Warm Autoimmune Hemolytic Anemia (wAIHA)

Other names
Types
Causes
Symptoms
Diagnostic tests
Non-pharmacological treatments (therapies & other measures)
Drug treatments
Dietary molecular supplements
Drugs labeled as “immunity booster / regenerative / stem-cell”
Surgeries
Preventions
When to see a doctor immediately
What to eat and what to avoid
FAQs

Warm autoimmune hemolytic anemia (wAIHA) is a disease where your immune system makes IgG antibodies that attach to your red blood cells (RBCs) at normal body temperature (“warm”). These coated RBCs are then removed mainly by macrophages in the spleen, leading to anemia (low RBCs). Doctors confirm the diagnosis with a direct antiglobulin test (DAT/Coombs) that is typically positive for IgG (and sometimes C3). Common signs are tiredness, shortness of breath, yellow skin/eyes (jaundice), dark urine, and a fast heartbeat. wAIHA can occur by itself (primary) or with other conditions like autoimmune diseases, some cancers (e.g., CLL), infections, or drugs. The first-line treatment is usually steroids, with rituximab and splenectomy and other immunosuppressants used if needed. Transfusions are used for severe anemia and are safe when carefully matched. BSH+3PMC+3ASHP Publications+3

In wAIHA, IgG antibodies bind to proteins on your RBC surface. Spleen macrophages recognize the antibody “tags” via Fc receptors and remove parts of the RBC membrane, turning cells into spherocytes that are fragile and get destroyed (mostly extravascular hemolysis in the spleen). Complement may add to the damage. Your bone marrow tries to keep up by releasing more young RBCs (reticulocytes), but cannot fully replace ongoing loss. This is why tests show low hemoglobin, high LDH, high indirect bilirubin, low haptoglobin, and reticulocytosis, with a positive DAT (IgG ± C3). NCBI+1

Warm autoimmune hemolytic anemia (wAIHA) is a blood disorder where your own immune system makes antibodies that attach to your red blood cells at normal body temperature (around 37 °C). These antibodies mark the red cells for destruction mainly in the spleen and liver, causing anemia (low hemoglobin). Doctors confirm wAIHA by showing evidence of hemolysis (breakdown of red cells) and a positive direct antiglobulin test (DAT, or direct Coombs test) for IgG, sometimes with complement (C3) on the red cells. Most cases are “primary” (no clear trigger), but wAIHA can also be “secondary” to other diseases, medicines, or cancers of the blood. Treatment often starts with steroids, and may use rituximab or other therapies if steroids don’t work. ASHP Publications+3PMC+3PMC+3

Other names

Warm antibody autoimmune hemolytic anemia
IgG-mediated autoimmune hemolytic anemia
Warm-type AIHA / wAIHA
Warm autoantibody hemolysis
(These refer to the same condition in which antibodies react best at 37 °C.) PMC

Types

By cause

Primary (idiopathic) wAIHA: no underlying disease is found. PMC
Secondary wAIHA: linked to another condition (for example, lupus or chronic lymphocytic leukemia) or to a drug. PMC

By antibody and complement on DAT

IgG only positive (most common in warm type).
IgG + C3 positive (mixed coating).
C3 only positive usually suggests a cold-antibody mechanism; clinicians use the full clinical picture to classify. PMC+1

By clinical course

Acute (sudden drop in hemoglobin) or chronic/relapsing. ASHP Publications

Causes

In many people, no cause is found (primary). When there is a cause, it is often one of the following.

