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Thursday, July 28, 2011

Pfizer’s Zyvox and Antidepressants May Be Fatal Combination

Pfizer’s Zyvox and Antidepressants May Be Fatal Combination
Pfizer Inc. (PFE)’s Zyvox antib
iotic can cause potentially fatal central nervous system reactions in patients who also take antidepressants that increase levels of the brain chemical serotonin, U.S. regulators said.
Pfizer’s Zoloft and Pristiq, Eli Lilly & Co. (LLY)’s Cymbalta andGlaxoSmithKline Plc (GSK)’s Paxil and Wellbutrin are among 29 psychiatric drugs that patients may need to stop taking temporarily when they require treatment with Zyvox, the Food and Drug Administration said today in a drug safety communication.
Zyvox, used to treat some types of drug-resistant bacteria including MSRA or methicillin-related Staphylococcus aureus, skin infections and nosocomial pneumonia, can interact with the antidepressants to cause a toxic reaction known as serotonin syndrome in which excess amounts of the chemical build up in the brain, according to the FDA.
Some deaths among patients who suffered such a reaction were reported to the FDA’s adverse-event database, the agency said. Pfizer, based in New York, reported $1.18 billion in revenue from Zyvox last year.

Excess Serotonin

Confusion, memory issues, hyperactivity, excessive sweating and muscle twitching are among the symptoms of excess serotonin levels. Patients taking psychiatric drugs shouldn’t stop using them without first consulting a health-care professional, the FDA said.
The current U.S. package insert for Zyvox “already includes prominent information regarding the potential for serotonergic interactions, the risk of serotonin syndrome and the need for careful observation of patients prescribed Zyvox who are on such agents,” Kristen Neese, a Pfizer spokeswoman, said today in an e-mail. The company hasn’t identified any new safety signals related to those drug interactions, she said.
“In an ongoing commitment to ensure patient safety, Pfizer continually monitors all relevant safety information including information pertaining to the concomitant use of Zyvox and serotonergic antidepressant medications,” Neese said.
To contact the reporter on this story: Molly Peterson in Washington atmpeterson9@bloomberg.net
To contact the editor responsible for this story: Adriel Bettelheim at abettelheim@bloomberg.net

Tuesday, July 26, 2011

CF associated changes in lung stem cells may contribute to disease progression

Cystic fibrosis-associated changes in lung stem cells may contribute to disease progression

Researchers at the University of Iowa's Roy J. and Lucille A. Carver College of Medicine have discovered that in cystic fibrosis (CF) patients, the airway glands are depleted of a specific population of airway stem cells that participate in airway repair following injury.
Their results are published in the July 18 issue of Journal of Clinical Investigation.
The research team was led by John F. Engelhardt, Ph.D., Roy J. Carver Chair in Molecular Medicineand professor and head of anatomy and cell biology, and graduate student Weiliang Xie, UI Molecular and Cellular Biology Program.
Extensive research carried out on cystic fibrosis over the past two decades has firmly established that loss of a functional chloride channel called CFTR leads to chronic bacterial lung infections associated with recurrent injury and repair of the airways. One feature of the lung that helps to fightinfection is the presence of airway glands, which secrete bacteria-killing factors into the airway.
These glands are also neighborhoods, or niches, for adult airway stem cells, sheltering them from toxic insults that bombard the airway surface. Without functional CFTR these glands fail to secrete these antibacterial factors, making the lung particularly susceptible to infection and to the tissue damage that accompanies it. A question about CF that remains to be resolved is whether the repair processes normally triggered by infection-associated damage remain intact in the CF lung.
The UI research team discovered that airway glands from CF humans and three CF animal models -- pig, ferret and mouse -- aberrantly express a "neuropeptide" that both activates CFTR and controlsstem-cell responses in airway glands following lung injury. Neuropeptides are small molecules that help the nervous system direct functions in tissues. This increase in neuropeptide causes stemcells to abandon their protected glandular niches, and the airway to adapt by establishing new niches for stem cells in the more dangerous setting of the airway surface.
"This is the first demonstration that lung stem cell niches may be altered in CF," Engelhardt said.
In their study, the researchers hypothesized that when it comes to CFTR dysfunction the nervous system may try to compensate by overproducing one of several neuropeptides. Their research shows that the neuropeptide called CGRP is excessively produced by glands in an attempt to activate CFTR, but because of the lack of CFTR activity in cystic fibrosis the CGRP signal remains on.
"Imagine the axle is broken on a car and because the driver senses he is not moving he pushes the accelerator more; when the car still doesn't move he pushes down even further," Engelhardt said. "Eventually the engine overheats and bursts into flames."
In this analogy, CFTR is the broken axle, CGRP is the fuel that feeds the engine, and the centralnervous system is the driver who senses that thing are not functioning properly. CF airways thus produce more CGRP in an attempt to reactive the broken CFTR channel—the untoward side effectbeing that this pathway also stimulates stem cells in the gland to divide.
It remains unclear why the CGRP pathway is selectively hyperactivated in the CF lung, since other neuropeptides can also stimulate CFTR. Engelhardt and Xie hypothesize that this may be due to airway-gland injury caused by the lack of CFTR, since CGRP is transiently induced even in healthy glands following injury, to spur stem cells into action.
"The future excitement of these findings relates to the potential of manipulating lung stem cellsthrough neuropeptides or their inhibitors," Engelhardt said. He cautioned that "the identity of lungstem cell is a matter of hot debate, and it remains unclear how the majority of functional studies we conduct in mice will translate to humans. However, given the similar findings of CGRP dysregyulation in four CF species, this pathway appears to be important in CF."

