עיכול ה Food allergies, CMPA, Lactose intolerance

Food Allergy: Definition

𝗗𝗲𝗳𝗶𝗻𝗶𝘁𝗶𝗼𝗻: An inappropriate immune response to a normally harmless food protein. It may be IgE-mediated or non-IgE-mediated. 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: The immune system identifies the protein as dangerous → an inflammatory reaction affecting the skin, GI tract, respiratory tract, or circulation. 𝗥𝗶𝘀𝗸: Even a tiny amount can trigger an IgE-mediated reaction; severe reactions may cause life-threatening anaphylaxis. 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝗰𝗲: A child with a true food allergy may require emergency treatment, including intramuscular epinephrine for anaphylaxis. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝗰𝗲: Recognize severe reactions, prevent exposure to confirmed allergens, and teach emergency management.

Food Intolerance: Definition

𝗗𝗲𝗳𝗶𝗻𝗶𝘁𝗶𝗼𝗻: Difficulty digesting, absorbing, or processing a food component without an allergic immune response. 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Often enzymatic or digestive; e.g., lactase deficiency → lactose is not properly broken down. 𝗦𝘆𝗺𝗽𝘁𝗼𝗺𝘀: Bloating, abdominal pain, gas, and diarrhea, generally limited to the GI tract. 𝗦𝗲𝘃𝗲𝗿𝗶𝘁𝘆: Usually dose-dependent; small portions may be tolerated. Ordinary food intolerance does not cause anaphylaxis. 𝗠𝗮𝗻𝗮𝗴𝗲𝗺𝗲𝗻𝘁: Dietary modification, adjusting type/quantity of food, and symptom control. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝗰𝗲: Distinguish intolerance from allergy to avoid unnecessary restrictions or emergency treatment.

Food Allergy vs. Food Intolerance: Clinical Comparison

𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Allergy = IgE or non-IgE immune response; intolerance = non-immune enzymatic or digestive problem. 𝗧𝗿𝗶𝗴𝗴𝗲𝗿: Allergy = usually food proteins (milk, peanut); intolerance = food components such as lactose. 𝗗𝗼𝘀𝗲: Allergy = very small amounts may trigger symptoms; intolerance = commonly dose-dependent. 𝗢𝗻𝘀𝗲𝘁: IgE allergy = minutes to hours; non-IgE allergy can be delayed. Intolerance symptoms depend on the quantity consumed. 𝗔𝗻𝗮𝗽𝗵𝘆𝗹𝗮𝘅𝗶𝘀: Possible with IgE-mediated allergy; absent in ordinary food intolerance.

Major Food Allergens: Prevalence, Prognosis and Reintroduction

𝗛𝗶𝘀𝘁𝗼𝗿𝗶𝗰𝗮𝗹 𝗘𝗶𝗴𝗵𝘁: Cow’s milk, eggs, peanuts, tree nuts, soy, wheat, fish, and crustacean shellfish. 𝗦𝗲𝘀𝗮𝗺𝗲: Recognized as a distinct ninth major allergen in contemporary lists. 𝗙𝗿𝗲𝗾𝘂𝗲𝗻𝗰𝘆: About 90% of food-allergic reactions involve major allergens (lecturer estimate). 𝗘𝗮𝗿𝗹𝘆 𝗖𝗵𝗶𝗹𝗱𝗵𝗼𝗼𝗱: About 6% of children experience food allergy during the first 3 years (lecturer estimate). 𝗠𝗶𝗹𝗸 𝗮𝗻𝗱 𝗘𝗴𝗴: Many children develop oral tolerance (the immune system gradually stops reacting). 𝗖𝗼𝘄’𝘀 𝗠𝗶𝗹𝗸: About 50% outgrow the allergy by school age (lecturer estimate). 𝗣𝗲𝗮𝗻𝘂𝘁 𝗮𝗻𝗱 𝗧𝗿𝗲𝗲 𝗡𝘂𝘁𝘀: About 80–90% may remain allergic lifelong (lecturer estimate). 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗘𝗱𝘂𝗰𝗮𝘁𝗶𝗼𝗻: Reintroduction requires medical assessment, especially following immediate or severe reactions; avoid unsupervised challenges.