Systemic lupus erythematosus (SLE): autoimmune activity makes antibodies that target red cells. ScienceDirect
Other autoimmune diseases (e.g., rheumatoid arthritis, autoimmune hepatitis, thyroid autoimmunity): immune mis-targeting can include red cells. PMC
Chronic lymphocytic leukemia (CLL): abnormal B-cells can produce autoantibodies. PMC
Non-Hodgkin lymphomas: similar mechanism as CLL with autoantibody production. PMC
Common variable immunodeficiency (CVID): immune dysregulation increases risk of autoantibodies. PMC
Evans syndrome (AIHA with immune thrombocytopenia): body attacks both red cells and platelets. NCBI
HIV infection: chronic immune activation may trigger AIHA. PMC
Hepatitis C and other chronic infections: immune activation may cross-react with red cells. PMC
Mycoplasma and other atypical infections: can shift immune responses; warm type is less common than cold, but reported. PMC
Solid tumors (less common): paraneoplastic autoimmunity may include AIHA. PMC
Pregnancy/post-partum immune changes: rare trigger of AIHA via immune shifts. PMC
Allogeneic stem-cell or organ transplant: immune reconstitution or allo-/autoimmunity may cause hemolysis. PMC
Drugs—methyldopa: classic drug that can cause true autoantibody-mediated warm AIHA. Merck Manuals
Drugs—penicillin/cephalosporins (hapten type): drug binds to red cell and antibodies target the complex. Merck Manuals
Immune checkpoint inhibitors (e.g., nivolumab): can unleash autoimmunity, including AIHA. PMC
Other medications (rare): include certain antibiotics and anti-inflammatory agents reported in case series. Merck Manuals
Post-viral immune activation (case reports): immune cross-reactivity after infections may precipitate AIHA. PMC
Autoimmune thyroid disease: broader autoimmunity can include red cell antibodies. PMC
Ulcerative colitis/IBD (rare): systemic autoimmunity occasionally involves red cells. PMC
Mixed warm–cold antibody states: warm component drives hemolysis at 37 °C even if C3 is also present. Medscape

Symptoms

Tiredness and weakness: fewer red cells carry less oxygen to tissues. NCBI
Shortness of breath on exertion: low hemoglobin makes activity feel harder. NCBI
Fast heartbeat (palpitations): the heart compensates for low oxygen delivery. NCBI
Pale skin and inner eyelids (pallor): the classic sign of anemia. NCBI
Jaundice (yellow eyes/skin): bilirubin rises as red cells break down. NCBI
Dark urine (tea-colored): excreted pigments from hemolysis can darken urine. NCBI
Upper left abdominal fullness or pain: an enlarged spleen from extra red-cell clearance. NCBI
Headache or dizziness: reduced oxygen delivery to the brain. NCBI
Chest discomfort on exertion (in older adults): anemia can stress the heart. NCBI
Fever during severe hemolysis: inflammatory response to rapid breakdown. PMC
Poor exercise tolerance: everyday tasks feel harder due to anemia. NCBI
New or worsening gallstones (history): pigment stones form from excess bilirubin over time. NCBI
Worsening symptoms after infections or certain drugs: triggers can accelerate hemolysis. PMC
Bruising or nosebleeds if Evans syndrome: low platelets together with AIHA. NCBI
Symptoms of an underlying disease (e.g., joint pain in lupus): point to a secondary cause. ScienceDirect

Diagnostic tests

A) Physical examination

General inspection for pallor and jaundice: doctors look at skin and eyes to spot anemia and bilirubin buildup. NCBI
Heart rate and blood pressure: tachycardia is common; severe anemia may lower blood pressure. NCBI
Spleen and liver palpation: feeling for enlargement that suggests increased red-cell removal. NCBI
Review of medication bottles and history (the “drug test” at bedside): careful history can uncover drug-induced wAIHA. Merck Manuals

B) “Manual”/bedside tests

Urine dipstick and visual check: looks for dark urine and blood pigments from hemolysis. NCBI
Capillary refill and nailbed assessment: quick clue to perfusion in anemic states. NCBI
Point-of-care hemoglobin (finger-stick): rapid screen for anemia severity. NCBI

C) Laboratory & pathology

Complete blood count (CBC): shows anemia; MCV often normal; platelets may be low in Evans syndrome. NCBI+1
Reticulocyte count: usually high because bone marrow tries to replace destroyed red cells. NCBI
Serum bilirubin (indirect/unconjugated): rises with red-cell breakdown. NCBI
Lactate dehydrogenase (LDH): increased in hemolysis. NCBI
Haptoglobin: low or undetectable because it binds free hemoglobin released during hemolysis. NCBI
Peripheral blood smear: often shows spherocytes in wAIHA and “polychromasia” (young cells). PMC
Direct antiglobulin test (DAT, direct Coombs): the key test—positive for IgG (± C3). Monospecific DAT helps define which is present. PMC+1
Elution studies: strip antibodies off red cells to confirm warm autoantibody. NCBI
Antibody screen and identification: helps blood bank find compatible blood and characterize autoantibodies. NCBI
Tests for causes: e.g., ANA for lupus, flow cytometry for CLL, HIV/HCV serology—to identify secondary wAIHA. PMC
Bone marrow exam (selected cases): if the diagnosis is unclear or to evaluate marrow response or another blood cancer. PMC

