Living Well with a Bad Diagnosis - Lung Disease

Saturday, June 30, 2012

Foggy Day

A summer wet fog arrived and Michael's sinus are recovering. I don't know what it was that got to him, but it made for a few difficult days. He was without any medication yesterday and even looked pretty good.

We are going to spend the afternoon together.

In our little town, at the center of Main Street, sits an old market. It has some wooden shelves and old wide-planked wooden floors that creak when walked upon. It smells of a different era. It had been owned by the same family since the 1800s, the family sold it over five years ago to a newcomer who heavily leveraged it and it closed just over a week ago. It was a sad moment for the town.

It was a shock to everyone that it was reopened yesterday by a family who owns several smaller markets. They know what they are doing. The reviews are good. We are going to take a peak today. The town also has a farmer's market every Saturday, but I am usually working in the gardens. I have been just twice. So, today, we are going to check that out as well.

I know the rest of the country is suffering with oppressive heat but we are cold and foggy and wet here on the coast. No sunshine for us today! It is even too wet to work outside. So, that is our excuse to explore our little town and just spend some quiet time together because it is going to be a crazy busy week ahead.

Friday, June 29, 2012

Join New Pirfenidone Trial If You Have IPF


I received the below from the good folks at the Coalition for Pulmonary Fibrosis regarding the ASCEND trial opened to people with Idopathic Pulmonary Fibrosis. This is the second Pirfenidone trial, which seems so hopeful in treating pulmonary fibrosis. There are several people in my ILD Support Group who have been in the earlier trial and have shown amazing results.
The information below is about the new trial and, if you meet the criteria, how to be a part of this trial. All the information is below:
In an effort to keep you informed about active clinical trials in Pulmonary Fibrosis (PF), the Coalition for Pulmonary Fibrosis (CPF) would like to share updated information on the ASCEND trial, a Phase 3 trial investigating the potential therapeutic use of Pirfenidone. Please see information on the trial pasted for you below.  We also encourage you to see a listing of current Phase 1, 2 and 3 trials listed on our website at http://coalitionforpf.org/cpf_research_clinical.php  as well as the complete listing of PF related trials via www.clinicaltrials.gov.  

If you are a Pulmonary Fibrosis (PF) patient and would like to help find answers to PF, the CPF urges you to consider being involved in clinical trials. No treatments or cures can be discovered without these trials.  


If you are interested in being involved in the ASCEND trial, inform your physician and contact InterMune Medical Information at 1-888-486-6411.  If you're interested in other clinical trials, visit the CPF website's listing at http://coalitionforpf.org/cpf_research_clinical.php and use the contact information below the trial description for the trial in which you're interested.  


To view Frequently Asked Questions about Clinical trials, please refer to the National Institutes of Health (NIH) website on the subject at:http://clinicaltrials.gov/ct2/info/understand.  Please also feel free to contact the CPF with questions about the trials. Call or email us - 1-888-222-8541, ext. 702 or tbarnes@coalitionforpf.org.  
Sincerely,
Mishka Michon, CPF Chief Executive Officer 


ASCEND is a large clinical trial currently enrolling patients in the United States, Mexico, Australia, New Zealand, and select South American countries. This trial is designed to assess the efficacy and safety of the investigational use of pirfenidone in patients with idiopathic pulmonary fibrosis (IPF).


What Treatment is Being Tested?
Eligible patients will receive either pirfenidone (an investigational medication for IPF in the U.S., Mexico, Australia, New Zealand, and select South American countries) or placebo for one year (52 weeks). Patients who complete the entire 52-week study period will be offered the opportunity to continue taking pirfenidone treatment (or switch from placebo to pirfenidone) as part of an open-label rollover study. Patients may also be offered participation in the rollover study if they are able to follow their dosing regimen during the initial clinical trial.


Objectives
Clinical trials must be designed to address specific objectives. The objectives of the ASCEND Trial are to:
  • Assess the effect of pirfenidone compared with placebo on change in a lung function measure (percent predicted forced vital capacity, or %FVC)
  • Assess the safety of pirfenidone compared with placebo
Select Inclusion Criteria
Clinical trials must also set specific criteria for patient enrollment. To participate in the ASCEND Trial, the main requirements are:
  • The diagnosis of IPF (definite or probable) must have been made within 4 years (48 months) of study randomization — the time at which patients will be randomly assigned to receive either pirfenidone or placebo
  • At the time of study randomization, the patient must be between 40 and 80 years of age
  • Lung function, measured by a test of the ability to exhale (forced vital capacity, or FVC) must fall within a specific range (50% to 90%)
  • Another measure of lung function, called carbon monoxide diffusing capacity (DLCO), must be within the range of 30% to 90%
  • The patient must be able to walk at least 150 meters (about 500 feet) within 6 minutes
Select Exclusion Criteria
In order to produce scientifically meaningful results, the ASCEND Trial cannot admit all people with IPF. Patients with any of the following criteria are not eligible to participate in the ASCEND Trial:
  • At the time of study randomization, the patient is either expecting to receive a lung transplant within one year or, for patients in the United States, is on a lung transplant waiting list
  • The interstitial lung disease has a known explanation
  • There is a history of asthma or chronic obstructive pulmonary disease
  • The patient has an active infection
  • The patient is already receiving ongoing IPF treatment such as an investigational therapy, immunosuppressant, or a cytokine modulating agent
  • Within the past 6 months, the patient has had unstable or deteriorating cardiac disease or a pulmonary disease other than IPF
  • History of unstable or deteriorating cardiac or pulmonary disease (other than IPF) within the previous 6 months
Study Details:
  • Screening period (up to 56 days)
  • 52 Week Treatment Period
  • All treatment-compliant patients who complete 52 weeks will be offered participation in an open-label rollover study
Learn More About the ASCEND Trial
If you would like more detailed information about the ASCEND Trial, please go to www.ascendtrial.com, or call InterMune Medical Information at 1-888-486-6411

Thursday, June 28, 2012

Fish Oil and Lung Function?

I am breathing so well that it is a bit scary. No noises. Very little shortness of breath during exertion. I am walking quickly, forgetting to slow down. I am lying in bed at night without feeling the "work" of breathing.

It is so good that I find I don't even think about it.

What has happened? What has changed? The doctors keep telling me that they cannot understand the constant ups and downs of lung function with a disease. It just is.

