TGI Friday! Our weekly round-up of recently published abstracts | 20 December 2013

From Psychosomatics, published on 8 December 2013.

Original article

Chronic fatigue in adult survivors of childhood cancer: Associated symptoms, neuroendocrine markers and autonomic cardiovascular responses

Bernward Zeller(a), Ellen Ruud(a), Jon Havard Loge(b.c), Adriani Kanellopoulos(a), Hanne Hamre(b), Kristin Godang(d), Vegard Bruun Wyller(a)
a) Department of Pediatric Medicine, Oslo University Hospital, Oslo, Norway
b) National Resource Center for Late Effects after Cancer Treatment, Department of Oncology Oslo University Hospital, Oslo, Norway
c) Department of Behavioral Sciences in Medicine, University of Oslo, Norway
d) Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Oslo, Norway

Abstract

PURPOSE

Chronic fatigue (CF) is a common late effect after childhoodcancer. Based upon findings among patients with the chronic fatigue syndrome (CFS), this study explored symptoms, neuroendocrine markers and autonomic cardiovascular responses associated with CFS in childhood cancer survivors.

METHODS

Long-term survivors of childhood lymphoma and acute lymphoblastic leukemia reporting CF were compared to survivors without CF. Data included patient-reported outcomes, clinical examination, head-up tilt test (HUT) and neuroendocrine markers in blood and urine.

RESULTS

Of 102 included survivors, 15 were excluded from comparative analyses due to significant comorbidity or pregnancy. Of the remaining 87 participants (median age 33.0 years, follow-up time 25.2 years), 35 had CF and 52 did not have CF. Compared to non-CF controls, CF cases reported significantly (p<.01) higher frequency of symptoms typical of the chronic fatigue syndrome (muscle and/or joint pain, feeling confused/disoriented) and symptoms of autonomic dysfunction (palpitations, feeling intermittently heat and cold, watery diarrhea). CF cases and controls did not differ regarding autonomic cardiovascular responses to orthostatic stress, but the CF group had lower levels of plasma ACTH (p=.002), and higher levels of urine norepinephrine (p=.017). CONCLUSIONS Survivors with CF reported a high symptom-burden compared to controls. There were few differences between the two groups regarding biomarkers, but slight alterations of the hypothalamus-pituitary-adrenal axis and sympathetic nervous activity were detected. CF in cancer survivors has features in common with the chronic fatigue syndrome, but further efforts are required to clarify the pathophysiology.


From Psihologijske Teme, December 2013.

Brief report

Writing about chronic fatigue increases somatic complaints

Marko Jelicic(*), Mincke Frederix, Harald Merckelbach
– Department of Clinical Psychological Science, Faculty of Psychology and Neuroscience, Maastricht University, The Netherlands
* Corresponding author. Marko Jelicic, Department of Clinical Psychological Science, Faculty of Psychology and Neuroscience, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. E-mail: m.jelicic@maastrichtuniversity.nl

Abstract

Participants were instructed to imagine that either they or a friend were suffering from chronic fatigue syndrome (CFS) and were asked to fabricate a story about how CFS affected their own or their friend’s daily functioning. Control participants were not given an imagination exercise but were asked to write about their study choice. After the writing exercise, all participants completed the Symptom Checklist-90 (SCL-90). Participants who had written a story about how CFS symptoms affected daily life (either their own life or that of a friend) had higher scores on the Somatization subscale of the SCL 90 than controls. This finding resembles the misinformation effect documented by memory research, and suggests that elaborative writing about illness, through its symptom-escalating power, has iatrogenic potential.


From International Immunology, published 16 December 2013.

The Role of Adaptive and Innate Immune Cells in Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis

Ekua Weba Brenu(1,2,*), Teilah K. Huth(2), Sharni L. Hardcastle(2), Kirsty Fuller(2), Manprit Kaur(2), Samantha Johnston(2), Sandra B. Ramos(2), Don R. Staines(2,3) and Sonya M. Marshall-Gradisnik(1,2)
1) School of Medical Science, Griffith University, Gold Coast, Australia
2) The National Centre for Neuroimmunology and Emerging Diseases, Griffith Health Institute, Griffith University, Gold Coast, Australia
30 Queensland Health, Gold Coast Public Health Unit, Robina, Australia
↵*Corresponding author: Ekua Brenu Contact email: e.brenu@griffith.edu.au Griffith University, Medical Science, 16 High Street, 16 High Street, Southport, Queensland, Australia, 4215, Phone: +61 7 5678 9282

Abstract

Perturbations in immune processes are a hallmark of a number of autoimmune and inflammatory disorders. Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis (CFS/ME) is an inflammatory disorder with possible autoimmune correlates, characterised by reduced Natural Killer (NK) cell activity, elevations in regulatory T cells (Tregs)and dysregulation in cytokine levels.

The purpose of this paper is to examine innate and adaptive immune cell phenotypes and functional characteristics that have not been previously examined in CFS/ME patients. 30 patients with CFS/ME and 25 non-fatigued controls were recruited for this study. Whole blood samples were collected from all participants for the assessment of cell phenotypes, functional properties, receptors, adhesion molecules, antigens and intracellular proteins using flow cytometric protocols.

The cells investigated included NK cells, dendritic cells (DCs), neutrophils, B cells, T cells, γδT cells and Tregs. Significant changes were observed in B cell subsets, Tregs, CD4+CD73+CD39+ T cells, cytotoxic activity, granzyme B, neutrophil antigens, TNF-α and IFN-γ in the CFS/ME patients in comparison to the non-fatigued controls.

Alterations in B cells, Tregs, NK cells and neutrophils suggest significant impairments in immune regulation in CFS/ME and these may have similarities to a number of autoimmune disorders.


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