Immune-Mediated Protracted Diarrhea of Infancy

Other names
Types
Causes
Symptoms and signs
Diagnostic tests
Non-pharmacological treatments
Drug treatments
Dietary molecular supplements
Therapies for “immunity-booster / regenerative / stem-cell
Procedures/surgeries
Prevention tips
When to see a doctor urgently
What to eat & what to avoid (10 quick pointers)
FAQs

Immune-mediated protracted diarrhea of infancy means a baby has diarrhea that lasts for more than two weeks because the immune system is attacking or overreacting inside the gut. The stools are frequent and watery. Babies may not gain weight and can become dehydrated or malnourished. This problem often starts in the first months of life and does not improve with simple diet changes. It can come from autoimmune diseases (where the body attacks its own intestine), immune-allergic reactions to foods (like non-IgE milk allergy or FPIES), very-early-onset inflammatory bowel disease, or immune-regulation disorders such as IPEX. Doctors first exclude infections. Then they look for immune causes using blood tests, stool markers, endoscopy, biopsies, and sometimes genetic testing. Treatment depends on the cause and may include special diets, medicines that calm the immune system, or targeted therapies for any genetic immune problem. NCBI+3PMC+3PMC+3

Immune-mediated protracted diarrhea of infancy means a baby has ongoing diarrhea that lasts many weeks and is driven largely by immune problems rather than a simple infection. In some babies, the immune system attacks the gut lining (autoimmune enteropathy). In others, the immune system over-reacts to food proteins like cow’s milk or soy (non-IgE food allergy such as FPIES), or there is a genetic immune regulation defect (e.g., IPEX). These conditions damage the small-bowel villi, reduce absorption, and cause malnutrition, dehydration, and vitamin/mineral losses. Treatment focuses on hydration and nutrition first, then treating the immune cause (dietary elimination, immunosuppressive medicines, or—rarely—transplant). Children’s Hospital of Philadelphia+3PMC+3PMC+3

Other names

Doctors and researchers have used several names for similar clinical pictures in infants:

Intractable diarrhea of infancy / Protracted diarrhea of infancy (older terms for severe, chronic, unexplained diarrhea beginning in early infancy). NASPGHAN+1
Autoimmune enteropathy (AIE) (autoimmune damage to small intestine causing severe diarrhea and malabsorption). PMC+1
IPEX-associated enteropathy (intestinal autoimmunity as part of FOXP3 mutation syndrome). NCBI+1
Non-IgE-mediated cow’s milk protein allergy (CMPA) (immune-mediated, not antibody-IgE type). ESPGHAN+1
Food protein–induced enterocolitis syndrome (FPIES) (non-IgE food allergy; acute and chronic forms). PMC+1
Very-early-onset inflammatory bowel disease (VEO-IBD) (IBD presenting before age 6, often monogenic immune defects). PMC
Enteropathy of common variable immunodeficiency (CVID-related enteropathy) (malabsorption/diarrhea from primary immunodeficiency). PMC

Types

Autoimmune enteropathy (AIE) – Autoantibodies and T-cell–driven damage to intestinal lining; severe malabsorption and watery diarrhea; biopsy critical. PMC+1
IPEX enteropathy – Part of a systemic immune-regulation defect (FOXP3). Babies develop early-onset diarrhea, eczema, endocrine autoimmunity; requires genetic confirmation. NCBI
Non-IgE-mediated CMPA – Immune reaction to milk proteins without IgE; symptoms improve on elimination diet; diagnosis is clinical plus diet trials and, if needed, challenge. ESPGHAN+1
Chronic FPIES – Ongoing exposure to trigger food causes persistent diarrhea, poor weight gain; removal of trigger resolves symptoms. PMC
VEO-IBD / monogenic IBD – Immune defects cause colitis/enteritis in infants; often severe and therapy-resistant without targeted treatment. PMC
CVID-related enteropathy – Hypogammaglobulinemia with chronic diarrhea and villous atrophy that mimics celiac disease but is immune-defect related. PMC
Post-infectious immune-mediated enteropathy – After an infection clears, an abnormal immune response keeps the gut inflamed and leaky. PMC
Eosinophilic gastroenteritis/enterocolitis (non-IgE predominant variants) – Eosinophil-rich inflammation from immune dysregulation; can present with diarrhea and protein loss. PMC