I have been thinking back to my meeting with Dr. M., my endocrinologist, who is managing my cholesterol levels. He not only prescribed Lipitor but also instructed me to take the Trader Joe's fish oil with the blue/green label. I am up to five per day. That is 5,500 units. That is a lot of fish oil!

He mentioned that what he was most interested in, as a researcher, was the positive effects of the anti-inflammatory fish oil on my lung disease. It that what is happening?

Wednesday, June 27, 2012

Downtime

I need some downtime. Sweet Michael went to work late this morning so I could sleep in to almost 7:30. Unheard of! So today, I am hitting the yards and going no where other than into town with Michael for his hair cut later today.

He is suffering with horrible, out of control sinus. Red eyes, runny nose, sneezing, They are out of control. Even an over-the-counter allergy drug is not helping very much. He slept on the couch last night as he wanted to try and sit up to help the draining. Poor guy.

Yesterday, Mom's doctor ordered a full run of Pulmonary Function Tests to check her lungs. She is so short of breath especially on exertion and has had a runny nose for years. Both are signs of an ILD, which makes me very worried. Hopefully, they will schedule it soon.

Tomorrow, I am going to an EDD office in a horrible area to check on the possibility of receiving the $2500 from the WC Lawsuit that somehow fell through the cracks. I'll hit the other rehab afterwards.

So, today is downtime. Next week begins some more madness: my hair appointment, a fabulous party at a magnificent restaurant right along the ocean thrown by the owner and a wedding. All in one week!

Tuesday, June 26, 2012

Aviation Museum

We met Barbara and her lovely day care kids at the aviation museum near mom's house. It was spectacular. Old planes from the late 1800's, a copy of the Wright plane, old photos, jets, helicopters. Everything was hands-on. We loved it. The kids loved it. We even climbed into a 747 and into its cockpit.

My mom
We climbed into a lot of planes, up and down a lot of stairs and kept up with the kids! Here is a photo of her climbing into one of the cockpits!

Within minutes, I will be meeting mom for an appointment with her primary doctor. I am concerned that she might have an ILD along with the sinus issue. She has been complaining about a drippy nose for years. Nothing seems to work. Lately, she seems to desaturating when walking up stairs, especially if she is carrying packages. So classic. The doctor had talked with her about arranging a full set of pulmonary function tests so I want to follow through with that today.

I didn't go with her to their last meeting as I was giving the speech for the American Thoracic Society that day. The doctor asked about me and mom gave him a thumbnail sketch of my ILD. He was intrigued. So, I am going to bring a copy of speech, in case he asks. Educating doctors, that's my goal!

I did talk with the Employment Department yesterday and will be in their office on Friday to speak with a specific person. That person will direct me through the maze of how or even if I can collect the $2500 I just discovered that may be available to me. It may be too late but at least I will have tried.

Monday, June 25, 2012

Recommitting to Rehab

Rehab. So important. Everyday.

But, with mom moving closer to me, I have not been as vigilant in going to rehab. Her doctor appointments, my doctor appointments and the recent visit with Michael's sister have conspired to waylay my rehab plans.

This week, I am determined to workout each day. Yes, mom has a doctor appointment on Tuesday but we should be back in time to make the rehab class.

Last week, I thought I was having hip problems with suddenly a lot of pain. Oh no! Another round of doctors! Then, I realized that I probably overworked at the gym and in the garden and the pain did go away after two days. Yesterday, my sister and I walked just over seven miles but I don't have any pain this morning. Thank goodness.

Today will start at the other rehab, a Trader Joe run then Mom and I are playing with Barbara and her daycare kids again. We are meeting at a local small airport to tour their museum. We hear that it is interesting and appropriate for the kids. Barbara takes her kids out into the world everyday during the summer. It may just be a trip to Chucky Cheese or swimming at a pool, but they are out of their routine and enjoying the freedom of summer. But, she also has them doing five pages in their workbooks every morning so they don't lose anything during the summer. Love that.

Sunday, June 24, 2012

Weekend Visitors

I am late writing today. My sister Lee and her husband Jeff arrived yesterday afternoon for a short visit. We sat in the garden with cocktails and appetizers then drove 12 miles down the coast to the famous dive for the best, freshest fish. The ocean was a deep glorious blue and we could see forever. We had calamari fresh from the ocean lightly grilled, artichokes picked from their garden and served with an aioli sauce, raw oysters, hot sourdough French bread then crab for me, Prime Rib for Michael (at a fish place?!?), prawns for Lee and scallops for Jeff both with amazing potatoes and veggies straight from the garden.

This morning, Michael and Jeff went to a very high end car show while Lee and I walked along the ocean for just about 7 miles. We made a quick lunch and they just took off for home. What a lovely weekend.

We are watching a recording of the F1 race from Spain, I know who won and am trying so hard not to tell Michael. We will have a quiet dinner tonight and into bed early!

Rather quiet week ahead with a doctor appointment for mom on Tuesday and rehab all week.

Saturday, June 23, 2012

Social Security Disability and Retirement and Workers' Comp

Why, oh why, does bad news seem to always arrive in the mail on a Friday afternoon? No time to take care of it and a worry all weekend.

Yesterday, I received a notice that I have been overpaid by the Social Security Disability Administration for a total of $1,089.00 since January 2007 through December 2011. Why?

They figured that the money I received from Social Security Disability and workers' compensation payments added up to more that 80 percent of my monthly average current earnings while I was still employed. They then went back to the original amount, figured in the cost of living adjustments and will now reduce my monthly checks.

So, they have reduced my monthly benefits from $1,294.00 to $1,186.00. But, that is before Medicare costs are deducted. The actual monthly benefits were $1,204.00 and now I will receive $1,096.00. Only a $108.00 difference.

Also, I have to pay back the $1,089.00, which will be held back from my September check. That month's check will only be $97.00 minus the $90.00 for Medicare and....Starbucks!

Now, do I fight it? There is a section in the letter that states that I can challenge it if the mistake was not my fault in any way. When I was out on leave from the school before I was declared disabled by the doctors, I would give the workers' comp checks to the school and they would give me my normal paycheck amount because I had lots of sick pay and vacation time saved up. All was well until they discovered they paid me over $7,000.00 extra income. Apparently, they had not kept track of my sick pay and vacation time and just kept paying me. After the overpayment was discovered, they allowed me to keep it. Thus, is the reason for the current problem. 

For $108.00 a month, I am not going to challenge their decision. 

The good news is that at the age of 62, I can receive Social Security Retirement Benefits, which will be much more than I am receiving now. Good information!

