This document discusses several types of skin conditions that can occur during pregnancy including Pemphigoid Gestationis, Pruritic Urticarial Papules and Plaques of Pregnancy (PUPPP), Polymorphic Eruption of Pregnancy (PEP), and Prurigo of Pregnancy. It provides details on the clinical presentation, pathogenesis, diagnosis, and treatment options for each condition. The document emphasizes that most of these skin conditions do not pose risks to the fetus or mother, but may recur in subsequent pregnancies. Topical corticosteroids and oral antihistamines are usually first-line treatments.

1. 피부과 김은형

4.  Predominantly a disease of women in their 1st
pregnancy in the 3rd trimester
 Pruritic urticarial papules ; microvesiculation, target
like, annular, polycyclic, no bullae
 Begin on the abdomen (in the striae in 2/3 of the cases)
 Usually sparing the periumbilical area, palms, soles, and
face
 Recurrence in subsequent pregnancies, with menses or
with the use of oral contraceptives; uncommon

5.  10 times more common in women with
twins or triplets
 Other : primiparous, male fetus, rapid or
excessive weight gain
 Prognosis
 unassociated with fetal or maternal morbidity and
mortality

6.  Unknown
 Sex hormones
 Campbell et al; Progesterone has been shown to aggravate the
inflammatory process at the tissue level.
 Im et al; increased progesterone receptor immunoreactivity in skin
lesions of PUPPP
 Damage to connective tissue within the striae distensae
 rapid abdominal wall distension → damage to connective tissue →
conversion of nonantigenic molecules to antigenic ones →
inflammatory process
 Fetal cell migration to the maternal skin
 Nelson et al ; Increased abdominal stretching → increased vascular
permeability → migration of chimeric cells into the maternal skin

7.  Histopathology
 Nonspecific perivascular lymphohistiocytic infiltrate
with some edema and eosinophils in the dermis
 DIF; negative
 Treatment
 Conservative therapies
 Topical emollients and topical corticosteroids
 Oral antihistamines
 Oral corticosteroids

8.  Prurigo of pregnancy
 Pruritic folliculitis of pregnancy
 Atopic dermatitis or eczema of pregnancy

9.  Prurigo gestationis
 Papular dermatitis of pregnancy
 Early onset prurigo of pregnancy

10.  Clinical feautres
 intensely pruritic rashes in the 2nd or 3rd trimester
 small, mostly excoriated, nonvesicular erythematous
papules
 grouped over the abdomen and the distal extensor
aspects of both upper and lower extremities
 propensity to resolve leaving residual PIH
 disappearance soon after delivery
 Histopathologic examination; nonspecific
 DIF; negative

11.  No risk to the fetus or to the mother
 Recurrences during subsequent pregnancies;
infrequent
 Treatment
 symptomatic
 topical steroids
 oral antihistamines
 systemic steroids

12.  Extremely itchy
erythematous follicular
papules, pustules localized
to the torso
≈ steroid induced acne
 Any trimester
(m/c 2nd or 3rd )
 May resolve before delivery

13.  No morbidity to the mother or fetus
 Biopsy; sterile folliculitis
 DIF; negative
 Treatment
 Topical corticosteroid
 Benzoyl peroxide
 Emollient
 UVB

14.  Eczema of pregnancy
 Eczematous lesion typically appear during the 1st and 2nd
trimester
 All parts of the body including the face, palms and soles
 Eczematous(50%), papular or prurigo-like features (30%)

15.  Etiology: Unknown
 20% exacerbation of atopic dermatitis
 80% have no past history
 Elevated serum IgE in app. 70% of patients
 Treatment : topical steroid

16.  Clinical features
 Markedly pruritic and/or urticarial plaques, papules or
vesicles beginning in the periumbilical region before
spreading across the trunk and body, forming bullae
 during the 2nd or 3rd trimester
 sparing of the face, mucous membranes, palms, and
soles

18.  Pathology
 subepidermal vesicles, spongiotic epidermis
 some perivascular lymphocyte and histiocyte infiltrates
with a preponderance of eosinophils
 DIF; C3 with or without IgG in a linear band along the
BMZ

19.  Immunologic response against class II antigens of paternal
haplotype at the placenta, which then cross-reacts with the
skin
 Associations with HLA DR3 (61%-80%), DR4 (52%), or
both (43%-50%)
 Immunology
 HG factor; IgG1 subclass
 Epitope mapping; common antigenic site within the
noncollagenous domain (NC16A) of the transmembrane
180-kD HG Ag (BP Ag 2)

20.  Clinical course
 Remit before delivery or regresses spontaneously over
weeks or months after delivery
 Flares
 At the time of delivery
 During menstruation
 Oral contraceptives
 Occurrences in subsequent pregnancies
 earlier
 more severe clinical picture
 prolonged postpartum duration

21.  No maternal risk
 but an increased risk of Graves’ disease, other
autoimmune diseases
 Mild increase in fetal morbidity or mortality
 small-for-gestational-age infants
- associated with presence of blisters and disease onset
in 2nd trimester but not antibody titer or systemic
corticosteroid treatment
 prematurity

22.  Treatment
 Early urticarial lesions
 topical corticosteroids in addition to oral antihistamines
 First line; (bullae)
 systemic corticosteroids (0.5 mg/kg or 30mg/d of
prednisolone daily)
 Chronic HG
 plasmapheresis
 박 등 (2000); Cyclosporine으로 호전을 보인 임신성 포진 1예
 IVIG combined with cyclosporine
 Refractory cases; adjuvant medications, especially in the
postpartum period (methotrexate, azothioprine,
gold,pyridoxine, cyclophosphamide)
 Alternative ; dapsone, sulfapyridine, pyridoxine, cyclosporine

23.  Classification
 a rare form of generalized pustular psoriasis in
pregnancy
 an entity distinct from psoriasis
 Onset; most commonly in the 3rd trimester
 Systemic symptoms; malaise, fever, delirium, diarrhea,
vomiting, tetany
 Usually no personal or family history of psoriasis
 Often associated with hypocalcemia or low serum levels of
vitamin D

24.  Erythematous patches with grouped pustules at their
margins starting in the intertriginous or flexural areas and
extend centrifugally

25.  Pustular psoriasis occurring during pregnancy tends to
worsen as the pregnancy progresses and resolves rapidly
at delivery or termination.
 Obstetric complications
 placental insufficiency; increased risk of stillbirths, fetal
abnormalities, neonatal death
 fluid and electrolyte imbalance; increased morbidity
and mortality

26.  Treatment
 systemic corticosteroids; usually effective at a relatively low
dose of 15 to 30 mg/day of prednisone
 oral cyclosporin (category C)
 parenteral calcium with vitamin D
 postpartum administration of oral retinoids
 Recurrence in successive pregnancies
 earlier onset and increased morbidity
 increase in morbidity with each successive pregnancy

29.  The safety of topical glucocorticoids (C) varies with the
strength of the agent and the specific vehicle employed.
 high potency topical steroids used on large body surface areas
- increased potential for systemic absorption
 Not more than 45g/week of potent or 100g /week of weak
or moderately potent topical corticosteroid should be
applied (without occlusion) if systemic absorption is to be
avoided.

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