Causes

Autoimmune enterocyte injury (AIE) – Body makes antibodies and activated T cells that attack intestinal lining, leading to villous atrophy and severe malabsorption. PMC+1
IPEX syndrome (FOXP3 mutation) – Regulatory T cells fail; widespread autoimmunity hits the gut first, causing early, persistent diarrhea. NCBI
Non-IgE cow’s milk protein allergy – Delayed immune inflammation to milk proteins; diarrhea resolves with strict elimination and appropriate formula. ESPGHAN+1
Chronic FPIES to milk/soy/grains – Repeated exposure to a trigger food (e.g., cow’s milk, rice, oat) keeps inflammation active, causing chronic diarrhea and poor weight gain. PMC
Very-early-onset IBD – Single-gene immune defects (e.g., IL-10 pathway) drive colitis/enteritis starting in infancy. PMC
Common variable immunodeficiency (CVID) enteropathy – Defective antibody production with immune-mediated small bowel injury leading to diarrhea. PMC
Post-infectious immune enteropathy – After acute gastroenteritis, an abnormal immune response persists, keeping the intestine inflamed. PMC
Eosinophilic gastrointestinal disease – Immune-mediated eosinophil infiltration of bowel causes diarrhea, sometimes with protein loss. PMC
Autoimmune polyendocrine syndromes with gut involvement – Systemic autoimmunity that includes enteropathy. PMC
Drug-triggered immune colitis (rare in infants) – Immune reaction to medications (e.g., antibiotics) can injure mucosa and cause diarrhea. PMC
Immune dysregulation from primary immunodeficiencies (non-CVID) – Several inborn errors of immunity present with chronic, immune-mediated diarrhea. PMC
Gluten-sensitive enteropathy in very young infants (uncommon) – Rare before weaning, but immune-mediated villous atrophy can occur in certain contexts. PMC
Food protein–induced allergic proctocolitis – Immune reaction, usually to milk/soy proteins; mucus/blood in stools of young infants. ESPGHAN
Allergic enteropathy beyond milk (multiple foods) – Non-IgE immune reactions to various foods can cause persistent diarrhea until triggers are removed. PMC
Autoimmune small-bowel predominant disease (AIE variants) – Seronegative variants still behave like autoimmune mucosal injury. PMC
Enteropathy in immune checkpoint dysregulation (monogenic) – Specific gene defects (e.g., CTLA4, LRBA) cause immune-mediated gut inflammation in early life. CGH Journal
Protein-losing enteropathy of immune cause – Immune injury increases leakiness, leading to low albumin and edema with diarrhea. PMC
Autoimmune colitis overlap with small-bowel disease – Combined small and large bowel immune inflammation drives persistent symptoms. PMC
Enteropathy after severe cow’s-milk intolerance in preterm infants (immune-mediated component) – Some cases have immune mechanisms that prolong diarrhea. ESPGHAN
Mixed immune-allergic gut disorders – Children may have overlapping conditions (e.g., FPIES plus atopy) that sustain chronic diarrhea. PMC

Symptoms and signs

Watery, frequent stools – Main feature; often persists despite routine care. PMC
Failure to thrive / poor weight gain – Malabsorption prevents normal growth. PMC
Dehydration – Dry mouth, sunken eyes, poor skin turgor in prolonged diarrhea. PMC
Vomiting (especially with food triggers) – Common in FPIES and some milk allergies. PMC
Blood or mucus in stool – Suggests colitis or allergic proctocolitis. ESPGHAN
Abdominal distension and cramps – From inflammation and gas. PMC
Irritability or lethargy – Due to dehydration or electrolyte changes. PMC
Skin eczema or atopic signs – Common in non-IgE allergy and IPEX. NCBI+1
Mouth ulcers / perianal rash – Seen in IBD-like inflammation. PMC
Edema (swelling) – Protein-losing enteropathy lowers albumin. PMC
Anemia (pallor) – From chronic inflammation or nutrient loss. PMC
Nutrient deficiencies (e.g., iron, vitamins) – Villous damage reduces absorption. PMC
Fever (sometimes) – More likely with colitis or secondary infection exclusion phase. PMC
Electrolyte disturbances (e.g., low sodium) – From ongoing fluid loss. PMC
Endocrine autoimmunity (in IPEX) – Diabetes or thyroid disease may co-occur. NCBI

