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NTM/MAC/MAI: We must advocate for ourselves
Throughout the US & its territories, a total of 8580 people are infected with Zika, a virus that is easily prevented and does not harm adults - it can cause birth defects in unborn children of infected people, but that can be prevented. The US is spending hundreds of millions of dollars to search for a vaccine.
In contrast, 1 of every 100,000 people (not including people with HIV) in the US are diagnosed with some form of NTM, most prevalent is MAC/MAI, and that figure is increasing. Under "NTM Facts, A Growing Problem" (https://www.ntmfacts.com/prevalence), here's a few alarming statistics:
"Currently, there are an estimated 86,000 cases of NTM lung infections in the US, and that number continues to grow more than 8% in prevalence every year. (with no requirement to report NTM infections as there is for TB, most researchers believe the number is far higher).
With the rise of NTM infections, data has shown that NTM is now more prevalent than TB in the US...it has been found that incidences of NTM are increasing while TB is decreasing around the US. ...The rates of NTM infection are increasing in patients aged 65 and over, a population
that is expected to double by the year 2030."
The infection went from one considered as opportunistic (effects mostly those who are very compromised, like the HIV infected) to one that has now invaded the general population.
Yet, by all research and medical standards, treatment with first 2, and now 3 (and in some cases 4) extremely powerful antibiotics is grueling (side-effects similar to those experienced with chemotherapy) thus difficult (for some impossible) to sustain as it must be taken 3X/day for at least 1 year, thus its effectiveness as a cure in many patients is spotty; for an increasing number it can only manage the infection, causing them to be on strong antibiotics for the rest of their lives.
In essence, the bug has become more prevalent (and perhaps stronger), and the medical community's response has been minimal research to ID current antibiotics that may work better than others, then increase the number used to treat it rather than find more appropriate treatments designed to kill this particular bacteria. Exacerbating the problem is the medical conundrum that taking these medications orally has a reduced impact on this infection deep in the lungs. Most researchers agree that the best solution is something that can be introduced directly to the lung via aerosol or inhalant.
Over the past 18 years, no significant research beyond that mentioned above has been conducted to find a more effective cure. The only clinical trial conducted over the past 5 years for an inhaled treatment, Amikacin, is generally being tested on those who have already failed traditional treatments, thus not supplanting them.
I believe that patients who endure the impact of this medical vacuum must push for more research, and better treatments, not just more clinically effective, but with far less side-effects. We can start by contacting top research facilities for this condition (U TX, National Jewish, Mayo Clinic, and the NIH, FDA) asking for more research. We can also talk with our physicians about better treatments, asking them to push for more research. Finally, we can continue to search for, and share, information on clinical trials for new NTM treatments, and our ideas for treatments that could work.
If these facilities continue to hear from a great number of people suffering from this insidious infection, it may have the "squeaky wheel" effect. Most assuredly if we remain silent, willing to trudge along with the existing treatments without asking for something better, we are likely to get nothing better.
I believe patients themselves can have a great impact on improving research. But...only if they hear from us.
Thoughts? Ideas?
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thanks for that terrid, i will have a look
I had what most doctor consider the "spit test" .. the 23andme.com genetic test it showed the below. For the heck of it I printed out my report .. showed it to my Mayo Clinic doctor, Dr. Timothy Aksamit .. WOW! He actually asked for a copy of it! Frankly I have ALWAYS felt that nearly ALL mental and physical aspects of diseases will be found to have at least in part a genetic component. I certainly feel that my MAC/MAI did! Here is what my "spit test" reveal BEFORE I was diagnosed .. that I had the gene .. Alpha-1 Antitrypsin Deficiency. By the way .. I never smoked a day in my life!
Alpha-1 Antitrypsin Deficiency The alpha-1 antitrypsin (AAT) protein protects the body, especially fragile lung tissues, from the damaging effects of a powerful enzyme called neutrophil elastase that is released from white blood cells. In AAT deficiency, a genetic mutation reduces levels of the protective protein in the bloodstream. AAT deficiency can lead to chronic obstructive pulmonary disease (COPD), specifically emphysema, and liver disease. Smoking, which can inhibit what little AAT protein an affected person does have, increases the risk of lung disease.
Kay, I am 5'3 .. have always been slim. Was diagnosed in 2007 with MAC .. age 64.. Been on thyroid medication since mid 40's. Hormones after menopause for about 5-6 years.
In 2003 had TERRIBLE pneumonia .. the doctor did NOT culture my sputum (I didn't know better back then to require it) .. so was horribly sick for 3 months .. 5 round of antibiotics and 3 rounds of steroids. I always felt this weakened my lungs .. BUT my Mayo doctor said it did not. He has to be the better judge. They just do NOT know how the mycobacterium gets into our lungs.
Hi there! I have been on a bi-monthly treatment of inhaled tobramycin for two alt months now. it has knocked down my MAC infection to a minimal amount. No more coughing!
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1 ReactionHello! I believe I caught my MAC in a hot tub that was up to par with the chemicals. I remember it smelling kind of funky and was diagnosed two weeks later.
Hi Katherine. I am a carrier for the alfa-1 gene. Are you a carrier as well or are you full blown double gene?
Hello @windwalker, Welcome to our Forum, we are glad you found us! Do you have a first name .. makes it so much more personal! For your question .. I do not have a CLUE if I am a carrier or not .. I really don't know much beyond what I read in the 23andme report which pretty much stated:
Youhave one M and one Z form of the SERPINA1 gene. People of this combination may be at increased risk for liver disease, and may experience decreased lung function if they smoke. Variants detected: PI*Z. AAT deficiency is a genetic disorder that reduces circulating levels of a protein that protects the lungs by trapping it in the liver, where the protein is produced. AAT deficiency can lead to COPD.
Since I have never smoked a day in my life I really just found it interesting that perhaps there definitely was a genetic link to our disease. Question .. were you told there was a genetic link and that you also have that gene? Interesting! Katherine
Yes, I have one of the two genes for Alfa-1 deficiency I am MS I believe. I have low levels of the antitriptin but not considered deficient. I believe they still don't know a whole lot about Alpha-1. Especially why carriers tend to get the diseases of full-blown positives.
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1 ReactionCan I ask what your Alpha alleles are? Are you totally positive for it or a carrier?
My first name is Terri.
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