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Short Communication - Journal of Pulmonology and Clinical Research (2021) Volume 4, Issue 6
Chronic Rhinosinusitis and Structural Remodeling
CRS places a significant burden on the health care system and significantly alters a CRS patient?s quality of life. Discharge, nasal blockage, loss of smell, migraine, facial pain, and other symptoms of upper-airway inflammation are well recognized; however, the fact that 40% of patients with CRS are clinically depressed. Moreover, the impact of CRS on quality of life and social functioning is greater than that of back pain, chronic heart disease, or even chronic obstructive pulmonary disease (COPD). It is estimated that 31 million Americans suffer from CRS, and the financial costs?both direct (due to medical care) and indirect (for example, due to lost work) are estimated at 22 billion. This does not take into account money spent on overthe-counter therapies or other alternative and complementary remedies that are used in all-too-often failed attempts to gain control over symptoms. The fact that patients rely on such complementary or alternative approaches suggests that our current therapies are not particularly effective. For instance, Newton and colleagues found that 63% of patients had used some form of complementary or alternative therapy (6), and this is likely an underestimate. One such therapy, nasal irrigation, has been around for over a hundred years, and the rationale for this is supported by a recent Cochrane Collaboration review suggesting a possible benefit. Lastly, there are many well-recognized diseases that are associated with CRS, including aspirin-exacerbated respiratory disease (also known as aspirin idiosyncrasy or Samter?s Triad), cystic fibrosis, asthma, and even COPD. CRS is also a known risk factor for asthma, and there is currently a debate as to whether it is a cause or a coexistent phenomenon (according to the united airways disease hypothesis) (8). Smoking is also a wellknown risk factor for CRS, which may explain the connection of CRS to COPD. CRS is frequently divided into two distinct phenotypes: CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP). The latter tends to be associated with asthma and more severe disease expression, whereas CRSsNP is associated with collagen deposition. The immunological mechanisms underlying CRS with and without NPs differ. CRSsNP is thought to be regulated via a TH-1 pathway disorder, with increased expression of that is associated with collagen deposition and has been linked to bacterial infection. Conversely, CRSwNP is considered a TH-2 pathway response with increased levels, and an eosinophil predominance. Careful studies on the molecular pathways of CRS in the literature, however, are relatively sparse.
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