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Hypoxaemia in sickle cell disease: biomarker modulation and relevance to pathophysiology.

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Title: Hypoxaemia in sickle cell disease: biomarker modulation and relevance to pathophysiology.
Authors: Setty BNY (AUTHOR), Stuart MJ (AUTHOR), Dampier C (AUTHOR), Brodecki D (AUTHOR), Allen JL (AUTHOR), Setty, B N Yamaja (AUTHOR), Stuart, Marie J (AUTHOR), Dampier, Carlton (AUTHOR), Brodecki, Darcy (AUTHOR), Allen, Julian L (AUTHOR)
Source: Lancet. 11/1/2003, Vol. 362 Issue 9394, p1450-1455. 6p.
Abstract: Background: Nocturnal oxyhaemoglobin desaturation might have a role in CNS complications related to sickle cell disease, and rates of painful crises. We attempted to examine the biological relations, and describe the haematological risk factors for oxyhaemoglobin desaturation. Methods: The study population included children with sickle cell disease and controls. Cellular activation was assessed by measurement of soluble vascular cell adhesion molecule 1, P-selectin, L-selectin, and leukotriene B4. Erythrocyte-endothelial adhesion and routine haematological variables were assessed. Oxygen saturation (SaO2) was measured by pulse oximetry while children were awake and asleep. Children with a mean sleeping SaO2 of < or =93% were identified as hypoxaemic. Children were divided into four groups: controls (ten children), HbSC (nine, all normoxic), HbSS normoxic (13), and HbSS hypoxaemic (15). Findings: Among haematological variables, sleeping SaO2 correlated only with packed-cell volume (r=0.7; p<0.0001). Inverse relations were noted between sleeping SaO2 and adhesion (-0.45; p<0.01), and markers of white-cell (-0.51; p<0.01), platelet (-0.61; p<0.001), and endothelial activation (-0.46; p<0.01). In the HbSS group who had sleeping hypoxaemia, waking SaO2 measurements showed continuing hypoxaemia, with similar correlation between SaO2 and cell activation markers. Interpretation: Our adhesion-related findings suggest a potential mechanism for the increased occurrence of clinical vaso-occlusive crises in individuals with sickle cell disease who have oxyhaemoglobin desaturation. Release of cellular mediators in hypoxaemia, and the relation between anaemia and oxyhaemoglobin desaturation, suggest that risk factors for stroke, including anaemia, might have a role in CNS-vasculopathy through hypoxia-mediated pathways. Further more, hypoxaemia in the older child also occurs during the day; such mild untreated hypoxia could lead to an increased risk of vaso-occlusive episodes. [ABSTRACT FROM AUTHOR]
Copyright of Lancet is the property of Lancet and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Hypoxaemia in sickle cell disease: biomarker modulation and relevance to pathophysiology.
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  Data: &lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Setty+BNY%22&quot;&gt;Setty BNY&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Stuart+MJ%22&quot;&gt;Stuart MJ&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Dampier+C%22&quot;&gt;Dampier C&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Brodecki+D%22&quot;&gt;Brodecki D&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Allen+JL%22&quot;&gt;Allen JL&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Setty%2C+B+N+Yamaja%22&quot;&gt;Setty, B N Yamaja&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Stuart%2C+Marie+J%22&quot;&gt;Stuart, Marie J&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Dampier%2C+Carlton%22&quot;&gt;Dampier, Carlton&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Brodecki%2C+Darcy%22&quot;&gt;Brodecki, Darcy&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Allen%2C+Julian+L%22&quot;&gt;Allen, Julian L&lt;/searchLink&gt; (AUTHOR)
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  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22Lancet%22&quot;&gt;Lancet&lt;/searchLink&gt;. 11/1/2003, Vol. 362 Issue 9394, p1450-1455. 6p.
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: &lt;bold&gt;Background: &lt;/bold&gt;Nocturnal oxyhaemoglobin desaturation might have a role in CNS complications related to sickle cell disease, and rates of painful crises. We attempted to examine the biological relations, and describe the haematological risk factors for oxyhaemoglobin desaturation. &lt;bold&gt;Methods: &lt;/bold&gt;The study population included children with sickle cell disease and controls. Cellular activation was assessed by measurement of soluble vascular cell adhesion molecule 1, P-selectin, L-selectin, and leukotriene B4. Erythrocyte-endothelial adhesion and routine haematological variables were assessed. Oxygen saturation (SaO2) was measured by pulse oximetry while children were awake and asleep. Children with a mean sleeping SaO2 of &lt; or =93% were identified as hypoxaemic. Children were divided into four groups: controls (ten children), HbSC (nine, all normoxic), HbSS normoxic (13), and HbSS hypoxaemic (15). &lt;bold&gt;Findings: &lt;/bold&gt;Among haematological variables, sleeping SaO2 correlated only with packed-cell volume (r=0.7; p&lt;0.0001). Inverse relations were noted between sleeping SaO2 and adhesion (-0.45; p&lt;0.01), and markers of white-cell (-0.51; p&lt;0.01), platelet (-0.61; p&lt;0.001), and endothelial activation (-0.46; p&lt;0.01). In the HbSS group who had sleeping hypoxaemia, waking SaO2 measurements showed continuing hypoxaemia, with similar correlation between SaO2 and cell activation markers. &lt;bold&gt;Interpretation: &lt;/bold&gt;Our adhesion-related findings suggest a potential mechanism for the increased occurrence of clinical vaso-occlusive crises in individuals with sickle cell disease who have oxyhaemoglobin desaturation. Release of cellular mediators in hypoxaemia, and the relation between anaemia and oxyhaemoglobin desaturation, suggest that risk factors for stroke, including anaemia, might have a role in CNS-vasculopathy through hypoxia-mediated pathways. Further more, hypoxaemia in the older child also occurs during the day; such mild untreated hypoxia could lead to an increased risk of vaso-occlusive episodes. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: &lt;i&gt;Copyright of Lancet is the property of Lancet and its content may not be copied or emailed to multiple sites without the copyright holder&#39;s express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
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        Value: 10.1016/s0140-6736(03)14689-2
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              Text: 11/1/2003
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