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-   -   Shortness of Breath (https://www.neurotalk.org/peripheral-neuropathy/169275-shortness-breath.html)

Idiopathic PN 06-12-2012 07:52 PM

Quote:

Originally Posted by echoes long ago (Post 888361)
SE= side effects

Oh, thank you!!!

Idiopathic PN 06-12-2012 08:05 PM

Quote:

Originally Posted by echoes long ago (Post 888274)
i dont know why your pulmonary doctor told you your results were normal. anything below 80% of predicted is below normal. Both your fev1 and fev/fvc ratio are significantly below 80%. 59% and 73% respectively. 59 % is moderately obstructed as i wrote before. shortness of breath is a common symptom with this number. an fev1/fvc ratio below 70% is a basis for a diagnosis of chronic obstructive pulmonary disease. you are inching closer to that number, maybe he or she means that you arent there yet for a firm diagnosis of chronic obstructive pulmonary disease but you are definitely not normal and are obstructed.

i have chronic bronchitis and asthma (chronic obstructive pulmonary disease /reactive airway disease) since 2001. i also have numerous nodules on my lungs which i have to keep track of via cat scans to make sure they arent growing.
if you have insurance, i would ask for a prescription for a nebulizer for home for those times you are short of breath. it has saved me from many a scary and uncomfortable experience not to mention trips to the Emergency room.

The doctor saw 2 small scars in one of my lungs. he said it may have been from the ileocecal T.B. i had in 2000. I will have another CT scan when I get the schedule.
Are there certain exercise that we can do to prevent the progression? or supplements or food?

Thank you echoes!

Idiopathic PN 06-12-2012 08:09 PM

Quote:

Originally Posted by mrsD (Post 888291)
For what it is worth.... there are drugs that can lower breathing capacity... that gabapentin for one. Also the family of beta blockers will do it.

Lowered ability to breathe, will lower oxygen to your body, and therefore also your nerves will suffer.

I'd try the inhaler...the doctor probably wants to see if airway inflammation is the the culprit. If it does not help, that tells the doctor something, as well.

Oh, I just remember, when the staff assistant got the oxygen level (the one they clip in your finger), mine was 99. She did not comment, nor I asked if that was normal. I used to be so inquisitive about results and numbers...I dont know...:eek:

zygopetalum 06-12-2012 08:29 PM

I'm sorry, we must have been posting at the same time and I didn't see your question re: SE. Exercise is good because fit muscle uses oxygen more efficiently. I take D3 which is supposed to be good for your lungs. there was some research with probiotics and rats that looked promising but was not replicated or something, I think its good to take them anyhow, it won't hurt and may help in some way they haven't discovered.

99% )2 saturation is normal, they prescribe oxygen if you drop below 88% consistantly but you really want to try to stay at least 92-94% .

judi

echoes long ago 06-12-2012 08:42 PM

if you have trouble doing aerobic exercizes, an incentive spirometer may help you with your shortness of breath. Incentive spirometers are those things they give you in the hospital that you blow into to prevent pneumonia. you can give your lungs a decent workout with it.

http://en.wikipedia.org/wiki/Incentive_spirometer

Idiopathic PN 06-12-2012 10:17 PM

Quote:

Originally Posted by echoes long ago (Post 888377)
if you have trouble doing aerobic exercizes, an incentive spirometer may help you with your shortness of breath. Incentive spirometers are those things they give you in the hospital that you blow into to prevent pneumonia. you can give your lungs a decent workout with it.

http://en.wikipedia.org/wiki/Incentive_spirometer

I can tolerate doing exercises. I walk at least 30mins a day (but just relatively slow walking due to my painful feet), then I rest my feet for a while, then do the stationary bicycle for another 30 minutes. When I do this, I dont gasp for air.

How can you be tested for Alpha-1 Antitripsin?
Thank you.

Idiopathic PN 06-12-2012 10:23 PM

Quote:

Originally Posted by zygopetalum (Post 888374)
I'm sorry, we must have been posting at the same time and I didn't see your question re: SE. Exercise is good because fit muscle uses oxygen more efficiently. I take D3 which is supposed to be good for your lungs. there was some research with probiotics and rats that looked promising but was not replicated or something, I think its good to take them anyhow, it won't hurt and may help in some way they haven't discovered.

99% )2 saturation is normal, they prescribe oxygen if you drop below 88% consistantly but you really want to try to stay at least 92-94% .

judi

I take D3 too at 2000mg - 3x a week. I also take Calcium at 750mg (it has D3 too) at 4x a week for my osteopenia.
I am taking Kefir for the probiotics.
What is your lung condition? I am sorry if I asked you this question already? My memory is becoming really bad - i blame it to Gabapentin (or maybe simply age:D)

Thank you.

echoes long ago 06-13-2012 08:54 AM

From Wikipedia http://en.wikipedia.org/wiki/Alpha_1-antitrypsin

Analysis
As protein electrophoresis is imprecise, A1AT is analysed by isoelectric focusing (IEF) in the pH range 4.5-5.5, where the protein migrates in a gel according to its isoelectric point or charge in a pH gradient.

