Tag: 2005

Acupuncture and Chinese patent drugs for treatment of chronic fatigue syndrome

We have, in recent years, treated 84 cases of chronic fatigue syndrome with acupuncture therapy and Chinese patent drugs and obtained quite good clinical therapeutic effects. A report follows.

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Source: Lijue Z. Acupuncture and Chinese patent drugs for treatment of chronic fatigue syndrome. J Tradit Chin Med. 2005 Jun;25(2):99-101. http://www.journaltcm.com/modules/Journal/contents/stories/052/6.pdf (Full article)

 

The Chronic Fatigue Syndrome Activities and Participation Questionnaire (CFS-APQ): an overview

Abstract:

Chronic fatigue syndrome (CFS) is characterized by severe fatigue and a reduction in activity levels. The purpose of this study was to provide an overview of design, reliability, and validity of the CFS Activities and Participation Questionnaire (CFS-APQ).

The CFS-APQ was constructed based on a retrospective analysis of the Karnofsky Performance Status Questionnaire and the Activities of Daily Living Questionnaire (n = 141). In a reliability study of 34 participants the test-retest reliability coefficient of the CFS-APQ was 0.95. In two different studies, the Cronbach alpha coefficient for internal consistency varied between 0.87 (n = 88) and 0.94 (n = 47). The CFS-APQ was administered to 47 patients who listed 183 activities that had become difficult due to their chronic symptoms, and 157 (85.8%) answers matched the content of the CFS-APQ.

The outcome of a cross-sectional study (n = 88) studying the correlations between the Medical Outcomes Short Form 36 Health Status Survey subscale scores and the CFS-APQ supported the validity of the CFS-APQ. The CFS-APQ scores correlated with a behavioural assessment of the patients’ performance of activities encompassed by the questionnaire (r = 0.29-0.55; n = 63), and correlated with exercise capacity parameters (r = 0.26-0.39; n = 77) obtained during a maximal exercise capacity stress test. Finally, the CFS-APQ correlated with visual analogue scales for pain (r = 0.51) and fatigue (r = 0.50; n = 47).

It is concluded that the CFS-APQ generates reliable and valid data, and can be used as a clinical measure of disease severity in patients with CFS. Future studies should aim at examining the sensitivity of the CFS-APQ.

 

Source: Nijs J, Vaes P, De Meirleir K. The Chronic Fatigue Syndrome Activities and Participation Questionnaire (CFS-APQ): an overview. Occup Ther Int. 2005;12(2):107-21. http://www.ncbi.nlm.nih.gov/pubmed/16136868

 

Chronic fatigue syndrome, exercise, cortisol and lymphadenopathy

Dear Sir,

As in the past [1], the effects of exercise in the treatment of chronic fatigue syndrome (CFS) are conflicting. Indeed, while Powell et al. [2], in 2004, reported that graded exercise was beneficial to CFS patients, Black et al. [3] have lately written that ‘overall mood, muscle pain intensity, and time spent each day with fatigue worsened following increased activity’ [3] in CFS patients, despite the fact that their increase in daily physical activity was rather moderate (28%) [3]. The virtually opposite effects of exercise in different groups of CFS patients [1–3] may reflect their different cortisol levels [1], which, just as occurred some years ago [1], continue to be contradictory. For example, Inder et al. [4], in March 2005, reported that cortisol levels were normal in their patients with CFS, whereas Segal et al. [5], in the same month, reported that their subjects with CFS had hypocortisolism.

Considering that most features of CFS, such as ‘debilitating fatigue, an abrupt onset precipitated by a stressor, feverishness, arthralgias, myalgias, adenopathy, postexertional fatigue, exacerbation of allergic responses, and disturbances in mood and sleep are all characteristic of glucocorticoid insufficiency’ [6], it is not surprising that hypocortisolism has been convincingly shown to be implicated in the pathophysiology of CFS [7]. Therefore, especially the postexertional fatigue caused by glucocorticoid insufficiency [6] strongly suggests that exercise could be of benefit to CFS patients with high [1] or normal cortisol levels [4], whereas it could be harmful to CFS patients with hypocortisolism [1, 5, 6]. Unfortunately, because of the misleading coexistence of quite different diagnostic criteria for CFS [1], it is difficult to predict the patients with CFS who are more likely to have hypocortisolism and which would worsen with exercise. However, it is arguable that the presence or absence of lymphadenopathy [8], which is a sign of hypocortisolism [6, 9] and is one of the 43 clinical features that CFS shares with Addison’s disease [10–12], could reliably discriminate CFS patients who may worsen with exercise from those who may improve with it. Indeed, lymphadenopathy, unlike other symptoms of CFS [11, 12], many of which are non-specific and can also be found in depression and other affective disorders [11, 12], is far from being common in physical diseases and is absent in psychiatric conditions.

