Tag Archives: researchers

COPDers Most Accurate Measurement of Disease Severity is the 6-Minute Walk According to Netherlands Study

COPDers (Chronic Obstructive Pulmonary Disease) are familiar with the 6-minute walking test but the following study presented recently at the American Thoracic Society ATS 2011 Denver is the best explanation I’ve seen of what the test result really means in the progression of the disease.

COPD is the 3^rd leading cause of death in the US, 5^th in the world. For many of us it means don’t waste time. Most of us already know we might be short timers based on other folk’s reactions – like my wonderful dentist doesn’t mention fixing my lower teeth – he just kindly replaced the upper teeth insert my dog, Dean chewed up.

Mr. Dean is a notorious thief of night guards (three) and now he is a pick pocket of false teeth inserts. He can’t be trusted around teeth in an pocket or loose anywhere he can jump. I thought he wanted petting – ha! Seven tiny pieces were found scattered in his cushioned pad and carefully carried to Dr. Robinson.

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Harrison Medical Center, Silverdale Better Breather’s (American Lung Association) upcoming meeting is a super place to ask the questions – more about the meeting in Monday’s blog post.

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American Thoracic Society

‘Walking distance’ test an accurate indicator of disease severity in patients with COPD

ATS 2011, DENVER – The six-minute walking distance test (6MWD), a test that measures a patient’s ability to tolerate exercise and physical activity, is an effective tool for understanding disease severity in patients with chronic obstructive pulmonary disease (COPD), according to a three-year global study of patients with COPD sponsored by drug manufacturer GlaxoSmithKline.

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“We found that baseline 6MWD was predictive of hospital admission with an acute COPD exacerbation, was relatively stable in milder COPD, and has a steady rate of decline in patients with severe disease,” said study author Martijn Spruit, PhD, scientific advisor and research leader at the Centre of Expertise for Chronic Organ Failure (CIRO+) in Horn, the Netherlands. “This confirms prior observations that the results of the 6MWD are related to the risk of death in patients with COPD, and that the test is a useful tool in understanding disease severity in patients with COPD.”

Researchers studied 2,110 patients with moderate to severe COPD who underwent a supervised 6MWD at study enrollment to provide a baseline value and annually for 3 years. Death and exacerbation-related hospitalization were recorded.

During 3 years of observation, 200 patients died and 650 were hospitalized for exacerbations. Mortality rates and exacerbation-related hospitalization were higher in COPD patients as baseline 6MWD decreased. Researchers found that a 6MWD threshold of 357 meters was optimal to predict increased risk of hospitalization; while a 6MWD threshold of 334 meters was optimal to predict an increased risk of death. The mean rate of deterioration of the 6MWD was 5.7 meters per year and was primarily limited by the ability of the patient to breathe easily.

“Exercise tolerance is an important clinical aspect of COPD which can be easily and reliably measured with the 6MWD test,” Dr. Spruit said. “These data confirm the power of the 6MWD to identify subsets of the COPD population at higher risk of exacerbation-related hospitalization or death.

“The ability to group COPD patients according to their functional status disease severity should enable healthcare providers to better tailor therapy for their patients and optimize use of medical resources,” he added. “Patient grouping is also useful for those designing interventional studies in COPD; for example, if the aim of an intervention were to reduce the rate of exacerbation related admission, then a study can be designed by including primarily patients at higher risk of that outcome.”

Dr. Spruit also noted that the 6MWD test offers benefits over a more traditional test of COPD disease severity, the FEV1 (forced expiratory volume in the first second) which measures a patient’s ability to forcefully exhale air in one second. “The FEV1 has limitations as a marker of disease severity in COPD because it fails to capture systemic manifestations of the disease,” he said. “This study was designed to determine if the 6MWD could be an additional measure of disease severity, and the results confirmed that it can.”

