dermatology changes in pregnancy

2. Introduction
•Pregnancy is a time of significant and complex physiological changes
•Some of these changes are due to denovo production of hormones by feto-
placental unit
&
•Increased activity of maternal pituitary, thyroid and adrenals

3. Endocrine changes
• Developing trophoblast begins to secrete chorionic gonadotrophin
Placenta produces lactogen,(hPL) with somatotrophic and lactogenic properties
• Thyroid enlarges and takes up more iodine
• Pituitary enlarges and inc., output of ACTH, prolactin and gonadotrophins
•Cortisol level rises, due to its decreased clearance and and increased Cortisol
binding globulin

4. SKIN CHANGES IN PREGNANCY
•Physiological changes of pregnancy
•Skin diseases modified by pregnancy
•Specific dermatoses of pregnancy

5. PHYSIOLOGICAL CHANGES
Pigmentary changes
Most common physiologic changes
Due toMSH,Estrogen and Progesterone
•Diffuse hyperpigmentation
•Selective hyperpigmentation (genitalia, axillae, recent scars)
•Secondary areolae
•Linea nigra
• Melasma (chloasma, mask of pregnancy)-m/c in 2nd half of pregnancy
•Darkening of melanocytic nevi
•Freckles or lentigenes may darken

6. Structural Changes
• Striae distensae (striae gravidarum)
• Molluscum fibrosum gravidarum (acrochordons)-neck,axillae
Vascular
• Spider angiomas (spider nevi, nevi aranei)-due to ed estrogen(2nd trimester)
• Palmar erythema-pink mottling of whole palm or confined to thenar and
•hypothenar eminences,digits are spared
• Non pitting edema (hands, ankles, feet, face)
•Varicosities-saphenous,vulvar,hemorrhoidal veins-m/c in 3rd month

7. • Vasomotor instability-facial flushing,hot and cold sensation,cutis marmorata
•Dermographism/pruritus
• Purpura
• Gingival hyperemia or hyperplasia
• Pyogenic granuloma (granuloma gravidarum, pregnancy epulis)
• Hemangiomas, hemangioendotheliomas, glomangiomas
• Unilateral nevoid (unilateral dermatomal superficial) telangiectasia.
•Carpal tunnel syndrome
Mucosa
Gingivitis,Jacquemier–Chadwick sign,Goodell’s sign

8. Glandular
•Decreased apocrine function-improvement of hydradenitis suppurativa and Fox
Fordyce disease
• Increased eccrine function (except palms) (miliaria, dyshidrotic eczema,
hyperhidrosis)
•Increased sebaceous function (growth in Montgomery’s tubercles)
•Elevated thyroid activity with resultant relative iodine deficiency
Hair
• Hirsutism
•Thickening of scalp hair-ed no.of anagen hairs

9. •Postpartum telogen effluvium
•Postpartum androgenetic alopecia in fronto parietal region
Nails
•Accelerated growth
• ed Brittleness
• Subungual hyperkeratosis
•Distal onycholysis
•Transverse grooving
• Longitudinal melanonychia
Cracked and sore nipples

10. SPECIFIC DERMATOSES OF PREGNANCY
Pemphigoid gestationalis
Polymorphic eruption of pregnancy
Intrahepatic cholestatis of pregnancy
Atopic eruption of pregnancy

11. Classification of specific dermatoses
HOLMES AND BLACK CLASSIFICATION
1. Pemphigoid gestationis
2. Polymorhic eruption of pregnancy
3. Prurigo of pregnancy
4. Pruritic folliculitis of pregnancy
AMBROS RUDOLPH CLASSIFICATION
1. Pemphigoid gestationis
2. Polymorphic eruption of pregnancy
3. Atopic eruption of pregnancy
4. Intrahepatic cholestasis of pregnancy

