Antiplasmin Deficiency (Alpha-2-Antiplasmin Deficiency, α2-AP Deficiency)

Antiplasmin deficiency is a rare bleeding disorder. In healthy blood, clots form to stop bleeding and then slowly dissolve when healing is done. A protein called alpha-2-antiplasmin (α2-antiplasmin) protects the clot from breaking down too early. In antiplasmin deficiency, there is not enough of this protein or it does not work well. Because the clot is not protected, it dissolves too fast. The result is easy or prolonged bleeding, especially after dental work, minor surgery, injury, or during periods in people who menstruate. The medical gene behind the inherited form is SERPINF2. When SERPINF2 has harmful changes (mutations), the body cannot make a normal antiplasmin protein. The disorder is often inherited in an autosomal recessive pattern (you need two faulty copies to have the disease). NCBI+2NCBI+2

Your body stops bleeding by making a blood clot and then, later, slowly dissolving it. The “clot-dissolving” system is called fibrinolysis. The main enzyme that breaks clots is plasmin.
Alpha-2-antiplasmin (A2AP) is the natural “brake” on plasmin. It binds plasmin very fast and shuts it down so clots are not dissolved too early. In antiplasmin deficiency, there is too little A2AP or it does not work well. As a result, clots dissolve too soon, and bleeding lasts longer than normal. Routine clotting tests (like PT and aPTT) can be normal because the problem is not making the clot but keeping it in place. Inherited cases happen when changes (variants) in the SERPINF2 gene stop the body from making normal A2AP. Acquired cases happen when disease or medicines lower A2AP or use it up. NCBI+2Orpha+2

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Other names

• Alpha-2-antiplasmin deficiency

• Alpha-2-plasmin inhibitor deficiency

• Antiplasmin deficiency (congenital/acquired)

• SERPINF2-related bleeding disorder

• A2AP (or A2PI) deficiency
  These names all point to the same basic problem: not enough working alpha-2-antiplasmin to control plasmin. National Organization for Rare Disorders+2DrugBank+2

• It is made mainly in the liver and circulates in blood. When a clot forms, Factor XIII cross-links A2AP into the fibrin mesh to make the clot more resistant to breakdown. Without enough working A2AP, fibrinolysis runs “too hot,” and clots melt away early. Rare Coagulation Disorders+1

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Types

1. Congenital (inherited) antiplasmin deficiency

   • Caused by SERPINF2 gene variants.

   • Can be severe (little to no activity; often homozygous) or partial (reduced activity; often heterozygous). Severe forms may bleed like hemophilia, including joint bleeds; partial forms can have milder or procedure-related bleeding. NCBI+1

2. Acquired antiplasmin deficiency

   • Happens when A2AP is not produced well (e.g., significant liver disease), consumed during conditions with ongoing clot breakdown (e.g., DIC/sepsis, major trauma), lost (e.g., nephrotic syndrome), or blocked/overwhelmed by medicines that trigger fibrinolysis (e.g., thrombolytic drugs like tPA). Rare Coagulation Disorders+1

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Causes

Congenital (genetic) causes

1. SERPINF2 gene variants (biallelic) – The classic inherited form; very low A2AP activity leads to strong bleeding tendency from early life. NCBI

2. SERPINF2 variants (monoallelic/heterozygous) – Partial deficiency; many people bleed only during surgery, dental work, or major trauma. ASHA Publications

Acquired (non-genetic) causes

3. Advanced liver disease/cirrhosis – The liver makes A2AP; when it fails, levels can fall and fibrinolysis may become excessive. Merck Manuals

4. Disseminated intravascular coagulation (DIC), especially with sepsis – Ongoing clotting and lysis consume A2AP faster than it can be replaced. ASHA Publications

5. Major trauma with shock or tissue injury – Bursts of fibrinolysis can use up A2AP. (Often tracked with viscoelastic tests). Practical Haemostasis

6. Thrombolytic therapy (e.g., tPA, urokinase, streptokinase) – These drugs drive plasmin generation and can deplete/overwhelm A2AP. PMC

7. After cardiac or major surgery (e.g., cardiopulmonary bypass, liver surgery) – Transient hyperfibrinolysis and dilution can reduce functional A2AP. ScienceDirect

8. Nephrotic syndrome – Urinary protein loss can lower some inhibitors; acquired A2AP deficiency has been reported. Rare Coagulation Disorders

