ALLERGY IN PREGNANCY

Literature Reading
Sally Mahdiani

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 INTRODUCTION

20% of
pregnancy

allergic disease
1% of
pregnancy
asthma

32% pregnant women  frequent/constant nasal problems

2
Effect of pregnancy Effect of allergy
to allergy to pregnancy

The optimal way

to manage  The chances to
the baby

The methods that available

to lower the risk

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INTRODUCTION

Biochemical

Pregnancy Physiologic Affect allergies

Immunologic

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5
HORMONAL & METABOLIC CHANGES

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HORMONAL & METABOLIC CHANGES
HCG
Placenta, 60-90 days of
gestation
Luteotropic role
Maintaining corpus luteum
& steroidogenesis
Thyroid-stimulating activity
HCS
Placental protein, 1st trimester
Major metabolic hormone
GH-like, antiinsulin effect 
impaired glucose use, prot
synthesis, ↑ lipolysis 
hypoglycemia,
hyperinsulinemia,
hyperlipidemia,
hypoaminoacidemia
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HORMONAL & METABOLIC CHANGES

Progesterone Esterogen Corticosteroids

Circulating Placenta Free cortisol (2-3

maternal x)
cholesterol
Relaxation of Estriol  maintain Pulmonary effects
smooth muscle placental blood
flow
Immunosuppressi Softening cervical
ve effect connective tissue
↑ ventilatory
respones
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CIRCULATORY PHYSIOLOGIC CHANGES
• ↑ weight
• ↑ total body water (6-8 l  4-6 l extracellular)
• Sodium retention
• ↑ blood volume  hemodilution
• ↑ stroke volume  cardiac output

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PULMONARY PHYSIOLOGIC CHANGES

• ↑ ventilation  ↑ metabolic demands  renal

compensation  respiratory alkalosis
• Progesterone  ↑ respiratory center  sensitive to CO2
• ↑ O2 consumption

↓ pCO2, ↑ pO2, N/↑ pH

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PREGNANCY-INDUCED-
HYPERVENTILATION
• ↑ pressure on diaphragm  dyspnea

Acute asthma: bronchial obstruction

Asthmatic pregnancy patients:
Good: ↓ bronchomotor tone in large central airway
Not good: changes in smaller peripheral airways

Maternal alkalosis hypoxia

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 IMMUNOLOGIC CHANGES

Immunoanatomic barrier No fetal

Maternal immune hyperresponsiveness rejection

• Biochemical rx.  fc inhibitory maternal cellular immune

response
• Lymphoid tissues  ↓ (size, cellularity, germinal centers)
• AFP, hormones  changes in B and T cell inhibit maternal
IgG & IgA, changes in IgE
• Histamine in fetal tissue ↑  maternal serum histamine ↑
• PGF, PGA, PGE ↑

PG administrration  bronchoconstriction
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 Histamine, Histamine, Histamine Histamine,
IL-1, TNF-
PGD2 acetylcholine, protease,
acetylcholine
PGD2 Leukotrienes, prostaglandine
PGD2,
PGD2
Leukotrienes, Neuropeptide (SP,VIP)
platelet activating factor

SOMNOGENIC CEFALGIA DISCHARGE SNEEZING NASAL ITCHING

NASAL OBSTRUCTION

SLEEPING DISORDERS

PSYCHOMOTOR AND COGNITIVE FUNCTION 

(DAYTIME SLEEPINESS)

QUALITY of LIFE 

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 THERAPEUTIC PRINCIPLES
Psychologic Management
• Ventilation • Support
• Education • Reassurance

Immunologic Management
• Ag & irritant avoidance
• Immunotherapy  contradiction
lower maintenance dose not begun during pregnancy
do further dosage increases
• Skin testing only for therapeutic impact
RASTs
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THERAPEUTIC PRINCIPLES

Pharmacologic Management
• Not the ideal
1. The developmental state of the fetus
2. Specific agents act in specific ways
3. The chemical nature of an agent
4. The doses
5. The route
6. The duration