More good news, I thought this problem might be connected to my Workers' Comp Settlement agreement, so I pulled the letter from the lawyer out of the files to read it all again. In the letter, dated 2.18.09, I missed something big:

"The settlement also provides for the Employment Development Department to accept $2500 payable by the defendant as payment in full on the lien. It may be possible for you to withdraw this amount, upon appropriate medial certification. You may reapply for said benefits after you received the settlement funds. However, this is solely within the discretion of the Employment Development Department, and I have given you no guarantee that you will in fact be able to withdraw said funds."

Ta-Da! Guess where I am going on Monday morning?

Friday, June 22, 2012

Magical Morning

I took the day off from my Thursday routine yesterday. I didn't go to the rehab class. Again. Instead, Natalie and I had been talking about taking the kids for a hike on the ped walk heading north along the ocean.

Good plan but suddenly, the weather had turned wet, windy and cold. By the time they were here at 9AM, it had calmed down a bit but still cold. Oliver was in his stroller and Winnie walked with us. We were heading to a restaurant for hot chocolate and coffee but there was just one problem, they weren't opened. Oops.

I suddenly remembered a coffee shop/plant nursery just up a street heading away from the ocean. We walked there for the best hot chocolate and lattes then started the return trip back to my house. It was a total walk of just over three miles. Oliver was getting restless on the way home. Enough of this stroller! He wanted to run! The only problem was that he never stopped when told to, which made his freedom rather dangerous as we often crossed roads going into the state parks.

So when we passed the final state park entrance, we let him loose. He loved the dirt road, loved the rocks which ended up in his pockets, he loved to run along side of us, he loved looked at the plants along the road and he spotted a beetle and a rabbit. I also taught Winnie how to throw - stepping into the throw - and we threw some rocks into the weeds and wild roses and wild fennel.

It was a pretty magical morning.

Suddenly, I realized that I missed the rehab class. Our walk had taken much longer than I had planned. The housekeepers arrived while we were walking home so I couldn't stay there. We all went to lunch together, I ran some errands then arrived home to the clean house.

But, the walk had energized me, so I painted my closet and moved my clothes back into it. It is now a beautifully organized closet thanks to the Elfa system.

Today will find me in the yards, pulling weeds, cutting the grass, trimming some bushes and making it close to perfect for visitors! My sister and her husband are due tomorrow early evening and will leave later Sunday. I so wish the weather was better! Maybe a bit of sun is not too much to ask?

Thursday, June 21, 2012

Dependent


A burden. I am feeling like I am a burden. I can’t earn any money, as I would lose my Medicare through SSI Disability. I don’t think I could physically work more than one day a week anyway because I would have to take the next four days off to recover!

A burden. I have never felt this way before. Even when I stayed home with William for nine years, I felt I was holding up my end of our lives.

Though I deal with the house and gardens and bills and food, somehow I suddenly feel like I am a burden to Michael.

Am I holding him back from pursuing his dreams? Has he become resentful being the only earner and having to support us, as I am totally dependent?

It has been bothering me for a few days. We sat in the sunshine after work yesterday when I brought up the subject.

He said, ”No. We are doing this together.”

Me, “But don’t you feel like I am a burden?”

It was a quick, “No. Not at all. Not once.”

I asked, “Really, honestly, truly?”

“Truly.”

Michael’s sister was a stay-at-home mom most of her married life. We were talking about this when she was here and she totally got it. She, too, at times has felt this same issue creeping into her brain.

I hope I can shake it soon. 

Wednesday, June 20, 2012

Donkeys and Chickens and Sheep, Oh My!

     Recovering today. Mom and I met Barbara and her childcare group at a working farm owned by a university in the canyons south of us. I hadn't been there since William was in 4th grade. It is opened to groups of children only and just one group at a time. She brought eight kids with her plus one set of parents and uncles from Missouri.
Now, the coastside can be very cold and foggy this time of year. The forecast was for fog through the morning and a high of 58 degrees. I was worried. We brought heavy coats with us. HA! They were wrong again! It was a beautiful 75 degrees and sunny! Even right at the water's edge!
     We met everyone at the ranch which is just minutes south of us. Barbara has a lovely group of kids and the docent keep commenting that they were amazing. Everything she presented to them, they took the initial ideas and ran with them. All were totally engaged.
     It began with learning how to pick up chickens. Even the most scared "city kid" was successful. They even picked flowers from the garden to feed them as well as a little "scratch." They also gathered eggs, feed goats, brush goats, talk to donkeys, feed the sheep, carded the wool and made bracelets with it. 
     Afterwards, we drove to the closest beach and the kids had so much fun digging in the sand and getting soaked. Barbara brought tons of sand buckets and shovels and towels and extra clothes for all the kids. So prepared! Thirty years of experience!
     Mom and I arrived home around 3:30, had cocktails in the garden with Michael then I made a quick dinner of Mongolian Beef, rice and broccoli. We drove mom home and I snored all night. I was tired but it was exhilarating to be around a group of children for the day. I so miss their energy and wisdom and kindness. We had lovely conversations with each of them throughout the day but I especially enjoyed sharing a lunch table with a few of them. Charming. 
     So my job today? I am going to spread the "miracle soil" I bought there. Fresh! Smelly! My garden is going to be very happy!

Tuesday, June 19, 2012

Sharing the Blog


My mom had some biopsies taken from her elbow, hand, face and ear a couple of weeks ago. The spot on her elbow came back pre-cancerous so we went to the doctor yesterday to removed the entire growth with an application of liquid nitrogen. They also did a full exam of her body and found two other benign but bothersome ones that they also removed.

As Mom was at a teaching university clinic, a first year resident did the initial exam and asked all the questions then she left to reviewed all she had learned with the dermatologist. They both returned to the room where the doctor examined mom again and was lovely to her. They agreed to freeze the three spots and asked mom to return in three months. It as so interesting to watch the resident use the liquid nitrogen. She used what looked like a little torch and just danced around the edges of the scab of the biopsy of her elbow and completely covered the other two moles. They turned pink but we were told they would turn black and eventually just fall off. Mom said it was all rather painless.

Afterwards, the resident said something about prednisone and both mom and I moaned. Yes, we know all about prednisone. The resident began to ask questions and a quick version of my story came out. She seemed very interested so I told her about this blog, something I very rarely do. Michael, who never reads my blog, was beginning to tell people about it if they were having some minor medical problems. I reminded him that it was VERY personal and not something I wanted to share with a lot of people we know. It's funny that I have to keep it anonymous in order to be completely honest about what we are facing. 

