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Pregnancy, Dermatoses


Basics


Description


There are 5 dermatoses considered specific to pregnancy. All tend to occur later in pregnancy and to resolve postpartum. ‚  
  • Pemphigoid gestationis (PG) " “ Also called "herpes gestationis " 
    • Rare autoimmune (AI) blistering disorder that is intensely pruritic; resembles bullous pemphigoid clinically and histologically
  • Polymorphic eruption of pregnancy (PEP)
    • Pruritic papulo-urticarial inflammatory disorder; also called "pruritic urticarial papules and plaques of pregnancy "  (PUPPP)
  • Impetigo herpetiformis
    • Rare pustular disorder; may be variant of pustular psoriasis; also called "generalized pustular psoriasis of pregnancy " 
  • Papular dermatoses
    • Prurigo, pruritic folliculitis, and atopic eruption of pregnancy (AEP)
  • Intrahepatic cholestasis of pregnancy (ICP)
    • Rare pregnancy-related liver disorder
    • Also called "cholestasis of pregnancy, "  "recurrent/idiopathic jaundice of pregnancy, "  and "pruritus/icterus gravidarum " 

Epidemiology


  • Pemphigoid gestationis
    • Incidence: 1 in 50,000 pregnancies in North America (some reports as high as 1 in 1,700)
  • Polymorphic eruption of pregnancy
    • Incidence: 1:160 to 1:240 pregnancies
    • Most common dermatosis of pregnancy
  • Impetigo herpetiformis
    • Incidence: Unknown; ¢ ˆ ¼200 reported cases
  • Papular dermatoses
    • Incidence: Prurigo of pregnancy: 1 in 300 pregnancies; pruritic folliculitis of pregnancy: 1 in 3,000 pregnancies
    • Prevalence: Among pruritic dermatoses of pregnancy, AEP has a prevalence of 50%
  • Intrahepatic cholestasis of pregnancy
    • Prevalence: Higher prevalence in South America (28% among Araucanian Indian in Chile; 9% in Bolivia), Scandinavia (2.4%)
      • Lower prevalence in North America, Australia, and Europe (0.1 " “1.5%)

Risk Factors


  • Pemphigoid gestationis
    • Genetic predisposition: More common in women with HLA-DR3 or HLA-DR4 positivity
    • Hormonal fluctuation implicated in flares
  • Polymorphic eruption of pregnancy
    • Primigravida status (80% cases)
    • Controversial: Male fetus, atopy, multiple-gestation pregnancy (twins or triplets)
  • Impetigo herpetiformis
    • No personal/family history of psoriasis
  • Papular dermatoses
    • Prurigo of pregnancy: Atopy (controversial)
    • Pruritic folliculitis of pregnancy: Unknown
    • AEP: Personal or family history of atopy
  • Intrahepatic cholestasis of pregnancy
    • Genetic predisposition: (+) Family history in ¢ ˆ ¼50%
    • Multiple-gestation pregnancy

Etiology


  • Pemphigoid gestationis
    • AI disorder in genetically predisposed pts, possibly triggered by hormonal factors.
    • Autoantibody targets component of basement membrane; immune complex deposition results in complement-mediated destruction of basement membrane and subepidermal blister formation.
  • Polymorphic eruption of pregnancy
    • Unknown. Theories include:
      • Maternal immunoreactivity: Abdominal distention causes damage to collagen within striae, triggering an inflammatory response.
      • Fetal cell microchimerism: Migration and persistence of fetal cells in maternal skin
      • Possible hormonal role, link with atopy
  • Impetigo herpetiformis
    • Unknown; debate as to whether it is a form of pustular psoriasis or a separate entity.
    • Inconsistently implicated: High levels of progesterone, hypocalcemia
  • Papular dermatoses
    • Prurigo of pregnancy: Unknown
    • Role of atopic diathesis implicated. Some consider a subset of PEP or AEP.
      • Pruritic folliculitis of pregnancy
    • Maternal androgens inconsistently implicated
      • Atopic eruption of pregnancy
    • Genetic predisposition (nearly 100% with personal or first-degree relative with atopy)
  • Intrahepatic cholestasis of pregnancy
    • Unclear, thought to be multifactorial
    • Genetic predisposition, hormonal factors, environmental and/or dietary factors

