Muscle Loss is Independent Predictor of Morbidity and Mortality in Patients with COPD

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide and by the year 2020, experts believe it will be the third leading cause of death. Patients with COPD frequently suffer from muscle wasting, a medical condition that occurs when the muscle tissue in the arms and legs atrophies. Peripheral muscle loss and muscle dysfunction is an independent predictor of morbidity and mortality.

Note: Despite all advances in stem cells research and the application of these therapies in many countries all over the world, stem cells therapies are not legally approved yet in San Diego, Los Angeles, Chicago, Dallas, New York, Jacksonville, Seattle, Houston, San Francisco, Salt Lake City, Miami, Beverly Hills and other US cities. However, stem cell treatments are legal in Costa Rica.

Patients with COPD frequently suffer from exercise intolerance however in approximately 40% of cases exercise is limited due to muscle loss or dysfunction and not pulmonary related problems. Limiting muscle wasting would reduce a patient’s risk of dying and improve his or her quality of life, however, it is not clear what causes the loss of muscle.  Exercise has been considered the most powerful tool for slowing or reversing muscle wasting in patients with COPD but not all patients respond the same to physical rehabilitation and some patients experience almost no benefit.

Muscle loss may be due to:

  • Lack of use
  • A low level of oxygen in the blood
  • Oxidative stress (an imbalance of free radicals and antioxidants)
  • Systemic inflammation
  • Impaired ability to repair DNA damage

To better understand the cause of muscle wasting and accelerated aging in patient with COPD, researchers in Edinburgh measured biomarkers associated with DNA repair. The results, published in May of 2018, showed a significant increase in cellular damage and muscle inflammatory markers and a significant decrease in proteins related DNA repair. The data from this research project supports the theory that muscle dysfunction, muscle loss and accelerated aging in patients with COPD is a result of impaired DNA repair and the body’s inability to maintain and regulate the necessary metabolic and physiological processes to maintain and grow muscle.

Patients with COPD that experience significant muscle atrophy are at an increased risk of falls, osteoporosis, and fractures as well as an increased need for healthcare services and a decreased quality of life. The experts at the Stem Cells Transplant Institute are using adipose derived mesenchymal stem cells to treat the symptoms associated with COPD.

Clinical trials have shown mesenchymal stem cells have the ability to differentiate, self-renew, suppress the immune system, reduce inflammation, and repair tissues.

Mesenchymal stem cells have the ability to:

  • Promote self-healing
  • Have potent anti-inflammatory capabilities
  • Modulate abnormal immune system responses
  • Prevent additional premature cell and tissue damage
  • Reduce scarring
  • Stimulate new blood vessel growth improving blood flow

The goal of stem cell therapy is to use your own healing cells to improve breathing, reduce inflammation and create an environment that is optimal for tissue repair and angiogenesis.  If you or someone you love has been diagnosed with COPD and would like to learn more about stem cell therapy, contact the Stem Cells Transplant Institute today.

Note: Despite all advances in stem cells research and the application of these therapies in many countries all over the world, stem cells therapies are not legally approved yet in San Diego, Los Angeles, Chicago, Dallas, New York, Jacksonville, Seattle, Houston, San Francisco, Salt Lake City, Miami, Beverly Hills and other US cities. However, stem cell treatments are legal in Costa Rica.

 

Reference:

Lakhdar, Ramzi et al., Role of accelerated ageing in limb muscle wasting of patients with Chronic Obstructive Pulmonary Disease (COPD), 2011-2015 [dataset]. Published May, 2018. University of Edinburgh. http://dx.doi.org/10.7488/ds/2352.

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