A low-intensity type of laser treatment may offer a non-invasive, drug-free treatment for thrombocytopenia—a potentially life-threatening shortage of the blood cells called platelets that are essential to blood clotting.
A research team from the Wellmen Center for Photomedicine at Massachusetts General Hospital (MGH) found that low-level laser therapy increased the generation of platelets from precursor cells called megakaryocytes (MKs) and had the same effect in several mouse models of the condition. They also identified the probable mechanism underlying this effect.
Among the conditions that can lead to thrombocytopenia are certain types of leukemia, an autoimmune disorder that attacks platelets, and side-effects of certain drugs, including some used for chemotherapy. The most established treatment is platelet transfusion, which since it risks complications including infection, allergic reaction and immunosuppression is limited to the most severe cases. Dosage levels of the FDA-approved drugs that increase platelet levels must be precisely controlled to avoid excessive platelet production that raises the risk of dangerous blood clots.
Low-level lasers (LLL) —sometimes called cold lasers—emit low-powered laser light that does not heat its target tissue. LLL has been used to improve wound healing, relieve pain, and treat conditions including stroke and neurodegenerative disorders. It is known to protect the function of mitochondria—cellular structures that provide cells with energy—and several conditions associated with impaired platelet production are characterized by abnormalities in mitochondria of the bone marrow cells that give rise to platelets.
The body responds to low platelet levels by rapid differentiation of MKs from hematopoietic stem cells and an exponential increase in the number of the cells. MKs expand in size, along with many rounds of DNA replication without cellular division, which results in giant cells containing multiple copies of each chromosome—a condition called polyploidy—instead of the two copies found in most cells. Each of these giant, polyploid MKs generates many long, branched, small tubular structures called proplatelets that eventually fragment into thousands of platelets.
The MGH/Wellman team conducted a number of experiments to investigate whether LLL’s ability to protect mitochondrial function could mitigate several forms of thrombocytopenia. Their results showed the following:
- LLL treatment of MKs increased their size, accelerated the formation of proplatelets and doubled the production of platelets. Infusion of LLL-treated MKs into mice led to greater platelet production than did infusion of MKs treated with normal light.
- One of the keys to determining the number of platelets generated from MKs was mitochondrial production of the energy molecule ATP.
- LLL treatment greatly increased mitochondrial generation in polyploid MKs, but the increase was only slight in less mature MKs with only two copies of each chromosome.
- Whole-body LLL treatment of mice with radiation-induced thrombocytopenia induced the rapid maturation of MKs and restored platelet levels in a light-dose-dependent fashion. Platelets from LLL-treated mice had normal structure and function. LLL treatment of normal mice did not raise levels of either MKs or platelets.
- LLL treatment also restored platelet levels in mice with the autoimmune form of thrombocytopenia or with thrombocytopenia caused by chemotherapy treatment.
- In cultured human MKs. LLL treatment at dosage levels similar to that used in mice increased ATP production and platelet generation.
Wu notes that LLL’s lack of an effect in animals without thrombocytopenia indicates it would probably avoid the potential complications of current drug treatments, which act by increasing the production of MKs from their progenitors in the bone marrow.
