie, previous pemphigoid gestationis, primigravida, onset between 28 and 36 weeks, onset before 28 weeks) and clinical findings (ie, umbilical involvement, rash in striae, bullae) are assigned a score ranging from -2 to +2. In a multicenter validation study that included 19 patients with pemphigoid gestationis and 39 with PEP, PDCSS was able to differentiate pemphigoid gestationis from PEP with a sensitivity of 79 percent and a specificity of 95 percent [54].

DIF – DIF of perilesional skin showing linear C3 deposition along the dermoepidermal junction is pathognomonic of pemphigoid gestationis. In PEP, DIF is usually negative or may show a nonspecific, granular deposition of C3 at the dermoepidermal junction.

Circulating antibodies – The demonstration of circulating antibodies against BP180 NC16A by ELISA test will confirm the diagnosis of pemphigoid gestationis. In PEP, BP180 NC16A antibodies are negative. (See 'Polymorphic eruption of pregnancy' above.)

Other skin eruptions

Dermatitis herpetiformis – Dermatitis herpetiformis is a very pruritic vesicular autoimmune skin eruption associated with gluten sensitivity. In contrast with pemphigoid gestationis, dermatitis herpetiformis lesions are typically located on the elbows, dorsal forearms, knees, scalp, back, and buttocks (picture 12A-B). DIF of perilesional skin showing granular deposits of IgA within the dermal papillae confirms the diagnosis of dermatitis herpetiformis. (See "Dermatitis herpetiformis".)

Erythema multiforme – Erythema multiforme, whether due to pregnancy, infection, or drugs, can mimic pemphigoid gestationis clinically, but routine histology usually distinguishes between these disorders. (See "Erythema multiforme: Pathogenesis, clinical features, and diagnosis".)

Allergic contact dermatitis and drug reactions – Allergic contact dermatitis and drug reactions can also appear similar to pemphigoid gestationis on physical examination. Thus, a careful history regarding use of medications and exposure to environmental agents may be helpful for the correct diagnosis [11,48]. (See "Allergic contact dermatitis: Clinical features and diagnosis" and "Drug eruptions".)

Treatment — The goals of treatment of pemphigoid gestationis are to decrease blister formation, promote the healing of blisters and erosions, and relieve pruritus. Due to its rarity, the therapies for pemphigoid gestationis have not been evaluated in randomized trials. Treatment is mainly based on clinical experience and evidence from studies on bullous pemphigoid [55-57]. (See "Management and prognosis of bullous pemphigoid".)

High-potency topical corticosteroids – We suggest high-potency topical corticosteroids (groups 1 to 3 (table 2)) rather than systemic corticosteroids for the initial treatment of pemphigoid gestationis. (See "Topical corticosteroids: Use and adverse effects", section on 'Use during pregnancy or lactation'.)

Systemic corticosteroids – If symptoms are not controlled by topical corticosteroids, systemic corticosteroids are usually effective.

AdministrationPrednisone is given at an initial dose of 0.5 mg/kg per day. Once the symptoms are stabilized, the dose may be tapered and even discontinued in some patients. However, postpartum reinstatement of treatment with higher corticosteroid doses or other immunosuppressive or immunomodulating agents will likely be needed [11,48].

Safety – The use of systemic corticosteroids during pregnancy appears to be relatively safe. Although early studies suggested an association between systemic corticosteroids and risk of miscarriage or congenital malformation (oral clefts), larger population-based studies have not confirmed these findings [58,59]. However, limited data suggest an increased risk of preterm birth or low birth weight for patients with pemphigoid gestationis or other autoimmune diseases exposed to systemic corticosteroids during pregnancy.

-A study of 61 individuals with pemphigoid gestationis found an increased risk of low birth weight in those treated with ≥60 mg prednisone per day after adjusting for maternal age and comorbidities (odds ratio [OR] 16.65, 95% CI 1.15-241.46) [4]. However, because of the small sample size and wide confidence interval, the magnitude of the risk remains uncertain.