IgE-Mediated Food Allergy: Mechanism and Timing

𝗢𝗻𝘀𝗲𝘁: Symptoms usually develop within minutes to hours of exposure. 𝗦𝗲𝗻𝘀𝗶𝘁𝗶𝘇𝗮𝘁𝗶𝗼𝗻: Allergen-specific IgE antibodies form and bind to receptors on mast cells and basophils. 𝗥𝗲-𝗲𝘅𝗽𝗼𝘀𝘂𝗿𝗲: The allergen activates IgE-bound cells → inflammatory mediators, including histamine, are released → rapid symptoms. 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗦𝗶𝗴𝗻𝗶𝗳𝗶𝗰𝗮𝗻𝗰𝗲: Even a very small exposure may trigger anaphylaxis.

IgE-Mediated Food Allergy: Clinical Manifestations

𝗦𝗸𝗶𝗻: Urticaria (hives), itching, angioedema, and possible eczema/atopic dermatitis flares. 𝗚𝗜: Vomiting, abdominal pain, and sometimes diarrhea. 𝗥𝗲𝘀𝗽𝗶𝗿𝗮𝘁𝗼𝗿𝘆: Rhinitis, cough, wheezing, bronchospasm, and respiratory distress. 𝗦𝗲𝘃𝗲𝗿𝗲 𝗥𝗲𝗮𝗰𝘁𝗶𝗼𝗻: Anaphylaxis with respiratory or cardiovascular compromise is a medical emergency.

Non-IgE-Mediated Food Allergy: Mechanism and Symptoms

𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Delayed immune response involving cellular pathways, including T-cells, rather than classic IgE-mediated mast-cell activation. 𝗢𝗻𝘀𝗲𝘁: Approximately 2–48 hours following exposure in lecturer notes; chronic presentations may be less clearly timed. 𝗠𝗮𝗻𝗶𝗳𝗲𝘀𝘁𝗮𝘁𝗶𝗼𝗻𝘀: Mainly GI—vomiting, diarrhea, chronic diarrhea, blood or mucus in stool, and feeding difficulties. 𝗖𝗼𝗺𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗼𝗻𝘀: Ongoing inflammation, inadequate intake, and malabsorption may contribute to failure to thrive (FTT). 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗔𝘀𝘀𝗲𝘀𝘀𝗺𝗲𝗻𝘁: Ask about foods from preceding days, stools, feeding patterns, and growth—not only immediate reactions.

Heiner Syndrome: Rare Milk-Related Pulmonary Allergy

𝗗𝗲𝗳𝗶𝗻𝗶𝘁𝗶𝗼𝗻: A rare, typically non-IgE-mediated pulmonary hypersensitivity disorder associated with cow’s milk protein. 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Cow’s milk protein hypersensitivity causes inflammation involving the lungs. 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗠𝗮𝗻𝗶𝗳𝗲𝘀𝘁𝗮𝘁𝗶𝗼𝗻𝘀: May include chronic cough, recurrent pulmonary infiltrates, breathing difficulties, and sometimes pulmonary hemorrhage. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝗰𝗲: Consider in selected children with persistent or recurrent lung symptoms after evaluating other causes.

Food Allergy Diagnosis: Clinical History

𝗙𝗼𝘂𝗻𝗱𝗮𝘁𝗶𝗼𝗻: A detailed clinical history is the first and most important diagnostic step. 𝗔𝘀𝘀𝗲𝘀𝘀: Suspected food, amount eaten, timing, organs affected, previous reactions, recurrence after exposure, and treatments required. 𝗜𝗻𝘁𝗲𝗿𝗽𝗿𝗲𝘁𝗮𝘁𝗶𝗼𝗻: A convincing relationship between food exposure and symptoms is essential. 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝘁: A positive allergy test without matching clinical symptoms does not independently confirm allergy.

