Alergia en Lactantes R.H. ZARAGOZA URDAZ, MD, PhD ALLERGY

Allergies and Breast Feeding
R.H. ZARAGOZA URDAZ, MD, PhD
ALLERGY/IMMUNOLOGY
DIAGNOSTIC IMMUNOLOGY
FAAAAI, FACAAI & FAAEM
AMPRO
9/04/04
MAYAGUEZ RESORT & CASINO
R.H. ZARAGOZA URDAZ, M.D.
College:
Washington University, St. Louis, Mo.
BS./ BA., 1983
Medical School: University of Puerto Rico
School of Medicine, San Juan, PR.
MD., 1987
Residency:
University of Miami, Jackson Memorial
Hospital, IM/Pediatrics, July, 1987 to
June, 1990
Fellowship:
National Jewish Center for Immunology
and Respiratory Medicine; Allergy and
Immunology, July 1990 to June 1994
National Jewish Center for Immunology
and Respiratory Medicine; Diagnostic
Laboratory Immunology, September
1992 to June 1994
OBJECTIVES
To review current views of the pathogenesis of
allergic reactions.
To review the materno-placento-fetal immune
interactions.
To review the role of Lactation in prevention
and/or induction of atopic disorders.
To review the role of allergen avoidance (both
food and aeroallergens) in the primary and
secondary prevention of atopic disorders.
INTRODUCTION
Atopy is defined as the genetic propensity to
develop IgE following allergen exposure
(sensitization) and manifests clinically as allergic
asthma, allergic rhinitis, atopic dermatitis and
IgE-mediated food allergy.
The exponential rise in the prevalence of asthma
and related allergic disorders in the last 30 years
has put an enormous burden on health care
resources and adversely affected the quality of
life of millions of children and adults.
This emphasizes the need for devising effective
methods for prevention in children at high risk of
Atopy.
INTRODUCTION
Developed nations are experiencing a marked increase
in prevalence of the familial allergic diseases including
asthma, allergic rhinitis, atopic dermatitis, and allergic
gastroenteropathy, which are often called atopic
diseases. No satisfactory explanation for this epidemic is
known, but it has been proposed that some facets of
modern life tend to bias immune responses away from
the Th1 cellular immune responses that protect against
many infections and toward Th2 responses that favor
atopy. There are 3 hypotheses to explain why this
epidemic is occurring now.
PATHOGENESIS
Allergic states pathogenesis are complex
polygenic disorders dependent on
multilayered gene-environment-time
interactions.
The genes relevant to the development of
allergic disorders might vary depending on
the environmental exposures present in a
given population; likewise, the relevant
environmental exposure will be dependent
on the genetic context.
PATHOGENESIS
The immunologic milieu at any given
time will be determined by the
individual’s cumulative environmental
exposures and his or her genetically
influenced responses to these
exposures.
Pathogenesis of Allergic Reactions
..\My DVDs\Asthma Pathophysiology\Asthma Pathophysiology2\Asthma
Pathophysiology2.dvd
ALLERGIC MARCH
The allergic march starts in the womb. The intrauterine
fetal sensitization is determined by the genetic
background and is modified by the maternal
environmental exposures including the diet.
There is recent evidence that suggest that neonatal
hygiene or early exposure to certain proteins, allergens
or infections may modified the balance of important Tcells regulators which may skew the disease expression
away from an allergic profile.
Later on in life, these infections and exposure to
pollutants may trigger a progressive evolution of allergic
symptoms in genetically predisposed individuals.
ALLERGEN AVOIDANCE &
PREVENTION OF ATOPY
Primary prevention
Development of atopic disease depends on an interaction between
genetic and environmental factors. Hence manipulation of
environmental risk factors may lead to a reversal of this trend.
– Allergen exposure and development of Atopy
Dose-dependent relationship between allergen exposure and sensitization
and between sensitization and the development of allergic disease is well
established.
– Allergens
Food Allergens-- early life– cow’s milk, egg and peanut.
Aeroallergens– humid climates–
house dust mite-arid climates-fungus spores
inner cities-cockroach
2-10 μg/g dust
– Time of contact with allergen
Evidence in dogs, early sensitization results in a higher level of IgE
production, influences the direction of immune responses such that
response to allergen exposure later in life is also more intense and leads to
bronchial hyperreactivity.