D) Electro-diagnostic

Electrocardiogram (ECG): anemia can stress the heart; ECG documents rate/rhythm and ischemic strain if present. NCBI
Pulse oximetry/telemetry as needed: monitors oxygenation and heart rate in more severe cases. NCBI

(Doctors may also order imaging—e.g., ultrasound—to check spleen or look for hidden causes when needed.) PMC

Non-pharmacological treatments (therapies & other measures)

Below are practical, supportive, and procedure-level options. Each includes purpose and mechanism in brief; I can expand any into ~150 words on request.

Education & trigger avoidance — Purpose: reduce flares; Mechanism: avoid suspect drugs/infections that can precipitate hemolysis. BSH
Folic acid dietary support — Purpose: support RBC production; Mechanism: folate replenishes substrate for marrow erythropoiesis during brisk turnover (often given as a supplement too). ASHP Publications
Vaccination planning — Purpose: reduce infection risk (especially if splenectomy/rituximab planned); Mechanism: immunization against pneumococcus/meningococcus/Hib, influenza; timing before B-cell depletion or splenectomy. BSH
Thrombosis risk mitigation — Purpose: lower clot risk (wAIHA raises VTE risk); Mechanism: early mobilization, hydrate, and pharmacologic prophylaxis when appropriate. NSSG Haematology
Transfusion (as needed) — Purpose: treat symptomatic/severe anemia; Mechanism: carefully selected crossmatch (least-incompatible if necessary), close monitoring. PMC+1
Bed rest and oxygen during crises — Purpose: stabilize severe anemia; Mechanism: decrease oxygen demand and increase delivery. PMC
Nutritional optimization — Purpose: support marrow; Mechanism: adequate protein, iron only if true deficiency, B12/folate intake. ASHP Publications
Infection control & prompt treatment — Purpose: avoid hemolysis triggers and treatment delays; Mechanism: fast evaluation for fevers; prophylaxis if immunosuppressed. BSH
Medication review/stop culprits — Purpose: remove drug-induced AIHA; Mechanism: discontinue suspect agents (e.g., certain antibiotics, immune drugs). BSH
Family planning counseling — Purpose: plan therapy around pregnancy; Mechanism: balance maternal disease control and fetal safety. BSH
Sunlight/jaundice skin care — Purpose: comfort for pruritus from cholestatic jaundice; Mechanism: gentle skincare, hydration. (Supportive.) Medscape
Activity pacing & rehab — Purpose: manage fatigue; Mechanism: graded exercise and rest to match oxygen capacity. Medscape
Psychological support — Purpose: reduce anxiety/depression burden; Mechanism: counseling; coping skills during chronic disease. Medscape
Fever/illness action plan — Purpose: reduce crisis severity; Mechanism: early labs, call team, fluids. BSH
Avoid extreme heat dehydration — Purpose: cut hemolysis stress; Mechanism: maintain hydration to protect circulation. Medscape
Perioperative planning — Purpose: safe surgery; Mechanism: pre-op optimization, crossmatch strategy, steroid cover. BSH
Bone health protection — Purpose: offset steroid effects; Mechanism: calcium/vitamin D, weight-bearing exercise, DEXA when indicated. BSH
Sun/heat-neutral clothing — Purpose: comfort; Mechanism: reduce fatigue and dehydration risk (supportive). Medscape
Smoking cessation — Purpose: improve oxygen delivery and vascular health; Mechanism: reduce carboxyhemoglobin and thrombosis risk. Medscape
Care coordination with hematology/transfusion medicine — Purpose: rapid access to blood and therapies; Mechanism: shared protocols. ASHP Publications

Drug treatments

I’m listing widely used and evidence-supported options first. Dosing is typical adult guidance; clinicians individualize. Please do not self-medicate.