(I exhale to just this side of fainting to get the best results – results hinge on the patient’s effort)

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“Reduced 6MWD Is Associated With Increased Mortality And Exacerbation-Related Hospitalization In COPD: The Eclipse Study” (Session A93, Sunday, May 15, 2:00-4:30 p.m., Room 505-506-507 (Street Level), Colorado Convention Center; Abstract 17736)

* Please note that numbers in this release may differ slightly from those in the abstract. Many of these investigations are ongoing; the release represents the most up-to-date data available at press time.

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http://patients.thoracic.org/

http://www.thoracic.org/

Thanks for reading… Sharon O’Hara

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Train the Brain? Reconsider the Pills?

Sharon O'Hara

The headline caught my eye…Anger amplifies clinical pain in women with and without fibromyalgia

I wondered if anger could choke off breathing as well. The researchers from Utrecht University in the Netherlands touched a chord…

Sensitizing effect of anger and sadness not limited to fibromyalgia patients

Researchers from Utrecht University who studied the effect of negative emotions on pain perception in women with and without fibromyalgia found that anger and sadness amplified pain equally in both groups…”

The other day I read a post causally commenting on the list of medications the poster takes. When I read ‘antianxiety’ pills, I wondered how anyone could take a pill when they are virtually helpless – seemingly in the middle of an anxiety attack.

A few weeks ago, I could no more have reached for a pill than fly to the moon with or without gossamer wings.

Tuesday, 31 August I had a doctor appointment. Already extremely short of breath a day or two – by the time I dressed and dragged myself up into the back seat of the roomy gas guzzler I was angry and disgusted. Gasping for air, weak, unable to move beyond a slight shift in position and braced against the side of the car door and the back seat of the car, I didn’t have enough air to purse lip breathe. (PLB) This was new stuff.

My husband had set up the stepper he’d made me to help get in the car and waited in the driver’s seat until I’d gotten myself in, pulled the stepper in and shut the car door.

The more I struggled to maneuver myself into the car, the angrier and more short of breathe. Slumped inside and in trouble I couldn’t breathe or talk.

My husband sat in the driver’s seat and drove off. I couldn’t tell him to take me to the hospital… I couldn’t talk. There was no way to communicate to him that I was in trouble. The only thing I had that could move was my mind.

Physically helpless my brain raced to hang on to something – anything. Touches of memory flitted by and were lost. I couldn’t hang on – until the memory of a toilet suspended over a ravine tickled my memory. The toilet was off to the right of the trail I was riding on. The memory touched my mind and. I grabbed hold and felt again the feeling of surprise and absurdity of seeing a toilet high in the Cascades.

I grabbed that memory and felt again the warm and windless Cascade mountain afternoon. I felt the warm sweat of Wixi’s neck and inhaled her sweet horse smell when I patted her and dismounted to take a closer look and a picture.

The halter rope felt pliable and soft coiled in my hand. The worn smooth edges of the leather reins slid through my fingers until I had enough rein to loop the ends around the saddle horn of my old roping saddle.

My mind pulled to relive every feeling and sight of that toilet set on the edge of space off a trail high in the Cascade mountain range. It sat out on the edge of a ravine overlooking space. Across the ridge, you could see the trail as it came around a bend and then disappeared again off to the right.

Focusing around that memory allowed me to breathe again.

Whoever hauled that toilet in – thanks for the memory.

It is a twenty minute drive to my doctor’s office. At some point during that drive, I began breathing again.

It is strange how desperation can pull past training up without conscious thought.

Focusing my mind to grab a memory and recall the sights, sound, smell in detail was something I’d learned during a week-end seminar more than thirty years ago. Lou Tice’s, Pacific Institute affirmation training saved the day.

Thanks Lou.

If that experience was an anxiety attack, a pill couldn’t have helped. I was helpless to move anything or to swallow if I had a pill to take.

Our minds are available year around. Maybe we should be trained to use our brain.