9. Malignancy with paraneoplastic hyperfibrinolysis (notably metastatic prostate cancer) – Tumor-driven fibrinolysis can lower effective A2AP; controlling the tumor can normalize levels. PubMed

10. Acute leukemia (e.g., APL) with hyperfibrinolysis – Intense plasmin activity consumes A2AP. Frontiers

11. Amyloidosis with bleeding diathesis – Reported association with fibrinolysis and reduced functional A2AP. Rare Coagulation Disorders

12. Severe obstetric complications with DIC (e.g., abruption, amniotic fluid embolism) – Consumptive coagulopathy can reduce A2AP. ASHA Publications

13. Massive transfusion/dilutional coagulopathy – Replacing blood with limited plasma can transiently lower inhibitors including A2AP. Practical Haemostasis

14. Severe systemic inflammation/sepsis without frank DIC – Surges in plasmin generation may outpace A2AP. PMC

15. Liver under-perfusion and injury during critical illness – Reduced synthesis adds to low levels. Medscape Reference

16. Hyperfibrinolysis from certain solid tumors (e.g., sarcoma, advanced lung/breast) – Elevated plasmin-A2AP (PAP) complexes show heavy plasmin use and relative A2AP shortfall. AHA Journals

17. High-dose plasmin or microplasmin exposure (research/therapeutic contexts) – Directly inactivates available A2AP by complexing. PMC

18. Major urogenital surgery (prostate/uterus) with high local plasminogen activator release – Local hyperfibrinolysis can exceed A2AP. Clinical Laboratory Diagnostics

19. Post-liver transplantation (early phase) – Temporary imbalance in fibrinolysis while the graft “settles” can reduce effective A2AP. ScienceDirect

20. Combined factor XIII issues (functional) – Not a true “cause,” but if FXIII cannot cross-link A2AP into clots, A2AP protection is weaker and mimics deficiency. (Important differential.) Rare Coagulation Disorders

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Symptoms

1. Easy bruising – Big or frequent bruises after minor bumps because clots dissolve early. Labcorp

2. Prolonged oozing after cuts – Bleeding may slow, then start again (delayed or “re-bleeding”) as fragile clots melt. Rare Coagulation Disorders

3. Nosebleeds – Recurrent epistaxis from delicate surface vessels that need stable clots. Labcorp

4. Gum bleeding – With tooth-brushing or dental work; oozing is often longer than expected. Labcorp

5. Heavy periods (menorrhagia) – Period flow can be heavier and last longer. Labcorp

6. Bleeding after dental extraction or surgery – Especially delayed oozing hours later. Rare Coagulation Disorders

7. Soft-tissue hematomas – Deep muscle or subcutaneous blood collections can form and expand because clots are unstable. Labcorp

8. Joint bleeds (hemarthrosis) – In severe inherited cases, joint bleeding similar to hemophilia may occur. ASHA Publications

9. Bleeding after childbirth – Post-procedure oozing can be prolonged if fibrinolysis dominates. ASHA Publications

10. Hematuria (blood in urine) – From fragile clots in urinary tract. Labcorp

11. Gastrointestinal bleeding – Oozing from the stomach or bowel, sometimes subtle but persistent.

12. Bleeding into closed spaces – Rare but serious, such as intracranial or retroperitoneal hemorrhage in severe cases.

13. Umbilical stump bleeding in newborns – A classic early clue in severe congenital deficiency. NCBI

14. Anemia from chronic blood loss – Tiredness, pallor, shortness of breath from slow ongoing bleeding.

15. Family pattern – Relatives with similar bleeding (in inherited cases). NCBI

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Diagnostic tests

A) Physical exam

1. Skin and mucosa check – Looks for large bruises, gum oozing, nosebleeds, or petechiae. In A2AP deficiency, bruises/oozing are common; petechiae suggest platelet problems and help with differential diagnosis.

2. Joint exam – Checks for warm, swollen, painful joints after minor injury; severe congenital cases can have hemarthrosis like hemophilia. ASHA Publications

3. Soft-tissue palpation – Finds deep muscle or subcutaneous hematomas that signal unstable clots.

4. Post-procedure wound check – Looks for delayed oozing after dental work, circumcision, or surgery—typical of overactive fibrinolysis. Rare Coagulation Disorders

5. Standardized bleeding history tools (e.g., ISTH-BAT) – A structured symptom score that flags a lifelong pattern pointing to an inherited bleeding disorder.

