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Noninvasive low-level laser therapy for thrombocytopenia
Qi Zhang1, Tingting Dong1, Peiyu Li1
1Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA 02114, USA. Department of Dermatology, Harvard Medical School, Boston, MA 02114, USA.
Science Translational Medicine
|July 29, 2016
Summary
Near-infrared laser therapy offers a novel, drug-free treatment for thrombocytopenia (low platelet count). This noninvasive approach accelerates platelet regeneration and prevents dangerous drops, presenting a paradigm shift in managing this hematologic disorder.
Area of Science:
- Hematology
- Biomedical Engineering
- Mitochondrial Biology
Background:
- Thrombocytopenia is a prevalent hematologic disorder often managed with platelet transfusions.
- Current treatments have limitations and potential side effects.
Purpose of the Study:
- To investigate the efficacy of noninvasive whole-body illumination with near-infrared laser (LLL) in treating thrombocytopenia.
- To elucidate the underlying mechanisms of LLL's effects on platelet regeneration.
Main Methods:
- Mice models of acute thrombocytopenia induced by gamma irradiation, anti-CD41 antibody, and chemotherapy were used.
- Whole-body low-level laser (LLL) therapy was applied.
- Mitochondrial biogenesis, megakaryocyte maturation, and platelet production were analyzed.
Main Results:
- LLL significantly accelerated platelet recovery in mice within 2 weeks, compared to 5 weeks in controls.
- LLL enhanced platelet regeneration under conditions of induced thrombocytopenia and protected megakaryocytes from stress-induced injury.
- LLL stimulated mitochondrial biogenesis in megakaryocytes, promoting maturation and increasing platelet output per megakaryocyte.
Conclusions:
- Noninvasive LLL is a safe, drug-free, and donor-independent modality for treating thrombocytopenia.
- LLL offers a paradigm shift in the prophylaxis and treatment of thrombocytopenia by stimulating endogenous platelet production.
- The mechanism involves enhanced megakaryocyte mitochondrial function and subsequent platelet biogenesis, regulated by existing platelet counts to prevent thrombosis.
