Stem Cell Treatment for Pulmonary Fibrosis and COPD are now available at ASCI
Pulmonary fibrosis is the formation or development of excess fibrous connective tissue (fibrosis) in the lungs. It is also described as "scarring of the lung."
Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation. A chest x-ray may or may not be abnormal, but high Resolution CT will frequently demonstrate abnormalities.
Symptoms of pulmonary fibrosis are mainly:
- Shortness of breath, particularly with exertion
- Chronic dry, hacking coughing
- Fatigue and weakness
- Chest discomfort
- Loss of appetite and rapid weight loss
Pulmonary fibrosis may be a secondary effect of other diseases. Most of these are classified as interstitial lung diseases. Examples include autoimmune disorders, viral infections or other microscopic injuries to the lung. However, pulmonary fibrosis can also appear without any known cause. In this case, it is termed "idiopathic". Most idiopathic cases are diagnosed as idiopathic pulmonary fibrosis. This is a diagnosis of exclusion of a characteristic set of histologic/pathologic features known as usual interstitial pneumonia (UIP). In either case, there is a growing body of evidence which points to a genetic predisposition in a subset of patients. For example, a mutation in Surfactant protein C (SP-C) has been found to exist in some families with a history of pulmonary fibrosis.
Diseases and conditions that may cause pulmonary fibrosis as a secondary effect include:
- Inhalation of environmental and occupational pollutants, such as in asbestosis, silicosis and exposure to certain gases. Coal miners, ship workers and sand blasters among others are at higher risk. Hypersensitivity pneumonitis, most often resulting from inhaling dust contaminated with bacterial, fungal, or animal products.
- Cigarette smoking can increase the risk or make the illness worse.
- Some typical connective tissue diseases such as rheumatoid arthritis and Scleroderma. Other diseases that involve connective tissue, such as sarcoidosis and Wegener's granulomatosis.
- Certain medications, e.g. amiodarone, bleomycin, busulfan, methotrexate, and nitrofurantoin
- Radiation therapy to the chest.
Stem Cell Treatments for Pulmonary Fibrosis and COPD. Pulmonary Fibrosis and COPD and Stem Cell studies and protocols from the NIH:
Influence of Rho kinase inhibitor fasudil on late endothelial progenitor cells in peripheral blood of COPD patients with pulmonary artery hypertension.
Related Articles Influence of Rho kinase inhibitor fasudil on late endothelial progenitor cells in peripheral blood of COPD patients with pulmonary artery hypertension. Bratisl Lek Listy. 2015;116(3):150-3 Authors: Liu P, Zhang HM, Tang YJ, Sheng CF, Liu JX, Zeng YJ Abstract OBJECTIVE: To investigate the influence of Fasudil, a Rho inhibitor on the number and functions of the late endothelial progenitor cells in peripheral blood of chronic obstructive pulmonary diseases (COPD) patients with pulmonary artery hypertension. BACKGROUND: It is not clear yet, whether Rho Kinase Inhibitor Fasudil can reduced pulmonary artery pressure through improving lung endothelial function. METHODS: 80 COPD patients with pulmonary artery hypertension were selected and divided into two groups: the treatment group and the control group, which had 40 patients, respectively. Changes in the number and function of the late endothelial progenitor cells in peripheral blood of the patients before and after the treatment were compared between the two groups. The changes on the pulmonary artery pressure were also compared. RESULTS: The number of the late endothelial progenitor cells in peripheral blood of the treatment group increased and the function was enhanced. The pulmonary artery pressure was reduced. The difference before and after the treatment and with the control group was statistically significant (p < 0.05). CONCLUSIONS: The Rho-kinase inhibitor Fasudil increased the number and enhanced the function of the late endothelial progenitor cells in peripheral blood of COPD patients with pulmonary artery hypertension (Tab. 3, Fig. 2, Ref. 17). PMID: 25869561 [PubMed - indexed for MEDLINE]Read more...