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Author Notes:

Manisha Newaskar: mnewaskar@mail.cho.org

Subjects:

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Environmental Sciences
  • Multidisciplinary Sciences
  • Environmental Sciences & Ecology
  • Science & Technology - Other Topics
  • sickle cell disease
  • asthma
  • obstructive lung disease
  • airway hyper-reactivity
  • proinflammatory state
  • arginase
  • nitric oxide
  • arginine metabolome
  • asthma therapy
  • ACUTE-CHEST-SYNDROME
  • EXHALED NITRIC-OXIDE
  • LOWER AIRWAY-OBSTRUCTION
  • PULMONARY-HYPERTENSION
  • METHACHOLINE CHALLENGE
  • ARGINASE ACTIVITY
  • VASOOCCLUSIVE CRISIS
  • PHOSPHOLIPASE A(2)
  • CHILDHOOD ASTHMA
  • LUNG-FUNCTION

Asthma in Sickle Cell Disease

Tools:

Journal Title:

Scientific World Journal

Volume:

Volume 11

Publisher:

, Pages 1138-1152

Type of Work:

Article | Final Publisher PDF

Abstract:

In recent years, evidence has increased that asthma predisposes to complications of sickle cell disease (SCD), such as pain crises, acute chest syndrome, pulmonary hypertension, and stroke, and is associated with increased mortality. An obstructive pattern of pulmonary function, along with a higher-than-expected prevalence of airway hyper-responsiveness (AHR) when compared to the general population, has led some researchers to suspect that underlying hemolysis may contribute to the development of a pulmonary disease similar to asthma in patients with SCD. While the pathophysiologic mechanism in atopic asthma involves up-regulation of Th2 cytokines, mast cell- and eosinophil-driven inflammation, plus increased activity of inducible nitric oxide synthase (iNOS) and arginase in airway epithelium resulting in obstructive changes and AHR, the exact mechanisms of AHR, obstructive and restrictive lung disease in SCD is unclear. It is known that SCD is associated with a proinflammatory state and an enhanced inflammatory response is seen during vaso-occlusive events (VOE). Hemolysis-driven acute-on-chronic inflammation and dysregulated arginine-nitric oxide metabolism are potential mechanisms by which pulmonary dysfunction could occur in patients with SCD. In patients with a genetic predisposition of atopic asthma, these changes are probably more severe and result in increased susceptibility to sickle cell complications. Early recognition and aggressive management of asthma based on established National Institutes of Health asthma guidelines is recommended in order to minimize morbidity and mortality.

Copyright information:

©2011 with author. Published by TheScientificWorld.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 3.0 Unported License (http://creativecommons.org/licenses/by/3.0/).

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