Objective: To evaluate the biochemical and vascular aspects of pediatric chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME).
Design Cross-sectional clinical study.
Setting: Tayside, Scotland, United Kingdom.
Participants: Twenty-five children with CFS/ME and 23 healthy children recruited from throughout the United Kingdom.
Interventions: Participants underwent a full clinical examination to establish a diagnosis of CFS/ME and were asked to describe and score their CFS/ME symptoms. Biochemical markers were measured. Arterial wave reflection was estimated to assess systemic arterial stiffness.
Main Outcome Measures: Markers of oxidative stress and free radicals, C-reactive protein level, white blood cell apoptosis, and arterial wave reflection.
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Children with CFS/ME had:
• Increased oxidative stress compared with control individuals (isoprostanes: 252.30 vs 215.60 pg/mL, P = .007; vitamin C, mean [SD]: 0.84 [0.26] vs 1.15 [0.28] mg/dL, P < .001; vitamin E, 8.72 [2.39] vs 10.94 [3.46] µg/mL, P = .01)
• And increased white blood cell apoptosis (neutrophils: 53.7% vs 35.7%, P = .005; lymphocytes: 40.1% vs 24.6%, P = .009).
Arterial stiffness variables did not differ significantly between groups (mean augmentation index, –0.57% vs –0.47%, P = .09);
However, the derived variables significantly correlated with total (r = 0.543, P = .02) and low-density lipoprotein (r = 0.631, P = .004) cholesterol in patients with CFS/ME but not in controls.
Conclusions: Biomedical anomalies seen in adults with CFS/ME – increased oxidative stress and increased white blood cell apoptosis [increased programmed death rate, associated with infection] – can also be observed in children with clinically diagnosed CFS/ME compared with matched controls.
Unlike in their adult counterparts, however, arterial stiffness remained within the reference range in these pediatric patients.
Source: Archives of Pediatric Adoescent Medicine, Sep 2010;164(9):817-823. doi:10.1001/archpediatrics.2010.157, by Kennedy g, Khan F, Hill A, Underwood C, Belch JJF. Author affiliations: Vascular and Inflammatory Diseases Research Unit, The Institute of Cardiovascular Research, Centre for Cardiovascular and Lung Biology, Division of Medical Sciences, Ninewells Hospital and Medical School, Dundee, Scotland, United Kingdom. [Email: firstname.lastname@example.org]