Journal of Chronic Fatigue Syndrome: Volume 4, Issue 4, 1998

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history

Titles and abstracts for the Journal of Chronic Fatigue Syndrome, Volume 4, Issue 4, 1998.

Volume 4, Issue 4, 1998[edit | edit source]

  • Editorial, by Nancy Klimas & Roberto Patarca
  • Increased Resting Energy Expenditure in the Chronic Fatigue Syndrome

    Abstract - "It has been suggested that resting energy expenditure may be raised in chronic fatigue syndrome due to an upregulation of transmembrane ion transport. We measured resting energy expenditure by indirect calorimetry in 11 women with chronic fatigue and in 11 healthy women. Total body potassium, by whole body counting, and total body water, extracellular water and intracellular water, by a bioelectrical impedance method, were also measured. When individual resting energy expenditure was predicted on the basis of total body potassium values for the chronic fatigue group, 5 out of 11 of these subjects had resting energy expenditure above the upper limit of normal as defined by the control group data. This is consistent with the hypothesis that there is upregulation of the sodium-potassium pump in chronic fatigue syndrome.[1]

  • Physiopathological Significance of 99mTc HMPAO SPECT Scan Anomalies in Chronic Fatigue Syndrome: A Replication Study

    Abstract - "Regional cerebral blood flow as measured by 99mTc SPECT imaging was compared between chronic fatigue syndrome (CFS) and healthy controls (HC). Larger right(R) > left(L) asymmetry at the parietotemporal level in CFS as compared to HC was observed in accordance with several previous studies. On the contrary, in most regions of interest, hypoperfusion was not confirmed in CFS, and hyperperfusion was demonstrated in several frontal and temporal regions. No significant correlations were found between frontal tracer uptake and R-L parietotemporal asymmetry, on the one hand, and clinically relevant CFS dimensions, on the other."[2]

  • Fatigue Syndromes and the Aetiology of Autoimmune Disease

    Abstract - "In the last decade or so, an impairment of Hypolhalamic-Pituitary-Adrenal (HPA) axis activity has been observed in fatigue syndromes. Elevated levels of glucocorticoids help to prevent the immune system from over-reacting and generating a damaging autoimmune process. The corollary should be that reduced activity of the HPA axis and diminished levels of plasma corlisol could be associated with autoimmune (AI) disease. Experimental work in mice and rats supports this view. Furthermore, plasma levels of cortisol have been found to be low in the early stages of rheumatoid arthritis. There is some clinical evidence that connective tissue disorders (many of which are regarded as autoimmune diseases) occur approximately one year after the onset of prolonged or chronic fatigue, with the implication that fatigue is not merely a symptom of these disorders but precedes them. Many workers have found changes in the immune system of subjects suffering from CFS (mainly immune activation) which could be conducive to the development of AI disease. It has recently been found that there is, in the CFS, some deficiency of another adrenal steroid, namely that of dehydroepiandrosterone. This steroid exerts a regulatory activity on the immune system and a deficiency may well be an additional factor in the genesis of AI disease. If an association can be established between fatigue syndromes and autoimmune disease then these syndromes will need to be addressed in a more concerned manner and prophylactic measures undertaken to forestall AI disease."[3]

  • Immunological and Haematological Parameters in Patients with Chronic Fatigue Syndrome

    Abstract - "Red and white blood cell parameter profiles and poke-weed mitogen responses were investigated in 57 CDC-dcfined CFS patients and 34 age-and sex-matched controls. CFS patients had significantly different red and white blood cell profiles compared with controls. Red cell distribution width (RDW) was the primary regression factor differentiating the groups. RDW was positively associated with mean platelet volume (MPV) in control subjects, but negatively correlated with MPV in CFS patients, indicating a reversal of the functional relationship between these parameters in CFS patients. Hematological parameters, and not the immunological parameters studied, were more important in differentiating CFS patients from healthy control subjects. Female CFS patients had significant increases in RDW and mean platelet volume, and decreases in the numbers of T-helper cells, T-cells and lymphocytes compared with control females. These alterations were not observed in corresponding mate comparisons. There were no differences in the pokeweed mitogen (PWM) response between the CFS and control groups. However, in control subjects, a significant association was observed between pokeweed mitogen responses and Rh(D) antigen status, whereas no similar association was measured in CFS patients. Rh(D)-negative control subjects had a significantly increased mitogen response compared with Rh(D)-positive subjects, whereas in CFS patients, no difference was found. It was concluded that future blood parameter and lymphocyte mitogen response studies in CFS patients should be controlled for sex and Rh status, respectively."[4]