Normal A1AT is termed M, as it is migrates toward the center of such an IEF gel. Other variants are less functional, and are termed A-L and N-Z, dependent on whether they run proximal or distal to the M band. The presence of deviant bands on IEF can signify the presence of alpha 1-antitrypsin deficiency. Since the number of identified mutations has exceeded the number of letters in the alphabet, subscripts have been added to most recent discoveries in this area, as in the Pittsburgh mutation described above.

As every person has two copies of the A1AT gene, a heterozygote with two different copies of the gene may have two different bands showing on electrofocusing, although heterozygote with one null mutant that abolishes expression of the gene will only show one band.

In blood test results, the IEF results are notated as in PiMM, where Pi stands for protease inhibitor and "MM" is the banding pattern of that patient.

Other detection methods include use of enzyme-linked-immuno-sorbent-assays in vitro and radial immunodiffusion.

Alpha 1-antitrypsin levels in the blood depend on the genotype. Some mutant forms fail to fold properly and are, thus, targeted for destruction in the proteasome, whereas others have a tendency to polymerise, being retained in the endoplasmic reticulum. The serum levels of some of the common genotypes are:

PiMM: 100% (normal)
PiMS: 80% of normal serum level of A1AT
****: 60% of normal serum level of A1AT
PiMZ: 60% of normal serum level of A1AT
PiSZ: 40% of normal serum level of A1AT
PiZZ: 10-15% (severe alpha 1-antitrypsin deficiency)
PiZ is caused by a glutamate to lysine mutation at position 342
PiS is caused by a glutamate to valine mutation at position 288
Other rarer forms have been described; in all there are over 80 variants.



http://en.wikipedia.org/wiki/Isoelectric_focusing

Idiopathic PN 06-13-2012 12:13 PM

Whew, that was a lot to understand! Back in my country I mentioned this to my pulmonologist but she shrugged me off by saying:"you are ASian, you are not predisposed to it". I'm starting to doubt it now. I will mention it again to my new doctor.

Thank you.
Quote:

Originally Posted by echoes long ago (Post 888482)
From Wikipedia http://en.wikipedia.org/wiki/Alpha_1-antitrypsin

Analysis
As protein electrophoresis is imprecise, A1AT is analysed by isoelectric focusing (IEF) in the pH range 4.5-5.5, where the protein migrates in a gel according to its isoelectric point or charge in a pH gradient.

Normal A1AT is termed M, as it is migrates toward the center of such an IEF gel. Other variants are less functional, and are termed A-L and N-Z, dependent on whether they run proximal or distal to the M band. The presence of deviant bands on IEF can signify the presence of alpha 1-antitrypsin deficiency. Since the number of identified mutations has exceeded the number of letters in the alphabet, subscripts have been added to most recent discoveries in this area, as in the Pittsburgh mutation described above.

As every person has two copies of the A1AT gene, a heterozygote with two different copies of the gene may have two different bands showing on electrofocusing, although heterozygote with one null mutant that abolishes expression of the gene will only show one band.

In blood test results, the IEF results are notated as in PiMM, where Pi stands for protease inhibitor and "MM" is the banding pattern of that patient.

Other detection methods include use of enzyme-linked-immuno-sorbent-assays in vitro and radial immunodiffusion.

Alpha 1-antitrypsin levels in the blood depend on the genotype. Some mutant forms fail to fold properly and are, thus, targeted for destruction in the proteasome, whereas others have a tendency to polymerise, being retained in the endoplasmic reticulum. The serum levels of some of the common genotypes are:

PiMM: 100% (normal)
PiMS: 80% of normal serum level of A1AT
****: 60% of normal serum level of A1AT
PiMZ: 60% of normal serum level of A1AT
PiSZ: 40% of normal serum level of A1AT
PiZZ: 10-15% (severe alpha 1-antitrypsin deficiency)
PiZ is caused by a glutamate to lysine mutation at position 342
PiS is caused by a glutamate to valine mutation at position 288
Other rarer forms have been described; in all there are over 80 variants.



http://en.wikipedia.org/wiki/Isoelectric_focusing


mrsD 06-13-2012 01:46 PM

Incidence: Alpha 1-antitrypsin


http://www.ncbi.nlm.nih.gov/pubmed/12426287
Quote:

CONCLUSIONS:

The database presented indicates that in a total population of 4.4 billion in the countries surveyed worldwide, there are at least 116 million carriers (PiMS and PiMZ) and 3.4 million deficiency allele combinations (****, PiSZ, and PiZZ). Furthermore, this database demonstrates that AAT deficiency is found in various populations of African blacks, Arabs and Jews in the Middle East, whites in Australia/New Zealand, Europe, and North America, central Asians, far east Asians, and southeast Asians. These data demonstrate that AAT deficiency is not just a disease of whites in Europe, but that it affects individuals in all racial subgroups worldwide. In addition, AAT deficiency may be one of the most common serious hereditary disorders in the world.


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