-In a nationwide Danish cohort study of 900 pregnant individuals with Crohn disease exposed to various treatments, 73 received systemic corticosteroids [60]. In this group, there were nine preterm births (12 percent) and one low birth weight (1.4 percent) at term.

Other therapies – In patients with pemphigoid gestationis that is not fully responding to systemic corticosteroids and in patients in whom corticosteroids are contraindicated, intravenous immunoglobulin (IVIG) at a dose of 2 g/kg/cycle is a treatment option [61,62]. In several case reports, dupilumab has been successfully used for the treatment of pemphigoid gestationis uncontrolled by systemic corticosteroids [63-66].

Postpartum treatment of severe, persistent disease — Severe, persistent postpartum pemphigoid gestationis may require higher doses of systemic corticosteroids or alternative immunosuppressant agents. Prednisone up to 2 mg/kg per day can be given until a clinical response is achieved and then tapered and maintained at the lowest effective dose.

Alternative therapies that have been successfully used in a few patients with severe, persistent postpartum pemphigoid gestationis include:

Azathioprine

High-dose IVIG (2 g/kg per cycle) [61,67-69]

Cyclosporine [70]

Cyclophosphamide [71]

Doxycycline and nicotinamide [72]

Rituximab [73]

Immunoapheresis [74]

Omalizumab [75]

The first-generation oral antihistamine chlorpheniramine or second-generation loratadine and cetirizine may be helpful for the symptomatic control of pruritus. (See "Recognition and management of allergic disease during pregnancy", section on 'Oral antihistamines'.)

Prognosis

Fetal prognosis – The fetal prognosis is generally good despite an increased risk of prematurity and small-for-gestational-age babies due to mild placental failure [4,76,77]. A review of 61 pregnancies complicated by pemphigoid gestationis reported 20 preterm births (34 percent) [4]. There is no increased risk of miscarriage.

A few newborns present with blisters (neonatal pemphigoid gestationis) due to the transplacental passage of maternal IgG autoantibodies. The eruption has a mild course and resolves within weeks without treatment [78-80]. There is minimal risk of adrenal suppression in the newborn even if the mother has been maintained on high-dose corticosteroids.

Maternal prognosis – The mother is at high risk of recurrent pemphigoid gestationis with subsequent pregnancies.

INTRAHEPATIC CHOLESTASIS OF PREGNANCY — 

Intrahepatic cholestasis of pregnancy (obstetric cholestasis) is the only pregnancy dermatosis without primary skin changes [81]. Intrahepatic cholestasis of pregnancy usually develops during the late second or third trimester. Due to elevated levels of bile acids, patients experience severe, generalized pruritus that involves the palms and soles and may present with excoriations secondary to scratching. (See "Intrahepatic cholestasis of pregnancy", section on 'Clinical findings'.)

Intrahepatic cholestasis of pregnancy carries significant morbidity for the fetus, including prematurity, meconium-stained amniotic fluid, intrauterine demise, and an increased risk for neonatal respiratory distress syndrome. (See "Intrahepatic cholestasis of pregnancy", section on 'Fetal effects'.)

The maternal prognosis is generally favorable, although one study suggests that affected individuals have an increased risk of later hepatobiliary disease [82]. (See "Intrahepatic cholestasis of pregnancy", section on 'Fetal effects' and "Intrahepatic cholestasis of pregnancy", section on 'Maternal treatment'.)

PUSTULAR PSORIASIS OF PREGNANCY — 

Pustular psoriasis of pregnancy (PPP), formerly called impetigo herpetiformis, is an exceedingly rare variant of generalized pustular psoriasis occurring during pregnancy or triggered by pregnancy [83]. It typically presents during the third trimester but may occur earlier or in the immediate postpartum period. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis" and "Pustular psoriasis: Management".)