Anyway, I hope the information will be helpful to the resident in the coming years as she becomes a practicing physician. She was one smart cookie. I know she will do well.

Monday, June 18, 2012

More Company

Well, I have had a couple of days to just enjoy putting the house back together and working in the garden after Michael's sister's visit. But, last night my own sister phoned and is coming for a visit this coming weekend!

More company!

Lee and Jeff are suffering with high temperatures in their area and need a break! They also have not visited mom in her new apartment. We have two extra bedrooms and an extra bathroom so I invited them to spend the night here. Along the coast. Cool air. Clean air.

So, back to list making. Need to wash both sets of sheets and iron them, of course! (Jeff has sleep apnea and the noise from the machine has my sister fleeing to another room!) The yards will need to be done before they come and I will make the famous Ancho Macho Chili Friday for Saturday night's dinner. We will plan walks along the coast and appetizers in the garden. It will be nice to have them here without a holiday. Just for fun.

Sunday, June 17, 2012

Happiness and Tears

Father's Day. Happiness to all fathers today and all year!

I was going through some old stuff in my closet last night when I ran across a letter my dad had written to me in Chicago from the Bay Area. He had been transferred to a job six months before we packed up the house and moved during summer vacation.

I was twelve years old.

It was a sweet letter about how he was touched that I had written to him. Apparently, my other siblings had not. Between the lines of that letter, I felt the relationship that we had together as adults that was so special and so real. I burst into tears. I was suddenly reminded of how special he was and how lucky I was to have him as a dad.

I deeply miss my dad this Father's Day.

Saturday, June 16, 2012

Just Us

Home alone again. Anna left last evening but we really did enjoy her company. On Friday morning, we chatted in our pjs until noon then drove into town to the organic market. I wanted to buy enough food to last the weekend and also put together some lunch for us.

She found some very dense dark crackers which we topped with Harley Farm goat cheese and a touch of fig jam. We also chose some unique olives and freshly grilled chicken teriyaki. Add a bowl of chopped veggies and we had some lunch. Afterwards, we headed over the hill to hand her off to Michael's twin. She flies home on Sunday.

She wants to come back for a weekend visit with her husband next time.

The weather is going to be warm along the ocean today so we are expecting lots of tourists. I plan to work in the gardens, pull the house together and maybe enjoy a chapter or two of my book.

Friday, June 15, 2012

No Fly Zone

Flying. Can't do it. Banned. Dr. K. made it very clear to me back in 2005 that I cannot travel via planes. Ever. I thought it had something to do with oxygen issues but later learned that it was a much bigger issue.

Paris. Michael and I have travelled so much together through the years but somehow missed Paris. It was going to be our next trip before I became ill. When I met Dr. K. I told her about our goal to visit Paris. Our final trip. She smiled and said, "We'll get you there someday but not now."

What I later learned was that the issue was everyone else on the plane and being immune suppressed. She said that she could get me to Paris but if I contracted something during the flight and my lungs crashed, she couldn't get me home. Being stuck in Paris needing lung transplants is not a happy thought. We put Paris on the very back burner.

But, I would begin to dream about Paris again while sitting in the ILD Support Group meeting and hearing everyone around me telling about their upcoming trips - Ireland! Rome! Hawaii! I was so jealous.

I met Marty in the support group on my first visit. We both were the first people we met who had our disease, Hypersensitivity Pneumonitis. We bonded. We shared PFT numbers. We shared our stories. Last time I saw him, he was headed to Hawaii for a much needed vacation.

I got an e-mail from him today. On the trip to Hawaii, he contracted a virus. A bad virus. After his return, he needed to be on supplemental oxygen 24/7 for the first time. They took an x-ray. No PFTs. No CT Scan. Does he have a blood clot? He is now off of all prednisone and cellcept. But, his saturation numbers are still horrible. Is this his new normal?

He was heartened to hear about my fight with the virus in March and my recent dramatic recovery from it and wanted the full details. I also encouraged him to ask for full PTFs and CT scan. Clearly, something is going on.

Communications. Sharing of information. So powerful.

Thursday, June 14, 2012

More Fun

Anna and I walked three miles along the ocean up the coast to Sam's. It was still a bit foggy when we left home, which made the walk a little easier for me. I did wear my oxygen because that hike was the longest I have walked since my diagnosis.

The coastal trail winds through some fields of wild fennel and other gloriously smelling plants. The views of the ocean were stunning and she kept remarking about the freshness of the air. We arrived and were seated right at a window facing the water and she ordered, at my suggestion, a huge 1.25 pound Maine Lobster Rolls with the best cole slaw and potato chips. She loved it. I had a cup of gumbo. Delicious.

As we were sitting there, the fog began to burn off to reveal the bluest ocean with waves breaking with stunning beauty against the shore. Rather perfect, I must say. The three mile hike home took only 45-minutes, which was rather a surprise as we took an hour to get to the restaurant. We were moving!

After we got home, we drove into town and had her fingernails and my toe nails done. It was only the second time in her life that she has had her nails done. I think she will now do it more often!

For dinner, we drove to the top of the pass and long the ridge for appetizers and cocktails at a very elegant fancy but comfortable restaurant. The bartender was hilarious and made both of them excellent drinks, Anna and Michael shared an appetizer portion of fettuccine Alfredo and a jumbo shrimp cocktail. I sat on the other side of the table protecting my Oysters Rockefeller from any poachers.

Another busy day ahead including lunch with my mom. Should be more fun!

Wednesday, June 13, 2012

Way Too Much Fun


I love family. We are having fun with Michael's sister. All went well at the airport then we headed home where Michael met us for cocktails and appetizers in the garden. With different types of music playing in the background, Michael BBQed the prime cut steaks, I cooked the artichokes and we had a simple dinner. With wine. Oh my. Suddenly, Junior Brown's CD started playing. We jumped up, cranked it up, hauled her into the living room and gave her the prime seat on the couch. "Highway Patrol!" She's a Venom Wearing Denim!" "...You are wanted by the police and my wife thinks you're dead!" She loved it and got to dancing. Then, she is a total Beatles freak, Michael played that CD then showed her the Mustang in the garage. We talked about lungs and husbands and children and laughed a lot before falling into bed at 9:30! Late for me!

Today, we are going to walk off dinner with a three mile walk along the ocean to lunch. Then back. Other plans for tonight.

