GITNUXREPORT 2026

Hemophilia A Statistics

Hemophilia A is a rare bleeding disorder with varied global prevalence and treatments.

Min-ji Park

Research Analyst focused on sustainability and consumer trends.

First published: Feb 13, 2026

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Statistic 1

Severe hemophilia A patients have factor VIII levels <1% of normal

Statistic 2

Moderate hemophilia A is defined by factor VIII levels of 1-5% of normal activity

Statistic 3

Mild hemophilia A features factor VIII levels of 6-49% of normal

Statistic 4

Spontaneous joint bleeds occur in 80-90% of severe hemophilia A patients without prophylaxis

Statistic 5

The most common initial bleed in hemophilia A is post-circumcision in neonates, in 10-20% cases

Statistic 6

Prolonged bleeding after dental extraction affects 70% of untreated hemophilia A patients

Statistic 7

Muscle hematomas are reported in 50-60% of moderate hemophilia A episodes

Statistic 8

Diagnosis of hemophilia A is confirmed by aPTT prolongation and low FVIII activity

Statistic 9

Genetic testing confirms diagnosis in 95% of hemophilia A families

Statistic 10

Hemarthrosis of the knee occurs in 60% of first joint bleeds in children with hemophilia A

Statistic 11

Epistaxis is a presenting symptom in 20-30% of mild hemophilia A cases

Statistic 12

Intracranial hemorrhage risk is 5-10% lifetime in severe hemophilia A

Statistic 13

von Willebrand factor levels are normal in hemophilia A, distinguishing from VWD

Statistic 14

Thrombin time is normal in hemophilia A diagnostic panels

Statistic 15

Pretest probability using family history predicts 90% of hemophilia A diagnoses

Statistic 16

Joint pain precedes visible swelling in 40% of hemarthrosis episodes

Statistic 17

Umbilical stump bleeding occurs in 10% of neonatal hemophilia A presentations

Statistic 18

FVIII inhibitor screening is positive in 25-30% of severe cases post-treatment

Statistic 19

ECOG score correlates with bleed frequency in hemophilia A assessment

Statistic 20

FISH testing detects intron 22 inversions in 50% of severe cases rapidly

Statistic 21

Bethesda assay quantifies inhibitors at >5 BU/mL as high-titer in hemophilia A

Statistic 22

Median age at diagnosis for severe hemophilia A is 9 months

Statistic 23

GI bleeding from angiodysplasia occurs in 2-5% of mild hemophilia A adults

Statistic 24

Pseudotumors develop in 1-2% of untreated severe hemophilia A patients

Statistic 25

Annual joint bleeds reduced from 55 to 1.9 with prophylaxis

Statistic 26

Life expectancy in severe hemophilia A with prophylaxis approaches normal at 70+ years

Statistic 27

Arthropathy develops in 50% of patients without early prophylaxis by age 30

Statistic 28

HIV transmission via clotting factors affected 50-70% pre-1985 cohort

Statistic 29

HCV prevalence in hemophilia A is 20-40% from past plasma products

Statistic 30

Inhibitor development risk is 25-30% in severe hemophilia A first 50 exposure days

Statistic 31

Synovitis leads to target joint status in 20% of non-prophylaxed patients yearly

Statistic 32

Cardiovascular disease mortality increased 2-3 fold in hemophilia A

Statistic 33

Pseudotumor complication rate is 1.5-2% in severe untreated cases

Statistic 34

Nephropathy from retroperitoneal bleeds affects 5% long-term

Statistic 35

Malignancy risk not elevated but cancer survival poorer due to bleeds, 10-15% higher mortality

Statistic 36

Quality of life scores (HAEM-A-QoL) improve 20-30% with prophylaxis

Statistic 37

Annualized bleed rate (ABR) <2 with modern prophylaxis in 80% patients

Statistic 38

Orthopedic surgery needed in 40% by age 40 without prophylaxis

Statistic 39

Inhibitor eradication failure leads to 5x higher bleed rates

Statistic 40

Overweight/obesity in 40-50% hemophilia A adults worsens arthropathy

Statistic 41

Gene therapy trials show 90% reduction in FVIII usage post-infusion

Statistic 42

Mental health disorders 2x higher in hemophilia A (anxiety/depression 30%)