Clinical manifestations

Onset – PPP can occur anytime during pregnancy but typically presents in the late second or third trimester of pregnancy.

Skin lesion characteristics and distribution – The eruption begins in the flexural areas with symmetric, erythematous plaques studded at the periphery with sterile pustules in a circinate pattern (picture 4) [84]. The plaques then enlarge from the periphery as the center becomes eroded and crusted (picture 13B). There may be concentric rings of pustules. The pustules are typically sterile. The eruption spreads centrifugally involving the trunk and extremities while the hands, feet, and face are usually spared.

Systemic symptoms – Pruritus is usually absent. Systemic symptoms are severe and include malaise, fever, anorexia, nausea, vomiting, and diarrhea [85,86]. Hypocalcemia can lead to tetany, delirium, and seizures.

Extracutaneous manifestations – Oral and esophageal erosions may occur. The nails may become onycholytic (lifting of the nail plate from the nail bed) [85,86]. Pitting has also been described [87].

Laboratory findings – Leukocytosis and elevated erythrocyte sedimentation rate (ESR) are common. Hypocalcemia may be present, possibly related to hypoparathyroidism [85]. Albuminuria, hypoalbuminemia, pyuria, and hematuria occasionally occur. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Laboratory abnormalities'.)

Diagnosis

Clinical – The diagnosis can be made clinically, based on history and physical examination (picture 13A-B). However, we suggest histopathologic confirmation given the potential consequences of the disease to maternal and child health and the need for prompt institution of fetal monitoring and maternal treatment.

Pathology – The histopathologic features of PPP are the same as those of pustular psoriasis in the nonpregnant patient. Spongiform pustules with neutrophils are observed in the epidermis. Psoriasiform hyperplasia and parakeratosis also occur [85,86]. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Histopathology'.)

Laboratory tests – The initial laboratory evaluation includes a complete blood count (CBC) with differential and a complete metabolic panel to evaluate for hypocalcemia, other electrolyte abnormalities, hypoalbuminemia, and liver and renal function. Pustule cultures for bacteria or yeasts may be obtained.

Differential diagnosis — An infectious etiology for the pustular eruption (eg, candidiasis, tinea corporis, impetigo) should be excluded by appropriate cultures. Other dermatoses that should be considered in the differential diagnosis of PPP include:

Subcorneal pustular dermatosis – Subcorneal pustular dermatosis (picture 14) can mimic PPP clinically and histopathologically but is typically asymptomatic. The presence of severe systemic symptoms suggests PPP. (See "Subcorneal pustular dermatosis".)

Acute generalized exanthematous pustulosis – Acute generalized exanthematous pustulosis (picture 15) is a severe drug reaction that typically manifests with the rapid development of dozens to hundreds of nonfollicular, sterile, pinhead-sized pustules that usually occur a few hours to a few days after exposure to an offending drug (most often an antibiotic). The absence of a history of drug exposure helps in distinguishing PPP from acute generalized exanthematous pustulosis. (See "Acute generalized exanthematous pustulosis (AGEP)".)

Pruritic folliculitis of pregnancy – Pruritic folliculitis of pregnancy, an uncommon clinical variant of atopic eruption of pregnancy (AEP), is pruritic and exclusively perifollicular, neither of which is true of PPP. (See 'Atopic eruption of pregnancy' above.)

Pemphigoid gestationis – Pemphigoid gestationis can present with rings of vesicles or pustules. Histopathology clarifies the diagnosis. (See 'Pemphigoid gestationis' above.)

Management — Because of the associated risk for the fetus, PPP requires prompt dermatologic consult and institution of treatment. Fetal monitoring with nonstress tests or biophysical profiles and ultrasound assessment of fetal growth are indicated. (See "Fetal assessment: Overview of antepartum tests of fetal well-being".)

Patients with PPP sometimes require early delivery for relief of symptoms and for fetal safety [85,86,88]. Hypocalcemia must be corrected when present, and fluid and electrolyte balance should be maintained.

