Our regular Friday feature of summaries from research papers that have not already appeared on the MEA website.
Comment from Dr Charles Shepherd:
The US study relating to iron insufficiency and hypovitaminosis D in adolescents with orthostatic intolerance and the report from University College, London on 4 cases involving the misdiagnosis of ME/CFS in people who actually had Parkinson’s disease are two important contributions to the research literature. Both have practical implications for the clinical assessment and diagnosis of people with ME/CFS.
From the Southern Medical Journal, USA 2011 Aug;104(8):609-11.
Iron insufficiency and hypovitaminosis D in adolescents with chronic fatigue and orthostatic intolerance.
Antiel RM, Caudill JS, Burkhardt BE, Brands CK, Fischer PR.
Department of Pediatric & Adolescent Medicine, Division of General Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, MN 55905, USA. firstname.lastname@example.org
More than 10% of adolescents suffer from severe fatigue and/or orthostatic intolerance. Adult studies show correlations between iron insufficiency and fatigue as well as between hypovitaminosis D and non-specific pain. We sought to determine whether there were correlations between nutritional factors (iron status, and serum vitamin D levels) and chronic ill health.
We reviewed records of 188 adolescents with symptoms of fatigue and/or orthostatic intolerance and who underwent autonomic reflex screening.
Of the 188 patients, 130 patients (69%) had excessive postural tachycardia (PT) with a heart rate (HR) change of ¡Ý30 bpm. 62 patients (47%, n = 131) had iron insufficiency with low iron stores, and 29 patients (22%, n = 131) were iron deficient. HR change did not correlate to ferritin level (P = 0.15). 21 patients (22%, n = 95) had hypovitaminosis D (25-hydroxyvitamin D ¡Ü20 ng/mL). There was a significant association with hypovitaminosis D and orthostatic intolerance (P = 0.024).
In patients presenting with chronic fatigue and/or orthostatic intolerance, low ferritin levels and hypovitaminosis D are common, especially in patients with PT.
From Movement Disorders, 2011 Jun;26(7):1337-40. doi: 10.1002/mds.23563. Epub 2011 Mar 29.
Decades of delayed diagnosis in 4 levodopa-responsive young-onset monogenetic parkinsonism patients.
Ling H, Braschinsky M, Taba P, L¨¹¨¹s SM, Doherty K, Hotter A, Poewe W, Lees AJ.
Reta Lila Weston Institute of Neurological Studies, Institute of Neurology, University College London, London, United Kingdom.
We report 4 patients with young-onset monogenetic parkinsonism, each of whom was misdiagnosed with either a psychogenic movement disorder or chronic fatigue syndrome for 10 to 23 years after the onset of their first symptoms.
Once the diagnosis was eventually made, they all had a rapid and excellent response to levodopa, albeit with the early appearance of interdose dyskinesias in 3.
We discuss possible reasons for the missed diagnosis despite the relentless progression of their motor handicap. DAT scanning supported the revised clinical diagnosis of parkinsonism. © 2011 Movement Disorder Society.
Behavioural and Brain Functions. 2010 Dec 29;6:76.
Plasma neuropeptide Y: a biomarker for symptom severity in chronic fatigue syndrome.
Fletcher MA, Rosenthal M, Antoni M, Ironson G, Zeng XR, Barnes Z, Harvey JM, Hurwitz B, Levis S, Broderick G, Klimas NG.
Department of Medicine, University of Miami Miller School of Medicine, 1600 NW 10th Ave, Miami, FL USA. email@example.com
Chronic fatigue syndrome (CFS) is a complex, multi-symptom illness with a multisystem pathogenesis involving alterations in the nervous, endocrine and immune systems.Abnormalities in stress responses have been identified as potential triggers or mediators of CFS symptoms. This study focused on the stress mediator neuropeptide Y (NPY). We hypothesized that NPY would be a useful biomarker for CFS.
The CFS patients (n = 93) were from the Chronic Fatigue and Related Disorders Clinic at the University of Miami and met the 1994 case definition of Fukuda and colleagues. Healthy sedentary controls (n = 100)) were from NIH or VA funded studies. Another fatiguing, multi-symptom illness, Gulf War Illness (GWI), was also compared to CFS. We measured NPY in plasma using a radioimmunoassay (RIA). Psychometric measures, available for a subset of CFS patients included: Perceived Stress Scale, Profile of Mood States, ATQ Positive & Negative Self-Talk Scores, the COPE, the Beck Depression Inventory, Fatigue Symptom Inventory, Cognitive Capacity Screening Examination, Medical Outcomes Survey Short Form-36, and the Quality of Life Scale.
Plasma NPY was elevated in CFS subjects, compared to controls (p = .000) and to GWI cases (p = .000). Receiver operating characteristics (ROC) curve analyses indicated that the predictive ability of plasma NPY to distinguish CFS patients from healthy controls and from GWI was significantly better than chance alone. In 42 patients with CFS, plasma NPY had significant correlations (<0.05) with perceived stress, depression, anger/hostility, confusion, negative thoughts, positive thoughts, general health, and cognitive status. In each case the correlation (+ or -) was in the anticipated direction. CONCLUSIONS: This study is the first in the CFS literature to report that plasma NPY is elevated compared to healthy controls and to a fatigued comparison group, GWI patients. The significant correlations of NPY with stress, negative mood, general health, depression and cognitive function strongly suggest that this peptide be considered as a biomarker to distinguish subsets of CFS.