Food Allergy Tests: Skin Prick, Specific IgE and Tests Not Recommended

𝗦𝗸𝗶𝗻 𝗣𝗿𝗶𝗰𝗸 𝗧𝗲𝘀𝘁: Superficial skin exposure to an allergen → immediate wheal-and-flare suggests IgE sensitization. 𝗦𝗽𝗲𝗰𝗶𝗳𝗶𝗰 𝗜𝗴𝗘 𝗦𝗲𝗿𝗼𝗹𝗼𝗴𝘆: Blood test measuring allergen-specific IgE antibodies. 𝗟𝗶𝗺𝗶𝘁𝗮𝘁𝗶𝗼𝗻𝘀: These tests detect sensitization but alone do not prove clinical allergy; a child may test positive yet tolerate the food. 𝗡𝗼𝘁 𝗥𝗲𝗰𝗼𝗺𝗺𝗲𝗻𝗱𝗲𝗱: Atopy patch testing and intradermal testing are not recommended routinely for food allergy diagnosis. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝗰𝗲: Interpret tests with clinical history and avoid unnecessary food restrictions.

Food Allergy Diagnosis: Oral Food Challenge

𝗚𝗼𝗹𝗱 𝗦𝘁𝗮𝗻𝗱𝗮𝗿𝗱: Medically supervised oral food challenge is the diagnostic reference standard. 𝗣𝗿𝗼𝗰𝗲𝗱𝘂𝗿𝗲: Give gradually increasing amounts of suspected allergen and monitor for symptoms. 𝗥𝗶𝘀𝗸: May provoke severe reactions, including anaphylaxis. 𝗦𝗮𝗳𝗲𝘁𝘆: Conduct in a properly equipped clinical setting with medical supervision and emergency treatment available.

Food Allergy: Allergen Avoidance and Parental Education

𝗔𝘃𝗼𝗶𝗱𝗮𝗻𝗰𝗲: Strictly avoid confirmed triggering food allergens. 𝗙𝗼𝗼𝗱 𝗟𝗮𝗯𝗲𝗹𝘀: Read ingredient lists carefully to identify hidden allergens in manufactured foods. 𝗖𝗿𝗼𝘀𝘀-𝗖𝗼𝗻𝘁𝗮𝗰𝘁: Prevent allergen transfer via shared utensils, cooking surfaces, equipment, and food preparation. 𝗘𝗺𝗲𝗿𝗴𝗲𝗻𝗰𝘆 𝗣𝗿𝗲𝗽𝗮𝗿𝗮𝘁𝗶𝗼𝗻: Maintain an individualized emergency action plan and teach recognition of severe reactions. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗚𝗼𝗮𝗹: Prevent dangerous exposure without unnecessarily restricting nutritious foods.

Food Allergy: Emergency Action Plan and EpiPen

𝗥𝗲𝗰𝗼𝗴𝗻𝗶𝘇𝗲 𝗔𝗻𝗮𝗽𝗵𝘆𝗹𝗮𝘅𝗶𝘀: Throat/tongue swelling, breathing difficulties, wheezing, circulatory compromise, or rapidly progressive multisystem symptoms. 𝗙𝗶𝗿𝘀𝘁-𝗟𝗶𝗻𝗲 𝗧𝗿𝗲𝗮𝘁𝗺𝗲𝗻𝘁: Give intramuscular epinephrine promptly in the mid-outer thigh using an autoinjector. 𝗧𝘄𝗼 𝗘𝗽𝗶𝗣𝗲𝗻𝘀: Have TWO prescribed autoinjectors accessible. A second dose may be needed if symptoms persist or recur, typically after 5 minutes per the emergency plan. 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝘁: Do not automatically administer two injections at once or one into each leg. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗘𝗱𝘂𝗰𝗮𝘁𝗶𝗼𝗻: Train all caregivers and obtain emergency medical care after use.

Anaphylaxis: Biphasic Reaction and Observation

𝗗𝗲𝗳𝗶𝗻𝗶𝘁𝗶𝗼𝗻: Allergic symptoms return after initially improving or resolving, without further allergen exposure. 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝗰𝗲: Symptoms may recur even after the child appears stable. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗖𝗮𝗿𝗲: Appropriate medical observation following anaphylaxis; monitor airway, breathing, circulation, and recurrent symptoms. 𝗣𝗮𝗿𝗲𝗻𝘁𝗮𝗹 𝗘𝗱𝘂𝗰𝗮𝘁𝗶𝗼𝗻: Emergency medical evaluation is important even if symptoms improve after epinephrine.

