<마더리스크라운드> Dermatoses and pregnancy2
Upcoming SlideShare
Loading in...5
×
 

<마더리스크라운드> Dermatoses and pregnancy2

on

  • 837 views

김은형 교수(관동대 제일병원 피부과)

김은형 교수(관동대 제일병원 피부과)

Statistics

Views

Total Views
837
Views on SlideShare
687
Embed Views
150

Actions

Likes
0
Downloads
27
Comments
0

4 Embeds 150

http://www.kaog.org 82
http://blog.mothersafe.or.kr 62
http://kaog.org 4
http://www.hanrss.com 2

Accessibility

Upload Details

Uploaded via as Adobe PDF

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

 <마더리스크라운드> Dermatoses and pregnancy2 <마더리스크라운드> Dermatoses and pregnancy2 Presentation Transcript

  • 피부과 김은형
  •  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
  •  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
  •  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
  •  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
  •  Prurigo of pregnancy Pruritic folliculitis of pregnancy Atopic dermatitis or eczema of pregnancy
  •  Prurigo gestationis Papular dermatitis of pregnancy Early onset prurigo of pregnancy
  •  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
  •  No risk to the fetus or to the mother Recurrences during subsequent pregnancies; infrequent Treatment  symptomatic  topical steroids  oral antihistamines  systemic steroids
  •  Extremely itchy erythematous follicular papules, pustules localized to the torso ≈ steroid induced acne Any trimester (m/c 2nd or 3rd ) May resolve before delivery
  •  No morbidity to the mother or fetus Biopsy; sterile folliculitis DIF; negative Treatment  Topical corticosteroid  Benzoyl peroxide  Emollient  UVB
  •  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%)
  •  Etiology: Unknown  20% exacerbation of atopic dermatitis  80% have no past history Elevated serum IgE in app. 70% of patients Treatment : topical steroid
  •  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
  •  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
  •  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)
  •  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
  •  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
  •  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
  •  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
  •  Erythematous patches with grouped pustules at their margins starting in the intertriginous or flexural areas and extend centrifugally
  •  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
  •  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
  •  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.
  • 30