Diagnostic tests

A) Physical examination (bedside assessment)

Hydration status check – Looks for dry mucosa, sunken fontanelle, decreased urine; guides urgent fluid therapy. PMC
Growth and nutrition assessment – Plot weight, length, head circumference; persistent faltering suggests malabsorption. PMC
Skin and allergy signs – Eczema, urticaria absent/present, or chronic rash support an immune/allergic cause. ESPGHAN
Abdominal exam – Distension, tenderness, hyperactive bowel sounds in active enteritis. PMC
Perianal inspection – Fissures, ulcers, or dermatitis point to colitis/IBD features. PMC

B) “Manual/bedside” tests and clinical trials

Stool pH and reducing substances (bedside) – Suggest carbohydrate malabsorption; supportive but nonspecific. PMC
Fecal occult blood (point-of-care) – Detects microscopic bleeding in allergic colitis or IBD-like disease. PMC
Careful elimination diet trial – Removing suspected triggers (e.g., milk/soy) can clarify non-IgE allergy or chronic FPIES. ESPGHAN+1
Medically supervised oral food challenge (selected cases) – Gold standard for confirming FPIES/CMPA when safe and indicated. PMC+1
Stool output diary and intake monitoring – Quantifies severity and guides nutrition planning. PMC

C) Laboratory and pathological tests

Complete blood count (CBC) – Looks for anemia, eosinophilia, or infection signs; tracks illness severity. PMC
Electrolytes, kidney function, acid–base – Detects dehydration and metabolic imbalance from losses. PMC
Inflammatory markers (CRP/ESR) – Support inflammatory disease when elevated. PMC
Stool tests to exclude infection – Cultures, PCR panels; immune causes are considered only after pathogens are excluded. PMC
Stool calprotectin – Indicates intestinal inflammation; helpful in IBD-like disease and severe enteropathy. PMC
Serum Ig levels and vaccine titers – Screen for primary immunodeficiencies (e.g., CVID) that cause enteropathy. PMC
Autoantibodies to enterocytes (when available) – Support AIE diagnosis in context of biopsy findings. PMC
Celiac serology (age-appropriate) and total IgA – Rare cause in young infants, but part of structured work-up in persistent malabsorption. PMC
Upper/lower endoscopy with small-bowel and colonic biopsies – Essential to document villous atrophy, crypt apoptosis, lymphoplasmacytic infiltrates, or eosinophils; distinguishes AIE, IBD, eosinophilic disease, and others. PMC+1
Genetic testing (targeted panels or exome) – Looks for FOXP3 (IPEX) and other monogenic immune defects guiding precise therapy. NCBI+1

D) Electrodiagnostic/physiologic tools (used selectively)

Electrocardiogram (ECG) – Monitors for arrhythmias from severe electrolyte imbalance in dehydrated infants. PMC
24-hour esophageal pH-impedance (selected) – Helps when reflux/aspiration complicates feeding in chronic illness; clarifies differential but not always required. PMC

E) Imaging (to support diagnosis or rule out mimics)

Abdominal ultrasound – Noninvasive check for bowel wall thickening, ascites (protein loss), or hepatosplenomegaly. PMC
Contrast studies (upper GI) when indicated – Exclude anatomic problems (e.g., malrotation) in complex cases. PMC
Chest radiograph – Consider if immunodeficiency suspected (recurrent infections) or to assess lines/tubes. PMC
Nuclear medicine albumin scan (selected) – Confirms protein-losing enteropathy when serum albumin is low with edema. PMC

Non-pharmacological treatments

Below are brief, high-yield items. I can expand any into 150-word mini-essays with mechanisms and references on request.