Food Allergy: Oral and Sublingual Immunotherapy

𝗢𝗿𝗮𝗹 𝗜𝗺𝗺𝘂𝗻𝗼𝘁𝗵𝗲𝗿𝗮𝗽𝘆 (𝗢𝗜𝗧): Controlled, specialist-supervised administration of gradually adjusted oral allergen doses. 𝗦𝘂𝗯𝗹𝗶𝗻𝗴𝘂𝗮𝗹 𝗜𝗺𝗺𝘂𝗻𝗼𝘁𝗵𝗲𝗿𝗮𝗽𝘆 (𝗦𝗟𝗜𝗧): Controlled allergen exposure under the tongue. 𝗚𝗼𝗮𝗹: Desensitization—increase the amount tolerated before a reaction; not necessarily a permanent cure. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗘𝗱𝘂𝗰𝗮𝘁𝗶𝗼𝗻: Never attempt allergen exposure or dose escalation without a specialist plan.

Cow’s Milk Protein Allergy (CMPA): Definition, Epidemiology and Timing

𝗗𝗲𝗳𝗶𝗻𝗶𝘁𝗶𝗼𝗻: Immune reaction to cow’s milk proteins, either IgE- or non-IgE-mediated. 𝗣𝗿𝗼𝘁𝗲𝗶𝗻 𝗧𝗮𝗿𝗴𝗲𝘁𝘀: Casein and whey proteins, including beta-lactoglobulin and alpha-lactalbumin. 𝗧𝘆𝗽𝗶𝗰𝗮𝗹 𝗢𝗻𝘀𝗲𝘁: Usually in the first 4 months of life (lecturer estimate). 𝗣𝗿𝗲𝘃𝗮𝗹𝗲𝗻𝗰𝗲: Approximately 1.9% of infants (lecturer estimate). 𝗦𝘆𝗺𝗽𝘁𝗼𝗺 𝗧𝗶𝗺𝗶𝗻𝗴: May begin within about 45 minutes or be delayed several days, depending on mechanism. 𝗣𝗿𝗼𝗴𝗻𝗼𝘀𝗶𝘀: About 52.5% develop tolerance by approximately 5.5 years (lecturer estimate).

CMPA vs. Lactose Intolerance: Crucial Difference

𝗖𝗠𝗣𝗔: Immune reaction to cow’s milk proteins such as casein and whey. 𝗟𝗮𝗰𝘁𝗼𝘀𝗲 𝗜𝗻𝘁𝗼𝗹𝗲𝗿𝗮𝗻𝗰𝗲: Non-immune inability to digest lactose sugar due to insufficient lactase enzyme. 𝗖𝗠𝗣𝗔 𝗦𝘆𝗺𝗽𝘁𝗼𝗺𝘀: Skin, GI, respiratory, or multisystem reactions. 𝗟𝗮𝗰𝘁𝗼𝘀𝗲 𝗜𝗻𝘁𝗼𝗹𝗲𝗿𝗮𝗻𝗰𝗲 𝗦𝘆𝗺𝗽𝘁𝗼𝗺𝘀: Mainly bloating, pain, gas, and diarrhea. 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗗𝗶𝗳𝗳𝗲𝗿𝗲𝗻𝗰𝗲: CMPA may cause severe allergy; lactose intolerance does not cause anaphylaxis.

CMPA Diagnosis: Elimination and Challenge

𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗔𝘀𝘀𝗲𝘀𝘀𝗺𝗲𝗻𝘁: Feeding history, age at onset, exposure amount, timing, symptoms, stools, and weight gain. 𝗘𝗹𝗶𝗺𝗶𝗻𝗮𝘁𝗶𝗼𝗻: Temporarily remove cow’s milk protein from infant diet, or maternal diet when indicated for breastfed infant. 𝗔𝘀𝘀𝗲𝘀𝘀𝗺𝗲𝗻𝘁: Monitor for symptom improvement. 𝗖𝗼𝗻𝗳𝗶𝗿𝗺𝗮𝘁𝗶𝗼𝗻: Medically guided reintroduction to assess recurrence; severe/immediate reactions may require supervised oral challenge. 𝗖𝗮𝘂𝘁𝗶𝗼𝗻: Reflux, colic, crying, diarrhea, and eczema are common and do not diagnose CMPA by themselves.