  • Severe CFS/ME of Juvenile Onset— A Report from the CHROME Database

    Abstract - "CHROME has been collecting data since 1995 on very severely disabled patients in the UK with ME, in order to assess aspects of physical and cognitive levels of disability at the onset of the illness and to monitor progress. Results of the first two years data (225 cases) collection are reported.The modal age of onset for this severe group of patients was 11-15, and the proportion increased with more recent years of onset. Patients tended to deteriorate between onset and recruitment in cognitive and functional ability, and in sensory and sleep disturbance. Statistical significance was assessed using McNemar's Test for comparing correlated proportions."[5]

  • Review of Neuroendocrine Disturbances in the Chronic Fatigue Syndrome: Indications for a Role of the Growth Hormone-IGF-1 Axis in the Pathogenesis

    Abstract - "The investigation of the growth hormone (GH)-IGF-J. axis in patients with chronic fatigue syndrome (CFS) may be important for different reasons. Some of the disturbances of the hypothalamic-pituitary-adrenal axis and central serotonincrgic (5-HT) function in CFS will be reviewed, before elaborating on three hypotheses that may explain the role of a disturbed GH axis activity in CFS. Firstly, the disturbed central 5-HT receptor activity may be the cause of GH axis dysfunction. Secondly, CFS may be considered as a “stress-related illness,” in which the disturbed central 5-HT function is a result rather than the cause of impaired neuroendocrine stress responses. Finally, by analogy with fibromyalgia, sleep abnormalities in CFS may impair nocturnal GH secretion. Whether the disturbed GH axis activity is a primary or secondary phenomenon in the pathogenesis of CFS, should be elucidated by future clinical investigations."[6]

  • Letter to the Editor by Wells Goodrich

See also[edit | edit source]

References[edit | edit source]

  1. Walter S. Watson, Donald C. McMillan, Abhijit Chaudhuri & Peter O. Behan. (1998). Increased Resting Energy Expenditure in the Chronic Fatigue Syndrome Journal of Chronic Fatigue Syndrome, Vol. 4, Iss. 4, pp. 3-14 . http://dx.doi.org/10.1300/J092v04n04_02
  2. Benjamin Fischler, Patrick Flamen, Hendrik Everaert, Axel Bossuyt & Kenny De Meirleir. (1998). Physiopathological Significance of 99mTc HMPAO SPECT Scan Anomalies in Chronic Fatigue Syndrome: A Replication Study. Journal of Chronic Fatigue Syndrome, Vol. 4, Iss. 4, pp. 15-30. http://dx.doi.org/10.1300/J092v04n04_03
  3. Benjamin Fischler, Patrick Flamen, Hendrik Everaert, Axel Bossuyt & Kenny De Meirleir. (1998). Physiopathological Significance of 99mTc HMPAO SPECT Scan Anomalies in Chronic Fatigue Syndrome: A Replication Study. Journal of Chronic Fatigue Syndrome, Vol. 4, Iss. 4, pp. 31-49. http://dx.doi.org/10.1300/J092v04n04_04
  4. Timothy K. Roberts, Neil R. McGregor, R. Hugh Dunstan, Mark Donohoe, Raymond N. Murdoch,D. Hope, S. Zhang, Henry L. Butt, Jennifer A. Watkins, and Warren G. Taylor. (1998). Immunological and Haematological Parameters in Patients with Chronic Fatigue Syndrome. Journal of Chronic Fatigue Syndrome, Vol. 4, Iss. 4, pp. 51-65. http://dx.doi.org/10.1300/J092v04n04_05
  5. R. Gibbons, D. F. H. Pheby, C. Richards & F. I. Bray. (1998). Severe CFS/ME of Juvenile Onset— A Report from the CHROME Database.Journal of Chronic Fatigue Syndrome, Vol. 4, Iss. 4, pp. 67-80. http://dx.doi.org/10.1300/J092v04n04_06
  6. Joris Berwaerts, Greta Moorkens & Roger Abs. (1998). Review of Neuroendocrine Disturbances in the Chronic Fatigue Syndrome: Indications for a Role of the Growth Hormone-IGF-1 Axis in the Pathogenesis.Journal of Chronic Fatigue Syndrome, Vol. 4, Iss. 4, pp. 81-91. http://dx.doi.org/10.1300/J092v04n04_07