You can read the rest of this comment here: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01526.x/full

 

Source: Baschetti R. Chronic fatigue syndrome, exercise, cortisol and lymphadenopathy. J Intern Med. 2005 Sep;258(3):291-2. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01526.x/full (Full article)

 

Prevalence of chronic fatigue and chronic fatigue syndrome in Korea: community-based primary care study

Abstract:

There have been many epidemiological and clinical researches on chronic fatigue (CF) and chronic fatigue syndrome (CFS) since the 1990s, but such studies have been quite limited in Korea. The aim of this study was to investigate the point prevalence of CF and CFS in patients who visited community-based eight primary care clinics in Korea. The study subjects were 1,648 patients aged 18 yr and over who visited one of eight primary care clinics in Korea between the 7th and 17th of May 2001. The physicians determined the status of the subjects through fatigue-related questionnaires, medical history, physical examination, and laboratory tests. The subjects were categorized into no fatigue, prolonged fatigue, CF and then CF were further classified to medically explained CF (Physical CF and Psychological CF) and medically unexplained CF (CFS and idiopathic chronic fatigue). The point prevalence of CF and CFS were 8.4% (95% CI 7.1-9.7%) and 0.6% (95% CI 0.2-1.0%). Medically explained CF was 80.5% of CF, of which 57.1% had psychological causes. The clinical characteristics of CFS were distinguished from explained CF. CF was common but CFS was rare in community-based primary care settings in Korea.

 

Source: Kim CH, Shin HC, Won CW. Prevalence of chronic fatigue and chronic fatigue syndrome in Korea: community-based primary care study. J Korean Med Sci. 2005 Aug;20(4):529-34. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782143/ (Full article)

 

CFSUM1 and CFSUM2 in urine from patients with chronic fatigue syndrome are methodological artefacts

Abstract:

McGregor et al. reported increased levels of an unidentified urinary compound (CFSUM1) in patients with chronic fatigue syndrome (CFS), with reduced excretion of another unidentified compound (CFSUM2), and suggested the possibility of chemical or metabolic ‘markers’ for CFS. The identity of CFSUM1 as reported was erroneous and the identities of these compounds have remained unknown until now.

Urine samples were obtained from 30 patients with ME/CFS, 30 age- and sex-matched healthy controls, 20 control patients with depression and 22 control patients with rheumatoid arthritis. Samples were prepared using the published methods of McGregor et al. to produce heptafluorobutyryl-isobutyl derivatives of urinary metabolites. Alternative preparations utilised isopropyl, n-butyl and trifluoroacetyl derivatives. These were separated and identified using gas chromatography-mass spectrometry.

CFSUM2 was identified as being partially derivatised [isobutyl ester-mono-heptafluorobutyryl (HFB)] serine. CFSUM1 was identified as partially derivatised pyroglutamic acid, being the isobutyl ester without formation of a HFB derivative.

Both CFSUM1 and CFSUM2 are artefacts of the sample preparation procedure and previously reported quantitative abnormalities of CFSUM1 and CFSUM2 in urine from patients with ME/CFS are also artefactual. Pyroglutamic acid may be of primarily dietary origin. The methods used cannot provide reliable qualitative or quantitative data on urinary metabolites. No clinical or biochemical significance can be drawn between these compounds in ME/CFS or any other clinical conditions.

 

Source: Chalmers RA, Jones MG, Goodwin CS, Amjad S. CFSUM1 and CFSUM2 in urine from patients with chronic fatigue syndrome are methodological artefacts. Clin Chim Acta. 2006 Feb;364(1-2):148-58. Epub 2005 Aug 10. http://www.ncbi.nlm.nih.gov/pubmed/16095585

 

The definition of disabling fatigue in children and adolescents

Abstract:

BACKGROUND: Disabling fatigue is the main illness related reason for prolonged absence from school. Although there are accepted criteria for diagnosing chronic fatigue in adults, it remains uncertain as to how best to define disabling fatigue and Chronic Fatigue Syndrome (CFS) in children and adolescents. In this population-based study, the aim was to identify children who had experienced an episode of disabling fatigue and examine the clinical and demographic differences between those individuals who fulfilled a narrow definition of disabling fatigue and those who fulfilled broader definitions of disabling fatigue.