ALLERGEN AVOIDANCE &
PREVENTION OF ATOPY
– Food allergens avoidance
Maternal dietary allergen avoidance during pregnancy does not
prevent atopic disease in children and may be harmful to the
fetus.
Recent WHO report states that exclusive breast feeding and
avoidance of solid food for 4 mo. seems to be effective for allergy
prevention.
Differential effect of breast feeding on the development of atopy,
such that, children with atopic heredity, breast feeding reduced
the risk of atopy while it increased the risk in those without atopic
heredity.
Cow’s milk protein is an important food allergen in early life. The
incidence of allergic manifestations, such as AD, food allergy or
allergic urticaria, was significantly reduced by using an
extensively hydrolyzed casein formula compared with a cow’s
milk formula. Use of partially hydrolyzed whey formula reduced
the incidence of AD.
ALLERGEN AVOIDANCE &
PREVENTION OF ATOPY
– Avoidance of aeroallergens
To prevent the development of atopy (primary prevention),
allergen avoidance has to be instituted before sensitization
occurs. Avoidance measures would have to be applied from
birth (or even during pregnancy).
– Combined approach
The Isle of Wight allergy prevention study was the first to
show that a combination of strict avoidance of food and
reduction in house dust mite allergens during infancy could
have a profound effect on the development of atopy in
genetically at risk children. There was a reduction in the
incidence of asthma, atopic dermatitis and food allergy in
early childhood.
ALLERGEN AVOIDANCE &
PREVENTION OF ATOPY
Secondary prevention
– Environmental allergen control is
recommended as an essential part of most
asthma management guidelines. Patients
with asthma and aeroallergen sensitivities are
appropriate advice on allergen avoidance and
such measures can indeed reduce asthma
symptoms, the need for medication, and
airway hyperresponsiveness.
Breastfeeding and allergic disease: a multidisciplinary review of
the literature (1966-2001) on the mode of early feeding in
infancy and its impact on later atopic manifestations
RESULTS: Of the 132 studies selected, 56 were
regarded as conclusive. Several factors contributed to
the exclusions. The studies considered conclusive by the
review group were categorized according to population
and study design.
CONCLUSIONS: The review group concluded that
breastfeeding seems to protect from the development of
atopic disease. The effect appears even stronger in
children with atopic heredity. If breast milk is unavailable
or insufficient, extensively hydrolysed formulas are
preferable to unhydrolysed or partially hydrolysed
formulas in terms of the risk of some atopic
manifestations.
van Odijk et al., Allergy 2003;58:8332003;58:833-43.
Recommendations for Atopy
Prevention in high risk children:
DIET
– MATERNAL
ROTARY DIET (4 DAYS CYCLE)
INCREASE THE INTAKE OF n-3 FATTY ACIDS (FISH OILS)
PROBIOTICS SUPPLEMENTATION
AVOID OR MINIMIZE THE USE OF ORAL ANTIBIOTICS
– INFANT
EXCLUSIVE BREAST FEEDING FOR 4-6 MO
AVOID INTRODUCTION OF SOLID FOODS
AVOID INTRODUCTION OF ALLERGENIC FOODS FOR THE FIRST
YEAR i.e. cow’s milk, egg, peanut.
ALLERGEN AVOIDANCE
– IMPLEMENT STRICT PERENNIAL AEROALLERGENS REDUCTION
MEASURES DURING PREGNANCY (i.e. HDM, Molds, Insects
(Cockroaches) and Pets) WITH HEPA AIR PURIFIERS,
ACAROCIDES,FUNGIZIDES, TANNIC ACID AND HUMIDITY
CONTROL.
– IMPLEMENT STRICT PERENNIAL AEROALLERGENS BARRIER
METHODS WITH MITE PROOF COVERS
Recommendations for Atopy
Prevention in high risk children:
IMMUNOTHERAPY
– START C.I.T. IN HIGH RISK MOTHER
PRIOR TO PREGNANCY.
– USE N.I.T. OR TEMP. DM C.I.T.
– USE S.L.I.T. IN HIGH RISK INFANTS
INFANTS FROM ATOPIC MOTHERS.
INFANTS WITH SYMPTOMATIC SENSITIVITY.
INFANTS WITH INCREASED IgE, IgG1 or TH2