It is fun to hang out, tell family tales we hadn't heard and just connect in person. Michael is keeping an eye on me to make sure I don't over do anything. I really don't want to get sick, again.

So, dear reader, I am having way too much fun. 

Tuesday, June 12, 2012

Life After a Fatal Diagnosis

After accepting that I had a very limited future, a sense of calm worked its way into my body. I slowed down to enjoy moments. I became more polite, oddly enough. I smiled more often. I refused to waste one moment of the limited moments I had left on depression.

All plans changed. We closed our circle of friends and relatives with whom we shared our medical information. We removed people from our lives who were negative or pulled on our positive strength. We noticed that we didn't sweat the small stuff anymore. It didn't matter. We were dealing with life and death issues.

After burying my aunt in Indiana in 2007, we drove back home on Highway 40 and were able to visit my brother and his wife in New Mexico. We had a ball and while driving away from their home, I vowed to develop a better relationship with them. We had to fix it before I died. There had been no problem but we never phoned or chatted or had anything other than a distant relationship. After we got home, I began to build our friendship. Phone calls, texts, e-mails. It didn't take long and now we are dear friends, not just relatives.

I believe that this never would have happened if I had not received a fatal diagnosis.

To live life with relationships all in order, no anger or depression and with a deeper appreciation of the small moments reflecting the goodness of life is a wonderful gift. It is a lovely way to live a life. Sadly, it took a major illness to get me here but I vow to focus on living every moment with kindness and joy.

Monday, June 11, 2012

Final Countdown

I am almost ready for Anna's visit. Michael's sister is flying in from Southern California around noon tomorrow. It has been a long weekend of preparations including finishing the gardens, washing the windows, cleaning the front door, food shopping and a final cleaning of the house this morning.

Also this morning, mom is having another shot in her eye to treat her Macular Degeneration. We will probably have a lovely lunch together somewhere afterwards.

Having Anna with us will be sort of a vacation for me, too. No cooking. No rehab. Nothing but talking and taking walks along the ocean and relaxing. A change of routine.

The weather will be perfect here on the coast with highs around 68 degrees.

Last evening, We finally met the new tenant across the street and, of course, I looked a total mess from doing the yard work! She is either newly separated or divorced and is loving our little community along the ocean. She was heading on a bike ride with friends to dinner up the coast when we met. I really liked her a lot. A new friend!

Sunday, June 10, 2012

The Music Babes

The Music Babes. Three of us. Taking over.

The music department at the school where I got sick was huge. The woman who ran the program for over thirty years was brilliant. The program included music education, choir and instrumental lessons taught during the day. Children left classes to have a lesson every week or two times a week if they where in a special program. There were 17-19 instrumental teachers on staff who where highly respected musicians in their own careers. One had to be a performing musician to be on the staff as it was a performance oriented program. How could one teach a child to prepare for an audition, competition or performance if one had never done it? It was that experience that we expected them to share and teach to the children. And they did. Even taking children to international competitions. She expanded the program in every direction including a competition that drew young musician from hundreds of miles away. She worked with another program that she founded, which brought high level music education into public schools.

But, when she was getting older, she was losing patience with the students. She was always a bit of a bristle and would sometimes yell at the kids but mostly, she was amazing with them. But suddenly, there was a lot more yelling and frustration. It was time for her to retire before she thought she was ready. She hand-picked her replacement who I hated. He was horrible to the children, had no sense to change the rules when needed, smelled of body odor to the point where I would gag and he thought he was the smartest person and best musician ever.

I was not going to work for him as I didn't want my name connected to his in any way within the music community. I was offered another job with a highly respected private youth orchestra. The afternoon before the final interview with their board, I told one of the parents who was connected with this other organization. She asked if she could tell the head of the school that I was having this final interview. I told her yes and with that, the head of the school begged me not to sign anything and to meet him in his office the next morning.

He offered me the position of being head of the music program at the school and that the woman would be forced to retire. Moved to a separate office, she would be given a couple of years to sort her huge pile of files to be handed over to the school archives.

I accepted. The smelly guy stayed my first year but was not happy. It was so difficult working with him, as you can imagine. Every time I tried to move the program forward or streamline it, the now former head would sit in my office for an afternoon while I explained why I changed some aspect of the program until she agreed it would be fine. It was a hard year.

Finally, we fired the smelly guy after that year and I was able to hire a new Pre-k through 5th grade classroom/choir music teacher and a 6th through 8th grade classroom/choir music teacher. I went through a huge number of applications and interviews. Through the process, I hired Natalie (now the mother of Winnie and Oliver) and Jeannette.

We were now in charge of this amazing program.

Natalie had never taught children but she had a wonderful education and had just received her Master of Music Degree from the Conservatory. She had and has a glorious voice. She was young and willing to learn the program. She was the best hired I ever made and we became best friends!

Jeanette had taught vocal lessons and also worked with private choruses. She had a great education. What I learned through her hire was to go with my gut about a person. It was most important to like the person. To have to work with someone like the smelly guy made the working environment difficult. Ultimately, it didn't matter how good of a teacher or musician he was, I just didn't like him. But, I really liked Jeannette.

She was the one who named us - The Music Babes.

There was a reunion of the Music Babes yesterday at a place near Natalie's house. The three of us sat and had cocktails and chatted for almost three hours. They have grown both personally and professionally this past decade. It was so satisfying to sit and listen and laugh and remember all of our long hard days working together.

It was the best time of my professional life.

Saturday, June 9, 2012

GERD and Lung Disease - Day 3


Now that we understand what GERD is, we can look at the possible connection between IPF and Microaspirations. It is heavy reading but worth the effort.
The article with graphics can be found here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851633/?tool=pubmed
Or you can read below:
 Does Chronic Microaspiration Cause Idiopathic Pulmonary Fibrosis?

The publisher's final edited version of this article is available at Am J Med
See other articles in PMC that cite the published article.