Prednisone (corticosteroid) — Dose/time: often 1–2 mg/kg/day then slow taper over weeks; Purpose: first-line to stop hemolysis; Mechanism: broad immune suppression, reduces autoantibody production and macrophage Fc activation; Side effects: high sugars, weight gain, mood change, infection, osteoporosis, hypertension. ASHP Publications+1
Methylprednisolone IV pulses — Dose: e.g., 500–1000 mg/day for 1–3 days in severe crises; Purpose: rapid control; Mechanism: high-dose steroid immunosuppression; Risks: same as steroids plus transient psychosis, myopathy. ASHP Publications
Rituximab (anti-CD20) — Dose/time: 375 mg/m² weekly x4 (or 1000 mg day 1 & 15); Purpose: second-line or added to steroids to improve remission; Mechanism: depletes B cells producing autoantibodies; Side effects: infusion reactions, infections, hepatitis B reactivation, hypogammaglobulinemia. PMC+1
IVIG — Dose: 1–2 g/kg total over 2–5 days; Purpose: short-term rescue (esp. severe hemolysis or before surgery); Mechanism: Fc receptor blockade and immune modulation; Side effects: headache, thrombosis risk, renal dysfunction (rare). BSH
Splenectomy (see surgery) often considered after steroids/rituximab failure; perioperative antibiotics and vaccines are vital. Drug note: not a drug, but a key step interacting with medical therapy. BSH+1
Azathioprine — Dose: 1–2 mg/kg/day; Purpose: steroid-sparing; Mechanism: purine antimetabolite suppressing lymphocyte proliferation; Adverse: myelosuppression (check TPMT), liver toxicity, infection, malignancy risk. BSH
Mycophenolate mofetil — Dose: 500–1000 mg twice daily; Purpose: alternative steroid-sparing; Mechanism: inhibits inosine monophosphate dehydrogenase (lymphocyte DNA synthesis); Adverse: GI upset, leukopenia, infections, teratogenicity. ASHP Publications
Cyclophosphamide — Dose: oral 1–2 mg/kg/day or intermittent IV; Purpose: refractory disease; Mechanism: alkylates DNA, suppresses autoantibody producing cells; Adverse: cytopenias, hemorrhagic cystitis, infertility, malignancy risk. BSH
Cyclosporine — Dose: 3–5 mg/kg/day in divided doses; Purpose: refractory AIHA; Mechanism: calcineurin inhibition reduces T-cell activation; Adverse: nephrotoxicity, hypertension, tremor, gingival hyperplasia. BSH
Tacrolimus — Dose: individualized troughs; Purpose: alternative calcineurin inhibitor in refractory cases; Mechanism: inhibits T-cell activation; Adverse: nephrotoxicity, neurotoxicity, diabetes. BSH
Sirolimus (rapamycin) — Dose: targeted troughs; Purpose: salvage therapy in autoimmune cytopenias; Mechanism: mTOR inhibition modulates T-cell responses; Adverse: hyperlipidemia, mucositis, cytopenias. PMC
Bortezomib — Dose: 1.3 mg/m² on days 1, 4, 8, 11 cycles; Purpose: severe refractory wAIHA (case series, off-label); Mechanism: proteasome inhibition reduces plasma cell antibody output; Adverse: neuropathy, cytopenias, infections. PMC
Daratumumab (anti-CD38) — Dose: oncology-style schedules; Purpose: refractory AIHA (case reports/series, esp. post-transplant or CLL-related); Mechanism: depletes plasma cells; Adverse: infusion reactions, hypogammaglobulinemia, infection. PMC
Ruxolitinib — Dose: 5–10 mg bid (off-label); Purpose: investigational refractory cases; Mechanism: JAK1/2 inhibition modulates cytokine signaling; Adverse: cytopenias, infections. PMC
Erythropoiesis-stimulating agents (ESAs) — Dose: per anemia protocols; Purpose: support marrow when under-producing or in steroid-sparing aims; Mechanism: stimulates RBC production; Adverse: hypertension, thrombosis risk. ASHP Publications
Folic acid (pharmacologic supplement) — Dose: 1 mg/day typical; Purpose: keep up with RBC turnover; Mechanism: replenishes folate for DNA synthesis; Adverse: minimal. ASHP Publications
Prophylactic anticoagulation (selected cases) — Dose: per VTE protocols; Purpose: mitigate elevated VTE risk during active hemolysis or high-dose steroids/IVIG; Mechanism: prevents clot formation; Adverse: bleeding. NSSG Haematology
Antimicrobials (as indicated) — Purpose: treat coexisting infections that can worsen hemolysis or complicate immunosuppression; Mechanism: eradication of pathogens; Adverse: drug-specific, some may trigger AIHA (review carefully). BSH
Pneumocystis jirovecii prophylaxis (selected on high-dose steroids/IS) — Dose: TMP-SMX regimens; Purpose: prevent opportunistic infection on immunosuppression; Mechanism: antimicrobial prophylaxis; Adverse: allergy, cytopenias. BSH
Emerging agents/clinical trials — Purpose: access novel pathways (e.g., FcRn inhibitors, BTK inhibitors); Mechanism: reduce pathogenic IgG or B-cell signaling; Adverse: under study; availability varies; note: some agents approved for other cytopenias or CAD, not wAIHA. PMC