Statistic 43

Post-surgical bleed complication <5% with optimal management

Statistic 44

Liver fibrosis in 30% of HCV+ hemophilia A from old factors

Statistic 45

Hemophilia A is an X-linked recessive disorder caused by mutations in the F8 gene located on the X chromosome at Xq28

Statistic 46

Over 2,000 unique mutations in the F8 gene have been identified in hemophilia A patients

Statistic 47

Inversions involving intron 22 (inv22) account for 45-50% of severe hemophilia A cases

Statistic 48

Intron 1 inversions (inv1) cause about 2-5% of severe hemophilia A mutations

Statistic 49

Point mutations represent 20-30% of F8 gene defects in hemophilia A

Statistic 50

Deletions in the F8 gene occur in approximately 5% of severe hemophilia A cases

Statistic 51

The F8 gene spans 186 kb and contains 26 exons encoding factor VIII protein of 2,332 amino acids

Statistic 52

Missense mutations are the most common type in mild/moderate hemophilia A, comprising 50-60%

Statistic 53

Nonsense mutations lead to severe hemophilia A in 15-20% of cases

Statistic 54

Splicing mutations account for 10-15% of F8 gene alterations in hemophilia A

Statistic 55

Large gene rearrangements cause 5-10% of hemophilia A mutations

Statistic 56

The carrier detection rate using genetic testing reaches 95-99% for known family mutations

Statistic 57

Skewed X-inactivation in female carriers leads to symptomatic hemophilia A in 10-20% of cases

Statistic 58

CRM-negative severe hemophilia A is 90% due to gross gene defects

Statistic 59

The F8 gene inversion breakpoint in intron 22 is precisely mapped to a 9.5 kb region

Statistic 60

Promoter mutations in F8 gene are rare, occurring in less than 1% of hemophilia A

Statistic 61

Frameshift mutations comprise 10% of F8 defects in moderate hemophilia A

Statistic 62

Haplotyping reveals founder effects in 20-30% of hemophilia A populations

Statistic 63

RNA-based analysis detects 98% of F8 mutations in hemophilia A

Statistic 64

De novo mutations account for 30% of severe hemophilia A cases with no family history

Statistic 65

The F8 gene has a high mutation rate of 3.1 x 10^-5 per generation

Statistic 66

Complex rearrangements like duplications occur in 3% of F8 mutations

Statistic 67

Genotype-phenotype correlation is strong in severe hemophilia A with null mutations

Statistic 68

Female hemophilia A due to X-autosome translocations is extremely rare, <0.5%

Statistic 69

NGS sequencing identifies novel F8 variants in 5-10% of undiagnosed cases

Statistic 70

Hemophilia A affects approximately 1 in 5,000 to 1 in 10,000 male births worldwide

Statistic 71

In the United States, about 20,000 males are living with hemophilia A as of recent estimates

Statistic 72

The prevalence of severe hemophilia A is around 45-52% of all hemophilia A cases

Statistic 73

In Europe, the incidence of hemophilia A is reported at 11.7 per 100,000 males

Statistic 74

Hemophilia A accounts for 80-85% of all hemophilia cases globally

Statistic 75

In India, the prevalence of hemophilia A is estimated at 1 in 7,500 male births

Statistic 76

African American males have a slightly higher prevalence of hemophilia A at 13.1 per 100,000 compared to 12.6 for white males