Abstract
Idiopathic pulmonary fibrosis is a diffuse fibrotic lung disease of unknown etiology with no effective treatment. Emerging data support a role for chronic microaspiration (i.e. subclinical aspiration of small droplets) in the pathogenesis and natural history of idiopathic pulmonary fibrosis. However, the precise relationship between chronic microaspiration and idiopathic pulmonary fibrosis remains unknown. Gastroesophageal reflux, a presumed risk factor for microaspiration, has been strongly associated with idiopathic pulmonary fibrosis with an estimated prevalence of 90%. This review aims to describe the relationship between chronic microaspiration and idiopathic pulmonary fibrosis by laying out the clinical and biologic rationale for this relationship and exploring the scientific evidence available. The gaps in our current understanding of the diagnosis of chronic microaspiration and idiopathic pulmonary fibrosis and the ongoing uncertainties in management and treatment will be highlighted. Defining the role of chronic microaspiration in idiopathic pulmonary fibrosis is essential as it has potential clinical, pathobiological and treatment implications for this deadly disease.
Keywords: pulmonary fibrosis, respiratory aspiration, gastroesophageal reflux, etiology, diagnostic techniques and procedures

INTRODUCTION
Idiopathic pulmonary fibrosis, often abbreviated as IPF, is a chronic, fibrotic lung disease.1 There is no proven therapy and the median survival is between 2 and 3 years from the time of diagnosis.2 By definition, the cause of idiopathic pulmonary fibrosis is unknown, although several associations have been described: cigarette smoking; exposure to wood and metal dusts; chronic viral infection; exposure to some drugs (e.g. antidepressants); and hereditary factors (e.g. mutations in the genes encoding telomerase components).1, 3, 4
Recent focus has shifted to the potential role of chronic silent microaspiration (i.e. subclinical aspiration of small droplets) in the pathogenesis of idiopathic pulmonary fibrosis.1 Further, it has been suggested that the acute respiratory decompensation (i.e. acute exacerbation) manifested by some patients with idiopathic pulmonary fibrosis may be due to microaspiration.5 As a result, there is a growing consensus that elucidating the impact of microaspiration on the pathogenesis and natural history of idiopathic pulmonary fibrosis is important.
This review aims to explore the relationship between microaspiration and idiopathic pulmonary fibrosis, highlighting the scientific evidence supporting a potential causative role. Our hope is to raise awareness of this topic among clinicians and scientists, establish a solid foundation for future scientific investigation in this field, and emphasize the need for further studies to determine the significance of microaspiration in idiopathic pulmonary fibrosis.
SILENT MICROASPIRATION AND LUNG DISEASE
Aspiration is defined as the inhalation of oropharyngeal or gastric contents into the larynx and lower respiratory tract.6 The clinical syndrome due to aspiration (e.g. aspiration pneumonitis, aspiration pneumonia) depends on the nature and volume of aspirated material, the frequency of aspiration, and the host’s response to the aspirated material.
The term “silent” microaspiration is used when patients have asymptomatic aspiration of small volumes of oropharyngeal secretions or gastric fluid into their lungs. Approximately half of all healthy adults aspirate small amounts of oropharyngeal secretions during sleep7 and other co-morbidities may increase the risk of aspiration (e.g. scleroderma, cerebrovascular disease, and degenerative neurologic disease).6, 8, 9 However, normal host defenses (e.g. glottis closure, cough reflex) are usually able to compensate.10 Depending on the frequency and intensity of the silent microaspiration, and, perhaps, genetic predisposition, patients may manifest with cough, wheeze, or mild gas exchange abnormalities.11
Gastroesophageal reflux and silent microaspiration is associated with several lung diseases and among those who have had lung transplantation.12, 13 Lipoid pneumonia is caused by the silent microaspiration of exogenous lipid (usually a complication of long-term ingestion of oil-based compounds) that leads to a chronic inflammatory pneumonitis that often progresses to fibrosis.10 Silent microaspiration has also been suggested as a cause of chronic bronchiolar and interstitial lung disease.14 Lastly, data from the lung transplantation literature strongly suggests that chronic silent microaspiration is associated with post-transplantation bronchiolitis obliterans, the primary lesion in chronic organ rejection.15 In fact, several studies have suggested that early fundoplication improves survival and decreases chronic allograft rejection in this population, presumably through reducing the frequency of silent microaspiration.16, 17
SILENT MICROASPIRATION AND PULMONARY FIBROSIS
Evidence from experimental models in animals and descriptive studies in humans support the concept of microaspiration as a potential cause of pulmonary fibrosis.
Animal data
Acute aspiration
Gastric juice is found to have rapid distribution in the lungs and is detected in the subpleural zones within 20 seconds following instillation in the main bronchus of dogs.18 Delivery of a single dose of acid solution to the lungs of rabbits and dogs leads to a wide array of histopathologic changes including alveolar hemorrhage, pulmonary edema, and neutrophilic inflammation.19, 20 A low-mortality acid aspiration lung injury model demonstrated loss of normal parenchymal architecture and wide-spread collagen deposition at 2 weeks.21 In addition, acid treated rodent lungs have demonstrated increased transforming growth factor (TGF)-beta 1 expression in the lung lavage and increased expression of collagens III/IV and fibronectin in the lung tissue, suggesting profibrotic mechanisms may be involved in aspiration-induced lung fibrosis.22
Chronic aspiration
Histologic specimens from rodent models of repetitive gastric fluid aspiration exhibited prominent giant cells, lymphocytic and obliterative bronchiolitis, and parenchymal fibrosis.23 Cytokine analysis showed increased production of TGF-beta. The effects of whole gastric fluid as well as its individual components were also studied using a similar chronic aspiration model.24 Interestingly, their findings, characterized by granulomatous interstitial pneumonitis, were independent of gastric fluid pH.
Human data
In vitro studies
There are limited in vitro data on the effects of gastric fluid aspiration on human epithelial cells, alveolar macrophages, and resident fibroblasts. A component of bile acid, chenodeoxycholic acid, has been shown to induce TGF-beta production from human airway epithelial cells via a p38 MAP-kinase dependent pathway.25 Fibroblast cell proliferation was also increased with exposure to chenodeoxycholic acid, a response which was inhibited by dexamethasone and anti-TGF-beta antibodies.
Clinical studies
There is no direct data demonstrating that microaspiration leads to pulmonary fibrosis in humans. Instead, studies have focused on investigating risk factors for microaspiration – primarily gastroesophageal reflux. Pearson and Wilson described the presence of gastroesophageal reflux and hiatal hernia, a risk factor for gastroesophageal reflux, in patients with diffuse pulmonary fibrosis,26 and Mays et al suggested that repeated small tracheobronchial aspiration of gastric secretions over a long period of time could lead to lung fibrosis.27
Recently, a strong association between gastroesophageal reflux and idiopathic pulmonary fibrosis has been reported.28-32 Esophageal 24-hour pH monitoring has estimated the prevalence of gastroesophageal reflux in idiopathic pulmonary fibrosis at 67-88% for distal esophageal reflux and 30-71% for proximal esophageal reflux. These studies also demonstrated that typical symptoms of reflux (e.g. heartburn, regurgitation) are poor predictors for the diagnosis of gastroesophageal reflux in this population.
Despite a strong association between idiopathic pulmonary fibrosis and gastroesophageal reflux, a causal relationship is unclear. A retrospective case series described 4 patients with idiopathic pulmonary fibrosis whose clinical course stabilized over several years with primarily medical therapy targeted at adequate suppression of gastroesophageal reflux.33 A second retrospective review of 14 patients with idiopathic pulmonary fibrosis awaiting lung transplantation showed stabilization of oxygen requirements in those patients who had undergone a laparoscopic Nissen fundoplication, but no difference in change in pulmonary function.34
SILENT MICROASPIRATION AND IDIOPATHIC PULMONARY FIBROSIS
The above animal and human data support the concept of silent microaspiration leading to pulmonary fibrosis, but many questions remain. Perhaps the most significant is how to reconcile the observed histopathology of aspiration-related lung injury (i.e. airways injury and granulomatous inflammation) with that of idiopathic pulmonary fibrosis (i.e. usual interstitial pneumonia pattern).
Usual interstitial pneumonia pattern is characterized by histologic heterogeneity of fibrosis, with alternating areas of normal lung and dense, mature collagen deposition with evidence of microscopic honeycomb change and characteristic aggregates of spindle-shaped cells beneath hyperplastic alveolar lining (i.e. fibroblastic foci).35 The fibrosis of usual interstitial pneumonia is anatomically located at the periphery of the secondary pulmonary lobule and is predominantly subpleural. Inflammation and granuloma formation, as described in some aspiration models, are not prominent features of usual interstitial pneumonia and may suggest alternative diagnoses, such as hypersensitivity pneumonitis. Hypersensitivity pneumonitis is due to the inhalation of organic antigens that, like microaspiration, can lead to inflammation and fibrosis in the lung parenchyma.
In clinical practice, distinguishing some cases of usual interstitial pneumonia from hypersensitivity pneumonitis is not straightforward, as both can demonstrate diffuse fibrotic lung disease. 36, 37 A recent study describing the role of surgical lung biopsy in separating chronic hypersensitivity pneumonitis from idiopathic pulmonary fibrosis demonstrated that while most patients with chronic hypersensitivity pneumonitis had histologic evidence of bronchiolocentric inflammation and/or granuloma formation, 2 patients had a usual interstitial pneumonia pattern on surgical lung biopsy.37 Interestingly, one of these patients had a previous surgical lung biopsy that showed features more typical of hypersensitivity pneumonitis. Histopathologic findings of interstitial fibrosis and parenchymal distortion have also been described in lipoid pneumonia, another example of microaspiration leading to peripheral lung disease.10 These data support the hypothesis that chronic microaspiration could lead to the histopathologic pattern of usual interstitial pneumonia.
MAKING THE DIAGNOSIS OF MICROASPIRATION
Several approaches for diagnosing microaspiration have been suggested, each having its own set of advantages and disadvantages (Table 1). We describe a few of these methods below.

