FOOD
ALERGY, INTOLERANCE,
MALABSORPSI
Food a great pleasure but some unfortunate people:
Food unpleasant, distressing, dangerous symptoms.
These symptoms are triggered by
food allergy (FA)
food intolerance (FI) reactions, caused by a
pharmacological or drug-like reaction to 1 food
chemicals.
Malabsorption: gastrointestinal symptoms caused by
incomplete digestion and absorption of food substances,
ex: milk )lactose) or fruit (fructose),
Etc
Food intolerance (FI)
more common than food allergy (FA):
5-10% population
wide range of chemicals reactions, such
as salicylates (an aspirin-like substance),
etc (see below table )
FI
Mechanism is not well understood, but similar:
act as irritants on nerve endings
side-effects of drugs in sensitive people.
histamine can be released
symptoms can be similar with FA
except neurological and behavioural problems
(not normally in FA)
FI
Symptoms: vary (look below table)
If there is no other medical cause for these
symptoms, FI is a possibility for exploring.
Occasionally, FI will exacerbate (worsen
symptoms) of other medical conditions
Identification of FI
FI sometime difficult to identify because:
Reactions may not happen straight away.
Reactions FI : rapidly days.
Even reactions are dose-dependant, but
reactions can be inconsistent. The same food
chemical : wide variety
People can have problems with more than one
food chemical.
The level of sensitivity of a person also vary at
different times, depending on factors such as
stress, hormone cycles, exposure to
environmental chemicals, use of medications
etc.
FI
The only proven way to investigate FI is
Elimination diet Challenge
In some cases: 2 or 3 times,
if improve: a possibility.
If no improvement: FI none or problem the
other chemicals substance
If partial improvement: there are other
non-food triggers involved
FI management in the long-term
Foods: lack the problem substances.
If desired, a gradual reintroduction of
foods gradually increasing the dose in a
systematic way help identify the
tolerance level. Over time (months or
years), the tolerance level can increase
Avoiding unnecessary restriction of the
diet, particularly in children. Special
attention needs to be paid to ensure an
adequate nutrient intake.
Food allergy (FA)
FA : immune system reacts to a protein in a
certain food, causing the release of
antibodies and histamine.
Prevalence developed countries: 68%
young children, 3.5% adults
> 90% occur in infants
FA
young children: cows milk, egg, peanut, soybean,
wheat, tree nuts, fish and shellfish.
Adults : shellfish, peanut, tree nuts and fish
Allergies to cows milk, egg, wheat and soy are
typically outgrown by age 35 years;
peanut allergy may resolve by age 5 years only
20%
Most children will grow out of FA by school age
Classification of Food Allergy Disorders
Based on the role of IgE antibody:
IgE-mediated, non-IgE-mediated (cell-mediated)
and mixed (IgE- and cell mediated) (look below
table)
Based on Allergen
Class 1 : GIT sensitization, heat- and acid-stable
glycoproteins and cause systemic reactions.
Class 2 : respiratory sensitization, very heat-labile
and tend to induce oral allergy symptoms. In
contrast, plant nonspecific lipid transfer proteins
are heat resistant and tend systemic reactions.
Based on Allergen
Class 1 : peanut, egg white, and cows
milk;
Class 2 Food allergens are homologous
to proteins in birch tree pollen
Pathophysiology FA
FA results from failed oral tolerance that is
characterized by suppression of immune
responses toward food proteins by the gut-
associated lymphoid tissue
FA
Symptoms begin: within minutes to 1 hour
of eating.
Symptoms : mild to severe, very severe :
anaphylaxis
Symptoms : eczema, hives, facial swelling,
itching or swelling of the lips, tongue or
mouth, vomiting, diarrhoea, itching or
tightness in the throat, and difficulty
breathing, etc.
FA
Allergic eosinophilic esophagitis (AEE) and
gastroenteritis (AEG)
characterized by infiltration of the GIT with
eosinophils.
AEE
most frequently in infants, children, and
adolescents
presents with symptoms of GER
Esophageal biopsy: > 1020 eosinophils
per 40/hpf
Allergic eosinophilic esophagitis (AEE) and
gastroenteritis (AEG)
AEG can occur at any age,
in young infants: failure to thrive
AEG may cause pyloric stenosis.
Symptoms: abdominal pain, emesis, diarrhea,
blood loss in the stool, anemia, and protein-
losing gastroenteropathy.
50% of patients have atopic
Allergic proctocolitis
Typically starts in the first few months of life, with
blood-streaked stools, healthy-looking infants.
Highly prevalent in breastfed infants,
Pathologic are limited to the colon
focal acute inflammation with epithelial erosions
and eosinophilic. Infiltration of the lamina
propria, the epithelium and lamina muscularis.
Most infants respond well to casein hydrolysate
and only few require amino acidbased formulas.
After 912 months of age, the infants typically
tolerate an unrestricted diet.
Food protein-induced enterocolitis syndrome
(FPIES)
most frequently in young infants
with irritability, protracted vomiting, and diarrhea .
Vomiting (13 h after feeding), bloody diarrhea,
anemia, abdominal distention, and failure to thrive.
typically caused by cows milk or soy-based formula
other foods: grains (rice, oat), meats (turkey,
chicken), and vegetables (pea)
Infantile colic
: unexplained paroxysms of irritability, fussing or
crying that persist for > 3 h/day, >3 days/ week,
at least 3 weeks.