B) Manual tests (bench/bedside)

6. Euglobulin Clot Lysis Time (ECLT) – Classic global screen of fibrinolysis. In antiplasmin deficiency, the clot lyses faster (shortened ECLT), although many labs now use newer assays. Practical Haemostasis+2specialtytesting.labcorp.com+2

7. Whole-blood clot-lysis observation in a tube – Simple lab setup that watches how quickly a formed clot dissolves; a very fast lysis supports excessive fibrinolysis. (Crude but illustrative where advanced testing is unavailable.)

8. Urea clot-solubility (FXIII screen) – Ensures Factor XIII is normal, because poor FXIII cross-linking also makes clots fragile (an important look-alike to A2AP deficiency). Rare Coagulation Disorders

C) Laboratory & pathological tests

9. PT and aPTT – Often normal in isolated A2AP deficiency, which helps separate it from factor deficiencies; the main issue is not forming the clot but keeping it. ScienceDirect

10. Fibrinogen level – Usually normal in isolated cases; may drop if there is concurrent DIC/consumption. PMC

11. D-dimer – Tends to be elevated when fibrinolysis is brisk; antifibrinolytics lower D-dimer, which supports the mechanism. PMC

12. Plasmin-A2AP (PAP) complex – High PAP shows plasmin is being rapidly neutralized by what A2AP remains; very high levels signal hyperfibrinolysis. AHA Journals

13. Alpha-2-antiplasmin activity assay (chromogenic) – The key functional test; low activity confirms deficiency (screen and monitor). Mayo Clinic Laboratories

14. Alpha-2-antiplasmin antigen (immunologic) level – Distinguishes low quantity (type I) from dysfunctional (type II) patterns when paired with activity. Labcorp

15. SERPINF2 genetic testing – Confirms the congenital diagnosis and helps with family counseling. NCBI

16. PAI-1 level (to exclude PAI-1 deficiency) – Another rare cause of premature clot lysis; testing helps sort the fibrinolytic disorders. Orpha

17. Plasminogen and tPA levels – Optional context tests; abnormal results point to other fibrinolytic imbalances rather than primary A2AP deficiency.

D) Device-based “electrodiagnostic” (viscoelastic) testing

18. Thromboelastography (TEG) – Dynamic clot-formation/lysis tracing; LY30 or similar lysis endpoints rise when fibrinolysis is excessive, supporting A2AP deficiency. Practical Haemostasis

19. ROTEM – A related viscoelastic method; maximum lysis (ML) or reduced clot-firmness over time signals hyperfibrinolysis and helps guide therapy in real time. Practical Haemostasis

E) Imaging

20. Targeted imaging when needed – Ultrasound for soft-tissue hematomas, MRI/CT for deep muscle, joint, or internal bleeds; endoscopy for GI bleeding. Imaging confirms where bleeding is occurring and its size so treatment can be aimed properly.

Non-pharmacological treatments

1. Direct pressure on bleeds for at least 10–15 minutes to help the clot set. JTH Journal

2. Ice/cold packs for nose or soft-tissue bleeds (vasoconstriction slows fibrinolysis locally). JTH Journal

3. Elevation and rest of injured limb to reduce blood flow and oozing. JTH Journal

4. Nasal care: humidification and saline sprays to prevent crusting/epistaxis. JTH Journal

5. Dental prevention plan: meticulous oral hygiene, regular cleanings to reduce gingival bleeding. WFH

6. Local hemostatic materials during dental/surgical care (gelatin sponge, oxidized cellulose, sutures). AGD

7. Topical fibrin sealant (fibrin glue) applied by clinicians during procedures to stabilize clots. AGD

8. Nasal cautery by ENT for recurrent nosebleeds. JTH Journal

9. Menstrual management devices (e.g., menstrual cup/pads with tracking) to monitor flow and plan care. (Supportive; clinical management still needed.) JTH Journal

10. Compression bandaging for soft-tissue bleeds/hematomas. JTH Journal

11. Pre-procedure planning with a hematologist; write a clear plan for dental/surgical teams. WFH

12. Medical alert ID noting “hyperfibrinolytic bleeding/α2-antiplasmin deficiency—needs antifibrinolytics.” JTH Journal

13. Avoidance of high-risk drugs/supplements (aspirin, NSAIDs, fish oil, high-dose vitamin E) unless prescribed. JTH Journal

14. Safe exercise and protective gear to reduce trauma. JTH Journal

15. Iron repletion through diet if iron-deficiency anemia is present from chronic loss (with clinician input). JTH Journal

16. Post-procedure tamponade (dental socket packs; nasal packing as needed). AGD

17. Cold saline mouth rinses 24–48 h after dental work (alongside prescribed antifibrinolytics). WFH

18. Wound care education—what to do if oozing restarts at home. WFH

19. Specialist-guided pregnancy/delivery plan to prevent post-partum hyperfibrinolysis. JTH Journal

20. Genetic counseling for families with confirmed SERPINF2 mutations. NCBI

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Drug treatments

Doses are typical ranges used by clinicians for hyperfibrinolytic bleeding. Always individualize with a hematologist, adjust for age/kidney function, and follow country-specific labels.

