Journal of Chronic Fatigue Syndrome: Volume 12, Issue 1, 2004

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Listing of articles and abstracts published in the Journal of Chronic Fatigue Syndrome, Volume 12, Issue 1, 2004.

Journal of Chronic Fatigue Syndrome[edit | edit source]

Volume 12, Issue 1, 2004[edit | edit source]

  • Editorial by Kenny De Meirleir & Neil McGregor
  • Clinical and Biochemical Characteristics Differentiating Chronic Fatigue Syndrome from Major Depression and Healthy Control Populations: Relation to Dysfunction in the RNase L Pathway (Full Text)
    "Abstract - Patterns of immune dysfunction have emerged in chronic fatigue syndrome (CFS) that include an immune activation state (evidenced by increased activated T lymphocytes and circulating cytokines) and poor cellular function (low natural killer (NK) cell cytotoxicity and impaired T lymphocyte response to mitogens). Therefore, the aim of the current study was to examine the relationship between clinical and functional characteristics, immune abnormalities and status of the RNase L pathway in CFS compared with healthy control and depression control populations. All study participants were assessed with respect to their general health, functional status, blood count and chemistry, biochemical and immune parameters. The CFS group (N = 66) demonstrated clinical, functional and biochemical abnormalities distinct from the healthy (N = 62) and depression (N = 51) control groups. The CFS group showed marked functional impairment compared with both control groups (P <.001) as measured by the Medical Outcomes Study 36-Item Short Form Health Survey (SF-36) (P <.001). The CFS group also showed decreased cognitive performance on a computerized test battery compared to healthy (P <.001) and depression controls (P <.009) and significantly higher 37/80 kDa RNase L ratio (P <.001) compared with both control groups. The odds ratios of a 37/80 kDa RNase L ratio > 2 compared with the CFS patients were 3.9 for the healthy controls (95% confidence limit (CL) 1.0-15.2, P <.05) and 65.8 for the depression controls (95% CL 10.7-406.6, P <.001). The CFS group demonstrated low NK cell cytotoxicity compared to healthy controls (P= .045). The correlation between abnormalities in the RNase L pathway and impaired NK cell function (r = .21, P <.006) suggests that both may be part of the same underlying disease mechanism, at least in this homogeneous population of very disabled CFS patients. Healthy contact-control subjects who had exposure to CFS patients showed a number of characteristics similar to the CFS patients, including an increased mean 37/80 kDa RNase L ratio (P <.04) and prevalence of the 37/80 kDa RNase L ratio > 2 (P <.03). In these contact-control subjects, the 37/80 kDa RNase L ratio was correlated with the interferon-a levels (r = .58, P <.02), suggestive of activation of the interferon pathway. The results of the present study support the cytokine/ immune activation model in this well-characterized CFS patient group."[1]
  • Comparing the Fukuda et al. Criteria and the Canadian Case Definition for Chronic Fatigue Syndrome (Full Text)
    "Abstract - Because the pathogenesis of Chronic Fatigue Syndrome (CFS) has yet to be determined, case definitions have relied on clinical observation in classifying signs and symptoms for diagnosis. The selection of diagnostic signs and symptoms has major implications for which individuals are diagnosed with CFS and how seriously the illness is viewed by health care providers, disability insurers and rehabilitation planners, and patients and their families and friends. Diagnostic criteria also have implications for whether research based on varying definitions can be synthesized. The current investigation examined differences between CFS as defined by Fukuda et al. (1994) and a set of criteria that has been proposed for a clinical Canadian Case definition. There were twenty-three participants who met the Canadian criteria, 12 in the CFS (Fukuda et al. (7) criteria) group and the 33 from the chronic fatigue (CF)-psychiatric group. Dependent measures included: work status, psychiatric comorbidity, symptoms, and functional impairment (measured by the Medical Outcomes Study). People meeting the Fukuda et al. and Canadian criteria were compared with people who had a chronically fatiguing illness explained by a psychiatric condition. Statistical tests used included binomial logistic regression and analysis of variance. The Canadian criteria group, in contrast to the Fukuda et al. criteria group, had more variables that statistically significantly differentiated them from the psychiatric comparison group. Overall, there were 17 symptom differences between the Canadian and CF-psychiatric group, but only 7 symptom differences between the CFS and CF-psychiatric group. The findings suggest that both the Canadian and Fukuda et al. case definitions select individuals who are statistically significantly different from psychiatric controls with chronic fatigue, with the Canadian criteria selecting cases with less psychiatric co-morbidity, more physical functional impairment, and more fatigue/weakness, neuropsychiatric, and neurological symptoms."[2]
  • The Fennell Phase Inventory in a Belgian Sample (Full Text)
    "Abstract: The present study is a follow-up of the research conducted by Jason, Fennell et al. (1995, 1999, 2000) on a multistage theory for chronic fatigue syndrome (CFS). This multistage model is a very promising method for the evaluation of patients suffering from CFS and could facilitate the appropriate selection of various psychosocial therapies that improve the patient’s ability to cope with their illness. Four predictive factors emerged with moderate to excellent reliability. A Spearman’s rank correlation revealed positive correlations between our four-factor model and the three-factor model identified by Jason et al.(1999). A correlation matrix between the dimensional psychological investigation and the Fennell Phases revealed characteristics as suggested by previous research. Biological parameters varied over the different phases suggesting an important interaction between body and psyche."[3]
  • Abnormal Pain Processing in Patients with Fibromyalgia Syndrome
    "Abstract: Fibromyalgia syndrome (FMS) is characterized by widespread pain, fatigue, sleep abnormalities, and distress. Because FMS lacks consistent evidence for tissue abnormalities, recent investigations have focused on central nervous system mechanisms of pain. Abnormal temporal summation of second pain (“windup”) and central sensitization (CS) have recently been described in FMS patients. Windup (WU) and central sensitization, which rely on central pain mechanisms, occur after prolonged C-nociceptor input and depend on activation of nociceptor specific neurons as well as wide dynamic range neurons in the dorsal horn of the spinal cord. The important role of WU is also supported by its ability to predict the clinical pain intensity of FMS patients. Furthermore, brain-imaging techniques that can detect neuronal activation following nociceptive stimuli have provided additional evidence for abnormal central pain mechanisms in FMS. Most importantly, brain images have corroborated the augmented reported pain experience of FMS patients during experimental pain stimuli. These findings may have important implications for future research as well as the treatment of FMS pain."[4]
  • Gulf War Veterans: Evidence for Chromosome Alterations and Their Significance[5]