Low-osmolality oral rehydration (ORS) – Use WHO-recommended 245 mOsm/L ORS for dehydration. It lowers need for IV fluids and reduces stool output vs older formulas. Purpose: correct fluids/electrolytes safely. Mechanism: glucose-sodium cotransport speeds water uptake. UNICEF DATA+1
Zinc with diarrhea episodes – WHO/UNICEF recommend 10 mg/day (<6 mo) or 20 mg/day (≥6 mo) for 10–14 days to shorten diarrhea and prevent recurrences. Purpose: support mucosal healing and immunity. Mechanism: enzyme cofactor, improves transporters and barrier. World Health Organization+1
Continue feeding – After rehydration, keep breastmilk or appropriate formula going to prevent malnutrition; avoid unnecessary fasting. Purpose: preserve gut function. Mechanism: nutrients stimulate villus recovery. PubMed
Targeted elimination diet – If cow’s-milk protein allergy suspected, use an amino acid-based formula (AAF) in severe cases; eHF may be used for milder cases per guidelines. Purpose: remove offending antigen. Mechanism: eliminates protein triggers of cell-mediated inflammation. ESPGHAN+1
Dietitian-led feeding plan – Structured caloric goals, step-wise formula trials (eHF → AAF), and micronutrient repletion. Purpose: regain weight/length. Mechanism: tailored macro/micro delivery to reverse deficits. ESPGHAN
Breastfeeding optimization – If maternal diet helps (rare), a short supervised maternal elimination may be tried; otherwise maintain breastmilk while investigating other causes. Purpose: maintain ideal nutrition and immunity. Mechanism: human milk oligosaccharides support mucosa and microbiome. PMC
Enteral tube feeding (NG/G-tube/J-tube) – For poor intake or severe growth faltering, continuous pump feeds can stabilize gains. Purpose: ensure reliable calories. Mechanism: bypass feeding fatigue; steady nutrient delivery. PGHN+1
Infection control – Hand hygiene, safe water, and vaccine updates (e.g., rotavirus when eligible). Purpose: prevent superimposed infections. Mechanism: reduces pathogen exposure in vulnerable infants. PubMed
Probiotics (selected cases) – Certain strains (e.g., Lactobacillus rhamnosus GG) may shorten persistent diarrhea modestly; use with caution in immunocompromised infants. Purpose: microbiome support. Mechanism: competitive inhibition, SCFA production. PMC+1
Micronutrient repletion – Iron, fat-soluble vitamins, folate, B12, and electrolytes guided by labs. Purpose: correct common deficits from malabsorption. Mechanism: restores enzyme systems and growth. PMC
Lactose management – Temporary lactose-free formula may help when severe mucosal damage causes secondary lactase deficiency. Purpose: reduce osmotic load. Mechanism: avoids unabsorbed lactose drawing water. ESPGHAN
MCT-rich feeds – Medium-chain triglycerides are absorbed more easily and can support weight gain when fat malabsorption coexists. Purpose: improve energy absorption. Mechanism: portal vein uptake without bile micelles. ESPGHAN
Energy-dense feeds – Calorie concentration under supervision to reach catch-up growth targets. Purpose: rapid nutritional recovery. Mechanism: higher kcal/mL intake. PGHN
Allergen education – Clear label reading, cross-contact avoidance, and emergency plans for FPIES-type reactions. Purpose: prevent flares. Mechanism: strict antigen avoidance. PubMed
Frequent growth monitoring – Plot weight/length and head circumference to detect failure-to-thrive early. Purpose: track response. Mechanism: objective anthropometry. PMC
Stool-diary and trigger tracking – Record feeds, symptoms, and exposures to guide iterative diet changes. Purpose: precision elimination. Mechanism: pattern recognition. PMC
Oral rehydration teaching at home – Caregiver training on signs of dehydration and correct ORS mixing. Purpose: prevent ER visits. Mechanism: early at-home correction. WHO Apps
Psychosocial and caregiver support – High caregiver stress is common; connect families with specialist nurses and support groups. Purpose: adherence and resilience. Mechanism: education and coping resources. fpies.org
TPN when needed (short-term) – If enteral nutrition fails, parenteral nutrition via central line prevents life-threatening malnutrition while therapy begins. Purpose: bridge to gut recovery. Mechanism: IV macro/micronutrients. PMC
Specialist center referral – Early involvement of pediatric gastroenterology/immunology for testing (endoscopy, genetics) speeds diagnosis and targeted care. Purpose: treat the exact cause. Mechanism: precision medicine. PMC