Important clarifier: Complement C1s inhibition (e.g., sutimlimab) is for cold agglutinin disease, not standard for wAIHA. Avoid extrapolation without specialist input. PMC

Dietary molecular supplements

Folic acid — Dose: ~1 mg/day; Function: DNA synthesis to support RBC production; Mechanism: cofactor for nucleotide synthesis; strong rationale in hemolysis. ASHP Publications
Vitamin B12 — Dose: per deficiency status; Function: erythropoiesis support; Mechanism: cofactor for DNA synthesis; correct deficiency if present. ASHP Publications
Iron — Dose: only if proven deficiency; Function: hemoglobin synthesis; Mechanism: replaces iron stores; avoid if not deficient. ASHP Publications
Vitamin D — Function: bone protection, immune modulation; Mechanism: supports bone against steroid effects; deficiency correction. BSH
Calcium — Function: bone health under steroids; Mechanism: supports mineralization. BSH
High-quality protein (dietary) — Function: substrate for marrow; Mechanism: provides amino acids for hemoglobin and enzymes. Medscape
Omega-3 fatty acids (food-based) — Function: general anti-inflammatory support; Mechanism: eicosanoid balance; modest, nonspecific. Medscape
B-complex (dietary) — Function: energy metabolism; Mechanism: coenzymes for RBC production; use to correct deficits. ASHP Publications
Antioxidant-rich foods — Function: reduce oxidative stress burden; Mechanism: supports RBC membranes; evidence indirect. Medscape
Hydration (not a molecule but essential) — Function: support circulation and kidney bilirubin clearance; Mechanism: maintains plasma volume. Medscape

Drugs labeled as “immunity booster / regenerative / stem-cell”

Transparency note: for wAIHA, there are no proven “immunity boosters” that cure the disease, and stem-cell therapy is not routine. Below are contexts where these terms arise, with caution.

Hematopoietic stem cell transplant (HSCT) — Use: extremely rare salvage in catastrophic, refractory autoimmune cytopenias often tied to another hematologic disorder; Dose: oncology protocols; Function/Mechanism: replaces dysfunctional immune system; Risks: significant morbidity/mortality; specialist only. PMC
Daratumumab (plasma-cell–targeting; see above) — sometimes framed as “regenerative” via removing autoantibody sources; mechanism: anti-CD38 plasma-cell depletion; caution off-label. PMC
Bortezomib — proteasome inhibitor that reduces antibody-secreting cells; used off-label in refractory wAIHA. PMC
Ruxolitinib — immune-signaling modulator; experimental; case-based evidence. PMC
Sirolimus — mTOR inhibitor reshaping immune responses; salvage option in autoimmune cytopenias. PMC
Clinical-trial biologics (e.g., FcRn or BTK inhibitors) — aim to reduce pathogenic IgG or B-cell activation; investigational for wAIHA. PMC

Surgeries

Laparoscopic splenectomy — Procedure: remove spleen through small incisions; Why: the spleen is the main RBC-clearing organ in wAIHA; removing it can reduce hemolysis when drugs fail; Notes: vaccinate pre-op, infection prophylaxis post-op. PMC
Open splenectomy — Procedure: traditional open approach when anatomy or urgent circumstances require; Why: same rationale as above. PMC
Splenic artery embolization (selected cases) — Procedure: interventional radiology blocks splenic blood flow to reduce function; Why: bridge or alternative when surgery is high-risk. PMC
Cholecystectomy — Procedure: remove gallbladder; Why: chronic hemolysis can cause pigment gallstones and biliary symptoms; indicated if gallstone complications occur. Medscape
HSCT (see above) — Procedure: transplant of hematopoietic stem cells; Why: last-resort in exceptional refractory autoimmune cytopenias linked to underlying hematologic disease. PMC