12. PEMPHIGOID GESTATIONIS
•Herpes gestationis(MILTON)
•Gestational pemphigoid
•Acute onset ,intensely pruritic,vesiculo bullous disorder that presents mainly in
late pregnancy(2nd /3rd trimester) or the immediate postpartum period
•Associated with trophoblastic tumours (choriocarcinoma, hydatidi-form mole).
• Rare autoimmune disease- incidence 1 :50 00
• Increased risk of developing other organ‐ specific autoimmune diseases, Graves
(mostcommon),hypothyroidism,vitiligo,alopecia areata
•HLA haplotypes DR3 and DR4 .
I

13. ETIOPATHOGENESIS
• Breakdown of the protective immunity of the fetoplacental unit from maternal
allogeneic recognition.
•Most patients develop autoantibodies against two hemidesmosomal proteins,
BP180, and less frequently, BP230.236
•BP180 - basement membranes of the skin and amniotic epithelium of placental
tissues.
• In normal pregnancy, MHC class II antigens are not expressed on the
trophoblast (“silencing”)
• PG- aberrant expression of MHC class II molecules in amniochorionic stromal
cells &trophoblast, results in exposure of BP180 (collagen XVII) to the maternal
immune system
.

14. •Aberrant self-antigen presentation  triggers the production of antibodies 
Ab cross-react with collagen XVII in the skin  form immune complexes 
activate complement and recruit inflammatory cells tissue damage and
blister formation, or recruit other inflammatory cells.
• predominant antibody subclass identified is IgG1.
• Progesterone, depresses antibody production, while estrogen enhances
antibody production.
• PG usually improves just before delivery(last 6wks), with an immediate
postpartum flare.
• Low-progesterone levels in the premenstrual phase and the estrogen content
of oral contraceptive pills can explain the flares of PG in these two scenarios.

15. CLINICAL FEATURES
•Intense itching is a prominent feature.
• The patient initially presents with pruritic urticarial papules, annular plaques,
and targetoid lesions, followed by vesicles, and finally, large tense bullae.
• Periumbilical area is the most common initial site of eruption; later lesions
spread to the rest of the abdomen, thighs, palms, and soles .
• Face and mucous membranes are generally spared.
•Almost half of cases develop in the first pregnancy.
• Duration of active disease ranges from 2 weeks postpartum to 12 years PP
Neonatal pemphigoid- resolves spontaneously

17. PROGNOSIS
•The majority of patients are disease-free after about 6 months postpartum.
In less than 5% of patients, the disease persists and converts to BP
• Prolonged diseasesae- older maternal age, multiparity, mucosal involvement.
• PG -Recurs, with an even earlier onset, in subsequent pregnancies.
• 8% of patients have “skip” pregnancy following a previously affected pregnancy.
• Recurrences can occur during the premenstrual period or with OCP in 25%
•Abortion (20%), premature delivery and stillbirths
• small forgestationalage babies,prematurity- low-grade placental insufficiency
•The fetal prognosis is worse with early onset of the disease and blistering

18. DIFFERENTIAL DIAGNOSIS
PG - absence of involvement of striae gravidarum, and the presence of skin
lesions in the periumbilical area
Most Likely
• urticarial pemphigoid gestationis
• Pruritic urticarial papules and plaques of pregnancy
• Contact dermatitis
• Drug eruption
Consider
• urticaria
• Erythema multiforme
• Dermatitis herpetiformis
Rule Out
• Pemphigus vulgaris,Varicella

19. INVESTIGATIONS
Histopathology
•Early urticarial lesions are characterized by eosinophilic spongiosis, spongiotic
vesicles, marked papillary dermal edema and mixed perivascular inflammatory
infiltrate of lymphocytes, histiocytesand numerous eosinophils.
• The bullous lesions show necrosis of the basal cell layer, subepidermal bulla
with numerous eosinophils in the blister cavity and edema along with mixed
inflammatory infiltrate in the dermis.
• The split is through the lamina lucida.
• Severe edema may cause a teardrop appearance of the dermal papillae.
•The placenta may show evidence of villitis.