Statistic 77

The number of registered hemophilia A patients in the UK is approximately 6,000

Statistic 78

In Canada, hemophilia A prevalence is 13.5 per 100,000 males

Statistic 79

Global carrier frequency for hemophilia A is about 1 in 5,000 females

Statistic 80

Australia reports 2,500 individuals with hemophilia A

Statistic 81

In Brazil, there are over 12,000 registered hemophilia A patients

Statistic 82

Hemophilia A incidence in China is 5.6 per 100,000 males

Statistic 83

Japan has about 3,000 hemophilia A patients

Statistic 84

In South Africa, prevalence is 11.9 per 100,000 males for hemophilia A

Statistic 85

Russia estimates 15,000 hemophilia A cases

Statistic 86

Mexico reports 6,000 hemophilia A patients

Statistic 87

In Egypt, incidence is 1 in 12,000 male births for hemophilia A

Statistic 88

Saudi Arabia has a prevalence of 10.3 per 100,000 males

Statistic 89

Turkey registers about 5,000 hemophilia A patients

Statistic 90

In Iran, over 3,000 hemophilia A cases are documented

Statistic 91

Thailand prevalence is 6.8 per 100,000 males

Statistic 92

Nigeria reports lower diagnosis rates with estimated 1,000 known hemophilia A patients

Statistic 93

In France, 7,000 individuals live with hemophilia A

Statistic 94

Germany has around 8,000 hemophilia A patients

Statistic 95

Italy registers 5,500 hemophilia A cases

Statistic 96

Spain prevalence is 12.4 per 100,000 males

Statistic 97

Sweden has 900 hemophilia A patients

Statistic 98

Netherlands reports 1,200 hemophilia A cases

Statistic 99

Prophylactic factor VIII replacement therapy maintains levels >1% in 85% of severe cases

Statistic 100

Extended half-life FVIII products extend dosing intervals to every 5-7 days

Statistic 101

Emicizumab prophylaxis reduces bleed rates by 87% in inhibitor patients

Statistic 102

Bypassing agents like rFVIIa control 90% of bleeds in inhibitor hemophilia A

Statistic 103

Immune tolerance induction succeeds in 60-80% of pediatric inhibitor cases

Statistic 104

Gene therapy with AAV5-hFVIII achieves sustained FVIII >5% in 80% of adults

Statistic 105

DDAVP increases FVIII levels 2-6 fold in 80% of mild hemophilia A patients

Statistic 106

Weekly prophylaxis dosing is 25-40 IU/kg for severe hemophilia A children

Statistic 107

FEIBA (aPCC) hemostatic efficacy is 80-90% per bleed episode

Statistic 108

Valoctocogene roxaparvovec gene therapy normalizes FVIII in phase 3 trials for 96 weeks

Statistic 109

Tranexamic acid adjunct reduces bleed duration by 30% in dental procedures

Statistic 110

Pegylated FVIII (BAY 94-9027) has 1.5-fold longer half-life than standard

Statistic 111

ITI with high-dose FVIII (200 IU/kg/day) eradicates inhibitors in 70% cases

Statistic 112

Fitusiran RNAi therapy reduces bleeds by 90% in non-inhibitor patients

Statistic 113

Orthopedic surgery success rate is 95% with adequate perioperative FVIII

Statistic 114

Concizumab subcutaneous dosing prevents 98% of treated bleeds

Statistic 115

AAV8-hFVIII gene transfer sustains expression >3% for 5+ years in trials

Statistic 116

RFVIII-SingleChain has 2-fold longer half-life and 93% efficacy

Statistic 117

Checkpoint inhibitors like anti-C2 domain emicizumab mimic FVIII

Statistic 118

Bispecific antibodies (ACE910) prophylaxis ABR <1 bleed/year

Statistic 119

Liver-directed AAV gene therapy corrects 30% of circulating FVIII

Statistic 120

rurioctocog alfa pegol prophylaxis dosing every 7 days in 90% patients

Statistic 121

Porcine FVIII for rescue in inhibitors achieves 85% response rate

Statistic 122

Eloctate (rFVIIIFc) extends intervals to 5 days in 75% of patients

1/122

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While thousands of men across the globe navigate the daily realities of Hemophilia A, this X-linked bleeding disorder rooted in over 2,000 unique genetic mutations presents a complex tapestry of both global burden and groundbreaking scientific progress.