1. Tranexamic acid (TXA) – antifibrinolytic.
   Dose/time: Common oral prophylaxis 1–1.5 g 2–3×/day; dental extraction 10 mL of 5% mouthwash swished 4×/day for 7–10 days; IV 10 mg/kg before procedures (examples from reviews/guidance).
   Purpose: First-line for mucosal/post-procedural bleeding and dental/surgical prophylaxis.
   Mechanism: Lysine analog; blocks plasminogen binding to fibrin → stabilizes clot.
   Side effects: Nausea, rare visual changes; use caution with history of thrombosis. BioMed Central+2NCBI+2

2. Aminocaproic acid (EACA; Amicar) – antifibrinolytic.
   Dose/time: Oral 5 g once, then 1 g hourly for 8 h or until controlled; alternative 50–100 mg/kg every 4–6 h while awake (max per local guidance).
   Purpose: Alternative to TXA for mucosal and dental bleeds.
   Mechanism: Lysine analog; blocks plasminogen–fibrin interaction.
   Side effects: GI upset, rare hypotension with rapid IV use; dose adjust in renal impairment. NCBI+2Mayo Clinic+2

3. Fresh frozen plasma (FFP) – plasma protein source.
   Dose/time: Typical 10–20 mL/kg for active bleeding or before procedures (per transfusion guidance).
   Purpose: Supplies exogenous α2-antiplasmin when bleeding is severe or antifibrinolytics are not enough.
   Mechanism: Replaces missing inhibitor proteins.
   Side effects: Transfusion reactions, volume overload; ABO-compatible only. Medscape+1

4. Topical TXA mouthwash (4.8–5%) – local antifibrinolytic.
   Dose/time: 10 mL swish 2 minutes, then spit; repeat up to 4×/day after dental work as directed.
   Purpose/Mechanism/AE: Local version of #1, fewer systemic effects. NCBI

5. Topical EACA mouthwash (5%) – local antifibrinolytic.
   Dose/time: 10 mL in mouth 2 minutes before procedure; then every 2 h for 6–10 doses post-procedure as needed.
   Purpose/Mechanism/AE: As above; compounded per protocol. University of Washington

6. Fibrin sealant (fibrin glue; topical biological) – topical hemostatic.
   Dose/time: Applied by clinician to the wound bed during procedures.
   Purpose: Creates a stable fibrin layer; helpful in dental/ENT/surgical fields.
   Mechanism: Provides fibrin matrix that is less prone to washout when combined with antifibrinolytics.
   Side effects: Rare allergy; theoretical infection risk (screened products). AGD

7. Hormonal therapy for heavy menstrual bleeding – combined oral contraceptive pills (COCPs).
   Dose/time: Cyclic or continuous regimens per gynecologist.
   Purpose: Reduces menstrual blood loss in those who menstruate.
   Mechanism: Thins endometrium and stabilizes uterine lining.
   Side effects: Nausea, VTE risk in predisposed patients—screen first. (Guideline-based approach for heavy menses.) JTH Journal

8. Levonorgestrel intrauterine system (LNG-IUS) – local hormonal device.
   Dose/time: Intrauterine device effective up to 3–5 years.
   Purpose: Strong reduction of menstrual flow; useful adjunct to antifibrinolytics.
   Mechanism: Local progestin → endometrial suppression.
   Side effects: Irregular spotting at start. JTH Journal

9. High-dose oral progestin (e.g., norethindrone/medroxyprogesterone) – hormonal.
   Use: For acute or cyclic heavy bleeding when COCPs not suitable.
   Mechanism/AE: Endometrial stabilization; watch mood changes, fluid retention. JTH Journal

10. Antifibrinolytic prophylaxis around procedures (TXA or EACA, scheduled).
    Use: Start before dental/surgical work and continue several days after per specialist plan.
    Rationale: Prevents early clot dissolution at the wound. PMC