20. Immunofluorescence
•Gold standard -DIF of perilesional skin-bright linear deposition of C3 along the
BMZ in 100%. IgG deposition in 25%–30%
• On salt-split skin- deposits bind to the epidermal side of the split.
•Conventional IIF - C3 binding to the BMZ in 90% ,IgG is positive in less than 25%.
• IgG ab against BMZ structures detected on IIF were earlier known as HG factor
•ELISA is more sensitive than IIF to detect circulating antibodies
• IgG antibodies are most commonly targeted against collagen XVII (BP180); in
particular against the NC16A domain.
• Immunoblotting -antibodies to other antigens (i.e., BP230).
• Immunoelectron microscopic studies confirm IgG deposition along BMZ,
chiefly within lamina lucida and localized to proximal part of anchoring
167

21. TREATMENT
• Main goal of treatment is to reduce the intense pruritus and to prevent new
blister formation.
• In mild preblistering forms or premenstrual flares- potent topical
corticosteroids +emollients ±oral antihistamines.
• 1st trimester,-older sedating antihistamines-chlorpheniramine
• 2&3rd trimisters- nonsedating antihistamines -loratadine and cetirizine
• Newer nonsedating antihistamines such as desloratadine, levocabastine, or
levocetirizine are not recommended in pregnancy.
• When blisters have arisen, a cautious approach with systemic corticosteroids
is recommended. Moderate disease responds to 20–30 mg/day of
prednisolone; severe disease may need 0.5–1 mg/kg/day

22. • Systemic corticosteroids are relatively safe during pregnancy (category C).
• A placental enzyme inactivates 88% of prednisolone that crosses the placenta.
• Prednisolone is excreted in breast milk in small amounts, but doses up to 40 mg
are considered safe.
• Immunoapheresis, a new variant of plasmapheresis - circulating antibodies are
removed from the serum of the patient, is a safe complementary therapy for
severe cases during pregnancy.
• Dapsone
• immunosuppressives- cyclosporine, cyclophosphamide ;
• IVIG and rituximab have also been used successfully, mainly postpartum.

23. POLYMORPHIC ERUPTION OF PREGNANCY
•Pruritic urticarial papules and plaques of pregnancy (PUPPP) is the most
common specific dermatoses of pregnancy.
.Benign intensely pruritic dermatoses that occurs almost exclusively in
primigravidas during late pregnancy(3rd trimester).
• Recurrences in subsequent pregnancies is unusual
Synonyms
• PUPP
• Bourne’s toxemic rash of pregnancy
• Toxic erythema of pregnancy
• Nurse’s late onset prurigo of pregnancy

24. ETIOLOGY AND PATHOGENESIS
•Increased abd cutaneous distension altered collagen/elastic tissue
conversion of nonantigenic molecules to antigenic ones skin eruption
•More common in women with twins or triplets
•Increased risk in pegnant women with male fetuses and maternal fetal weight
gain
•IHC –T helper cells
•edCD1a+,CD54+,dendritic cells,CD1aepidermal LHCdelayed HS
•Deposition of fetal DNA in maternal skin containing damaged collagen

25. CLINICAL FEATURES
•PEP typically starts on the abdomen, often within the striae gravidarum
• severely pruritic urticarial papules that coalesce into plaques, spreading
to the buttocks and proximal thighs ,breast and arms
Later on, the morphology become more polymorphic ,vesicles(neverbullae) ,
purpura,targetoid,eczematous lesions that become confluent
• Pruritus generally parallels with the eruption and is localized to the involved
skin
• In contrast to pemphig-oid gestationis, umbilical sparing is characteristic.
•Face,palms ,soles and mucosal surfaces are unaffected.
•Lesions resolve near term or in the early postpartum period
•Maternal and fetal prognosis is good