Key Takeaways

Hemophilia A affects approximately 1 in 5,000 to 1 in 10,000 male births worldwide
In the United States, about 20,000 males are living with hemophilia A as of recent estimates
The prevalence of severe hemophilia A is around 45-52% of all hemophilia A cases
Hemophilia A is an X-linked recessive disorder caused by mutations in the F8 gene located on the X chromosome at Xq28
Over 2,000 unique mutations in the F8 gene have been identified in hemophilia A patients
Inversions involving intron 22 (inv22) account for 45-50% of severe hemophilia A cases
Severe hemophilia A patients have factor VIII levels <1% of normal
Moderate hemophilia A is defined by factor VIII levels of 1-5% of normal activity
Mild hemophilia A features factor VIII levels of 6-49% of normal
Prophylactic factor VIII replacement therapy maintains levels >1% in 85% of severe cases
Extended half-life FVIII products extend dosing intervals to every 5-7 days
Emicizumab prophylaxis reduces bleed rates by 87% in inhibitor patients
Annual joint bleeds reduced from 55 to 1.9 with prophylaxis
Life expectancy in severe hemophilia A with prophylaxis approaches normal at 70+ years
Arthropathy develops in 50% of patients without early prophylaxis by age 30

Hemophilia A is a rare bleeding disorder with varied global prevalence and treatments.

Clinical Presentation and Diagnosis

Severe hemophilia A patients have factor VIII levels <1% of normal
Moderate hemophilia A is defined by factor VIII levels of 1-5% of normal activity
Mild hemophilia A features factor VIII levels of 6-49% of normal
Spontaneous joint bleeds occur in 80-90% of severe hemophilia A patients without prophylaxis
The most common initial bleed in hemophilia A is post-circumcision in neonates, in 10-20% cases
Prolonged bleeding after dental extraction affects 70% of untreated hemophilia A patients
Muscle hematomas are reported in 50-60% of moderate hemophilia A episodes
Diagnosis of hemophilia A is confirmed by aPTT prolongation and low FVIII activity
Genetic testing confirms diagnosis in 95% of hemophilia A families
Hemarthrosis of the knee occurs in 60% of first joint bleeds in children with hemophilia A
Epistaxis is a presenting symptom in 20-30% of mild hemophilia A cases
Intracranial hemorrhage risk is 5-10% lifetime in severe hemophilia A
von Willebrand factor levels are normal in hemophilia A, distinguishing from VWD
Thrombin time is normal in hemophilia A diagnostic panels
Pretest probability using family history predicts 90% of hemophilia A diagnoses
Joint pain precedes visible swelling in 40% of hemarthrosis episodes
Umbilical stump bleeding occurs in 10% of neonatal hemophilia A presentations
FVIII inhibitor screening is positive in 25-30% of severe cases post-treatment
ECOG score correlates with bleed frequency in hemophilia A assessment
FISH testing detects intron 22 inversions in 50% of severe cases rapidly
Bethesda assay quantifies inhibitors at >5 BU/mL as high-titer in hemophilia A
Median age at diagnosis for severe hemophilia A is 9 months
GI bleeding from angiodysplasia occurs in 2-5% of mild hemophilia A adults
Pseudotumors develop in 1-2% of untreated severe hemophilia A patients

Clinical Presentation and Diagnosis Interpretation

While severe hemophilia A is often diagnosed after a baby's first cut or a toddler's swollen knee, the underlying math is a grim tally where less than 1% of normal clotting factor can lead to a lifetime where over 80% of patients face spontaneous joint destruction, a 10% risk of fatal brain bleeds, and where the very treatment creates dangerous inhibitors in a quarter of the most severe cases.

