In terms of hemophilia C medication cyklokapron is often used for both treatment after an incident of bleeding and as a preventative measure to avoid excessive bleeding during oral surgery.

Treatment is usually not necessary, except in relation to operations, leading to many of those having the condition not being aware of it. In these cases, fresh frozen plasma or recombinant factor XI may be used, but only if necessary.

The afflicted may often suffer nosebleeds, while females can experience unusual menstrual bleeding which can be avoided by taking birth control such as: IUDs and oral or injected contraceptives to increase coagulation ability by adjusting hormones to levels similar to pregnancy.

Desmopressin (DDAVP) may be used in those with mild haemophilia A. Tranexamic acid or epsilon aminocaproic acid may be given along with clotting factors to prevent breakdown of clots.

Pain medicines, steroids, and physical therapy may be used to reduce pain and swelling in an affected joint.

While there is no cure for haemophilia, treatment improves outcomes.

Treatment is by intravenous infusion of factor IX, which has a longer half life than factor VIII and as such factor IX can be transfused less frequently. Blood transfusions may be needed, NSAIDS should be discontinued once the individual has been diagnosed with the condition. Any surgical procedure should be done "in concert" with tranexamic acid.

In regards to the treatment of this genetic disorder, most individuals with severe haemophilia require regular supplementation with intravenous recombinant or plasma concentrate Factor VIII. The preventative treatment regime is highly variable and individually determined. In children, an easily accessible intravenous port ( portacath) may have to be inserted to minimise frequent traumatic intravenous cannulation. These devices have made prophylaxis in haemophilia much easier for families because the problems of "finding a vein" for infusion several times a week are eliminated. However, there are risks involved with their use, the most worrisome being that of infection, studies differ but some show an infection rate that is high These infections can usually be treated with intravenous antibiotics but sometimes the device must be removed, also, there are other studies that show a risk of clots forming at the tip of the catheter.Some individuals with severe haemophilia and most with moderate and mild haemophilia treat only as needed without a regular prophylactic schedule. Mild haemophiliacs often manage their condition with desmopressin, which releases stored factor VIII from blood vessel walls.

In December 2017, it was reported that doctors had used a new form of gene therapy to treat haemophilia A.

In congenital FXII deficiency treatment is not necessary. In acquired FXII deficiency the underlying problem needs to be addressed.

There are several treatments available for factor VII deficiency; they all replace deficient FVII.

1. Recombinant FVIIa concentrate (rFVIIa) is a recombinant treatment that is highly effective and has no risk of fluid overload or viral disease. It may be the optimal therapy.

2. Plasma derived Factor VII concentrate (pdFVII) : This treatment is suitable for surgery but can lead to thrombosis. It is virus attenuated.

3. Prothrombin complex concentrate (PCC) containing factor VII: this treatment is suitable for surgery, but has a risk of thrombosis. It is virus attenuated.

4. Fresh frozen plasma (FFP): This is relatively inexpensive and readily available. While effective this treatment carries a risk of blood-borne viruses and fluid overload.

Fresh frozen plasma and cryoprecipitate are the mainstay of therapy for Factor XIII deficiency, but carry risk related to transfusion.

Recombinant factor XIII (rFXIII) is the only drug alternative to receiving blood transfusions, the traditional treatment for factor XIII deficiency. Novo Nordisk’s rFXIII, catridecacog, was approved by the US Food and Drug Administration in 2014. Although it is a recombinant protein, rFXIII subunit A is identical in structure and function to the A subunit of factor XIII naturally produced in the body by healthy individuals. These patients need exogenous subunit A of factor XIII since they have a mutation which prevents production of the A subunit. However, since the B-subunit is located on a separate chromosome, factor XIII deficient patients actually produce the B-subunit normally. When these two subunits interact in the plasma, the enzyme is activated and can act within the clotting cascade. rFXIII acts by inhibiting fibrinolysis factors which enzymatically cleave the fibrin matrix, leading to the ultimate formation of clots.

rFXIII is synthetically bio-engineered through a yeast expression system and administered intravenously. In clinical trials, the drug was administered once every four weeks or administered on-demand in order to treat bleeding episodes. The introduction of rFXIII as a treatment for factor XIII deficiency eliminates the risk of pathogenic infection present in plasma-based treatments. rFXIII treatment would also not be dependent on blood donations, consequently increasing availability and product quality. One of the biggest fears in developing rFXIII was that the body would mount an immune-response to the protein; however, several safety and pharmokinetics studies have reported no immunogenic response to rFXIII or associated yeast products.

Treatment is almost always aimed to control hemorrhages, treating underlying causes, and taking preventative steps before performing invasive surgeries.