Prevalence 519%.
possible role of an underlying transient
hypersensitivity to one or several foods
50% GER caused by hypersensitivity to dietary
food proteins, mainly cows milk and soybean .
Diagnosis FA
Medical history
Laboratory tests
Oral food challenges (OFCs), especially in
chronic disorders such as AD or AEG.
Skin prick test
laboratory immune assays
Biopsy
Laboratory techniques (e.g. peripheral
eosinophil count, serum albumin and total
protein level, fecal occult blood, fecal 1-
antitrypsin)
Management of Food Allergy
avoidance,
prompt recognition and treatment of food-allergic
reactions,
nutritional support. Hypoallergenic formulas are
well tolerated by children with IgE-mediated and
with cell-mediated food allergy. Hypoallergenic
formulas are also recommended for prophylaxis
of food allergy in infants at risk of atopy.
Food Malabsorption
Pattern :
Developed country: coeliac disease, cistic
fibrosis
Developing country: gastroenteritis,
malnourish, prematur baby, diarrhoea post
surgery
Carbohydrate maldigestion and
malabsorption
Normal digestion and absorption (Harriess):
1. Intraluminal hydrolysis: amylase
2. Brush border hydrolysis: maltase,
sucrose, isomaltase, lactase
3. Monosacharide translocation
4. Monosacharide exit from entrocite to
porta vein
CH
Carbohydrate undigestable osmotic
burden digested by colon bacteria
osmotic diarrhoea
Diagnosis
1. Clinical feature: equal with viral diarrhea
2. Laboratory
laboratory
Stool: Reducing substance (clinitest),
cromotography, stool pH.
Radiology: barium lactose meal with
contras media
Breath test,
Biopsy
etc
therapy
Secondary disacharide maldigestion and
malabsorption free disacharide diet
Secondary monosacharide malabsorption
free carbohydrate diet, parenteral
nutrition, polymer glucose formula
Fat maldigestion & malabsorption
With/without diarrhoea , Harriess classification:
1. Pancreatic lipolysis defect: deficiency of lipase,
chronic pancreatitis, cystic fibrosis, Schwachman's
syndrome
2. Micellar solubilization defect: bile salt deficent
3. Disorder of emulsification trigliserid : gastrectomy
and / or cange of gastric motility
Fat maldigestion & malabsorption
With/without diarrhoea , Harriess classification:
4. intake lipolytic result in mucosa : enteropathy,
intestinal resection, blind loop syndrome, saturated
enterocyte, intestinal transit time increase
5. Abnormality of intralumen intestine phase :
enteropathy, blind loop, a-(or beta)
lipoproteinemia.
6. Trouble of Annoyed* chylomicron jetting to
lymphatic channel : obstruksi of channel limfe,
limfangiektasi
Patophysiology of fat malabsorption
1. Pancreatic type
2. Hepatic type
3. Enteric type
4. Lymphatic type
FAT
1. Pancreatic type
Lipase decrease:
Prematuritas
Severe malnourish
Resection of illium and blind loop
syndrome
Cystic Fibrosis
(2) Hepatic type bile salt in gut lumen:
prematurity, severe malnourish, liver
cirrhosis, bacterial overgrowth, blind loop
(3) Enteric type, damage of mucosal small
intestine: GE, severe malnourish, bile salt
dekonjugation increase
( 4) Lymphatic type: intestine tuberculosis,
limfagiektasia .
Disease with fat maldigestion & malabsorption
Severe malnourish: pancreas and liver
function disorder, mucus epithelial atrophy
Prematurity: pancreas, intestinal and liver
function not perfect
Ileal resection: < 100 cm (compensated by
liver bile salt increase enterohepatic
cycle decrease cholerrhoic diarrhoea).
> 100 cm (fat malabsorption)
FAT
Lab
Vd Kamer
Lipiodol absorption
Miscoscopyc (Drumney)
FAT
Treatment
Treatment of underlying disease
Formula (MCT unsaturated fatty acid
low concentration of LCT)
Protein Maldigestion/malabsorption
2 condition:
1. Pancreas disorder
2. Intestinal mucous disorder
Location of disorder:
1. Intraluminal
2. Enterocite (brush border dan
intracelluler)
3. Porta vein (transport)
PROT
Intraluminal
Etio: Cistic Fibrosis, malnourish
Malnourish,
Mucous layer destroyed Pancreozimin
(cholecystokinin-pancreozimin)
secretion of pancreas enzyme
pancreas enzyme
PROT
Example:
1 Depression of Pancreas insuficiency 10%
maldigesti protein azotorrhea
2. Enterokinase deficiency : Clinical feature :
hipoproteinemia, malnnourish, edema, and
azotorrhea
Enterocyte (brush border and intracelluler)
Peptidase enzyme lays in brush border
and intracelluler
Example:
1. Enterokinase deficiency
2. Celiac sprue
3. Contraception drug
Porta vein (transport)
Absent of active transportation
Bile acid malabsorption
Bile acid hyperosmolar cholerhoic
diarrhea
Treatment: cholestiramine,