METHODS: Participants (aged 8-17 years) were identified from a population-based twin register. Parent report was used to identify children who had ever experienced a period of disabling fatigue. Standardised telephone interviews were then conducted with the parents of these affected children. Data on clinical and demographic characteristics, including age of onset, gender, days per week affected, hours per day spent resting, absence from school, comorbidity with depression and a global measure of impairment due to the fatigue, were examined. A narrow definition was defined as a minimum of 6 months disabling fatigue plus at least 4 associated symptoms, which is comparable to the operational criteria for CFS in adults. Broader definitions included those with at least 3 months of disabling fatigue and 4 or more of the associated symptoms and those with simply a minimum of 3 months of disabling fatigue. Groups were mutually exclusive.

RESULTS: Questionnaires were returned by 1468 families (65% response rate) and telephone interviews were completed on 99 of the 129 participants (77%) who had experienced fatigue. There were no significant differences in demographic and clinical characteristics or levels of impairment between those who fulfilled the narrower definition and those who fulfilled the broader definitions. The only exception was the reported number of days per week that the child was affected by the fatigue. All groups demonstrated evidence of substantial impairment associated with the fatigue.

CONCLUSION: Children and adolescents who do not fulfil the current narrow definition of CFS but do suffer from disabling fatigue show comparable and substantial impairment. In primary care settings, a broader definition of disabling fatigue would improve the identification of impaired children and adolescents who require support.

 

Source: Fowler T, Duthie P, Thapar A, Farmer A. The definition of disabling fatigue in children and adolescents. BMC Fam Pract. 2005 Aug 9;6:33. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1192794/ (Full article)

 

Oxidative stress levels are raised in chronic fatigue syndrome and are associated with clinical symptoms

Abstract:

The aetiology of chronic fatigue syndrome (CFS) is unknown; however, recent evidence suggests excessive free radical (FR) generation may be involved. This study investigated for the first time levels of 8-iso-prostaglandin-F(2 alpha)-isoprostanes alongside other plasma markers of oxidative stress in CFS patients and control subjects.

Forty-seven patients (18 males, 29 females, mean age 48 [19–63] years) who fulfilled the Centres for Disease Control classification for CFS and 34 healthy volunteers (13 males, 21 females, 46 [19–63] years) were enrolled in the study. The CFS patients were divided into two groups; one group had previously defined cardiovascular (CV) risk factors of obesity and hypertension (group 1) and the second were normotensive and nonobese (group 2). Patients had significantly increased levels of isoprostanes (group 1, P=0.007; group 2, P=0.03, unpaired t test compared to controls) and oxidised low-density lipoproteins (group 2, P=0.02) indicative of a FR attack on lipids. CFS patients also had significantly lower high-density lipoproteins (group 1, P=0.011; group 2, P=0.005).

CFS symptoms correlated with isoprostane levels, but only in group 2 low CV risk CFS patients (isoprostanes correlated with; total symptom score P=0.005; joint pain P=0.002; postexertional malaise P=0.027, Pearson). This is the first time that raised levels of the gold standard measure of in vivo oxidative stress (isoprostanes) and their association with CFS symptoms have been reported.

 

Source: Kennedy G, Spence VA, McLaren M, Hill A, Underwood C, Belch JJ. Oxidative stress levels are raised in chronic fatigue syndrome and are associated with clinical symptoms. Free Radic Biol Med. 2005 Sep 1;39(5):584-9. http://www.ncbi.nlm.nih.gov/pubmed/16085177

 

Effect of psychiatric disorders on outcome of cognitive-behavioural therapy for chronic fatigue syndrome

Abstract:

Psychiatric disorders have been associated with poor outcome in individuals with chronic fatigue syndrome (CFS). This study examines the impact of psychiatric disorders on outcome of cognitive-behavioural therapy (CBT). Psychiatric diagnoses were assessed with a structured psychiatric interview in a CBT trial of 270 people with CFS. Lifetime and current psychiatric disorders were found in 50 and 32% respectively. No significant differences in fatigue severity and functional impairment following treatment were found between participants with and without psychiatric diagnoses.