There is very limited evidence to support the choice of treatment for PPP. In a review from the medical board of the National Psoriasis Foundation, corticosteroids, cyclosporine, and infliximab were all listed as first-line treatments [89].

Systemic corticosteroids – We suggest systemic corticosteroids for the initial treatment of PPP. High-dose prednisone or prednisolone up to 60 to 80 mg per day are given for a few days and then slowly tapered as symptoms improve, with monitoring in case a flare occurs.

Oral cyclosporine – Low-dose cyclosporine (2 to 3 mg/kg per day) may be an alternative to systemic corticosteroids for patients with PPP [89-93]. Data from studies in pregnant patients with organ transplantation indicate that the risk of teratogenicity is low, but premature labor and infants small for gestational age have been reported [94]. (See "Safety of rheumatic disease medication use during pregnancy and lactation".)

Tumor necrosis factor (TNF) inhibitors – There are isolated reports of successful use of infliximab for PPP [95-98]. Adalimumab and certolizumab pegol have also been used in a few patients, the latter having the advantage of not crossing the placenta [99-101].

Other biologics – The interleukin (IL) 17 inhibitors secukinumab [102,103] and brodalumab [104] and the IL-12/23 inhibitor ustekinumab [105] have been used in pregnant patients.

Spesolimab, an IL-36 inhibitor, was approved in 2022 in the United States to treat generalized pustular psoriasis. There is one case report of successful use of spesolimab for PPP [106].

Other therapies – There are a few case reports from Japan of successful use of granulocyte and monocyte adsorption apheresis (GMA) for PPP [107,108].

For persistent cases, after delivery and in mothers who are not breastfeeding, systemic retinoids or methotrexate are additional therapeutic options [84].

Prognosis — PPP usually remits quickly postpartum but may flare after delivery [87,109,110]. Placental insufficiency with severe sequelae, such as miscarriage, fetal growth restriction, or stillbirth, may occur [111,112].

In patients exposed to a TNF inhibitor (eg infliximab), consider delaying live vaccines in the newborn until six months of age.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dermatoses of pregnancy".)

SUMMARY AND RECOMMENDATIONS

Evaluation of the pregnant patient with a pruritic eruption – Pruritus during pregnancy is a major symptom of specific dermatoses of pregnancy or common inflammatory skin diseases, infections, or infestations. A new pruritic skin eruption requires immediate evaluation and diagnosis to exclude conditions associated with fetal and/or maternal risk (eg, pemphigoid gestationis, intrahepatic cholestasis of pregnancy, generalized pustular psoriasis). (See 'Evaluation of the pregnant individual with a pruritic eruption' above.)

Specific dermatoses of pregnancy

Definition and clinical features – The specific dermatoses of pregnancy are a heterogeneous group of pruritic inflammatory dermatoses that occur exclusively during pregnancy and/or in the immediate postpartum period. They include (see 'Specific dermatoses of pregnancy' above):

-Atopic eruption of pregnancy (AEP) (picture 2).

-Polymorphic eruption of pregnancy (PEP; previously known as pruritic urticarial papules and plaques of pregnancy) (picture 5A-B).

-Pemphigoid gestationis (also called herpes gestationis) (picture 10A-C).

The relevant clinical features and the associated maternal and fetal prognosis are summarized in the table (table 1). (See 'Atopic eruption of pregnancy' above and 'Polymorphic eruption of pregnancy' above and 'Pemphigoid gestationis' above.)

When to suspect a specific dermatosis of pregnancy – A specific dermatosis of pregnancy can be suspected based on history and clinical features, including time of onset and type and distribution of lesions (table 1). (See 'When to suspect a specific dermatosis of pregnancy' above.)

Diagnosis – The diagnosis is clinical in most cases. A skin biopsy and laboratory tests are generally not necessary for diagnosis but may be performed in cases of diagnostic uncertainty and when there is suspicion for pemphigoid gestationis (algorithm 1 and algorithm 2 and table 1). (See 'Evaluation of the pregnant individual with a pruritic eruption' above.)