The research team included UI researchers from the UI Carver College of Medicine and UCSF.
The study was funded in part by grants from the National Institutes of Health, and the UI Center for Gene Therapy.
STORY SOURCE: UI Health Care Marketing and Communications, University of Iowa Health Care, 200 Hawkins Dr., W319 GH, Iowa City, Iowa 52242-1178

MEDIA CONTACT: Molly Rossiter, 319-356-7127, molly-rossiter@uiowa.edu


Tuesday, July 19, 2011

Treatment of Hemoptysis with Tranexamic Acid

Treatment of Recurrent Severe Hemoptysis in Cystic Fibrosis with Tranexamic Acid


Severity of Cystic Fibrosis Linked to Genetics

Such a fascinating debate in the CF community over to what extent CF genes influence clinical outcomes. This is such an amazingly cool study!

Dr. Garry Cutting, from the Institute for Genetic Medicine at Johns Hopkins, explains, “We already know which gene causes cystic fibrosis, but to a large extent that gene does not by itself explain how severe the condition will be.”


Severity of Cystic Fibrosis Linked to Genetics

Severity of Cystic Fibrosis Linked to Genetics

Researchers have found that the severity of cystic fibrosis, which is a life-threatening hereditary condition that affects the lungs and digestive system, is seemed to be influenced by genetic variations.
According to Dr. Garry Cutting, a professor of pediatrics and a member of the McKusick-Nathans Institute for Genetic Medicine at Johns Hopkins, most cystic fibrosis patients born today live to their mid-30’s but that’s an average. Some succumb to the disease before their 10th birthday, while others live into their 50s and we wanted to know why.
For the study, the researchers used and analyzed a data from 3,467 patients, which included unrelated patients from the Genetic Modifier Study out of the University of North Carolina at Chapel Hill, the Canadian Consortium for Genetic Studies out of the University of Toronto, and related patients and their parents from the CF Twin and Sibling Study at Johns Hopkins. With this study, the team aims to achieve help extend the life expectancy of the people having this kind of disease.
The team of the three studies collaborated and analyzed 600,000 sites of variation that is found within the genome, hoping to search common variations which are more frequently associated with severe cases of the disease.
After this, the researchers were “able to identify a region encompassed by two genes on chromosome 11 linked to severe cases of the disease.” Chromosome 20 on the second region was also identified.
Cutting explained, “We already know which gene causes cystic fibrosis, but to a large extent that gene does not by itself explain how severe the condition will be.” He further added that they’ve already discovered new genes that influence the course of disease and may enable prediction of the disease’s severity and, most importantly, the customization of treatments for patients with unfavorable genetic modifiers — this is the realization of individualized medicine.
Moreover, Cutting concluded that this study might be the first step in developing therapies for the patients with cystic fibrosis.

Sunday, July 10, 2011

Improved treatment response to dornase alfa in cystic fibrosis patients using controlled inhalation.

Anyone know what a "Smart Nebulizer" is? I have never heard of it and I'm trying to google but not really finding much....

Eur Respir J. 2011 Jul 7. [Epub ahead of print]

Improved treatment response to dornase alfa in cystic fibrosis patients using controlled inhalation.


Erasmus MC - Sophia Children's Hospital Rotterdam The Netherlands.


Better treatment of obstructed small airways is needed in CF. This study investigated whether efficient deposition of dornase alfa in the small airways improves small airway obstruction. In a multi-centre, double-blind, randomized controlled clinical trial, CF patients on maintenance treatment with 2.5 mL dornase alfa once daily were switched to a smart nebulizer and randomized to small airways deposition (n=24) or large airways deposition (n=25) for 4 weeks. 
The primary outcome parameter was Forced Expiratory Flow at 75% of Forced Vital Capacity (FEF75). FEF75 increased significantly by 0.7 SD (5.2% predicted) in the large airways group and 1.2 SD (8.8% predicted) in the small airways group. Intention to treat analysis did not show a significant difference in treatment effect between groups. Per protocol analysis, excluding patients not completing the trial or with adherence <70%, showed a trend (p=0.06) in FEF75 Z-score and a significant difference (p=0.04) between groups in absolute FEF75 (L·s(-1)) favouring small airways deposition. 
Improved delivery of dornase alfa using a smart nebulizer that aids patients in correct inhalation technique resulted in significant improvement of FEF75 in children with stable CF. Adherent children showed a larger treatment response for small airways deposition.

[PubMed - as supplied by publisher]

Friday, July 8, 2011

Replace Your Jacket!

Thanks to catboogie from www.cf2chat.com , I ordered a free replacement jacket from Respirtech. I have had my original jacket since 2006 so I figured it might be time for a replacement.

HUGS to catboogie for this tip because I had no idea what crappy shape my old jacket was in. WOW.

I would be able to do 100% pressure no problem with my old jacket - now I'm on 70% with this new jacket and it is MUCH more intense. wow wow wow! I'm guessing I had air leaking perhaps with my old jacket and just didn't notice it.

If you have a Respirtech vest, please make sure to replace it every so often to make sure you're getting the full effect (AND change the filter....something I also haven't done in a while). We use these devices way too often to not keep them in tip top shape.