Hypoprothrombinemia can be treated with periodic infusions of purified prothrombin complexes. These are typically used as treatment methods for severe bleeding cases in order to boost clotting ability and increasing levels of vitamin K-dependent coagulation factors.

1. A known treatment for hypoprothrombinemia is menadoxime.

2. Menatetrenone was also listed as a Antihaemorrhagic vitamin.

3. 4-Amino-2-methyl-1-naphthol (Vitamin K5) is another treatment for hypoprothrombinemia.

1. Vitamin K forms are administered orally or intravenously.

4. Other concentrates include Proplex T, Konyne 80, and Bebulin VH.

Fresh Frozen Plasma infusion (FFP) is a method used for continuous bleeding episodes, every 3-5 weeks for mention.

1. Used to treat various conditions related to low blood clotting factors.

2. Administered by intravenous injection and typically at a 15-20 ml/kg/dose.

3. Can be used to treat acute bleeding.

Sometimes, underlying causes cannot be controlled or determined, so management of symptoms and bleeding conditions should be priority in treatment.

Invasive options, such as surgery or clotting factor infusions, are required if previous methods do not suffice. Surgery is to be avoided, as it causes significant bleeding in patients with hypoprothrombinemia.

Prognosis for patients varies and is dependent on severity of the condition and how early the treatment is managed.

1. With proper treatment and care, most people go on to live a normal and healthy life.

2. With more severe cases, a hematologist will need to be seen throughout the patient's life in order to deal with bleeding and continued risks.

The first element of treatment is usually to discontinue the offending drug, although there have been reports describing how the eruption evolved little after it had established in spite of continuing the medication. Vitamin K1 can be used to reverse the effects of warfarin, and heparin or its low molecular weight heparin (LMWH) can be used in an attempt to prevent further clotting. None of these suggested therapies have been studied in clinical trials.

Heparin and LMWH act by a different mechanism than warfarin, so these drugs can also be used to prevent clotting during the first few days of warfarin therapy and thus prevent warfarin necrosis (this is called 'bridging').

Based on the assumption that low levels of protein C are involved in the underlying mechanism, common treatments in this setting include fresh frozen plasma or pure activated protein C.

Since the clot-promoting effects of starting administration of 4-hydroxycoumarins are transitory, patients with protein C deficiency or previous warfarin necrosis can still be restarted on these drugs if appropriate measures are taken. These include gradual increase starting from low doses and supplemental administration of protein C (pure or from fresh frozen plasma).

The necrotic skin areas are treated as in other conditions, sometimes healing spontaneously with or without scarring, sometimes going on to require surgical debridement or skin grafting.

For people who have severe congenital protein C deficiency, protein C replacement therapies are available, which is indicated and approved for use in the United States and Europe for the prevention of purpura fulminans. Protein C replacement is often in combination with anticoagulation therapy of injectable low molecular weight heparin or oral warfarin. Before initiating warfarin therapy, a few days of therapeutic heparin may be administered to prevent warfarin skin necrosis and other progressive or recurrent thrombotic complications.

Early stage sepsis-associated purpura fulminans may be reversible with quick therapeutic intervention. Treatment is mainly removing the underlying cause and degree of clotting abnormalities and with supportive treatment (antibiotics, volume expansion, tissue oxygenation, etc.). Thus, treatment includes aggressive management of the septic state.

Purpura fulminans with disseminated intravascular coagulation should be urgently treated with fresh frozen plasma (10–20 mL/kg every 8–12 hours) and/or protein C concentrate to replace pro-coagulant and anticoagulant plasma proteins that have been depleted by the disseminated intravascular coagulation process.

Protein C in plasma in the steady state has a half life of 6- to 10-hour, therefore, patients with severe protein C deficiency and presenting with purpura fulminans can be treated acutely with an initial bolus of protein C concentrate 100 IU/kg followed by 50 IU /kg every 6 hours. A total of 1 IU/kg of protein C concentrate or 1 mL/kg of fresh frozen plasma will increase the plasma concentration of protein C by 1 IU/dL. Cases with comorbid pathological bleeding may require additional transfusions with platelet concentrate (10–15 mL/kg) or cryoprecipitate (5 mL/kg).

Established soft tissue necrosis may require surgical removal of the dead tissue, fasciotomy, amputation or reconstructive surgery.

Two Dutch studies have followed hemophilia patients for a number of years. Both studies found that viral infections were common in hemophiliacs due to the frequent blood transfusions which put them at risk of getting blood borne infections such as HIV and hepatitis C. In the latest study which followed patients from 1992 to 2001, the male life expectancy was 59 years. If cases with known viral infections were excluded, the life expectancy was 72, close to that of the general population. 26% of the cases died from AIDS and 22% from hepatitis C.

