2. PRAGNANCY :
๏ข Pregnancy is a physiological
condition.
๏ข It is characterised by altered
endocrine,metabolic and
immunologic milius.
๏ข This dramatic alteration result
in multiple cutaneous changes,
both physiologic and
pathologic
3. DERMATOSES IN
PREGNANCY
๏ฑ Physiologic changes
associated with pregnancy
๏ฑ Preexisting dermatoses
affected by pregnancy
๏ฑ Dermatoses specific to
pregnancy
12. WELL-DEFINED DERMATOSES ASSOCIATED
WITH PREGNANCY
๏ข Pemphigoid (Herpes) Gestationis
๏ข Pruritic Urticarial Papules and Plaques of Pregnancy
๏ข Recurrent Cholestasis of Pregnancy (Prurigo
Gravidarum)
๏ข Impetigo Herpetiformis
INCOMPLETELY DEFINED ERUPTIONS
ASSOCIATED WITH PREGNANCY
๏ข Prurigo Gestationis (Besnier) ATOPIC ERRUPTION
๏ข Pruritic Folliculitis of Pregnancy OF PREGNANCY
๏ข Miscellaneous Disorders
13. ๏ฑPEMPHIGOID GESTATIONIS
(HERPES GESTATIONIS)
๏ข Incidence: approximately
1 in 50,000 pregnancies
๏ข Usually begins with
urticarial papules and
plaques around the
umbilicus and extremities.
๏ข Bullous lesions tend to
develop as the disease
progresses, and are often
not present on first
presentation.
๏ข Lesions of PG tend to spare
the face, palms, and soles.
๏ข Mucosal surfaces are
involved in fewer than 20%
of cases.
14. CONTINUE-
๏ข Mean onset at 21 weeks;
postpartum in 20% of cases
๏ข In about 75% of cases, PG
flares around the time of
delivery, regressing
spontaneously after the baby
is born.
๏ข Recurrence in subsequent
pregnancies: 8%
๏ข May be provoked by
subsequent menstrual
periods or OCPs
15. ๏ฑPATHOPHYSIOLOGY
๏ข An autoimmune bullous disorder
๏ข Involves IgG immune response directed at a 180-kDa
hemidesmosome transmembrane glycoprotein
๏ข IgG Abs bind to the lamina lucida and fix compliment
๏ข Activated eosinophils, neutrophils, T- cells (Th2
predominant) involved in blister formation
๏ข Increased frequency of HLA- DR3, DR4 and C4 null
alleles in PG patients
๏ข Black women rarely manifest PG (possibly due to low
incidence of HLA- DR4)
๏ข May be associated with menstruating women, those
taking OCPs
๏ข May be associated with hydatidiform mole and
choriocarcinoma
16. ๏ฑLABORATORY STUDIES
๏ข Histology: papillary dermal edema resulting in
subepidermal bulla with eosinophil-rich infiltrate, ยฑ
keratinocyte necrosis, perivascular infiltrate
๏ข DIF: linear C3 deposition ยฑ IgG at basement
membrane (c.f. PUPPP)
๏ข IIF: epidermal base (roof of blister like BP)
17. ๏ฑTREATMENT
๏ข Oral corticosteroids: 20 to 60 mg/d of
prednisone
๏ข Severe PG have required treatment with
rituximab, cyclophosphamide, MTX
๏ข Intravenous immunoglobulin (IVIG)
๏ข Cyclosporine in refractory cases
18. ๏ฑPRURITIC URTICARIAL PAPULES
AND PLAQUES OF PREGNANCY
๏ข Incidence: 1 in 120
to 1 in 240
pregnancies
๏ข Itchy, erythematous
papules that
coalesce into
plaques
๏ข Classically found on
the abdomen,
sparing the umbilical
area, and are found
primarily in the
abdominal striae
19. CONTINUE
๏ข Onset : Late in third
trimester
๏ข Resolves with delivery
and rarely recurrence
with subsequent
pregnancy
๏ข Fetus and mother are
not effected by this
eruption. Rarely
manifested transient
lesion of PUPPP
20. ๏ฑINTRAHEPATIC CHOLESTASIS OF
PREGNANCY
๏ข Onset after 30th week in
80% of patients
๏ข Steatorrhea often noted
by the patient, followed
by vitamin K deficiency
๏ข Resolves after delivery
๏ข Recurs with subsequent
pregnancies
๏ข Increased fetal
complication
21. CONTINUE-
๏ข No primary skin lesions
๏ข Present with sudden onset
of severe pruritus on palms
and soles which quickly
becomes generalized
๏ข Itching is often so severe
that it leads to chronic
insomnia
๏ข Secondary skin lesions:
erythema and excoriations
๏ข Observable jaundice occurs
10% to 20% of patients
22. ๏ข ICP is a disease of late pregnancy corresponding to
the period of highest placental hormone level
๏ข ICP spontaneously remits at delivery when
hormone concentration normalized
๏ข Twin and triplet pregnancy characterize by greater
rise in hormone concentration
ETIOLOGY
23. LABORATORY STUDIES
๏ข Gold standard:
serum bile acid level >11 ฮผmol/L (N: 6.6-11 ฮผmol/L)
๏ข Recent study: โ urine bile acids have 100% sensitivity
and 83% specificity for ICP.