11. FFP peri-operative optimization (planned cases).
    Use: One or more pre-op doses to raise α2-AP; individualized to labs and bleeding risk; described in case reports.
    Mechanism/AE: Replaces inhibitors; usual transfusion risks. PubMed

12. Topical thrombin – adjunct topical hemostat.
    Use: Surgeon-applied to oozing surfaces.
    Mechanism: Converts fibrinogen to fibrin locally.
    AE: Rare hypersensitivity. (General hemostasis reference.) AGD

13. Antifibrinolytic lozenges/sprays for oral bleeding (where available).
    Use: Minor gum bleeds/after dental cleaning.
    Rationale: Local plasmin blockade. AGD

14. TXA for epistaxis (topical/soaked nasal pledgets) – used by ENT.
    Use: Short courses for nosebleeds.
    Mechanism/AE: Local antifibrinolysis; minimal systemic exposure. JTH Journal

15. Antifibrinolytics for menorrhagia during menses only (e.g., TXA 1–1.5 g 3×/day for up to 5 days each cycle).
    Purpose: Reduce menstrual volume on heavy days.
    Caution: Avoid if high thrombosis risk; follow local labeling. BioMed Central

16. Antifibrinolytics for dental extractions (rinse + tablets as directed).
    Purpose: Prevent post-extraction oozing. PMC

17. Plasma-derived pooled plasma (Octaplas, where used) – alternative to FFP in some centers.
    Dose: Similar to FFP by volume; center-specific.
    Note: Discuss with transfusion medicine. Medscape

18. Avoid desmopressin (DDAVP) as primary therapy – it raises FVIII/VWF but does not fix hyperfibrinolysis; may help only if another disorder co-exists. (Rationale statement.) JTH Journal

19. Avoid routine platelet/cryoprecipitate unless specific indications – platelets don’t solve fibrinolysis; cryo is fibrinogen-rich but not a substitute for α2-AP. (Transfusion principles.) JTH Journal+1

20. Case-by-case specialist therapies in complex surgery/trauma (multimodal hemostasis with antifibrinolytics at the core). PMC

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Dietary / molecular supplements

There are no supplements that replace α2-antiplasmin. These are supportive for anemia or tissue healing and should be used only if deficient and approved by your clinician.

1. Oral iron (ferrous sulfate/other) – dose per labs; restores hemoglobin in chronic loss; too much causes GI upset. JTH Journal

2. Folate (0.4–1 mg/day if deficient) – supports RBC production. JTH Journal

3. Vitamin B12 (dose per deficiency) – supports RBCs/neurologic health. JTH Journal

4. Vitamin C (e.g., 200–500 mg/day) – improves iron absorption; collagen support. JTH Journal

5. Vitamin K – only if deficient or on warfarin reversal under medical advice; it does not treat α2-AP deficiency itself. NCBI

6. Zinc (as per RDA) – wound healing support; avoid excess. JTH Journal

7. Protein-adequate diet – building blocks for clotting proteins and repair. JTH Journal

8. Avoid high-dose vitamin E – can worsen bleeding. JTH Journal

9. Avoid fish-oil/omega-3 megadoses – antiplatelet effect can increase oozing. JTH Journal

10. Hydration and fiber – helps recovery after bleeding and prevents straining. JTH Journal

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Immunity booster / regenerative / stem-cell drugs

I can’t list “hard immunity booster,” regenerative, or stem-cell drugs for antiplasmin deficiency because no such therapies are proven, approved, or recommended for this condition. The problem is fibrinolysis, not immune failure or marrow failure, and current evidence-based care relies on antifibrinolytics and plasma support when needed. Claims of stem-cell or “immunity-boosting” cures for this disorder are not supported by clinical guidelines. Safer, science-based alternatives are the medicines and strategies already listed above (TXA/EACA; careful dental/surgical planning; FFP when indicated). PubMed+1

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Surgeries/procedures

Surgery does not cure α2-AP deficiency, but some procedures treat complications or recurrent bleeding. Always combine with antifibrinolytic plans.