Diagnosis


History


All pregnancy dermatoses are pruritic, with the exception of impetigo herpetiformis. ‚  
  • Questions to ask: Gestational age at onset, parity, personal/family history of dermatoses in pregnancy, AI diseases, atopy
  • Pemphigoid gestationis " “ Typically second or third trimester (34% of patients each trimester, respectively); can also occur during first trimester (18%) or postpartum (14%).
    • Often associated with AI diseases. Reported with trophoblastic tumors, hydatiform moles, choriocarcinoma. No association with parity, multiple-gestation pregnancy, or atopy.
  • Polymorphic eruption of pregnancy " “ typically late third trimester; can occur postpartum (15%) or late second trimester (rare).
    • Often with first pregnancy, multiple-gestation pregnancies, personal/family history atopy (no association with AI diseases)
  • Impetigo herpetiformis " “ typically second half of pregnancy (most commonly third trimester), but can occur in first trimester or postpartum.
    • Typically NON-pruritic
    • Often with constitutional symptoms (fever/chills, nausea/vomiting, malaise)
    • No known parity, multiple-gestation, autoimmunity or atopy associations
  • Papular dermatoses
    • Prurigo of pregnancy " “ typically at 25 " “30 weeks, but reported in all 3 trimesters
      • Possible associated atopy (no parity, multiple-gestation, AI disease association)
    • Pruritic folliculitis of pregnancy
      • Late second or third trimester; no associations
    • AEP " “ typically before third trimester (75%)
      • 80% with atopic skin changes for first time during pregnancy; 20% with exacerbation of preexisting atopic dermatitis.
      • Strong association with personal/family history of atopy (no association with parity, multiple-gestation, other AI diseases).
  • Intrahepatic cholestasis of pregnancy
    • Third trimester; associated with multiple-gestation pregnancy (no association with parity, autoimmunity, or atopy)
    • Pruritus starts on palms/soles then becomes generalized, persistent, pruritus " “ worse at night. +/ " “ mild GI symptoms.

Physical Exam


  • Pemphigoid gestationis
    • Abrupt onset of intensely pruritic urticarial papules/plaques (50% begin on abdomen, adjacent or within umbilicus); may become targetoid/polycyclic and spread centrifugally.
    • Rapidly progresses to generalized tense fluid-filled bullae (>5 mm) in days to weeks.
    • Face, mucous membranes, striae spared
  • Polymorphic eruption of pregnancy
    • Begins with intensely pruritic urticarial papules within/adjacent to abdominal striae, which coalescence into urticarial plaques.
    • 50% progress to develop polymorphous features, including pseudovesiculation over striae or urticarial lesions, targetoid lesions, annular/polycyclic wheals, or small bullae only rarely (due to coalescing vesicles).
    • Note: Face, palms and soles, periumbilical skin classically (but not always) spared
  • Impetigo herpetiformis
    • Erythematous plaques with small, clustered pustules ( "herpetiform "  distribution) studding margins. As plaques expand outward, pustules remain on leading edge, leaving central eroded/crusted central plaques.
    • Face, hands, feet spared (rarely involves mucous membranes, esophagus, nail beds)
  • Papular dermatoses
    • Prurigo of pregnancy
      • Erythematous papules and nodules on extensor surfaces of limbs and/or trunk. Can become polymorphic with crusted, excoriated, eczematous lesions; occasionally follicular papules (not blisters).
    • Pruritic folliculitis of pregnancy
      • Small (3 " “5 mm) erythematous papules on upper trunk. Becomes generalized with follicular, erythematous papules/pustules.
    • AEP
      • Prurigo and eczema-like lesions
      • May have features of atopic dermatitis (xerosis, ichthyosis, hyperlinear palms, keratosis pilaris).
  • Intrahepatic cholestasis of pregnancy
    • No primary lesions; secondary lesions (e.g., excoriations, lichenification) from scratching
    • Jaundice in 10% of cases

Tests


  • Specific tests to confirm diagnosis of PG, impetigo herpetiformis, and ICP
  • Diagnosis of other types of pregnancy dermatoses based only on clinical criteria
  • 2 skin biopsies " “ lesional and peri-lesional " “ used to confirm diagnosis of PG and impetigo herpetiformis.
  • Serum bile acids and transaminases
    • Total bile acids >11 mmol/L in absence of primary skin lesions is diagnostic for ICP.
    • Check transaminases in any pregnant female with pruritus