๏ข 55% to 60% of cases: mildly โ aspartate
aminotransferase and alanine aminotransferase
24. TREATMENT
๏ข Reduction of serum bile acid levels in order to prolong
pregnancy and reduce both fetal risks and maternal
symptoms
๏ข Ursodeoxycholic acid: reduces maternal pruritus and
improves fetal prognosis
๏ Dose: 15 mg/kg/day or, independent of body weight, 1
g/day either as a single dose or divided into two to three
doses until delivery
๏ข Antihistamines
๏ข Close obstetric surveillance and weekly fetal
cardiotocographic (CTG) registration at least from 34 weeksโ
gestation
๏ข Interdisciplinary management by dermatologists,
hepatologists, gynecologists, and pediatricians absolutely
mandatory
25. ๏ฑPRURITIC FOLLICULITIS OF
PREGNANCY
๏ข Prevalence: 1 in every
10,000 pregnancies
๏ข Presents as papules
and pustules
concentrated around
hair follicles
๏ข Often, lesions begin on
the abdomen and
spread to the
extremities.
๏ข May be pruritic
26. CONTINUE
๏ข Onset most often in third trimester
๏ข Resolves after 2/3 weeks of delivery
๏ข Increased incidence of (fetal) low birth weight
๏ข No associated fetal morbidity or mortality
27. ๏ฑPAPULAR DERMATITIES OF
PREGNANCY
๏ข Pruritic generalised
eruption of 3-5 mm
erythematous papule
surmounted by a
small,firm,central crust.
๏ข May erupt anytime
during pregnancy
๏ข Resolves with delivery
๏ข Recurrence in
subsequent pregnancy
28. ๏ฑIMPETIGO HERPETIFORMIS/
PUSTULAR PSORIASIS OF PREGNANCY
๏ข Impetigo herpetiformis is a form of pustular
psoriasis that occurs during pregnancy and may be
life-threatening
๏ข Many of the affected women have had no personal
or family history of psoriasis.
๏ข Recurrences in subsequent pregnancies have been
reported.
๏ข There may be an increased risk of fetal morbidity
and mortality associated with placental insufficiency
with risk of still birth.
๏ข The disease tends to remit promptly after delivery
29. CONTINUE-
๏ข The earliest lesions are
erythematous patches
occurring in the groin, axillae,
and anterior as well as
posterior neck. At their
margins these erythematous
patches are studded with tiny
superficial pustules
๏ข As plaques enlarge, the center
becomes eroded and crusted.
๏ข Mild pruritus, painful lesions
30. LABORATORY STUDIES
Most Common Laboratory dearangemant includes
๏ข Leucocytosis
๏ข Neutriphillia
๏ข Elevated ESR
๏ข Hypoferric anemia
๏ข Hypoalbuminemea
๏ข Calcium, phosphate ,Vit-D level is decreased
31. ๏ฑHISTOPATHOLOGY
๏ Neutrophilc inflammatory
infiltrate, epidermal
acanthosis and
papillomatosis with focal
parakeratosis
๏ Neutrophils collections,
forming intraepidermal
multilocular
microabscesses, called
spongiform pustules of
Kogoj
32. TREATMENT:
๏ข Systemic corticosteroids, 30-60mg of prednisolone per
day
๏ข Cyclosporin may be used in refractory cases
๏ข Even if the pustules are sterile, some authors recommend
adjuvant treatment with cephalosporin
๏ข Replacement of calcium, fluids and electrolytes due to
โ Levels of calcium, phosphate and albumin
33. ๏ฑPRURIGO GESTATIONIS
๏ถ ONSET :
Between 20th and 34th weeks of gestation
๏ถ Resolution :
Post-purtum period
๏ถ Recurrence:
Usually not occur.
๏ถ Site :
Proximal limb and upper trunk
34. ๏ข This eruption may
symply be an expression
of atopic dermatities of
pregnancy
๏ข 2/3rd present with
widespread eczematous
changes (so-called E-type
AEP) often affecting
typical atopic sites such
as face, neck, upper
chest, and the flexural
surfaces of the
extremities.
35. CONTINUE-
๏ข 1/3rd have papular
lesions (P-type AEP).
๏ข Small erythematous
papules disseminated on
trunk and limbs, as well
as typical prurigo
nodules, mostly located
on the shins and arms.
๏ข Extreme dryness of the
skin
36. TREATMENT:
๏ข Symptomatic treatment
๏ Topical corticosteroids
๏ Antihistamines
๏ข Severe cases
๏ Short course of systemic corticosteroids
and antihistamines
๏ Phototherapy (UVB) is a helpful additional
measure and considered safe in pregnancy
37. MISCELLANEOUS DISORDERS
Other eruptions thought to be associated with
pregnancy have been described.
Examples include :
๏ข Spangler's papular dermatitis,
๏ข autoimmune progesterone dermatitis of pregnancy,
and
๏ข linear IgM dermatosis of pregnancy.
These entities have neither been substantiated nor
elucidated. Accordingly, their existence is in doubt.
38. References
๏ถANDREWSโ disease of skin: clinical
dermatology
๏ถFITZ PATRICKS dermatology in general
medicine
๏ถ James WD, Elston DM. 2011. Andrewsโ
Diseases of The Skin: Clinical Dermatology.
(11th edn). Elsevier Inc: London
๏ถ Jain S. 2012. Dermatology: Illustrated Study
Guide and Comprehensive Board Review.
Springer Science: New York
๏ถ http://www.obgmanagement.com
๏ถ A Study on Dermatoses of Pregnancy. Our
Dermatol Online. 2013; 4(1): 56-60
๏ถ A Dermatoses of pregnancy- clues to
diagnosis, fetal risk and therapy. Ann
Dermatol. 2011 Aug; 23(3):265-75.
๏ถ Recent developments in the specific
dermatoses of pregnancy. Clin Exp
Dermatol. 2012 Jan; 37(1):1-4