27. DIAGNOSIS
Histopathology-nonspecific -parakeratosis, spongiosis, and occasional exocytosis
of eosinophils (eosinophilic spongiosis).
dermis - edematous and a perivascular infiltrate of lymphocytes admixed with
variable num-bers of eosinophils and neutrophils.
DIF -no specific immunoreactants
indirect immunoflu-orescence studies - negative.
PROGNOSIS
•It usually resolves within 10 days following childbirth.
•It does not cause risk to mother and fetus

28. • DIFFERENTIAL DIAGNOSIS
 Most Likely
Pemphigoid gestationis
Atopic eruption of pregnancy
Contact dermatitis
 Consider
Drug eruption
Viral exanthema
Pityriasis rosea
Exfoliative or eczematous dermatitis
 Always Rule Out
scabies

29. TREATMENT
First line
• Topical emollients: aqueous cream + 1–2% menthol
• Topical corticosteroids
• Oral antihistamines: loratadine and cetirizine (safe in 2nd &3rd trimester)
Second line
• Prednisolone (40-60mg/day)
Consider early induction of labour if patient is close to term

30. INTRAHEPATICCHOLESTASIS OF PREGNANCY
Synonyms and inclusions
• Obstetric cholestasis
• Cholestatic jaundice of pregnancy
• idiopathic Jaundice of pregnancy
• Pruritus/prurigo gravidarum
• Icterus gravidarum
•DEFINITION:generalized pruritis with or without jaundice& without active
hepatitis or hepatotoxic medicines; absence of primary lesions; presence of
biochemical abnormalities; spontaneous resolution of symptoms following
delivery;&recurrence in subsequent pregnancies

31. ETIOLOGY
•Multifactorial -hormonal, genetic, environmental, and alimentary factors is
thought to induce a biochemical cholestasis in susceptible individuals.
Hormonal : (1) ICP is a disease of late preg-nancy (corresponding to the period
of highest placen-tal hormone levels);
(2) ICP spontaneously remits at delivery when hormone conc normalize;
(3) twin and triplet pregnancies
(4) ICP recurs during subsequent pregnancies in 45%–70% of patients
•Family h/o of ICP is common
•Associated with HLA-A31,HLA-B8

32. •Geographic variation and familial clustering indi-cate a genetic predisposition.
•ICP appears to be a polygenetic condition. ABCB4(multidrug resistance gene3),
ABCB11and ATP8B1
• Environmental and alimentary factors.-A recent decline in preva-lence rates in
Chile, higher incidence in winter months, and relative reductions of selenium
levels in some ICP patients
•Hepatitis C seropositivity increase the risk of ICP

33. CLINICAL FEATURES
•. Classically present during third trimester
•Sudden onset of severe pruritus
• Localised to palms and soles, becomes generalised
• Extensor surfaces, back and abdomen are mainly involved
•More severe during nights
•No primary lesions
•Secondary excoriations are seen
•Constitutional symptoms may be present
•Steatorrhea,malabsorption vit K deficiencyrisk of hemorrhage

34. PROGNOSIS
•A hallmark of ICP is that symptoms and associated biochemical abnormality
typically resolve within 2–4 weeks of delivery.
• MILD ICP-TBA-40 μmol/ml-IOL at 36weeks
• SEVERE ICP-TBA>40 μmol/ml-IOL at 38 weeks
• Fetal risks - higher bile acid levelsfetal elimination acute placental
anoxia, cardiac depression and increased incidence of meconium stained
amniotic fluid . prematurity, intrapartal fetal distress, and fetal death.