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ANTIHISTAMINES
Chlorpheniramine Crosses placenta? Cleft palate
Dyphenhydramine Crosses placenta
Hydroxyzine Malformations
Tripelennamine Malformations
Cetirizine Human teratogens
Desloratadine Safe
DEKONGESTANTS
Oxymetazoline Contraction of myometrium, gastroschisis
Pseudoephedrine Gastroschisis, intestinal atresia
Phenylephrine Clubfoot, eye & ear
BRONCHODILATORS
Epinephrine Uteroplacental circulation
vasoconstriction
Ephedrine Preeclampsia, 16
CORTICOSTEROIDS
Cortisone Abortion, IUGR, cleft palate
Beclomethasone Cleft lip & palate, intranasal: safe
Budesonide Fetal loss, IUGR, malformations
Mometasone furoate Category C
ANTIBIOTICS
Penicillin Crosses placenta
Erythromycin Maternal hepatic toxicity
Cefadroxil

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 RHINITIS

• Vasomotor rhinitis of pregnancy

nasal mucosa congestion
vasomotor instability
• Preexisting for:
chronic rhinitis allergic rhinitis
eosinophilic nonallergic nasal polyps
chronic sinusitis primary vasomotor rhinitis

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RHINITIS
• Therapy:
intermittent obstruction: oxymetazoline drops/spray
at minimum dose
continuous obstruction: pseudoephedrine
30-60 mg
3-4 x 60 mg
2 x 120 mg
eosinophilic allergic
nonallergic rhinitis
sneezing, runny nose: antihistamine
tripelennamine 25-50 mg
50-100 mg
other after 1st trimester
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RHINITIS
• Therapy:
severe eosinophilic rhinitis: intranasal cromolyn
beclomethasone
oral corticosteroids
nasal polyps: antihistamine-decongestant
intranasal beclomethasone
400 µg/day  tapered
oral corticosteroid
nasal polypectomy/LA
chronic sinusitis: 2 x saline lavage
chronic antihistamine-decongestant

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RHINITIS

• Therapy:
nonpharmacologic: buffered saline nose spray
exercise
rhinitis medicamentosa: topical vasoconstrictor
antihistamine-decongestant
intranasal corticosteroids

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ALLERGIC SENSITIZATION &
ITS POTENTIAL PREVENTION
• Prevention of IgE-mediated disorders by:
1. Genetic engineering
alteration of genes of parents and/or infant
2. Cellular engineering
alteration of immunologic capabilities of infant
- antibody-producing system
- mediator cells
- target organ sensitivity
3. Environmental engineering
reduction of allergenic load
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GENETIC CONSTITUTION

90
80
70
60
50
40
Risk
30
20
10
0
both (-) (-)/(+) (+)/(-) both (+) both
strongly
(+) 23
ALLERGIC SENSITIZATION &
ITS POTENTIAL PREVENTION
IgE Sensitization in utero in development of allergic
disease
• Fetus synthesize IgE (11st & 21st week)
protecting fetus from maternal IgE
• Placental permeability  transfer of IgG, hormones,
enzymes, Ag, drugs

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POSTNATAL ENVIRONMENT IN
DEVELOPMENT OF ALLERGIC DISEASE
Environmental Modulation of IgE Responsiveness
1. Inhaled or ingested allergens
- induces specific & nonspecific IgE
- month of birth  risk of immediate hypersensitivity
- formula feeding in T cell-deficient  serum IgE ↑
2. Microorganisms
- Viral infection assc. with onset of specific IgE
- B. pertusis adjuvant  IgE
- S. aureus & C. albicans  IgE
- Tissue phase parasites  IgE
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Environmental Modulation of IgE Responsiveness
3. Drugs and other agents
- exogenous maternal progesterone  IgE
- corticosteroids  ↓IgE receptors
- immunotherapy  ↓ IgE
- smoking  ↑ IgE

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BREAST FEEDING VS OTHERS IN
DEVELOPMENT OF ALLERGIC RHINITIS

• Breast-fed infants  fewer infection

• Sequential changes in Ig (IgA), C3, C4, lysozyme,
lactoferrin, alpha antitrypsin

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 Recommendation for Prevention of Allergies in
Families at Risk

1. Allergic disorders are frequent

2. Identified immunologically (↑ serum IgE)
3. At-risk infants can be identified at birth (↑ cord serum
IgE)
4. Environmental engineering  ↓ allergens, potential
prevention, delay of onset, ↓ severity

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 HIGHLIGHTS

• Pregnancy is needing a special attention in the

correlation to the allergic disease.
• There are hormonal, metabolic, pulmonary,
circulatory and immunologic changes in pregnancy.
• We should consider on the test and right
management for the allergic pregnant patients.
• The prevention for the allergic children can be
planned before birth.

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