Summary of Diagnostic Tools for Microaspiration
Symptoms
Symptoms of microaspiration or of conditions that increase the risk for microaspiration (e.g. gastroesophageal reflux) are poor diagnostic tools. Sweet et al found symptom screening for proximal esophageal reflux had a sensitivity and specificity of 60% and 39%, respectively.31
Radiology
Several radiologic studies have been used to diagnose microaspiration and risk for microaspiration including barium swallow, computed tomography scan, and scintigraphy. Gastroesophageal-pulmonary scintigraphy involves ingesting a radio-labeled compound, typically technetium labeled hepatate or colloid. If this compound is subsequently aspirated by the subject, the presence of the radio-labeled compound can be detected in the lung.38 However, limitations include its poor sensitivity (due to potential infrequency of aspiration events), inter-observer variation, availability, and cost.
Esophageal studies
Esophageal studies, including 24-hour pH monitoring and pH-impedance testing have been used in the diagnosis of gastroesophageal reflux; 24-hour pH monitoring is currently considered the gold standard for this diagnosis.39 pH-impedance testing may provide some advantage in its ability to diagnose both acid and non-acid reflux events, as well as the height and volume of the refluxate.40 However, both of these measures can only assess the risk for microaspiration.
Biomarkers
Measurements of pepsin and bile salt in the airways have been investigated as direct biomarkers of microaspiration given their specificity to the gastrointestinal tract, being gastric and biliary in origin, respectively. Pepsin is not normally found in the lower respiratory tract41-43 and patients with gastroesophageal reflux do not necessarily have elevated pepsin levels in their bronchoalveolar lavage (BAL) fluid, suggesting that identifying gastroesophageal reflux is not sufficient for diagnosing microaspiration.42 Pepsin in BAL has been shown to be a highly specific (100%) and sensitive (80%) method for diagnosing gastroesophageal reflux -associated pulmonary aspiration in children.43 In another study, BAL pepsin level correlated with the number of proximal reflux events as measured by 24-hour pH monitoring.44 The limitations of this method include the lack of standardized methodology and unknown half-life and clearance mechanisms from the lower respiratory tract.
At this time, a diagnostic gold-standard for microaspiration remains unknown. However, based on the current data, the specificity of pepsin and bile salt to the gastrointestinal tract makes this diagnostic approach highly appealing.
CLINICAL MANAGEMENT
Until further evidence is available, we cannot recommend a specific screening, diagnostic, and/or management algorithm for microaspiration in idiopathic pulmonary fibrosis. Much has been written about the need to screen and treat gastroesophageal reflux in this population.45, 46 However, there is equipoise in the idiopathic pulmonary fibrosis community as to how aggressively to pursue this diagnosis. Even within this group of authors, there are differences in practice patterns. This is primarily because there are no convincing data demonstrating a clinical benefit to treatment of gastroesophageal reflux in idiopathic pulmonary fibrosis and there are risks to medical treatment. Studies have suggested an increased risk for community-acquired pneumonia in association with current use of proton pump inhibitors (PPI).47 PPIs have also been associated with an increased risk of hip fracture.48 Further, PPIs only change the acidity of the refluxate; they do not prevent reflux or microaspiration of gastric contents.
It is also unknown if other measures, such as lifestyle modifications (e.g. small meals, avoidance of certain foods and alcohol), other pharmaceutical interventions (e.g. prokinetics), and/or surgical barrier creation (e.g. Nissen fundoplication), have a role in the treatment of microaspiration. Collaboration with our gastroenterology and surgery colleagues will be essential in addressing all of these issues.
GAPS IN KNOWLEDGE
One possible mechanism of microaspiration leading to pulmonary fibrosis is illustrated in Figure 1. However, many questions need to be addressed in future studies to clarify the role of silent microaspiration in patients with idiopathic pulmonary fibrosis:
What is the true prevalence of microaspiration in patients with idiopathic pulmonary fibrosis? The finding of gastroesophageal reflux does not imply microaspiration and there is no consensus on a gold standard for the diagnosis of microaspiration in the pulmonary community. Respiratory symptoms are well recognized extra-esophageal manifestations of gastroesophageal reflux,49 and reflux extending into the proximal esophagus and cricopharyngeal region is thought to reflect a high risk for microaspiration,50-52 however, its sensitivity and specificity are unknown. The measurement of pepsin and bile salt in BAL may help clarify this issue.
If gastroesophageal reflux is an accurate biomarker for microaspiration in idiopathic pulmonary fibrosis, why is there such a discrepancy between the prevalence of gastroesophageal reflux (20,000 per 100,000) and the prevalence of idiopathic pulmonary fibrosis (approximately 14-43 per 100,000)?53, 54 Possibilities include variation in the degree or duration of microaspiration, the involvement of other co-morbidities (e.g. Helicobacter pylori infection), or differences in genetic predisposition to fibroproliferation. Perhaps in genetically predisposed individuals, the pulmonary parenchyma responds in an aberrant “pro-fibrotic” manner to epithelial injury (e.g. recurrent acid injury), resulting in the clinical development of idiopathic pulmonary fibrosis.55, 56
Which components of the gastric refluxate are most injurious to the lung? Depending on the origin of the refluxate (stomach, duodenum), contents that move retrograde past the lower esophageal sphincter could contain acid, bile salts, proteases (pepsin, trypsin) and upper gastrointestinal organisms. As noted previously, animal studies have suggested that lung injury from chronic aspiration is independent of pH, implying that non-acid reflux may also be relevant.
Should patients with idiopathic pulmonary fibrosis be treated for presumed microaspiration? We do not know if clinical outcomes for patients with idiopathic pulmonary fibrosis are improved by treatment of microaspiration. The studies described previously suggest a possible benefit with the treatment of gastroesophageal reflux;33, 34 however there is insufficient data at this time to recommend this strategy. The role of treatment can only be addressed once the precise relationship between microaspiration and idiopathic pulmonary fibrosis has been defined.
Does microaspiration cause idiopathic pulmonary fibrosis or does idiopathic pulmonary fibrosis cause microaspiration? The latter theory argues that idiopathic pulmonary fibrosis leads to progressive architectural distortion of the mediastinal structures, traction on the esophagus and the diaphragm, and weakening of the lower esophageal sphincter. Weakening of the lower esophageal sphincter would predispose patients to gastroesophageal reflux and microaspiration. Evidence contrary to this theory includes two studies that demonstrated no association between lung function and acid exposure times,29, 32 and a third showing an inverse relationship between lung function and the presence of gastroesophageal reflux.31 Regardless, a weakened lower esophageal sphincter could allow for chronic microaspiration, causing repetitive injury to the already diseased lung and leading to the accelerated decline and/or acute respiratory decompensation seen in some patients with idiopathic pulmonary fibrosis.
Does microaspiration cause acute exacerbations in idiopathic pulmonary fibrosis? Recent studies have reported on the clinical significance of acute exacerbations in increasing the morbidity and mortality of idiopathic pulmonary fibrosis.5 Acute exacerbations of idiopathic pulmonary fibrosis are characterized by the development of diffuse alveolar damage superimposed on underlying usual interstitial pneumonia pattern. Clinically occult aspiration may be a cause of acute exacerbations of idiopathic pulmonary fibrosis as aspiration of gastric contents is a known cause of diffuse alveolar damage.10