Drug treatments

For infants, exact doses/timing must be set by the child’s specialist. Below I explain what each medicine is for and how it works, with key evidence.

Oral/IV corticosteroids (e.g., prednisolone, methylprednisolone) – First-line for autoimmune enteropathy or immune flares to calm mucosal inflammation. Purpose: induce remission quickly. Mechanism: broad cytokine suppression. Common side effects: hyperglycemia, infection risk, hypertension, growth effects. PMC+1
Budesonide (topical steroid) – High first-pass hepatic metabolism gives more local gut effects with fewer systemic effects; used in milder or maintenance settings under specialist care. Side effects: milder steroid-type risks. Lippincott Journals
Tacrolimus (calcineurin inhibitor) – Effective in steroid-refractory AIE; case series suggest ~70–80% remission. Purpose: steroid-sparing control. Mechanism: T-cell activation blockade. Side effects: nephrotoxicity, tremor, infections; needs blood-level monitoring. PMC
Cyclosporine (calcineurin inhibitor) – Alternative to tacrolimus in refractory disease; similar mechanism and monitoring needs. Side effects: nephrotoxicity, hypertension, gum hyperplasia. eurannallergyimm.com
Mycophenolate mofetil (antimetabolite) – Used as adjunct or alternative immunosuppression to maintain remission in AIE when steroids cannot be tapered. Side effects: cytopenias, infection risk, GI upset. eurannallergyimm.com
Azathioprine/6-MP (thiopurines) – Classic steroid-sparing agents in autoimmune gut disease; require TPMT/NUDT15 consideration in older children. Side effects: leukopenia, liver enzyme rise, pancreatitis. CGH Journal
Infliximab (anti-TNF) – Reports show benefit in refractory AIE to lower inflammation and allow nutrition recovery. Side effects: infusion reactions, TB reactivation (screen first). Wiley Online Library+1
Ustekinumab (anti-IL12/23) – Case reports/series describe success in steroid-refractory autoimmune enteropathy when anti-TNF is unsuitable. Side effects: infection risk. Lippincott Journals
Sirolimus (mTOR inhibitor) – Helpful in immune-dysregulation enteropathies (e.g., LRBA deficiency, selected IPEX cases). Side effects: mucositis, hyperlipidemia, cytopenias. eurannallergyimm.com+1
IVIG (intravenous immunoglobulin) – Used in immune dysregulation or combined immunodeficiency phenotypes to modulate autoimmunity and reduce infections while the gut heals. Side effects: headache, aseptic meningitis (rare). Immune Deficiency Foundation
Antiemetics for FPIES episodes – Ondansetron may reduce vomiting during acute FPIES reactions in ED settings; used per consensus pathways. Side effects: constipation, QT prolongation (monitoring). PubMed
Epinephrine (context: IgE-mediated allergy only) – Not for FPIES, but essential if a child later develops IgE-mediated anaphylaxis. Side effects: pallor, tremor; life-saving in anaphylaxis. PubMed
Antibiotics (selected) – Only when there’s a documented bacterial infection or SIBO; not routine for immune-mediated causes. Overuse worsens dysbiosis. Side effects: diarrhea, resistance. PMC
Antivirals/antiparasitics (selected) – If testing finds specific pathogens (e.g., CMV in immunosuppressed infants), targeted therapy is used alongside immune control. Side effects depend on agent. PMC
Acid suppression (short-term if severe esophagitis/mucositis) – To protect upper GI tract during high-dose steroids/TPN; avoid long-term routine use (infection risk). PMC
Electrolyte solutions and supplements – Correct hyponatremia, hypokalemia, bicarbonate loss due to stool losses; individualized plans. Side effects: shifts if given too fast. WHO Apps
Vitamin D supplementation – Supports immunity and bone health in malabsorption; dosing per labs/age. Side effects: hypercalcemia if overdosed. PMC
Probiotic preparations (carefully selected) – Considered adjunctive in persistent diarrhea; evidence modest and strain-specific; avoid in severe immunodeficiency. Side effects: rare bacteremia in high-risk hosts. PMC
Amino acid–based formula as “medical food” – Not a drug, but prescribed like one in severe CMPA/FPIES or enteropathy to induce remission and support growth. Side effects: cost, palatability. ESPGHAN+1
Hematopoietic stem-cell transplant (HSCT)–conditioning meds – In IPEX and related immune-regulation defects, HSCT is the only curative therapy; conditioning and graft-versus-host prophylaxis regimens are individualized. Risks: infection, GVHD; benefits: long-term cure rates ~70–80% in series. Frontiers+1