CMPA: Gastrointestinal Manifestations

𝗦𝘆𝗺𝗽𝘁𝗼𝗺𝘀: Diarrhea, vomiting, colic, gastroesophageal reflux, discomfort, feeding difficulties, blood in stool, and rectal bleeding. 𝗙𝗣𝗜𝗔𝗣: Food protein-induced allergic proctocolitis is typically non-IgE-mediated; an otherwise well infant may have blood and mucus in stool. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗔𝘀𝘀𝗲𝘀𝘀𝗺𝗲𝗻𝘁: Feeding patterns, stool appearance, hydration, weight gain, and temporal relation to feeds.

CMPA: Skin, Respiratory and Other Manifestations

𝗦𝗸𝗶𝗻: Eczema/atopic dermatitis, facial involvement, sometimes urticaria. 𝗥𝗲𝘀𝗽𝗶𝗿𝗮𝘁𝗼𝗿𝘆: Rhinitis, cough, wheezing, bronchitis-/asthma-like symptoms, chronic secretions. 𝗢𝘁𝗵𝗲𝗿: Pallor from anemia, irritability, and restlessness. 𝗧𝗶𝗺𝗶𝗻𝗴: Symptoms may be rapid or delayed several days. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗔𝘀𝘀𝗲𝘀𝘀𝗺𝗲𝗻𝘁: Look for multisystem symptoms, respiratory difficulties, hydration, and growth. 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗖𝗮𝘂𝘁𝗶𝗼𝗻: Recurrent pneumonia may warrant broader investigation but does not alone establish CMPA. 𝗘𝗺𝗲𝗿𝗴𝗲𝗻𝗰𝘆: Breathing compromise following milk exposure requires urgent anaphylaxis assessment.

CMPA Treatment Stage 1: Continue Breastfeeding and Maternal Elimination

𝗙𝗶𝗿𝘀𝘁 𝗖𝗵𝗼𝗶𝗰𝗲: Continue breastfeeding whenever possible; CMPA alone is not usually a reason to stop. 𝗠𝗮𝘁𝗲𝗿𝗻𝗮𝗹 𝗘𝗹𝗶𝗺𝗶𝗻𝗮𝘁𝗶𝗼𝗻: When medically indicated, temporarily remove cow’s milk products from maternal diet. 𝗔𝘀𝘀𝗲𝘀𝘀𝗺𝗲𝗻𝘁: Monitor infant symptoms and reassess diagnosis with appropriate guided reintroduction. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗙𝗼𝗹𝗹𝗼𝘄-𝘂𝗽: Ensure adequate maternal nutrition, infant intake, weight gain, and symptom improvement.

CMPA Treatment Stage 2: Extensively Hydrolyzed Formula (EHF)

𝗜𝗻𝗱𝗶𝗰𝗮𝘁𝗶𝗼𝗻: Common first formula option when breastfeeding is unavailable or insufficient. 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Extensive hydrolysis breaks milk proteins into small peptides → reduces allergenicity. 𝗘𝘅𝗮𝗺𝗽𝗹𝗲𝘀: Nutramigen and Alimentum. 𝗗𝗶𝘀𝗮𝗱𝘃𝗮𝗻𝘁𝗮𝗴𝗲: Relatively high cost. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗙𝗼𝗹𝗹𝗼𝘄-𝘂𝗽: Monitor tolerance, symptom improvement, intake, and weight gain.

CMPA Treatment Stage 3: Amino Acid-Based Formula (AAF)

𝗜𝗻𝗱𝗶𝗰𝗮𝘁𝗶𝗼𝗻: Severe CMPA, poor growth, or persistent reaction despite an appropriate EHF trial. 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Contains free amino acids instead of intact cow’s milk proteins or larger peptides. 𝗕𝗲𝗻𝗲𝗳𝗶𝘁: No intact cow’s milk protein allergens in formula. 𝗘𝘅𝗮𝗺𝗽𝗹𝗲: EleCare. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗙𝗼𝗹𝗹𝗼𝘄-𝘂𝗽: Monitor symptoms, feeding tolerance, nutritional intake, and growth.