Management

-AEP – For most patients with AEP, we suggest topical corticosteroids rather than other therapies (Grade 2C). Low- to mid-potency topical corticosteroids (groups 4 to 6 (table 2)) can be applied once or twice daily until improvement. Patients should be encouraged to maintain adequate skin hydration through the frequent use of emollients. (See 'Treatment' above and "Treatment of atopic dermatitis (eczema)", section on 'Maintaining skin hydration' and "Treatment of atopic dermatitis (eczema)", section on 'Topical corticosteroids'.)

For patients with AEP uncontrolled with topical corticosteroids, we suggest narrowband ultraviolet B (NBUVB) therapy if feasible and acceptable to the patient rather than systemic therapies (Grade 2C). NBUVB is considered safe during pregnancy. It is usually administered two to three times per week for several weeks. (See "Treatment of atopic dermatitis (eczema)", section on 'Phototherapy'.)

-PEP – For patients with PEP, we suggest topical corticosteroids rather than systemic corticosteroids (Grade 2C). Mid- to high-potency topical corticosteroids (groups 2 to 4 (table 2)) are applied once or twice daily until improvement occurs. Oral antihistamines may be helpful for the symptomatic treatment of pruritus. (See 'Treatment' above.)

-Pemphigoid gestationis – For patients with pemphigoid gestationis, we suggest high-potency topical corticosteroids (groups 2 and 3 (table 2)) rather than systemic corticosteroids as initial treatment (Grade 2C). For patients whose symptoms are not controlled by topical therapy, we suggest oral corticosteroids rather than other immunosuppressive or immunomodulating treatments (Grade 2C). Prednisone is given at a dose of 0.5 mg/kg per day until symptom control (decrease of pruritus and blister formation) is achieved and then slowly tapered to end. (See 'Treatment' above.)

Severe, persistent postpartum pemphigoid gestationis may require higher doses of systemic corticosteroids or alternative immunosuppressant/immunomodulator agents. (See 'Postpartum treatment of severe, persistent disease' above.)

Intrahepatic cholestasis of pregnancy Intrahepatic cholestasis of pregnancy is characterized by intense pruritus that involves the palms and soles. It usually starts in late pregnancy and is associated with adverse fetal outcomes. Patients may present with secondary lesions due to scratching. The diagnosis and management of intrahepatic cholestasis of pregnancy is discussed elsewhere. (See "Intrahepatic cholestasis of pregnancy".)

Pustular psoriasis of pregnancy (PPP)

Clinical presentation PPP can occur anytime during pregnancy but typically presents in the late second or third trimester. The eruption begins in the flexural areas with symmetric, erythematous plaques studded at the periphery with sterile pustules (picture 4) and then spreads to involve the trunk and extremities. Systemic symptoms are severe and include malaise, fever, anorexia, nausea, vomiting, and diarrhea. (See 'Clinical manifestations' above.)

Diagnosis – The diagnosis of PPP can be made clinically, based on history and physical examination. However, histologic confirmation is usually required. (See 'Diagnosis' above.)

Management – Because of the associated fetal and maternal risks (miscarriage, fetal growth restriction, stillbirth), prompt dermatologic consult and institution of treatment and fetal monitoring are required for patients with PPP. We suggest systemic corticosteroids rather than other immunosuppressants for the initial treatment of PPP (Grade 2C). High-dose prednisone or prednisolone up to 60 to 80 mg per day are given for a few days and then slowly tapered as symptoms improve. Low-dose cyclosporine (2 to 3 mg/kg per day) is an alternative option. (See 'Management' above.)

Fetal monitoring with nonstress tests or biophysical profiles and ultrasound assessment of fetal growth are indicated. (See "Fetal assessment: Overview of antepartum tests of fetal well-being".)

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Topic 5564 Version 29.0

References

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