 

Source: Prins J, Bleijenberg G, Rouweler EK, van der Meer J. Effect of psychiatric disorders on outcome of cognitive-behavioural therapy for chronic fatigue syndrome. Br J Psychiatry. 2005 Aug;187:184-5. http://bjp.rcpsych.org/content/187/2/184.long (Full article)

 

Association of chronic fatigue syndrome with human leucocyte antigen class II alleles

Abstract:

BACKGROUND: A genetic component to the development of chronic fatigue syndrome (CFS) has been proposed, and a possible association between human leucocyte antigen (HLA) class II antigens and chronic fatigue immune dysfunction has been shown in some, but not all, studies.

AIMS: To investigate the role of HLA class II antigens in CFS.

METHODS: Forty nine patients with CFS were genotyped for the HLA-DRB1, HLA-DQA1, and HLA-DQB1 alleles and the frequency of these alleles was compared with a control group comprising 102 normal individuals from the UK. All patients and controls were from the same region of England and, apart from two patients, were white.

RESULTS: Analysis by 2 x 2 contingency tables revealed an increased frequency of HLA-DQA1*01 alleles in patients with CFS (51.0% v 35%; odds ratio (OR), 1.93; p = 0.008). HLA-DQB1*06 was also increased in the patients with CFS (30.2% v 20.0%; OR, 1.73, p = 0.052). Only the association between HLA-DQA1*01 and CFS was significant in logistic regression models containing HLA-DQA1*01 and HLA-DRQB1*06, and this was independent of HLA-DRB1 alleles. There was a decreased expression of HLA-DRB1*11 in CFS, although this association disappeared after correction for multiple comparisons.

CONCLUSIONS: CFS may be associated with HLA-DQA1*01, although a role for other genes in linkage disequilibrium cannot be ruled out.

 

Source: Smith J, Fritz EL, Kerr JR, Cleare AJ, Wessely S, Mattey DL. Association of chronic fatigue syndrome with human leucocyte antigen class II alleles. J Clin Pathol. 2005 Aug;58(8):860-3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770867/ (Full article)

 

 

Gene expression in peripheral blood mononuclear cells from patients with chronic fatigue syndrome

Abstract:

BACKGROUND: Chronic fatigue syndrome (CFS) is a multisystem disease, the pathogenesis of which remains undetermined.

AIMS: To test the hypothesis that there are reproducible abnormalities of gene expression in patients with CFS compared with normal healthy persons.

METHODS: To gain further insight into the pathogenesis of this disease, gene expression was analysed in peripheral blood mononuclear cells from 25 patients with CFS diagnosed according to the Centers for Disease Control criteria and 25 normal blood donors matched for age, sex, and geographical location, using a single colour microarray representing 9522 human genes. After normalisation, average difference values for each gene were compared between test and control groups using a cutoff fold difference of expression > or = 1.5 and a p value of 0.001. Genes showing differential expression were further analysed using Taqman real time polymerase chain reaction (PCR) in fresh samples.

RESULTS: Analysis of microarray data revealed differential expression of 35 genes. Real time PCR confirmed differential expression in the same direction as array results for 16 of these genes, 15 of which were upregulated (ABCD4, PRKCL1, MRPL23, CD2BP2, GSN, NTE, POLR2G, PEX16, EIF2B4, EIF4G1, ANAPC11, PDCD2, KHSRP, BRMS1, and GABARAPL1) and one of which was downregulated (IL-10RA). This profile suggests T cell activation and perturbation of neuronal and mitochondrial function. Upregulation of neuropathy target esterase and eukaryotic translation initiation factor 4G1 may suggest links with organophosphate exposure and virus infection, respectively.

CONCLUSION: These results suggest that patients with CFS have reproducible alterations in gene regulation.

 

Source: Kaushik N, Fear D, Richards SC, McDermott CR, Nuwaysir EF, Kellam P, Harrison TJ, Wilkinson RJ, Tyrrell DA, Holgate ST, Kerr JR. Gene expression in peripheral blood mononuclear cells from patients with chronic fatigue syndrome. J Clin Pathol. 2005 Aug;58(8):826-32. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770875/ (Full article)