Dietary molecular supplements

Zinc – Standard of care with diarrhea episodes (see doses above); shortens illness and lowers recurrence for months. World Health Organization+1
Oral rehydration salts (glucose-electrolyte) – Not a “supplement” in the herbal sense, but essential medical nutrition. UNICEF DATA
Specific probiotics (e.g., LGG) – Modest benefit in persistent diarrhea; discuss safety first if immunocompromised. PMC
Vitamin D – Correct deficiency; supports barrier and immune function. PMC
Iron – Replete if iron-deficiency anemia emerges; improves neurodevelopmental outcomes. PMC
Folate/B12 – Replace if malabsorption documented. PMC
Fat-soluble vitamins (A, E, K) – Needed in fat malabsorption; dosing by labs. PMC
Electrolyte packets (K/Mg as indicated) – Target stool-related losses safely. WHO Apps
MCT oil (as part of formula plan) – Easier fat absorption in damaged mucosa. ESPGHAN
Calcium/Phosphate – Bone protection during prolonged steroid/TPN courses. PMC

Always use supplements under pediatric supervision; dosing depends on age, labs, and growth.

Therapies for “immunity-booster / regenerative / stem-cell

Intravenous immunoglobulin (IVIG) – Provides pooled antibodies; can modulate autoimmunity and reduce infections while definitive therapy proceeds; dosing by weight and indication. Mechanism: Fc-mediated immune modulation. Immune Deficiency Foundation
Sirolimus – mTOR inhibitor that can calm immune over-activation in certain immune-dysregulation enteropathies, including some IPEX-like cases. Mechanism: T-cell proliferation block. eurannallergyimm.com
Tacrolimus – Potent T-cell inhibitor that often induces remission in steroid-refractory autoimmune enteropathy. Mechanism: calcineurin inhibition. PMC
HSCT (allogeneic stem-cell transplant) – Replaces defective immune system (curative for IPEX). Timing and donor match are crucial. Mechanism: new regulatory T-cell function via donor hematopoiesis. Frontiers
Ustekinumab / anti-TNF biologics – Advanced biologics to rebalance cytokine pathways when conventional agents fail. Mechanism: block IL-12/23 or TNF-α. Lippincott Journals+1
Nutritional rehabilitation as “regenerative” support – Adequate protein-energy, micronutrients, and AAF where indicated are essential for mucosal regeneration. Mechanism: fuels epithelial turnover and barrier repair. ESPGHAN

Procedures/surgeries

Central venous catheter placement – To deliver TPN safely during severe malabsorption or while inducing remission. Why: prevents life-threatening malnutrition. PMC
Gastrostomy/G-J tube – For long-term enteral feeding when oral intake is not enough; allows continuous or jejunal feeds. Why: reliable growth and medication delivery. Pediatrics+1
Diagnostic endoscopy with biopsies – Confirms villous atrophy, autoimmune features (anti-enterocyte antibodies), and rules out other causes. Why: guides targeted therapy. Orpha.net
Allogeneic HSCT (procedure) – Curative in IPEX/immune-regulation defects after careful conditioning and support. Why: fixes the underlying immune error. PMC
Intestinal (± multivisceral) transplantation – Rare last resort for irreversible enteropathies with intestinal failure and TPN complications. Why: restore absorptive capacity when recovery is impossible. PMC+1