September is Pain Awareness Month

What does anger and pain have to do with women? Lots it seems, with or without fibromyalgia.

Part 1 of 2 More later… Sharon O’Hara

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Why Pay $150,000 Year for a Lung Drug if it Does Not Work?

Sharon O'Hara

The Apha 1 group comprises about 10% of COPDers but they are the group who has made great organizational strides in bringing public awareness to COPD (Chronic Obstructive Pulmonary Disease)
They are politically astute and I like most of the folks I’ve met in the organization.

That said… the idea of paying $150,000. a year per person for a drug that, at best, does nothing for the patient is OUTRAGEOUS!

There is little to no research being done for regular COPDers…if this study is accurate, why can’t we use that wasted $150,000. Per patient for RESEARCH?

Roll the drug manufactures out of the profit at any cost bed and use the money where it will do the most good for the most people.
Why not?!

I am including the following verbatim for obvious reasons.

Wasted drug dollars? NO!
Research dollars for the COPD majority benefit? YES!

“Pricey lung disease drugs have no benefit: study

URL of this page: http://www.nlm.nih.gov/medlineplus/news/fullstory_100767.html (*this news item will not be available after 10/04/2010)

Tuesday, July 6, 2010
By Kate Kelland
LONDON (Reuters) – Recommendations for expensive treatments made for a genetic disorder called alpha-1 antitrypsin deficiency should be withdrawn because the drugs have no benefit, scientists said on Wednesday.

The disorder causes chronic lung disease and researchers who reviewed data from two trials on 140 patients with it found no evidence that alpha-1 antitrypsin medicines — made by various drugmakers including Talecris, Kamada, CSL and Baxter — do any good.

Based on this evidence, the researchers said the treatment, which costs up to $150,000 a year in the United States, should not be recommended by doctors and advocacy groups.

“The drug has not shown any clinical benefit, is extremely costly and has important adverse effects,” said lead researcher Peter Gotzsche of the Nordic Cochrane Center at Rigshospitalet in Copenhagen, Denmark.

“In view of the lack of evidence and high cost of treatment, treating alpha-1 antitrypsin deficiency by replacement therapy cannot be recommended.”

According to the team, whose work was published in The Cochrane Library journal, recommendations by the American Thoracic Society and European Respiratory Society that promote alpha-1 antitrypsin replacement are “misguided”.

“Both societies recommend augmentation therapy for patients with breathing problems related to alfa-1 antitrypsin deficiency. In our opinion, these recommendations are not reasonable,” said Gotzsche.

Alpha-1 antitrypsin deficiency affects less than one in 1,600 people. Those who inherit the disorder have low levels of the protein alpha-1 antitrypsin, also called alpha-1 proteinase inhibitor, which protects the tissue of the lungs from destruction by the body’s own white blood cells.

At a relatively young age, this can result in symptoms of emphysema, including shortness of breath and wheezing.

The aim of alpha-1 antitrypsin replacement therapy is to give the patient back the protective protein they are missing. This should limit damage to lungs and, ultimately, prevent early death. The protein is usually extracted from blood donated by healthy volunteers.

The researchers reviewed data from two trials involving a total of 140 people with the disorder, all of whom were at a high genetic risk of developing chronic lung disease.

In one trial, patients were given intravenous alpha-1 antitrypsin or a placebo every four weeks for three years and in the other, the treatment or a placebo was given weekly for a minimum of two years.

There was no difference between treatment and control groups in terms of exacerbations of lung disease, or quality of life, the researchers found. Combining the results from the trials, Gotzsche’s team also found no evidence of a clinically important effect on lung function.

“Indeed the results suggested modest harm, or at best no effect,” they wrote in their study. They added that while the treatment might cause a reduction in the deterioration of lung appearance on CT scan, it was “not clear whether this is a clinically meaningful difference.”

http://www.nlm.nih.gov/medlineplus/print/news/fullstory_100767.html

More later… Sharon O’Hara

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