Buerger’s Disease is a sort of auto-immune disease or inflammation of the blood vessels – think of it as a painful, alergic blistering around the smallest arteries and veins. It doesn’t cause “hardening of the arteries” (with calcium in the walls) but can cause them to become clogged.
There has never been another treatment before, other than trying to get ahead of the pain at each site.
Buerger’s disease is not like leukemia or many of the other diseases we’ve treated with umbilical cord stem cell transplants: it is not a disease of the blood or bone marrow.
After treatment with umbilical cord stem cells, this report notes that the men treated “suddenly” became pain-free and, over time, the ulcers on their skin healed. The blood vessels were found to be more open. It appears that the stem cells repaired the blood vessel walls, allowing circulation to the skin.
Just imagine if this would work for diabetic blood vessel disease!
ABSTRACT: Buerger’s disease, also known as thromboangiitis obliterans, is a nonatherosclerotic, inflammatory, vasoocclusive disease. It is characterized pathologically as a panangiitis of medium and small blood vessels including both arteries and adjacent veins, especially the distal extremities, the feet and the hands. There is no curative medication or surgery for this disease. In the present studies, we transplanted human leukocyte antigen (HLA)-matched human umbilical cord blood (UCB)-derived mesenchymal stem cells (MSCs) into 4 men with Buerger’s disease who had already received medical treatment and surgical therapies. After the stem cell transplantation, ischemic rest pain suddenly disappeared from their affected extremities. The necrotic skin lesions were healed within 4 weeks. In the follow-up angiography, digital capillaries were increased in number and size. In addition, vascular resistance in the affected extremities, compared with the preoperative examination, was markedly decreased due to improvement of the peripheral circulation. Because an animal model of Buerger’s disease is absent and also in order to understand human results, we transplanted human UCB-derived MSCs to athymic nude mice with hindlimb ischemia by femoral artery ligation. Up to 60% of the hindlimbs were salvaged in the femoral artery ligated animals. By situ hybridization, the human UCB-derived MSC was detected in the arterial walls of the ischemic hindlimb in the treated group. Therefore, it is suggested that human UCB-derived MSCs transplantation may be a new and useful therapeutic armament for Buerger’s disease and other similar ischemic diseases.