Possible Pathogenetic Mechanism for Chronic Microaspiration in Idiopathic Pulmonary Fibrosis

CONCLUSION
The data summarized in this review are provocative and implicate a potential role for microaspiration in the etiology and natural history of idiopathic pulmonary fibrosis. We firmly believe defining the precise relationship between microaspiration and idiopathic pulmonary fibrosis is critically important because of its potential pathobiological and therapeutic implications. In general, current treatment strategies in idiopathic pulmonary fibrosis have focused on modulating the fibrotic tissue response after the injury, not on preventing the injury itself. Microaspiration may represent a source of repetitive injury in idiopathic pulmonary fibrosis and may be modifiable with medical and/or surgical therapy. Perhaps combining treatment of microaspiration with biologic agents targeted at key cellular and biological aspects of inflammation and fibrosis would provide a synergistic approach to preventing further lung injury from microaspiration and controlling disease progression in these patients.
Acknowledgements
The authors wish to thank Simon Kimm for illustrating Figure 1.
Funding: NHLBI HL086516
Footnotes
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
CONFLICT OF INTEREST STATEMENT
This manuscript represents original work and all authors meet the criteria for authorship. Dr. Lee has no conflicts of interest to disclose. Dr. Collard has provided consulting services to Actelion, Amira, InterMune, Gilead Science, Genzyme, CV Therapeutics, Nektar Therapeutics, and Roche, has served on an advisory committee for InterMune, and speaks regularly about idiopathic pulmonary fibrosis. Dr. Raghu has given lectures on the diagnosis and management of interstitial lung diseases, and has discussed the potential role of chronic silent microaspiration in the pathogenesis of idiopathic pulmonary fibrosis. Dr. Sweet has no conflicts of interest to disclose. Dr. Hays has no conflicts of interest to disclose. Dr. Campos has no conflicts of interest to disclose. Dr. Golden has no conflicts of interest to disclose. Dr. King has given lectures on the diagnosis and management of interstitial lung diseases, and has discussed the recent papers that have discussed the potential role of chronic silent microaspiration in the pathogenesis of idiopathic pulmonary fibrosis and as a potential cause of the acute respiratory decompensation manifested by some patients with idiopathic pulmonary fibrosis. In 2007, Dr. King provided expert testimony that a patient’s diffuse parenchymal lung disease (lung fibrosis) was, more likely than not, caused by chronic aspiration.

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