Preventions

Vaccinate (timed before rituximab/splenectomy). BSH
Avoid drugs previously linked to hemolysis for you. BSH
Treat infections quickly. BSH
Protect bone health on steroids (calcium, vitamin D, DEXA as indicated). BSH
Reduce thrombosis risk: hydrate, move, and follow clinician advice on prophylaxis. NSSG Haematology
Keep hematology follow-ups and labs. BSH
Plan pregnancies with your care team. BSH
Wear medical ID if you’ve had severe reactions/transfusion complexities. ASHP Publications
Maintain balanced nutrition with adequate folate/B12/protein. ASHP Publications
Don’t stop steroids suddenly; taper as directed. BSH

When to see a doctor immediately

New or worsening tiredness, dizziness, breathlessness, chest pain, or very fast heartbeat.
Yellowing of eyes/skin or dark cola-colored urine.
Fever (especially if on steroids/rituximab).
Signs of a blood clot: one-sided leg swelling/pain, sudden chest pain/shortness of breath.
After starting a new medication if you feel acutely worse.
These may signal an active hemolysis episode or treatment complication and need urgent review. NSSG Haematology+1

What to eat and what to avoid

Eat: iron-rich foods only if iron-deficient (your doctor will tell you). ASHP Publications
Eat: folate sources (leafy greens, legumes) and consider prescribed folic acid. ASHP Publications
Eat: B12 sources (fish, meat, dairy) if not supplemented. ASHP Publications
Eat: protein with each meal to support marrow. Medscape
Drink: plenty of water daily. Medscape
Limit: alcohol, which can suppress marrow and worsen anemia. Medscape
Avoid: starting over-the-counter supplements without checking (some interact with meds). BSH
Avoid: unnecessary NSAIDs if you’re at bleeding risk on anticoagulants. BSH
Keep: calcium/vitamin D intake if you’re on steroids. BSH
General: balanced, regular meals to prevent fatigue dips. Medscape

FAQs

1) Is wAIHA the same as cold agglutinin disease?
No. wAIHA uses IgG at body temperature; cold agglutinin disease is mostly IgM active in the cold and uses complement differently. Treatments differ. PMC

2) What test proves wAIHA?
The direct antiglobulin test (DAT/Coombs), typically IgG-positive (± C3). Doctors also look at hemolysis labs and blood smear. PMC

3) Can transfusions be given if crossmatch is difficult?
Yes. Experts use least-incompatible units with close monitoring when anemia is severe/symptomatic. PMC+1

4) What is first-line treatment?
Prednisone with a careful taper. Many add or move to rituximab if response is incomplete or relapse occurs. ASHP Publications

5) When is splenectomy used?
For steroid/rituximab-refractory disease or frequent relapses, after vaccination planning. BSH

6) Will I need treatment forever?
Some patients enter remission; others need ongoing or intermittent therapy. Plans are individualized. ASHP Publications

7) Why folic acid?
Hemolysis increases RBC turnover and folate use; supplementation helps the marrow keep up. ASHP Publications

8) Are blood clots really a risk?
Yes, VTE risk is higher during active hemolysis and with certain treatments. Prevention steps may be used. NSSG Haematology

9) Can infections trigger wAIHA flares?
They can. Prompt evaluation and treatment are important, especially if immunosuppressed. BSH

10) What about pregnancy?
Management requires obstetric-hematology coordination; some drugs are avoided; transfusion and IVIG may be used. BSH

11) Are there new medicines coming?
Yes—trials are exploring FcRn, BTK, and other targets; ask about clinical trials in your region. PMC

12) Do I need to avoid cold?
Cold avoidance is critical in cold agglutinin disease; in wAIHA it’s not central, but general comfort measures help. PMC

13) Can diet cure wAIHA?
No. Diet supports health but does not replace immunotherapy. Follow medical treatment plans. BSH

14) Is wAIHA common?
It’s rare; incidence is about a few per 100,000 per year. PMC

15) Will I always test positive on the DAT?
DAT can fluctuate; clinical status plus labs guide decisions, not the DAT alone. ASHP Publications

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