The greatest distress and danger to any individual is dealing with a blood disorder or a family member suffering from it.
The painful history of haemophilia
Haemophilia cases have been known to people from time immemorial. The first signs were that some of the people bled differently. They could not be diagnosed or treated as they did not know anything about blood clots. During the Second World War, doctors learned about the blood clotting proteins in the blood and that the lack of factor VIII can cause haemophilia A.
In 1837 Haemophilia was named the ‘royal disease,’ as Queen Victoria of England carried the haemophilia gene. This was believed to be caused due to spontaneous mutation. The descendants later passed on the defective gene to the royal families of Russia, Germany, and Spain.
Advancements in the research, a timeline of haemophilia treatment:
1900’s
The real research on hemophilia started around the 1900s when scientists discovered that human blood could be divided into groups and types and blood transfusions were more successful.
1930’s
With further advancements in 1930, they learned how to separate the significant parts of the blood and learned about plasma and red cells.
1960’s
The most significant breakthrough in treating hemophilia was the development of factor concentrates. The clotting factor in the blood is freeze-dried into a powder that is easy to store, carry and transport. Factor concentrates made treating hemophilia quicker. It even enabled patients to treat their bleeding at home and helped them lead an everyday life.
A historic landmark- the first treatment of hemophilia
It is arguably said that the first hemophilia case would date back to ancient Egypt in the second century AD.
Did you know that one per 10,000 males is born haemophilic (suffering from hemophilia A)?
The spectrum of clinical advancements to serve hemophilia has evolved from a catastrophic and fatal disease to a manageable disorder.
The first successful medical treatment for hemophilia was recorded in 1940.
An 11-year-old boy, Lancet, suffered a major hemorrhage after squint surgery. The doctors experimentally treated him with a blood transfusion, which was a success, and the kid survived.
With the discovery of the cryoprecipitate fraction by Judith G. Pool in 1964, the treatment became quicker and easier. Moreover, it could be used by the patient himself, dissolving the barrier to emergency care. As a result, the life expectancy of a hemophilic patient reached an average of 60 years.
Later with Nilsson and Ahlberg pioneering the regular administration of Factor VII in the prophylactic scheme, the life expectancy of a hemophilic patient saw a sike of 8 more years, i.e., an average of 68 years.
In 2000 the research was more concerned with making the treatment cost-effective.
Most of the clinic treatment evidence on hemophilia A treatment is seen in High-Income Counties. Swasth Kare introduces a state-of-the-art revolutionary hemostatic agent in India that helps arrest bleeds within seconds!
SeraSeal™ is the World’s ONLY Primary Hemostatic Agent, which stops major hemorrhages in seconds, even in anticoagulant therapy or factor deficiencies, without the need for ANY of the traditional applications of pressure, elevation, tourniquets, or cauterization. SeraSeal™ is derived from bovine factors and can be applied by a syringe, spray, catheter, foam, trauma dressing, surgical sponge, bandage strip, or a swab. All products are stable with long shelf lives, require no preparation, and immediately apply to the patient. SeraSeal™ does not create chemical burns but instead accelerates healing for the patient.
How does SeraSeal™ help hemophilic patients?
The active agents in SeraSeal™ are agar, Factors IIa, VIIa, IXa, and Xa, which are effective in both Hemophilia A and Hemophilia B patients and all other forms of coagulopathy.
Agar in SeraSeal™ adds another layer of hemostasis to a bleeding wound by binding to the patient’s platelets to form a platelet plug to seal the wound. Agar is effective in patients on platelet inhibitor therapy by binding to the ions of platelet phospholipids and cations from amine groups in the fibrinogen/fibrin monomers and tissue proteins to form a gelatin barrier over the wound.
Additionally, Phase 1 clinical trial had 24 heparin patients in both SeraSeal™ and cauterization groups, where SeraSeal™ achieved a hemodialysis mean collective time of 0.72 min compared to a collective mean of 10.00 min in the cauterized group.