Differential Diagnosis


  • Above pregnancy-specific dermatoses
  • Other bullous AI diseases: Bullous lupus, linear IgA dermatosis, bullous pemphigoid
  • Contact dermatitis (bullous or eczematous)
  • Infestations such as scabies
  • Dermatoses unrelated to pregnancy
  • Other skin or internal causes of pruritus

Treatment


Pemphigoid Gestationis


First Line
  • Prednisone (1,2)[C] " “ response in few days; 20 " “40 mg/day titrated to clinical response
    • Once blister formation suppressed, taper (5 " “10 mg/day) or discontinue (2)[C].
    • Some increase dose prior to delivery to prevent anticipated postpartum flare (2)[C].
    • No evidence that any treatment can prevent fetal risks associated with PG, which seem milder than previously thought (2)[C].
    • Prednisone relatively safe, but avoid dexamethasone/betamethasone (2)[C].
    • Most advocate against early delivery because fetal risks appear mild (2)[C].
    • If neonate affected, local wound care (1,2)[C].
    • Breastfeeding may decrease duration (1)[C].

Polymorphic Eruption of Pregnancy


First Line
  • Symptomatic treatment (1,2,3)[C] and reassurance that self-limited
    • General measures: Emollients on wet skin, antipruritic topical agents (menthol-containing)
    • Mid-potency topical steroid ointment, first-generation oral antihistamines

Second Line
  • Oral prednisone; phototherapy (2)[C]

Impetigo Herpetiformis


First Line
  • Oral prednisone: Initiate at 15 " “40 mg/day; can increase to 60 " “80 mg/day (1,3)[C]

Second-Line
  • Cyclosporine (1)[C]

Other
  • Monitor and treat hypocalcemia to prevent tetany or seizures (1)[C]. After delivery, consider agents used in psoriasis as anticipate flare with steroid tapering (1)[C].

Papular Dermatoses


Prurigo of Pregnancy
First Line
  • Symptomatic relief (1,2)[C]
    • General measures (emollients on wet skin)
    • Moderately potent topical steroids (can be intralesional or under occlusion)
    • Oral antihistamines that are safe in gestation

Second Line
  • Phototherapy (UVB) (2)[C]
    • Rarely a short course of oral prednisone may be necessary if recalcitrant pruritus

Pruritic Folliculitis of Pregnancy


First Line
  • Benzoyl peroxide (pregnancy category C), mild-to-moderate topical steroids, topical antipruritic medications (e.g., menthol-containing)

Atopic Eruption of Pregnancy


First Line
  • Topical antipruritic agents (menthol-containing), mild-to-moderate topical steroids

Second Line
  • Oral antihistamines, prednisone, or phototherapy for more severe cases

Intrahepatic Cholestasis of Pregnancy


  • Goal: Decrease bile acid levels in order to sustain pregnancy and diminish prevalence of fetal risks and maternal symptoms

First Line
  • Ursodeoxycholic acid (1,2,3)[A]
    • Only treatment to decrease maternal pruritus and improve fetal prognosis; off-label despite unquestionable positive effect on fetal prognosis
    • 15 mg/kg/day (or 1 g/day independent of body weight) (1)[C]

Second Line
  • Other antipruritic drugs (cholestyramine, dexamethasone, antihistamines, anion exchange resins, S-adenosylmethionine)

Other
  • Monitor bilirubin and transaminases. Possible induction of labor at 36 weeks per obstetrician (1,2)[C]

Issues for Referral


  • To dermatologist for definitive diagnosis
  • To obstetrician or obstetric medicine internist

