EXPOSURE TO THE INTERIOR ENVIRONMENT OF WATER-DAMAGED BUILDINGS CAN ACTIVATE HIF 1A, INDUCE PROLIFERATIVE PHYSIOLOGY AND IMPAIR MITOCHONDRIAL METABOLISM: IMPLICATIONS FOR HYPOXIC PULMONARY HYPERTENSION IN CHRONIC INFLAMMATORY RESPONSE SYNDROME

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 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 well established but treatment is problematic, depending on its physiologic basis. Reduction of HIF 1A by other modalities does not approach the reduction of HIF 1A reported here. As shown by current literature, reduction of HIF 1A is crucial in PAH therapy. The additional problem of proliferative physiology in CIRS and PAH suggests a commonality of pathogenesis, with reduction of HIF 1A providing a salutary response. 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 and to improve molecular hypometabolism, suggesting a basis for a novel approach to treatment of PAH.

Symptom Clusters