1. Nasal cauterization for stubborn nosebleeds—seals bleeding vessels. JTH Journal

2. Dental surgical hemostasis (packing, sutures, local hemostats) during extractions—prevents socket oozing. AGD

3. Endometrial ablation for refractory heavy menses when medications fail—reduces uterine lining. JTH Journal

4. Hysterectomy (last resort) for life-altering bleeding after all conservative options. JTH Journal

5. Interventional radiology embolization for focal bleeding (e.g., pelvic/ENT)—blocks the bleeding artery. JTH Journal

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Prevention tips

1. Share a written care plan with dentists and surgeons well before procedures. WFH

2. Use antifibrinolytic prophylaxis around dental/surgical work exactly as prescribed. PMC

3. Avoid aspirin/NSAIDs and bleeding-promoting supplements unless your doctor says otherwise. JTH Journal

4. Protect from trauma (sports guards, seat belts, safe home). JTH Journal

5. Keep nasal mucosa moist to reduce nosebleeds. JTH Journal

6. Maintain excellent oral hygiene to limit gum bleeding and dental procedures. WFH

7. Track menstrual flow and treat early each cycle where advised. BioMed Central

8. Wear a medical alert ID. JTH Journal

9. Manage liver health (vaccines for hepatitis where appropriate, avoid hepatotoxins). JTH Journal

10. Family testing/counseling if SERPINF2 mutation is known. NCBI

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When to see a doctor urgently

• Bleeding that does not stop with 10–15 minutes of firm pressure.

• Heavy menstrual bleeding soaking pads/cups hourly, or passing large clots.

• Head injury, severe headache, confusion, or any sign of internal bleeding.

• Post-procedure oozing that restarts at home.

• Recurrent nosebleeds or gum bleeding despite local care.

• Planning any dental work, surgery, or pregnancy—see a hematologist in advance. JTH Journal

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What to eat and what to avoid

Eat more of:

• Iron-rich foods (lean red meat, liver, beans, lentils, spinach), vitamin C–rich foods (citrus, guava, bell pepper) to help iron absorption.

• Protein-adequate meals (eggs, fish, legumes, dairy) to support healing.

• Whole grains, fruits, and fluids to avoid constipation and straining. JTH Journal

Limit/avoid:

• Alcohol excess (can worsen bleeding and harm the liver).

• High-dose vitamin E, fish-oil/omega-3 megadoses, and garlic/ginger in very large supplemental doses—they can thin blood or impair platelets.

• Aspirin/NSAIDs unless a doctor specifically recommends them. JTH Journal

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FAQs

1. Is antiplasmin deficiency the same as a clotting factor deficiency?
   No. Your clot forms, but it dissolves too quickly (hyperfibrinolysis). JTH Journal

2. Which gene is involved?
   SERPINF2—it encodes the α2-antiplasmin protein. NCBI

3. How rare is it?
   Very rare; only small numbers of confirmed cases are published worldwide. Wikipedia

4. What’s the main treatment?
   Antifibrinolytics: tranexamic acid or aminocaproic acid; FFP for severe cases or procedures. PubMed+1

5. Will desmopressin (DDAVP) help?
   Usually not—it doesn’t stop fibrinolysis; it’s for other bleeding problems. JTH Journal

6. Do I need treatment every day?
   Often no. Many people use antifibrinolytics only when bleeding or around dental/surgical work. Follow your specialist’s plan. PMC

7. What about pregnancy and birth?
   Plan ahead with obstetrics and hematology to prevent post-partum bleeding; antifibrinolytics are central. JTH Journal

8. Can I have dental work safely?
   Yes—with a plan: local hemostatics plus TXA/EACA rinses and/or tablets as directed. PMC

9. Is plasma (FFP) safe?
   Modern screening reduces risks, but transfusion always has potential reactions; used only when needed. NCBI

10. Can children be affected?
    Yes; severe congenital cases often appear in childhood (e.g., umbilical stump bleeding). PreventionGenetics

11. How is the diagnosis confirmed?
    Low α2-antiplasmin activity/antigen and often SERPINF2 genetic testing. PMC+1

12. Does vitamin K cure it?
    No. Vitamin K affects clotting factors, not fibrinolysis; only use if deficient under medical advice. NCBI

13. Is there a concentrate or recombinant α2-antiplasmin?
    No specific commercial concentrate; FFP supplies α2-AP when necessary. ScienceDirect

14. Could my liver condition make bleeding worse even if I’m a carrier?
    Yes—liver disease lowers production of α2-AP and can unmask bleeding. Wikipedia

15. Where can my clinician read more?
    Recent reviews on inherited fibrinolytic disorders and α2-AP’s role in bleeding outline diagnosis and management. PubMed+

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Last Updated: September 13, 2025.

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