35. DIAGNOSIS
Elevation in serum bile acids is the single most sensitive indicator of ICP.
In healthy pregnant women, total bile acids (TBAs) are slightly elevated above
baseline and levels as high as 11.0 μM are accepted as normal in late pregnancy
. Brites et al identified the following common features of ICP:
(1) serum TBA concentrations >11.0 μM (normal range, 4.6–8.7 μM);
(2) cholic acid–chenodeoxycholic acid ratio > 1.5 (normal range, 0.7–1.5) or cho-
lic acid proportion of TBAs > 42%;
(3) gly-cine –taurine ratio <1.0 (normal range, 0.9–2.0) or glycocholic acid
concentration >2.0 μM (normal rang range, 0.6–1.5 μM)

36. •Mild abnormalities in LFTs-transaminases,alkalinephosphatase,5′nucleotidase,
cholesterol, triglycerides, phospholipids, and lipoprotein X
• Alanine transaminase is sensitive indicator
• γ-Glutamyl transferase, which is generally low in late gestation, is typically
normal or slightly elevated in ICP.
•Direct (or conjugated) fractions of bilirubin are most commonly elevated in ICP.
Albumin may be slightly reduced, whereas α2-globulins and β-globulins are 
Biopsy -intrahepatic cholestasis with dilated, plugged bile canaliculi and deposits
of bile pigment in centri-lobular hepatocytes.

37. TREATMENT
In mild cases-emollients and topical antipruritic agents.
Antihistamines and Ultra-violet B (UVB) phototherapy are variably effective.
Anion exchange resin, cholestyramine, may effectively reduce symptoms in up to
70% ofpatients with mild ICP.
Ursodeoxycholic acid(450-1200mg/day)
• TBA in cord blood,colostrum,amniotic fluid.
• biliary secretion of bile acids
• protects cholangiocytes and hepatocytes

38. ATOPIC ERUPTION OF PREGNANCY
• Nurse’s Early onset prurigo of pregnancy
• Besnier’s Prurigo gestationis
• Pruritic folliculitis of pregnancy
• Eczema in pregnancy
• AEP more common in primi with single gestation
• Lesions start in early pregnancy in first and second trimester
• Affects all parts of body including face,palms,soles
• Reduced cellular immunity and reduced production of Th1cytokines(IL‐2,
interferon‐γ, IL‐12)
•Dominant humoral immunity and increased secre-tion of Th2 cytokines
(IL‐4, IL‐10)

39. PATHOGENESIS
AEP include 3 entities
1. Eczema in pregnancy:
• m/c in primi gravida in 1st and 2nd trimester
• Wide spread eczematous changes affecting typical atopic sites;
• face, neck, upper back and flexures
• Raised total serum IgE levels

40. 2. Prurigo of pregnancy
• At 25 to 30 weeks of pregnancy
• May persist upto 3 months after delivery
• Tiny erythematous pruritic papules & nodules on extensor aspects abdomen
with excoriation marks
• Key finding is extreme dryness of the skin

41. 3. Pruritic folliculitis of pregnancy
•Second and third trimester
•Pruritus is not a major feature
•Erythematous follicular papule resembling steroid induced acne
•Shoulders, upper back, arms, chest and abdomen
•Resolves spontaneoulsy 1-2 months following delivery

42. •20% of patients suffer from an exacerbation of pre‐existing atopic eczema with a
typical clinical picture. The remain-ing 80% experience atopic skin changes for
the first time ever or after a long remission.
• Of these, 2/3 present with widespread eczematous changes (so‐called E‐type
AEP) often affecting typical atopic sites such as the face, neck, Upper chest and
flexural surfaces of the limbs ;
1/3 of patients have papular lesions (P‐type AEP) -characterized by small
erythematous papules disseminated on the trunk and limbs as well as typical
prurigo nodules, mostly located on the shins and arms.
AEP more common in primi with single gestation pregnancy

43. •Maternal prognosis is good even in severe cases as skin lesions usually respond
quickly to therapy.
• Recurrence in subsequent pregnancies is common.
• Fetal prognosis is unaffected, but the infant may be at risk of developing atopic
skin changes later on.
Investigations
•Histopathology is non‐specific
• Direct and indirect immunofluorescence are both negative.
• Laboratory tests may reveal elevated serum IgE levels in 20–70% of patients

44. TREATMENT
First line
• Topical emollients
• Topical corticosteroids (see section on general treatment
guidance)
• Oral antihistamines: loratadine and cetirizine
Second line
• Narrow‐band UVB phototherapy
Third line
• Prednisolone
• Azathioprine