Ongoing Care


Prognosis


  • Pemphigoid gestationis
    • Course: Variable course; alternating exacerbations with remissions during pregnancy. 50 " “75% flare at delivery. Self-limited; spontaneously remits weeks to months after delivery without therapy. Recurrences postpartum associated with menses (up to 18 months) or oral contraceptives (OCPs) (20 " “50%) common. Recurs during subsequent pregnancies with earlier onset and increased severity (5 " “8% skip pregnancies).
    • Maternal risk: Increased risk of Graves ' (10%)
    • Fetal risk: Increased risk of premature delivery and small-for-gestational age; borderline increase in spontaneous abortions. Secondary to mild placental insufficiency; debate regarding cause (disease vs. corticosteroids). Risk not reduced with treatment.
    • Neonate risk: 10% with cutaneous symptoms; typically mild, resolves in days to weeks. Increased risk for skin infections. Risk for adrenal insufficiency if mother with high/long courses of systemic steroids.
  • Polymorphic eruption of pregnancy
    • Course: Rapid, spontaneous resolution post-partum, often within 4 " “6 weeks. Rarely recurs.
    • Risk: No maternal or fetal risk. No cutaneous manifestations in newborn.
  • Impetigo herpetiformis
    • Course: Typically resolves postpartum. May recur in subsequent pregnancies.
    • Maternal risk: None; good prognosis even if severe.
    • Fetal risk: Extent of fetal risk is somewhat controversial. Risks include stillbirth, neonatal death, fetal abnormalities; mainly due to placental insufficiency. Risks not reduced with successful control of maternal disease with systemic steroids.
    • Neonate risk: No cutaneous manifestations
  • Papular dermatoses
    • All three typically resolve spontaneously at or shortly after delivery and may recur with subsequent pregnancies.
    • No maternal, fetal, or neonatal risks
  • Intrahepatic cholestasis of pregnancy
    • Course: Resolve within 1 " “2 days to up to 1 " “2 weeks postpartum. Possible recurrence in subsequent pregnancies or with OCP use.
    • Maternal risk: Good prognosis; increased risk of cholelithiasis.
    • Fetal risk: High prevalence of impaired fetal prognosis " “ premature delivery with increased rate of cesarean section and meconium staining, intrauterine fetal distress, stillbirth. Disease severity correlates with fetal prognosis. No risk for fetal malformation.
    • Neonate risk: High-risk antepartal fetal hemorrhage with concomitant extrahepatic cholestasis, vitamin K deficiency.

References


1Roth ‚  M. Pregnancy dermatoses: Diagnosis, management, and controversies. Am J Clin Dermatol.  2011;12(1):25 " “41. ‚  [View Abstract]2Kroumpouzos ‚  G. Specific dermatoses of pregnancy: Advances and controversies. Expert Rev Dermatol.  2010;5(6):633 " “648.3Tunzi ‚  M, Gray ‚  G. Common skin conditions during pregnancy. Am Fam Physician.  2007;75(2):211 " “218. ‚  [View Abstract]

Additional Reading


1Chin ‚  CC, Wang ‚  SH, Kirtsching ‚  G. Systemic review of the safety of topical corticosteroids in pregnancy. J Am Acad Dermatol.  2010;62(4):694 " “705.

Codes


ICD9


  • 054.10 Genital herpes, unspecified
  • 646.80 Other specified complications of pregnancy, unspecified as to episode of care or not applicable
  • 692.9 Contact dermatitis and other eczema, unspecified cause
  • 696.1 Other psoriasis
  • 691.8 Other atopic dermatitis and related conditions
  • 704.8 Other specified diseases of hair and hair follicles
  • 646.70 Liver and biliary tract disorders in pregnancy, unspecified as to episode of care or not applicable
  • 576.8 Other specified disorders of biliary tract

ICD10


  • L40.1 Generalized pustular psoriasis
  • O26.40 Herpes gestationis, unspecified trimester
  • O26.86 Pruritic urticarial papules and plaques of pregnancy (PUPPP)
  • L28.2 Other prurigo
  • L73.9 Follicular disorder, unspecified
  • O26.619 Liver and biliary tract disord in pregnancy, unsp trimester
  • K83.1 Obstruction of bile duct

SNOMED


  • 239101008 pregnancy eruption (disorder)
  • 86081009 Herpes gestationis (disorder)
  • 88697005 papular dermatitis of pregnancy (disorder)
  • 200973000 pustular psoriasis (disorder)
  • 239103006 prurigo of pregnancy (disorder)
  • 239104000 pruritic folliculitis of pregnancy (disorder)
  • 235888006 cholestasis of pregnancy (disorder)

Clinical Pearls


  • Pruritus is the leading symptom in most dermatoses of pregnancy and should be investigated and treated.
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