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Reactive airway disease and mitochondrial myopathy
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Reactive airway disease and mitochondrial myopathy

Hi there.

I've had doctors scratching their heads for years. Normally I have Normal PFT's with a FEV1 of >100% of predicted.... even when I'm having symptoms of wheezing, shortness of breath, with no obstructive pattern.

Only in the last two years have I shown progressive deterioration with lowering NIF (only intermittantly) (to 26 or less at times), lactic acidosis and respiratory failure requring intubation x1 and bipap at night due to respiratory fatigue.

Only recently did someone have an "aha" moment and send me to a dyspnea clinic where I was concurrently diagnosed with Mitochondrial myopathy that is mild.

Are the two of these together playing off eachother? after the CPET test I had a massive acute broncospasm episode requring ICU admission and heliox for 24 hours to break the broncospasm.

Usually I'm not on any meds becuase my methocholine challenge tests are negative (except at 16mg) and my PFT's are usually normal unless i'm acutely ill.

I wonder if it's possible that having both mitochondrial myopathy and reactive airway diseas is causing me to have explosive attacks and if long term bronchdilators/inhaled steroids would really make a difference in this case.Because I seem to have theories on both sides from doctors.

242587_tn?1355427710
I know of no demonstrated association between Mitochondrial Myopathies and Reactive Airways Disease.  In addition, I did a literature search and found no reports of a correlation.  However, I did come across the Abstract that follows.  It documents several physiologic changes that could conceivably have a broncho-constrictive effect on asthmatic airways, these being:  1) a hyperkinetic circulation (exaggerated systemic oxygen delivery relative to oxygen utilization, 2) metabolic acidosis, perhaps related to #1.

A more comprehensive literature search by one conversant with both asthma and mitochondrial myopathy might unearth details in support of a cause and effect association between these two entities.

Good luck

Authors Full NameHeinicke, Katja. Taivassalo, Tanja. Wyrick, Phil. Wood, Helen. Babb, Tony G. Haller, Ronald G.
InstitutionNeuromuscular Center, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, 7232 Greenville Ave., #435, Dallas, TX 75231-5129, USA. ***@****
TitleExertional dyspnea in mitochondrial myopathy: clinical features and physiological mechanisms.
SourceAmerican Journal of Physiology - Regulatory Integrative & Comparative Physiology. 301(4):R873-84, 2011 Oct.
Other IDSource: NLM. PMC3197343 [Available on 10/01/12]

Exertional dyspnea limits exercise in some mitochondrial myopathy (MM) patients, but the clinical features of this syndrome are poorly defined, and its underlying mechanism is unknown. We evaluated ventilation and arterial blood gases during cycle exercise and recovery in five MM patients with exertional dyspnea and genetically defined mitochondrial defects, and in four control subjects (C). Patient ventilation was normal at rest. During exercise, MM patients had low Vo(2peak) (28 +/- 9% of predicted) and exaggerated systemic O(2) delivery relative to O(2) utilization (i.e., a hyperkinetic circulation). High perceived breathing effort in patients was associated with exaggerated ventilation relative to metabolic rate with high VE/VO(2peak), (MM = 104 +/- 18; C = 42 +/- 8, P <= 0.001), and Ve/VCO(2peak)(,) (MM = 54 +/- 9; C = 34 +/- 7, P <= 0.01); a steeper slope of increase in [Greek capital Delta]VE/[Greek capital Delta]VCO(2) (MM = 50.0 +/- 6.9; C = 32.2 +/- 6.6, P <= 0.01); and elevated peak respiratory exchange ratio (RER), (MM = 1.95 +/- 0.31, C = 1.25 +/- 0.03, P <= 0.01). Arterial lactate was higher in MM patients, and evidence for ventilatory compensation to metabolic acidosis included lower Pa(CO(2)) and standard bicarbonate. However, during 5 min of recovery, despite a further fall in arterial pH and lactate elevation, ventilation in MM rapidly normalized. These data indicate that exertional dyspnea in MM is attributable to mitochondrial defects that severely impair muscle oxidative phosphorylation and result in a hyperkinetic circulation in exercise. Exaggerated exercise ventilation is indicated by markedly elevated VE/VO(2), VE/VCO(2), and RER. While lactic acidosis likely contributes to exercise hyperventilation, the fact that ventilation normalizes during recovery from exercise despite increasing metabolic acidosis strongly indicates that additional, exercise-specific mechanisms are responsible for this distinctive pattern of exercise ventilation.

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