45. SKIN INFECTIONS
Human papillomavirus infection
• Condyloma acuminata can be exacerbated, growing very rapidly particularly
in the second trimester and occasionally obstructing the birth canal.
• Infants born through an infected cervix are at increased risk for laryngeal
papillomatosis, usually associated with HPV types 6 and 11.
•Genital HPV infections should be treated during pregnancy and if
necessary a caesarean section performed
• Physical treatments- Cryotherapy , Electrocautery
• Avoid- Podophyllin ,Imiquimod , 5‐fl uorouracil

46. Herpes simplex virus infection
• Primary herpetic infection (HSV‐1 2) occurs in 2% of pregnancies and is often more severe
than in the non‐pregnant state.
• In babies of very low birth weight, infection with herpes simplex can be life threatening
• Primary or recurrent genital HSV infection is an indication for a caesarean section and
drug therapy.
• Systemic aciclovir, although rated as US Food and Drug Administration (FDA) pregnancy
category C is considered safe in pregnancy as it has been used extensively without
adverse effects
Varicella zoster virus infection
• Herpes zoster in pregnancy is not associated with viraemia,does not put the fetus at risk.
• Primary VZV infections may put both mother and child at risk of pneumonia and
encephalitis.
• Infections during weeks 1–20 (highest risk from weeks 13 to 20) can lead to fetal varicella
syndrome in a small percentage of cases (1–2%)

47. • Passive immunization with varicella zoster immunoglobulin to seronega-tive mothers
within 72 h post exposure may prevent or ameliorate maternal infection
• . Confi rmed varicella should be treated early with aciclovir either orally or
intravenously for pneumonia or other complications.
• Perinatal VZV infections pose considerable risk to the development of neonatal
varicella, particularly if the infant is exposed to infection is at or just after birth.
• The infant will then develop widespread cutaneous and visceral disease, usually with
severe pneumonia and a 30% mortality rate.
• Treatment of neo-natal varicella is with high‐dose intravenous acyclovir
complications
Fetal varicella syndrome
• Neurological defects
• Growth defects
• Pneumonia
• Encephalitis
Maternal varicella infection -Pneumonia , Encephalitis

48. HIV
HIV infection is often asso-ciated with dermatological manifestations, although
to a lesser extent since the advent of highly active antiretroviral therapy
In HIV‐positive pregnant women, antiretroviral therapy can be given and
continued during labour and delivery
Recommendations for HIV in pregnancy
• Caesarean section if there is a high viral load
• Avoid breastfeeding
• HIV‐positive infants need pneumocystis prophylaxis with co‐trimoxazole
• Normal infant immunizations can be given

49. SCABIES
•Infestation with scabies is common during pregnancy and this diagnosis should
always be considered when assessing a pregnant women with itchy skineruption
•First line treatment should be topical permethrin 5% and second line treatment
benzoyl benzoate25% .
• Repeat the treatment after a week to kill eggs and persistent mites as
cell‐mediated immunity is reduced.
•Antihistamines and mild to moderately potent topical steroids may be needed to
control the marked irritant dermatitis that often results when the mites are
destroyed in the skin.
• Oral antihistamines can be guven if pruritus is severe

50. LEPROSY
• Reduction in cell‐mediated immunity may have an adverse effect on leprosy
• .Erythema nodosum leprosum in pregnancy is associated with an early loss of
nerve function compared with non‐pregnants.
•. Without treatment there is a signifi cant risk of nerve damage and disability, so
regular neurological examinations must becarried out in pregnants.
• Leprosy reactions can be treated with prednisolone 40–60 mg daily for 2 weeks
followed by a steady reduction in the dose.
• The thalidomide cannot be used because of its teratogenicity and clofazimine
crosses the placenta and has been associated with mild pigmentation in
the infant and unexplained fetal death.