See also[edit | edit source]

References[edit | edit source]

  1. Suhadolnik, Robert J.; Peterson, Daniel L.; Reichenbach, Nancy L.; Roen, Gail; Metzger, Melodie; McCahan, John; O'brien, Karen; Welsch, Suzanne; Gabriel, Jerome; Gaughan, John P.; McGregor, Neil R. (2004). "Clinical and Biochemical Characteristics Differentiating Chronic Fatigue Syndrome from Major Depression and Healthy Control Populations: Relation to Dysfunction in the RNase L Pathway". Journal of Chronic Fatigue Syndrome. 12 (1): 5–35. doi:10.1300/J092v12n01_02.
  2. Jason, Leonard A.; Torres-Harding, Susan R.; Jurgens, Amber; Helgerson, Jena (2004). "Comparing the Fukuda et al. Criteria and the Canadian Case Definition for Chronic Fatigue Syndrome". Journal of Chronic Fatigue Syndrome. 12 (1): 37–52. doi:10.1300/J092v12n01_03.
  3. Van Hoof, Elke; Coomans, Danny; Cluydts, Raymond; De Meirleir, Kenny (2004). "The Fennell Phase Inventory in a Belgian Sample". Journal of Chronic Fatigue Syndrome. 12 (1): 53–69. doi:10.1300/J092v12n01_04.
  4. Staud, Roland (2004). "Abnormal Pain Processing in Patients with Fibromyalgia Syndrome". Journal of Chronic Fatigue Syndrome. 12 (1): 71–77. doi:10.1300/J092v12n01_05.
  5. Nijs, Jo; Nicolson, Garth L. (2004). "Gulf War Veterans: Evidence for Chromosome Alterations and Their Significance". Journal of Chronic Fatigue Syndrome. 12 (1): 79–83. doi:10.1300/J092v12n01_06.

T cell A type of white blood cell which is mostly produced or matured in the thymus gland (hence T-cell) and is involved in the adaptive immune response on a cellular level. Also known as a T lymphocyte. (Learn more: www.youtube.com)

cytokine any class of immunoregulatory proteins secreted by cells, especially immune cells. Cytokines are small proteins important in cell signaling that modulate the immune system. (Learn more: me-pedia.org)

T cell A type of white blood cell which is mostly produced or matured in the thymus gland (hence T-cell) and is involved in the adaptive immune response on a cellular level. Also known as a T lymphocyte. (Learn more: www.youtube.com)

Short Form 36-Item Health Survey (SF-36) - A 36-item patient-reported questionnaire, used to determine patient health status and quality of life.

chronic fatigue (CF) - Persistent and abnormal fatigue is a symptom, not an illness. It may be caused by depression, multiple sclerosis, fibromyalgia, chronic fatigue syndrome or many other illnesses. The term "chronic fatigue" should never be confused with the disease chronic fatigue syndrome.

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