There are several treatments available for bleeding due to factor X deficiency, however a specifi FX concentrate is not available (2009).

1. Prothrombin complex concentrate (PCC) supplies FX with a risk of thrombosis.

2. Fresh frozen plasma (FFP): This is relatively inexpensive and readily available. While effective this treatment carries a risk of blood-borne viruses and fluid overload.

3. If vitamin K levels are low, vitamin K can be supplied orally or parenterally.

Treatment of FX deficiency in amyloidosis may be more complex and involve surgery (splenectomy) and chemotherapy.

The treatment of primary immunodeficiencies depends foremost on the nature of the abnormality. Somatic treatment of primarily genetic defects is in its infancy. Most treatment is therefore passive and palliative, and falls into two modalities: managing infections and boosting the immune system.

Reduction of exposure to pathogens may be recommended, and in many situations prophylactic antibiotics or antivirals may be advised.

In the case of humoral immune deficiency, immunoglobulin replacement therapy in the form of intravenous immunoglobulin (IVIG) or subcutaneous immunoglobulin (SCIG) may be available.

In cases of autoimmune disorders, immunosuppression therapies like corticosteroids may be prescribed.

The diagnosis of haemophilia C (factor XI deficiency) is centered on prolonged activated partial thromboplastin time.One will find that the factor XI has decreased in the individuals body.In terms of differential diagnosis one must consider:factor VIII deficiency, lupus anticoagulant and heparin contamination.

Bone marrow transplant may be possible for Severe Combined Immune Deficiency and other severe immunodeficiences.

Virus-specific T-Lymphocytes (VST) therapy is used for patients who have received hematopoietic stem cell transplantation that has proven to be unsuccessful. It is a treatment that has been effective in preventing and treating viral infections after HSCT. VST therapy uses active donor T-cells that are isolated from alloreactive T-cells which have proven immunity against one or more viruses. Such donor T-cells often cause acute graft-versus-host disease (GVHD), a subject of ongoing investigation. VSTs have been produced primarily by ex-vivo cultures and by the expansion of T-lymphocytes after stimulation with viral antigens. This is carried out by using donor-derived antigen-presenting cells. These new methods have reduced culture time to 10–12 days by using specific cytokines from adult donors or virus-naive cord blood. This treatment is far quicker and with a substantially higher success rate than the 3–6 months it takes to carry out HSCT on a patient diagnosed with a primary immunodeficiency. T-lymphocyte therapies are still in the experimental stage; few are even in clinical trials, none have been FDA approved, and availability in clinical practice may be years or even a decade or more away.

Often, no treatment is required or necessary for reactive thrombocytosis. In cases of reactive thrombocytosis of more than 1,000x10/L, it may be considered to administer daily low dose aspirin (such as 65 mg) to minimize the risk of stroke or thrombosis.

However, in primary thrombocytosis, if platelet counts are over 750,000 or 1,000,000, and especially if there are other risk factors for thrombosis, treatment may be needed. Selective use of aspirin at low doses is thought to be protective. Extremely high platelet counts in primary thrombocytosis can be treated with hydroxyurea (a cytoreducing agent) or anagrelide (Agrylin).

In Jak-2 positive disorders, ruxolitinib (Jakafi) can be effective.

There are a multiple ways to treat Gunther's diseases, but one of the most crucial things that a person with this disease can do is limit themselves from sun exposure or eliminate sun exposure altogether. There are some sunscreens that have undesirable effects such as tropical sunscreens, but other sunscreens that have zinc oxide and titanium dioxide in them are shown to provide protection due to those light-reflective agents. To block the ultraviolet and visible light wavelengths and get the protection that patients with Gunther's disease require, physical barriers are needed. It is also advised that patients wear protective clothing to block the sun from their skin. Plastic films can be attached to car windows and homes to filter out some of the wavelengths that could cause harm to someone's skin suffering with this disease. Incandescent bulbs replace the normal fluorescent lamps. These bulbs release less light, which prevents the "porphyrin-exciting" wavelengths that fluorescent lights emit.

Other less beneficial treatments have been used to help treat Gunther's disease. These include oral beta-carotene and other treatments such as activated charcoal and cholestyramine, which are used to interrupt and stop the porphyrins from being reabsorbed in the body. The reason that these oral treatments are unreasonable is because they require an extremely large dose of medicine and therefore are not beneficial.

Erythrocyte transfusions have been shown to be a successful measure in decreasing the appearance of the disease by trying to lower the erythropoiesis and circulating porphyrin levels. Unfortunately, having chronic erythrocyte transfusions, it can be extremely harmful to the body and can cause severe complications.