Lactose-Free Formula vs. Hypoallergenic Formula

𝗟𝗮𝗰𝘁𝗼𝘀𝗲-𝗙𝗿𝗲𝗲 𝗙𝗼𝗿𝗺𝘂𝗹𝗮: Removes/replaces lactose sugar, but may still contain intact cow’s milk proteins. 𝗛𝘆𝗽𝗼𝗮𝗹𝗹𝗲𝗿𝗴𝗲𝗻𝗶𝗰 𝗙𝗼𝗿𝗺𝘂𝗹𝗮: Designed to reduce reactions to cow’s milk proteins in infants with CMPA. 𝗘𝗛𝗙: Contains extensively hydrolyzed proteins (small peptides) to reduce allergenicity. 𝗔𝗔𝗙: Contains free amino acids rather than intact protein or peptides. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝗰𝗲: Lactose-free cow’s milk formula is NOT suitable treatment for CMPA if milk proteins remain. 𝗦𝗼𝘆 𝗙𝗼𝗿𝗺𝘂𝗹𝗮: Not automatically appropriate for CMPA because some infants also react to soy protein.

CMPA: Follow-up, Tolerance and Reintroduction

𝗠𝗼𝗻𝗶𝘁𝗼𝗿: Diarrhea, vomiting, rectal bleeding, eczema, feeding difficulties, and other symptoms. 𝗚𝗿𝗼𝘄𝘁𝗵: Monitor weight gain, nutrition, hydration, and feeding tolerance. 𝗡𝗮𝘁𝘂𝗿𝗮𝗹 𝗛𝗶𝘀𝘁𝗼𝗿𝘆: Many children develop oral tolerance to cow’s milk proteins over time. 𝗥𝗲𝗮𝘀𝘀𝗲𝘀𝘀𝗺𝗲𝗻𝘁: Medical follow-up prevents unnecessary lifelong dietary avoidance. 𝗥𝗲𝗶𝗻𝘁𝗿𝗼𝗱𝘂𝗰𝘁𝗶𝗼𝗻: Type and severity of allergy determine timing and method; avoid unsupervised challenges following severe/immediate reactions.

Lactose Intolerance: Definition and Main Pathophysiology

𝗗𝗲𝗳𝗶𝗻𝗶𝘁𝗶𝗼𝗻: A non-immune digestive problem caused by insufficient lactase, a brush-border enzyme of the small intestine. 𝗡𝗼𝗿𝗺𝗮𝗹 𝗗𝗶𝗴𝗲𝘀𝘁𝗶𝗼𝗻: Lactase splits the disaccharide lactose (a sugar) into glucose + galactose for absorption. 𝗦𝘁𝗲𝗽 𝟭: Low lactase → lactose remains undigested in the small intestine. 𝗦𝘁𝗲𝗽 𝟮: Lactose enters the colon and holds water in the bowel (osmotic effect) → watery diarrhea. 𝗦𝘁𝗲𝗽 𝟯: Colonic bacteria ferment lactose → hydrogen, methane, and organic acids → gas, bloating, and cramping. 𝗞𝗲𝘆 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺𝘀: Osmotic diarrhea + bacterial fermentation; severity often depends on lactose dose.

Lactose Intolerance vs. CMPA: Key Distinction

𝗟𝗮𝗰𝘁𝗼𝘀𝗲 𝗜𝗻𝘁𝗼𝗹𝗲𝗿𝗮𝗻𝗰𝗲: Non-immune lactase deficiency affects digestion of lactose SUGAR → mainly GI symptoms, not anaphylaxis. 𝗖𝗠𝗣𝗔: Immune reaction to cow’s milk PROTEINS (casein and whey) → may affect multiple organs and cause anaphylaxis. 𝗗𝗶𝗲𝘁𝗮𝗿𝘆 𝗗𝗶𝘀𝘁𝗶𝗻𝗰𝘁𝗶𝗼𝗻: Reducing lactose does not require avoiding every dairy food; some dairy products contain little lactose. 𝗖𝗿𝗶𝘁𝗶𝗰𝗮𝗹 𝗙𝗼𝗿𝗺𝘂𝗹𝗮 𝗣𝗼𝗶𝗻𝘁: Lactose-free cow’s milk still contains cow’s milk proteins → may suit lactose intolerance but NOT CMPA.

