So as most of you know, I visited Warwick in Minnesota and immeditely started oral NAC 600mg QD.
I told my phsycian that I started this treatment, and he informed me that Dr. Moss at Stanford is actually actively conducting a study on NAC. I had no idea.
In case others aren't aware of the study, here is the info I found on PubMed. Phase I trial was just concluded and published, taking a look to see if Dr. Moss' hypothesis of NAC helping to increase glutathione concentrations in neutrophils.
The goal of this study wasn't to look at increases in lung function or decrases in exacerbations or to look at effective doses. The goal simply was ensure that the oral NAC did in fact effect glutathione concentrations in neutrophils.
The next stage will be to examine optimal dosing, safety, as well as to prove that NAC does improve pulmonary function or help avoid exacerbations.
I was pleased to discover that this is being studied and I'm sure you feel the same way!
<b>High-dose oral N-acetylcysteine, a glutathione prodrug, modulates inflammation in cystic fibrosis. </b>
Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA. tirouvan@stanford.edu
Neutrophilic airway inflammation is a hallmark of cystic fibrosis (CF). As high oxidant producers, airway neutrophils contribute largely to the systemic redox imbalance seen in CF. In turn, this chronic and profound imbalance can impact circulating neutrophils before their migration into airways. Indeed, in 18 CF patients with stable disease, blood neutrophils were readily deficient in the pivotal antioxidant glutathione (P = 0.003, compared with 9 healthy controls). In a phase 1 study, this deficiency was improved (P = 0.025) by the glutathione prodrug N-acetylcysteine, given orally in high doses (0.6 to 1.0 g three times daily, for 4 weeks). This treatment was safe and markedly decreased sputum elastase activity (P = 0.006), the strongest predictor of CF pulmonary function. Consistently, neutrophil burden in CF airways was decreased upon treatment (P = 0.003), as was the number of airway neutrophils actively releasing elastase-rich granules (P = 0.005), as measured by flow cytometry. Pulmonary function measures were not improved, as expected with short-term treatment. After excluding data from subjects without baseline airway inflammation, positive treatment effects were more pronounced and included decreased sputum IL-8 levels (P = 0.032). Thus, high-dose oral N-acetylcysteine has the potential to counter the intertwined redox and inflammatory imbalances in CF.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16537378&query_hl=8&itool=pubmed_docsum">http://www.ncbi.nlm.nih.gov/en...=8&itool=pubmed_docsum</a>
I told my phsycian that I started this treatment, and he informed me that Dr. Moss at Stanford is actually actively conducting a study on NAC. I had no idea.
In case others aren't aware of the study, here is the info I found on PubMed. Phase I trial was just concluded and published, taking a look to see if Dr. Moss' hypothesis of NAC helping to increase glutathione concentrations in neutrophils.
The goal of this study wasn't to look at increases in lung function or decrases in exacerbations or to look at effective doses. The goal simply was ensure that the oral NAC did in fact effect glutathione concentrations in neutrophils.
The next stage will be to examine optimal dosing, safety, as well as to prove that NAC does improve pulmonary function or help avoid exacerbations.
I was pleased to discover that this is being studied and I'm sure you feel the same way!
<b>High-dose oral N-acetylcysteine, a glutathione prodrug, modulates inflammation in cystic fibrosis. </b>
Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA. tirouvan@stanford.edu
Neutrophilic airway inflammation is a hallmark of cystic fibrosis (CF). As high oxidant producers, airway neutrophils contribute largely to the systemic redox imbalance seen in CF. In turn, this chronic and profound imbalance can impact circulating neutrophils before their migration into airways. Indeed, in 18 CF patients with stable disease, blood neutrophils were readily deficient in the pivotal antioxidant glutathione (P = 0.003, compared with 9 healthy controls). In a phase 1 study, this deficiency was improved (P = 0.025) by the glutathione prodrug N-acetylcysteine, given orally in high doses (0.6 to 1.0 g three times daily, for 4 weeks). This treatment was safe and markedly decreased sputum elastase activity (P = 0.006), the strongest predictor of CF pulmonary function. Consistently, neutrophil burden in CF airways was decreased upon treatment (P = 0.003), as was the number of airway neutrophils actively releasing elastase-rich granules (P = 0.005), as measured by flow cytometry. Pulmonary function measures were not improved, as expected with short-term treatment. After excluding data from subjects without baseline airway inflammation, positive treatment effects were more pronounced and included decreased sputum IL-8 levels (P = 0.032). Thus, high-dose oral N-acetylcysteine has the potential to counter the intertwined redox and inflammatory imbalances in CF.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16537378&query_hl=8&itool=pubmed_docsum">http://www.ncbi.nlm.nih.gov/en...=8&itool=pubmed_docsum</a>