Abstract
Hypoxia-inducible factor 1A (HIF 1A) is an oxygen-sensing nuclear transcription factor that regulates oxygen homeostasis in many illnesses ranging from, but not limited to, cancer, heart failure, premature infants to viral infections. We report here the measurement of HIF 1A using transcriptomics as a biomarker in Chronic Inflammatory Response Syndrome (CIRS), a systemic inflammatory and metabolic illness characterized by a multisystem, multi-symptom illness acquired following exposure to the interior environment of water-damaged buildings (WDB).
Pulmonary artery hypertension (PAH) is a well-established disease and is also associated with CIRS, but treatment is problematic, depending on its physiologic basis.
Both CIRS and PAH share a common pathogenesis of proliferative physiology. In the case of CIRS, genomic overexpression of the HIF 1A pathway represents a particularly concerning finding in our study population. Its re-regulation offers a salutary outcome, with the benefit of reducing the phenotypic expression represented by resolving PAH. By first reviewing the diverse pathophysiology of PAH, we present data that provide a basis for the demonstrated efficacy of our treatment protocol, which was used sequentially in CIRS patients to reduce HIF 1A by resolving aberrant mitochondrial transcriptomics associated with proliferative physiology and molecular hypometabolism. These data suggest a basis for a novel approach to treatment of PAH.
We demonstrate reduction of HIF 1A by a CIRS-treatment protocol with VIP therapy in the context of proper biotoxin treatment. Current literature shows that reduction of HIF 1A is crucial in PAH to avoid the significant morbidity and mortality associated with this condition.