Complications, Prognosis, and Research

Annual joint bleeds reduced from 55 to 1.9 with prophylaxis
Life expectancy in severe hemophilia A with prophylaxis approaches normal at 70+ years
Arthropathy develops in 50% of patients without early prophylaxis by age 30
HIV transmission via clotting factors affected 50-70% pre-1985 cohort
HCV prevalence in hemophilia A is 20-40% from past plasma products
Inhibitor development risk is 25-30% in severe hemophilia A first 50 exposure days
Synovitis leads to target joint status in 20% of non-prophylaxed patients yearly
Cardiovascular disease mortality increased 2-3 fold in hemophilia A
Pseudotumor complication rate is 1.5-2% in severe untreated cases
Nephropathy from retroperitoneal bleeds affects 5% long-term
Malignancy risk not elevated but cancer survival poorer due to bleeds, 10-15% higher mortality
Quality of life scores (HAEM-A-QoL) improve 20-30% with prophylaxis
Annualized bleed rate (ABR) <2 with modern prophylaxis in 80% patients
Orthopedic surgery needed in 40% by age 40 without prophylaxis
Inhibitor eradication failure leads to 5x higher bleed rates
Overweight/obesity in 40-50% hemophilia A adults worsens arthropathy
Gene therapy trials show 90% reduction in FVIII usage post-infusion
Mental health disorders 2x higher in hemophilia A (anxiety/depression 30%)
Post-surgical bleed complication <5% with optimal management
Liver fibrosis in 30% of HCV+ hemophilia A from old factors

Complications, Prognosis, and Research Interpretation

Modern prophylaxis has transformed hemophilia A from a life of relentless bleeds and early death into a managed condition where most patients can expect a near-normal lifespan, yet the shadow of past treatments and complex complications like inhibitors and mental health burdens remind us that a cure remains the ultimate goal.

Genetics and Molecular Biology

Hemophilia A is an X-linked recessive disorder caused by mutations in the F8 gene located on the X chromosome at Xq28
Over 2,000 unique mutations in the F8 gene have been identified in hemophilia A patients
Inversions involving intron 22 (inv22) account for 45-50% of severe hemophilia A cases
Intron 1 inversions (inv1) cause about 2-5% of severe hemophilia A mutations
Point mutations represent 20-30% of F8 gene defects in hemophilia A
Deletions in the F8 gene occur in approximately 5% of severe hemophilia A cases
The F8 gene spans 186 kb and contains 26 exons encoding factor VIII protein of 2,332 amino acids
Missense mutations are the most common type in mild/moderate hemophilia A, comprising 50-60%
Nonsense mutations lead to severe hemophilia A in 15-20% of cases
Splicing mutations account for 10-15% of F8 gene alterations in hemophilia A
Large gene rearrangements cause 5-10% of hemophilia A mutations
The carrier detection rate using genetic testing reaches 95-99% for known family mutations
Skewed X-inactivation in female carriers leads to symptomatic hemophilia A in 10-20% of cases
CRM-negative severe hemophilia A is 90% due to gross gene defects
The F8 gene inversion breakpoint in intron 22 is precisely mapped to a 9.5 kb region
Promoter mutations in F8 gene are rare, occurring in less than 1% of hemophilia A
Frameshift mutations comprise 10% of F8 defects in moderate hemophilia A
Haplotyping reveals founder effects in 20-30% of hemophilia A populations
RNA-based analysis detects 98% of F8 mutations in hemophilia A
De novo mutations account for 30% of severe hemophilia A cases with no family history
The F8 gene has a high mutation rate of 3.1 x 10^-5 per generation
Complex rearrangements like duplications occur in 3% of F8 mutations
Genotype-phenotype correlation is strong in severe hemophilia A with null mutations
Female hemophilia A due to X-autosome translocations is extremely rare, <0.5%
NGS sequencing identifies novel F8 variants in 5-10% of undiagnosed cases

Genetics and Molecular Biology Interpretation

While the F8 gene appears to be a chaotic workshop with over 2,000 unique glitches, from the notorious intron 22 inversion bossing half the severe cases to the point mutations gossiping in the corner, its disarray is mapped with such precision that we can now spot a carrier with near-perfect certainty, though the X-chromosome's whims still let symptoms slip through in a surprising number of women.