51. INFLAMMATORY SKIN DISEASES
•ACNE VULGARIS AND ROSACEA
• Acne vulgaris often improves in early preg-nancy but worsens in the third
trimester as maternal andro-gen levels increase.
• Severe acne conglobata may require treatment with systemic corticosteroids
in addition to oral antibiotics
• Acne neonatorum may occur due to the passive transfer of maternal
androgens across the placenta during the third trimester- transient eruption ,
does not require ongoing treatment.
• Rosacea often worsens during pregnancy as oestro-gen levels increase, and
may require systemic treatment.
• Rosacea ful-minans is a rare variant of rosacea that may flare severely in
pregnancy

52. TREATMENT
First line
• Topical therapy: azelaic acid 10–15%
• Benzoyl peroxide gel 2.5–10%
• Oral erythromycin (avoid in first trimester)
• Oral azithromycin
Second line
• Narrow‐band UVB (TL‐01)
Third line
• Prednisolone (can be combined with oral antibiotic therapy)
Topical and oral retinoids must be avoided in pregnancy

53. PITYRIASIS ROSEA-Pityriasis rosea is another infl ammatory skin condition that
mimic psoriasis or tinea corporis).
URTICARIA-mimic pre‐bullous phase of pemphigoid gestationis or PEP
ERYTHEMA NODOSUM- reactive inflammation of subcutaneous fat, secondary
to streptococcal infections,TB, leprosy, sarcoidosis and IBD
•Pregnancy and oral contraceptive therapy trigger EN
•It presents with tender erythematous nodules or plaques over the anterior
lower legs.
•Fever, malaise and arthral-gia often occur and the eruption typically lasts up to
6–8 weeks.
•Supportive treatment is required

57. AUTOIMMUNE SKIN DISEASES
SYSTEMIC LUPUS ERYTHEMATOSUS
• Flare of LE activity (60%) –m/c cutaneous
• Spontaneous abortion
• Fetal loss
• Antiphospholipid syndrome – venous thromboembolism
• Pre‐eclampsia
• Preterm delivery
• Intrauterine growth restriction
• Neonatal lupus erythematosus – annular rash face and scalp
• Congenital heart block (2–3%)
•Treatment-1st line –topcal corticosteroids,hydroxychloroquine,prednisolone

58. PEMPHIGUS VLGARIS AND FOLIACEUS
• Fetal skin shares the same desmoglein 3 profi le as adult oral mucosa so that
neona-tal pemphigus is more likely to occur if the mother has oral disease.
• Exacerbation of disease (TH‐2 mediated)
• Spontaneous abortion
• Stillbirth
• Caesarean section needed if there is severe vulvo‐vaginal disease
• Neonatal pemphigus with transient blistering –IgG4 transfer across placenta
• Perinatal mortality of 12% with placental dysfunction
•RX-1stline-prednisolone,2nd line –azathioprine,3rd line-plasmapheresis

59. Ehler danlos –types 1 and 4
Pseudoxanthoma elasticum
Dermatomyositis/polymyositis
Systemic sclerosis
Tumours
Bowenoid papulosis
Langerhan’s cell histiocytosis
Mycosis fungoides
neurofibromatosis

60. SKIN TUMOURS
MALIGNANT MELANOMA
• Most studies show no adverse effect of pregnancy on prognosis
• Melanoma may have increased Breslow thickness at presentation in pregnancy
• A low threshold is recommended for excising changing pigmented lesions
• Transplacental metastatic spread can occur – examine the placenta closely
• Ultrasound or MRI is preferable to CT
• Sentinel node biopsy can be done (avoid methylene blue dye as there is a risk
of intestinal atresia)
• 5‐year survival rate for stage II melanoma -56%; stage IV melanoma-17%