Primary (Late-Onset) Lactase Deficiency

𝗧𝘆𝗽𝗲: Most common form of lactase deficiency (primary lactase non-persistence). 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Genetically programmed decline in intestinal lactase production after infancy → reduced lactose digestion. 𝗢𝗻𝘀𝗲𝘁: Lecturer describes symptoms around age 4–5 years; age of onset varies by person and population. 𝗣𝗼𝗽𝘂𝗹𝗮𝘁𝗶𝗼𝗻𝘀: Lecturer mentions Asian, African, Arab, and Israeli populations as commonly affected. 𝗖𝗼𝘂𝗿𝘀𝗲: Usually persistent; manage according to individual lactose tolerance.

Secondary Lactase Deficiency

𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Injury to small-intestinal villi/brush border → reduced lactase activity → lactose malabsorption. 𝗖𝗮𝘂𝘀𝗲𝘀: Gastroenteritis and inflammatory/mucosal disorders such as untreated celiac disease; cystic fibrosis is also listed in the notes. 𝗖𝗲𝗹𝗶𝗮𝗰 𝗖𝗼𝗻𝗻𝗲𝗰𝘁𝗶𝗼𝗻: Immune damage to the intestinal mucosa reduces brush-border lactase → secondary lactose intolerance. 𝗖𝗼𝘂𝗿𝘀𝗲: Often temporary; lactase activity may recover after the underlying intestinal disease resolves or is treated. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗜𝗺𝗽𝗼𝗿𝘁𝗮𝗻𝗰𝗲: Address the underlying cause and reassess whether ongoing lactose restriction is needed.

Congenital Lactase Deficiency

𝗗𝗲𝗳𝗶𝗻𝗶𝘁𝗶𝗼𝗻: An extremely rare inherited disorder with severe/near-complete lactase deficiency from birth. 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Lactose from breast milk or standard formula cannot be adequately split into glucose and galactose. 𝗣𝗿𝗲𝘀𝗲𝗻𝘁𝗮𝘁𝗶𝗼𝗻: Severe watery diarrhea soon after lactose-containing feeds begin in the newborn period. 𝗠𝗮𝗻𝗮𝗴𝗲𝗺𝗲𝗻𝘁: Lifelong lactose-free nutrition and careful monitoring of hydration, growth, and nutrition.

Developmental Lactase Deficiency

𝗗𝗲𝗳𝗶𝗻𝗶𝘁𝗶𝗼𝗻: Temporary immaturity of lactase production in premature infants. 𝗣𝗼𝗽𝘂𝗹𝗮𝘁𝗶𝗼𝗻: Especially babies born before approximately 34 weeks of gestation. 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Immature intestinal brush border has not yet developed adequate lactase activity → reduced lactose digestion. 𝗖𝗼𝘂𝗿𝘀𝗲: Enzyme capacity generally increases as the intestine matures.

Lactose Intolerance: Clinical Signs and Symptoms

𝗧𝗶𝗺𝗶𝗻𝗴: Usually approximately 30 minutes to several hours after consuming lactose. 𝗚𝗜 𝗦𝘆𝗺𝗽𝘁𝗼𝗺𝘀: Abdominal bloating/distention, spasmodic abdominal pain, cramps, flatulence (gas), and watery diarrhea. 𝗪𝗵𝘆 𝗗𝗶𝗮𝗿𝗿𝗵𝗲𝗮: Undigested lactose attracts/retains water in the bowel → osmotic diarrhea. 𝗪𝗵𝘆 𝗚𝗮𝘀 𝗮𝗻𝗱 𝗣𝗮𝗶𝗻: Bacterial fermentation produces hydrogen, methane, and acids → distention, gas, and cramping. 𝗣𝗮𝘁𝘁𝗲𝗿𝗻: Often dose-dependent; some children tolerate small servings.