Prevalence and Epidemiology

Hemophilia A affects approximately 1 in 5,000 to 1 in 10,000 male births worldwide
In the United States, about 20,000 males are living with hemophilia A as of recent estimates
The prevalence of severe hemophilia A is around 45-52% of all hemophilia A cases
In Europe, the incidence of hemophilia A is reported at 11.7 per 100,000 males
Hemophilia A accounts for 80-85% of all hemophilia cases globally
In India, the prevalence of hemophilia A is estimated at 1 in 7,500 male births
African American males have a slightly higher prevalence of hemophilia A at 13.1 per 100,000 compared to 12.6 for white males
The number of registered hemophilia A patients in the UK is approximately 6,000
In Canada, hemophilia A prevalence is 13.5 per 100,000 males
Global carrier frequency for hemophilia A is about 1 in 5,000 females
Australia reports 2,500 individuals with hemophilia A
In Brazil, there are over 12,000 registered hemophilia A patients
Hemophilia A incidence in China is 5.6 per 100,000 males
Japan has about 3,000 hemophilia A patients
In South Africa, prevalence is 11.9 per 100,000 males for hemophilia A
Russia estimates 15,000 hemophilia A cases
Mexico reports 6,000 hemophilia A patients
In Egypt, incidence is 1 in 12,000 male births for hemophilia A
Saudi Arabia has a prevalence of 10.3 per 100,000 males
Turkey registers about 5,000 hemophilia A patients
In Iran, over 3,000 hemophilia A cases are documented
Thailand prevalence is 6.8 per 100,000 males
Nigeria reports lower diagnosis rates with estimated 1,000 known hemophilia A patients
In France, 7,000 individuals live with hemophilia A
Germany has around 8,000 hemophilia A patients
Italy registers 5,500 hemophilia A cases
Spain prevalence is 12.4 per 100,000 males
Sweden has 900 hemophilia A patients
Netherlands reports 1,200 hemophilia A cases

Prevalence and Epidemiology Interpretation

These numbers paint a global picture of a rare condition where geography, genetics, and healthcare access mean that for every one man confidently counted, there is likely another whose story remains statistically unseen.

Treatment Options and Therapies

Prophylactic factor VIII replacement therapy maintains levels >1% in 85% of severe cases
Extended half-life FVIII products extend dosing intervals to every 5-7 days
Emicizumab prophylaxis reduces bleed rates by 87% in inhibitor patients
Bypassing agents like rFVIIa control 90% of bleeds in inhibitor hemophilia A
Immune tolerance induction succeeds in 60-80% of pediatric inhibitor cases
Gene therapy with AAV5-hFVIII achieves sustained FVIII >5% in 80% of adults
DDAVP increases FVIII levels 2-6 fold in 80% of mild hemophilia A patients
Weekly prophylaxis dosing is 25-40 IU/kg for severe hemophilia A children
FEIBA (aPCC) hemostatic efficacy is 80-90% per bleed episode
Valoctocogene roxaparvovec gene therapy normalizes FVIII in phase 3 trials for 96 weeks
Tranexamic acid adjunct reduces bleed duration by 30% in dental procedures
Pegylated FVIII (BAY 94-9027) has 1.5-fold longer half-life than standard
ITI with high-dose FVIII (200 IU/kg/day) eradicates inhibitors in 70% cases
Fitusiran RNAi therapy reduces bleeds by 90% in non-inhibitor patients
Orthopedic surgery success rate is 95% with adequate perioperative FVIII
Concizumab subcutaneous dosing prevents 98% of treated bleeds
AAV8-hFVIII gene transfer sustains expression >3% for 5+ years in trials
RFVIII-SingleChain has 2-fold longer half-life and 93% efficacy
Checkpoint inhibitors like anti-C2 domain emicizumab mimic FVIII
Bispecific antibodies (ACE910) prophylaxis ABR <1 bleed/year
Liver-directed AAV gene therapy corrects 30% of circulating FVIII
rurioctocog alfa pegol prophylaxis dosing every 7 days in 90% patients
Porcine FVIII for rescue in inhibitors achieves 85% response rate
Eloctate (rFVIIIFc) extends intervals to 5 days in 75% of patients

Treatment Options and Therapies Interpretation

Modern hemophilia A management has evolved from a constant battle with bleeding into a strategic campaign, where gene therapy offers potential cures, clever biotechnologies like emicizumab outmaneuver inhibitors, and a growing arsenal of extended-life factors and adjuncts lets patients trade daily skirmishes for weekly, or even monthly, peace treaties.

Sources & References

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