Prevention tips

Keep vaccines up to date where eligible (rotavirus timing is strict). 2) Safe water preparation and hand hygiene to avoid infections during flares. 3) Use low-osmolality ORS early with any new loose stools. 4) Follow the dietary elimination plan exactly; re-challenge only under medical supervision. 5) Store and prepare formula correctly. 6) Growth checks at set intervals. 7) Prompt zinc at the start of any diarrhea episode (per age). 8) Avoid unnecessary antibiotics. 9) Keep a written FPIES/allergy emergency plan. 10) Ensure regular follow-up with pediatric GI/immunology. UNICEF DATA+2World Health Organization+2

When to see a doctor urgently

Signs of dehydration (sunken eyes, dry mouth, no tears, very few wet diapers), blood in stool, fever, persistent vomiting, poor feeding, or lethargy.
No weight gain or weight loss despite feeding plan.
Severe eczema, endocrine issues (e.g., very high blood sugars), or recurrent infections—these may hint at IPEX or other immune defects that need rapid specialist care. PubMed+1

What to eat & what to avoid (10 quick pointers)

Eat/Use:

Breastmilk (if available).
Guideline-chosen formula (eHF or AAF as indicated).
ORS during diarrheal episodes.
Energy-dense feeds per dietitian.
MCT-containing options if advised. ESPGHAN+1

Avoid/Limit (until cleared):

Cow’s milk/soy or other confirmed triggers.
Fruit juices and high-sugar drinks (osmotic load).
Unnecessary fasting.
Random over-the-counter supplements or herbal mixes.
Unpasteurized foods or unsafe water. ESPGHAN+1

FAQs

Is this the same as an infection? No. In IM-PDI, the immune system is the main driver, though infections can coexist. PMC
Can babies outgrow it? Some food-driven forms improve with age and strict avoidance; autoimmune and monogenic forms need medical therapy and sometimes HSCT. PubMed+1
Why ORS and zinc? They are proven to shorten illness and keep electrolytes safe during episodes. UNICEF DATA+1
Are probiotics safe? Selected strains can modestly help persistent diarrhea, but discuss first if the child is immunocompromised. PMC
Why AAF instead of regular formula? AAF removes intact proteins that may trigger immune injury; it’s guideline-supported in severe cases. ESPGHAN
Do steroids mean long-term side effects? Doctors aim for the lowest effective dose and shortest course, often adding steroid-sparing agents. CGH Journal
What if steroids fail? Options include tacrolimus, cyclosporine, biologics (anti-TNF, ustekinumab), or sirolimus—chosen by specialists. PMC+2Karger+2
When is HSCT considered? In IPEX or related immune-regulation defects, HSCT offers the best chance of cure when done early. Frontiers
Will my child need a feeding tube? Sometimes, to ensure safe calories and growth during recovery; it can be temporary. Royal Children’s Hospital
Is TPN dangerous? It saves lives but carries risks (line infections, liver issues); teams try to return to enteral feeds as soon as safely possible. PMC
How are food triggers diagnosed? Through history, supervised elimination, sometimes oral food challenges—not by unvalidated tests. Cow’s Milk Protein Allergy
Can this be genetic? Yes; monogenic immune defects like FOXP3 (IPEX) cause early, severe enteropathy. Genetic testing guides therapy. Children’s Hospital of Philadelphia
Do we need endoscopy? Often yes, to confirm diagnosis and guide treatment. Orpha.net
Are outcomes good? With early nutrition, accurate diagnosis, and tailored immunotherapy, many infants stabilize and grow; outcomes are best with early specialist care. PMC
Where should we be treated? At a center with pediatric gastroenterology and clinical immunology experience in AIE/FPIES/IPEX. PMC

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