There are three main types of hemophilia: hemophilia A, hemophilia B, and hemophilia C. Each type results from a deficiency in a different clotting factor, a protein your blood needs to form clots and stop bleeding. A fourth form, acquired hemophilia, is not inherited but develops later in life when the immune system attacks one of these clotting factors.
Hemophilia A: The Most Common Type
Hemophilia A is caused by low levels or a complete lack of clotting factor VIII. It’s the most common form, occurring three to four times more frequently than hemophilia B. Because it primarily affects males and runs in families through the X chromosome, it’s sometimes called “classic hemophilia.”
The severity of hemophilia A varies widely from person to person, depending on how much functional clotting factor VIII is circulating in the blood. Some people bleed excessively only after surgery or a serious injury, while others experience spontaneous bleeding into joints and muscles with no obvious trigger. Doctors determine severity through a clotting factor assay, a blood test that measures how active the clotting factor is.
Hemophilia B: Factor IX Deficiency
Hemophilia B involves a deficiency in clotting factor IX. It’s less common than hemophilia A but inherited the same way and produces nearly identical symptoms. The two types are distinguishable only through blood tests, not by how they look clinically. You might hear hemophilia B called “Christmas disease,” named after the first patient in whom it was formally identified.
Like hemophilia A, severity ranges from mild to severe based on how much factor IX activity is present. Someone with mild hemophilia B may not be diagnosed until adulthood, often after unexpectedly heavy bleeding during a dental procedure or surgery.
Hemophilia C: A Different Inheritance Pattern
Hemophilia C results from a deficiency of clotting factor XI. It’s quite different from types A and B in two important ways. First, it’s not linked to the X chromosome. Instead, it follows an autosomal inheritance pattern, meaning it affects males and females at equal rates. Second, the relationship between factor levels and bleeding severity is less predictable. Some people with very low factor XI levels have minimal bleeding problems, while others with higher levels bleed more than expected.
Hemophilia C is rarer than A or B and is most common among people of Ashkenazi Jewish descent. Bleeding tends to occur after trauma or surgery rather than spontaneously, and it’s generally considered a milder condition overall.
Acquired Hemophilia: Not Inherited
Acquired hemophilia is fundamentally different from the inherited types. It develops when the immune system produces antibodies that attack the body’s own clotting factor VIII, disabling it. This can happen to anyone at any age, even people with no personal or family history of bleeding disorders.
In roughly half of all cases, no clear cause is identified. The other half are linked to autoimmune diseases, certain cancers, or pregnancy (which accounts for most cases in younger adults). Symptoms tend to appear suddenly: large bruises, prolonged bleeding from minor cuts, or bleeding into soft tissues. Because it’s unexpected and unfamiliar to many doctors outside of hematology, acquired hemophilia can take time to diagnose.
How Hemophilia A and B Are Inherited
The genes for clotting factors VIII and IX both sit on the X chromosome. Males have one X and one Y chromosome, so a single altered copy of the gene is enough to cause hemophilia. Females have two X chromosomes, which typically means they need alterations on both copies to develop symptoms. That’s why hemophilia A and B overwhelmingly affect males.
However, some females with one altered copy do experience bleeding problems. This happens through a process called X-inactivation, where each cell randomly shuts off one of its two X chromosomes. If the chromosome carrying the normal gene gets shut off in more than half of cells, the woman produces less clotting factor than usual and can develop symptoms ranging from easy bruising to more significant bleeding. These women are sometimes called “symptomatic carriers,” though the term undersells the real impact on their daily lives.
One notable feature of X-linked inheritance: fathers cannot pass hemophilia A or B to their sons. A father passes his Y chromosome to sons and his X to daughters. So an affected father will have unaffected sons, but all of his daughters will carry the altered gene.
How the Types Are Diagnosed
The first clue usually comes from a test called the activated partial thromboplastin time (APTT), which measures how long it takes a blood sample to clot. This test is sensitive to factors VIII, IX, XI, and XII. If the APTT is prolonged, the next step is a clotting factor assay, which individually measures the activity level of each factor. This pinpoints both the specific type of hemophilia and its severity.
For hemophilia A or B, the factor assay result also guides treatment decisions. Someone with very low factor activity will typically need regular preventive treatment, while someone with mild deficiency may only need treatment before procedures that carry bleeding risk.
Treatment Options Today
The core treatment for hemophilia A and B is replacing the missing clotting factor, either through products derived from donated blood or through lab-made (recombinant) versions. For decades, this meant frequent intravenous infusions, sometimes multiple times per week.
That landscape has shifted considerably. Newer therapies work differently from traditional factor replacement. Some are antibody-based treatments that mimic what factor VIII does, allowing people with hemophilia A to inject a medication under the skin rather than into a vein. In 2024, the FDA approved two newer options for preventing bleeding episodes in both hemophilia A and B, including a subcutaneous injection for patients 12 and older, expanding the choices available for routine prevention.
Gene therapy represents the most fundamental shift. Rather than regularly replacing the missing factor, gene therapy aims to give the body’s cells the genetic instructions to produce it on their own. The first gene therapies for hemophilia A and B have received approval, though long-term durability and access remain open questions. For many patients, these therapies have reduced or eliminated the need for regular infusions, a dramatic change in quality of life for a condition that historically required constant management.