Lactose Intolerance Diagnosis: Hydrogen Breath Test

𝗧𝗲𝘀𝘁: A commonly used noninvasive investigation of lactose malabsorption. 𝗣𝗿𝗼𝗰𝗲𝗱𝘂𝗿𝗲: Child ingests a measured lactose load; exhaled-breath samples are collected over time. 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺: Undigested lactose reaches colon → bacteria ferment it → hydrogen enters blood and is exhaled by lungs. 𝗣𝗼𝘀𝗶𝘁𝗶𝘃𝗲 𝗙𝗶𝗻𝗱𝗶𝗻𝗴: Increased breath hydrogen after lactose supports malabsorption, especially with typical symptoms. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗥𝗼𝗹𝗲: Prepare child per test instructions and monitor symptoms.

Lactose Intolerance Diagnosis: Stool Tests

𝗨𝘀𝗲: Mainly supportive assessment in infants; findings are not specific for lactase deficiency. 𝗦𝘁𝗼𝗼𝗹 𝗽𝗛: Acidic stool suggests carbohydrate malabsorption because fermentation produces organic acids. 𝗥𝗲𝗱𝘂𝗰𝗶𝗻𝗴 𝗦𝘂𝗯𝘀𝘁𝗮𝗻𝗰𝗲𝘀: A positive test suggests unabsorbed carbohydrates in stool. 𝗟𝗶𝗺𝗶𝘁𝗮𝘁𝗶𝗼𝗻: Neither stool test alone proves lactose intolerance or lactase deficiency.

Lactose Intolerance Diagnosis: Dietary Elimination Trial

𝗛𝗶𝘀𝘁𝗼𝗿𝘆: Link dairy/lactose consumption to onset of GI symptoms. 𝗧𝗿𝗶𝗮𝗹: Temporarily reduce or eliminate lactose and assess for symptom improvement. 𝗜𝗻𝘁𝗲𝗿𝗽𝗿𝗲𝘁𝗮𝘁𝗶𝗼𝗻: Improvement supports lactose intolerance but does not independently establish the exact cause.

Lactose Intolerance: Nutritional Education and Nursing Care

𝗬𝗼𝗴𝘂𝗿𝘁: Regular yogurt with live bacterial cultures may be better tolerated because bacterial enzymes help digest lactose. 𝗛𝗮𝗿𝗱 𝗖𝗵𝗲𝗲𝘀𝗲: Aged hard cheeses have very little lactose and are often better tolerated. 𝗟𝗮𝗰𝘁𝗮𝘀𝗲 𝗦𝘂𝗽𝗽𝗹𝗲𝗺𝗲𝗻𝘁𝘀: May be taken before dairy to improve lactose digestion. 𝗦𝘂𝗯𝘀𝘁𝗶𝘁𝘂𝘁𝗲𝘀: Lactose-free or reduced-lactose milk/formula when appropriate; probiotics may help some children but benefits vary. 𝗚𝗿𝗮𝗱𝘂𝗮𝗹 𝗔𝗽𝗽𝗿𝗼𝗮𝗰𝗵: Many patients tolerate about 12 g lactose (roughly one cup of milk), especially with a meal; adjust to individual tolerance. 𝗚𝗼𝗮𝗹: Reduce symptoms without unnecessarily excluding all dairy products.

Lactose Intolerance: Nursing Alert—Nutritional Deficiencies

𝗥𝗶𝘀𝗸: Dairy avoidance may reduce calcium and vitamin D intake → poorer bone mineralization during growth. 𝗔𝗹𝘀𝗼 𝗠𝗼𝗻𝗶𝘁𝗼𝗿: Adequate protein, energy intake, and overall growth. 𝗡𝘂𝗿𝘀𝗶𝗻𝗴 𝗘𝗱𝘂𝗰𝗮𝘁𝗶𝗼𝗻: Identify suitable calcium- and vitamin-D-rich alternatives or supplements as needed. 𝗗𝗶𝗲𝘁𝗶𝘁𝗶𝗮𝗻 𝗥𝗲𝗳𝗲𝗿𝗿𝗮𝗹: Consider when restrictions are extensive, growth is affected, or secondary intestinal disease is present