61. PUSTULAR PSORIASIS OF PREGNANCY
IMPETIGO HERPETIFORMIS-by VON HEBRA
• Absence of a positive family history, abrupt resolution of symptoms at delivery,
and a tendency to only recur during subsequent pregnan-cies distinguish this
entity from generalized pustular Psoriasis.
• Moreover, factors known to trigger pustularpsoriatic flares, such as infection,
exposure to culprit drugs, or abrupt discontinuation of systemic corticosteroids
are lacking in all patients with pustular psoriasis of pregnancy.
ETIOLOGY
• ed levels of progesterone and other hormones.
• Hypocalcemia and hypoparathyroidism

62. •Acute eruption occurring as early as the 1st, but generally during the 3rd
trimester of an otherwise uneventful pregnancy.
• Erythematous patches with margins studded with subcorneal pus-tules in
concentric rings.
•pustules enlarge centrifugally and form a crust at their centers
• The eruption typically originates in flexural areas(m/c in inguino-genital ) ,
Spread to trunk,arms legs,oral and esophageal mucosa.
• Subungual lesions may result in onycholysis.
•The face, palms, and soles are commonly spared.
• The rash may be pruritic or painful.
• constitutional symptoms -fever, chills, malaise, diarrhea, nausea and arthralgias.

65. DIFFERENTIAL DIAGNOSIS
Most Likely
Pustular drug eruption (acute generalized exanthem-atous pustulosis)
Pemphigoid gestationis
Consider
Pemphigus vulgaris
Dermatitis herpetiformis
Subcorneal pustular dermatosis
Pustular eruption in inflammatory bowel disease
Always Rule Out
Infectious causes of pustular eruptions

66. • Histopathologic examination reveals classic features of pustular psoriasis
• epidermis-parakeratosis,elongation of rete ridges,spongiform pustules of kogoj
• .The most common laboratory derangements include leukocytosis,neutrophilia,
an elevated ESR, hypoferric anemia, and hypoalbuminemia.
• Less commonly Calcium, phosphate, vitamin D and PTH levels are decreased.
• Cultures of pustule contents and peripheral blood are negative
PROGNOSIS
•Placental insufficiencymiscarriage,stillbirths,IUGR
•Recurrences in subsequent pregnancies are common with earlier onset and
more severe course
Reur during mensturation and ocp use

67. TREATMENT
•Topical treatments include wet dressings and topical corti-costeroids
Systemic corticosteroids are the mainstay of therapy during pregnancy.
•Cyclosporine-pregnancy category “C,”- 5 mg/kg and 10 mg/kg daily
to treat cases refractory to high-dose systemic cortico-steroids.
•Narrowband UVB combined with topical steroids has been reported to be
successful.
• Inflix-imab, a TNF-αblocking agent has been successfully used without adverse
effect on the fetus.
• Infliximab,etanercept and adalimumab –category B drugs – in refractory pts

68. • In all, cases, fluid status and electrolytes should be monitored.
• Fetal monitoring is essential as decelerations in fetal heart rate may be the
earliest sign of fetal hypoxemia.
• Maternal cardiac and renal functions may be compromised with disease
progression and should be monitored as well.
• Induction of labor -no remission despite supportive &pharmacological therapy
• The therapeutic armamen-tarium available after pregnancy termination or after
delivery in a non-nursing mother include oral psoralen and ultraviolet A (PUVA),
• oral retinoids, clofazimine, methotrexate, sulfapyridine and sulfones

69. PREGNANCY DERMATOSES ASSOCIATED
WITH FETAL RISK
1.Pemphigoid gestationis
2.Intrahepatic cholestasis of pregnancy
3.Impetigo herpetiformis
PREGNANCY DERMATOSES WITH OUT FETAL
RISK
1.Polymorphous eruption of pregnancy
2.Atopic eruption of pregnancy

70. PREGNANCY DERMATOSES WITH
RECURRENCE
1.Pemphigoid gestationis
2.Intrahepatic cholestasis of pregnancy
3.Impetigo herpetiformis
4.Atopic eruption of pregnancy
PREGNANCY DERMATOSES WITHOUT
RCURRENCE
1.Polymorphous eruption of pregnancy