Haemophilia C is an autosomal genetic disorder involving a lack of functional clotting Factor XI. Haemophilia C is not completely recessive, as heterozygous individuals also show increased bleeding.The type of haemophilia known as parahaemophilia is a mild and rare form and is due to a deficiency in factor V. This type can be inherited or acquired.A non-genetic form of haemophilia is caused by autoantibodies against factor VIII and so is known as acquired haemophilia A. It is a rare but potentially life-threatening bleeding disorder caused by the development of autoantibodies (inhibitors) directed against plasma coagulation factors. Acquired haemophilia can be associated with cancers, autoimmune disorders and following childbirth. Management
There is no long-term cure. Treatment and prevention of bleeding episodes is done primarily by replacing the missing blood clotting factors. Clotting factors
Clotting factors are usually not needed in mild haemophilia. In moderate haemophilia clotting factors are typically only needed when bleeding occurs or to prevent bleeding with certain events. In severe haemophilia preventive use is often recommended two or three times a week and may continue for life. Rapid treatment of bleeding episodes decreases damage to the body.Factor VIII is used in haemophilia A and factor IX in haemophilia B. Factor replacement can be either isolated from human blood serum, recombinant, or a combination of the two.
Pai syndrome, also known as Median cleft of the upper lip-corpus callosum lipoma-midline facial cutaneous polyps syndrome, is a very rare genetic disorder which is characterized by nervous system, cutaneous, ocular, nasal and bucal anomalies with facial dysmorphisms. Signs and symptoms
List of common symptoms:
Depressed nasal bridge
Median cleft lip
Central nervous system lipomas. Nasal polyposis
Presence of skin tags
Subcutaneous noduleList of not-so-common symptoms:[2]

Oral frenulum abnormalities
Bifid uvula
Hypertelorism
TelecanthusList of uncommon symptoms:[2]

Missing/underdeveloped corpus callosum
Down-slanting parpebral fissures
Encephalocele
Coloboma
Nose defects
Frontal bossing
High palate

Causes
A specific, shared genetic cause hasnt been found. The closest thing to it was a case reported by Masuno et al. of a Japanese girl with symptoms of the disorder plus short stature and intellectual disabilities with a spontaneous reciprocal translocation. This translocation involved chromosome Xq28 and chromosome 16q11.2 (more specifically, 46,X,t(X;16)(q28;q11.2). Epidemiology
According to OMIM, 18 cases have been described in medical literature, but according to ORPHAnet, 67 cases have been described. == References ==