To help with dry eye symptoms and visual function, using topical lubrication can be used.

A more invasive way to help treat Gunther's disease would be to have surgery. There have been numerous studies that have stated that bone marrow transplantation is successful. This is a recently new development for Gunther's disease so the long-term effects are still unresourced. If a patient has a life-threatening infectious complication then bone marrow transplantation is no longer relevant for them.

There are also reports that stem cell transplantation is successful in a limited number of participants

The course of treatment and the success rate is dependent on the type of TMA. Some patients with atypical HUS and TTP have responded to plasma infusions or exchanges, a procedure which replaces proteins necessary for the complement cascade that the patient does not have; however, this is not a permanent solution or treatment, especially for patients with congenital predispositions.

One exploratory, and potential alternative method for the treatment of pernicious anemia is the use of transdermal patches. In one such system, the patches are composed of cyanocobalamin, its stabilizers, and epidermal penetration enhancers. The transdermal route allows the cobalamin derivative to passively diffuse through the stratum corneum, epidermis, and dermis, and ultimately entering the bloodstream; hence, the cobalamin avoids the hepatic first pass effect, and so offers the potential for improved bioavailability and efficacy. Slow release increases cobalamin half-life, offering the potential of decreases in required dosage required relative to oral delivery methods. In one such system, a drug-loaded polycaprolactone fiber that is prepared as a electrospun nanofiber can release hundreds of micrograms of cobabalmin per day.

A 28 month old girl, showed symptoms from 8 months of age and consisted of complaints of painful bruises over lower limbs, and disturbed, painful sleep at night. Family history revealed older brother also suffered similar problems and died at age of two years possibly due to bleeding - no diagnosis was confirmed. Complete blood count and blood smear was determined as normal. No abnormality in fibrinogen, liver function test, and bleeding time. However, prothrombin levels were less than 1% so patient was transfused with fresh frozen plasma (FFP). Post transfusion methods, patient is now 28 months old and living healthy life. The only treatment that is needed to date is for the painful bruises, which the patient is given FFP every 5-6 weeks.

Twelve day old boy admitted for symptoms consisting of blood stained vomiting and dark colored stool. Upon admission into hospital, patient received vitamin K and FFP transfusion. No family history of similarity in symptoms that were presented. At 40 days old, patient showed symptoms of tonic posturing and constant vomiting. CT scan revealed subdural hemorrhage, and other testing showed low hb levels of 7%, platelets at 3.5 lakhs/cu mm. PT examination was 51 seconds and aPTT at 87 seconds. Prothrombin activity levels were less than 1%. All other exams revealed no abnormalities. Treatment methods included vitamin K and FFP, as well as ventilator support and packed red blood cell transfusion (PRBC). At half a year of age, condition consisted of possible poor neurological outcome secondary to CNS bleeding. Treatment of very frequent transfusion was needed for patient.

Recent study illustrated a patient with 2 weeks of continuous bleeding, with presence of epistaxis, melena, hematuria, and pruritic rash with no previous bleeding history. Vitals were all within normal range, however, presence of ecchymoses was visible in chest, back and upper areas. Lab exams revealed prolonged prothrombin time (PT) of 34.4 and acquired partial thromboplastin time (aPTT) of 81.7, as well as elevated liver function tests. Discontinuation of atorvastatin, caused liver enzymes to go back to normal. Treatment of vitamin K, antibiotics, and fresh frozen plasma (FFP) did not have an impact on coagulopathy. Mixing of PT and aPTT was performed in order to further evaluate coagulopathy and revealed no correction. Factor activity assays were performed to determine the presence of a specific one. Testing revealed that factor II activity could not be quantified. Further studies showed that acquired factor II inhibitor was present without the lupus anticoagulant, with no clear cause associated with the condition. Aimed to control bleeding and getting rid of the inhibitor through directly treating the underlying disease or through immunosuppressive therapy. Corticosteroids and intravenous immunoglobulin improved the PT and aPTT. Did not improve bleeding conditions until treatment of transfusion with activated PCC. Treatment of inhibitor required Rituximab, which was shown to increase factor II levels to 264%. Study shows that when a patient with no history of coagulopathy presents themselves with hemorrhagic diathesis, direct testing of a factor II inhibitor should be performed initially.

Factor XII deficiency (also Hageman factor deficiency) is a deficiency in the production of factor XII (FXII), a plasma glycoprotein and clotting factor that participates in the coagulation cascade and activates factor XI. FXII appears to be not essential for blood clotting, as individuals with this condition are usually asymptomatic and form blood clots in vivo. FXII deficiency tends to be identified during presurgical laboratory screening for bleeding disorders.

The condition can be inherited or acquired.