Tag: 2001

Chronic fatigue and immune dysfunction syndrome associated with Staphylococcus spp. bacteraemia responsive to thiacetarsamide sodium in eight birds of prey

Abstract:

Chronic fatigue and immune dysfunction syndrome (CFIDS) is a recognized human illness with zoonotic implications that is rarely described in animals. Eight birds of prey examined between 1992 and 1995 and sharing common symptoms (asthenia, inability to fly, poor appetite and emaciation) underwent laboratory tests revealing immunodeficiency, anaemia, high creatine kinase levels and low serum magnesium levels. Diagnosis of CFIDS was based upon these features.

The effectiveness of an arsenic-based medication, thiacetarsamide sodium, administered intravenously for 2-3 days at low dosages (0.1 ml/kg/day) has been demonstrated by checks carried out 10, 20 and 30 days after therapy. The symptoms and the immune and haematological dysfunctions disappeared within 2-4 weeks of treatment. In all patients, micrococcus-like organisms found adhering to the outer surface of many red blood cells, had disappeared at post-treatment controls. Two of five blood cultures were positive for Staphylococcus spp. (S. intermedius and S. xilosus). Consideration is given to the pharmacological activity of an arsenic-based drug in animal illnesses resembling CFIDS.

 

Source: Tarello W. Chronic fatigue and immune dysfunction syndrome associated with Staphylococcus spp. bacteraemia responsive to thiacetarsamide sodium in eight birds of prey.  J Vet Med B Infect Dis Vet Public Health. 2001 May;48(4):267-81. http://www.ncbi.nlm.nih.gov/pubmed/15129582

 

Elevated nitric oxide/peroxynitrite mechanism for the common etiology of multiple chemical sensitivity,chronic fatigue syndrome, and posttraumatic stress disorder

Abstract:

Various types of evidence implicate nitric oxide and an oxidant, possibly peroxynitrite, in MCS and chemical intolerance (CI). The positive feedback loops proposed earlier for CFS may explain the chronic nature of MCS (CI) as well as several of its other reported properties. These observations raise the possibility that this proposed elevated nitric oxide/peroxynitrite mechanism may be the mechanism of a new disease paradigm, answering the question raised by Miller earlier: “Are we on the threshold of a new theory of disease?”

 

Source: Pall ML, Satterlee JD. Elevated nitric oxide/peroxynitrite mechanism for the common etiology of multiple chemical sensitivity,chronic fatigue syndrome, and posttraumatic stress disorder.  Ann N Y Acad Sci. 2001 Mar;933:323-9. http://www.ncbi.nlm.nih.gov/pubmed/12000033

 

Controlled exposures to volatile organic compounds in sensitive groups

Abstract:

Sensitivities to chemicals are characterized by symptoms in multiple organ systems in response to low-level chemical exposures. This paper reviews studies of controlled exposures to odorants and to mixtures of volatile organic compounds. Sensitive subgroups include subjects who met Cullen’s 1987 criteria for multiple chemical sensitivity (MCS), Gulf War veterans with chronic fatigue syndrome and chemical sensitivity (CFS/CS), and subjects with specific self-reported sensitivities to methyl terbutyl ether (MTBE) in gasoline (MTBE-sensitive). All studies include comparison of age- and sex-matched healthy controls.

Studies of olfaction did not support unusual sensitivity, defined as lower odor thresholds, among MCS subjects; however, a dose-response pattern of symptoms was observed in response to suprathreshold concentrations of phenyl ethyl alcohol. In blinded, controlled exposures to clean air, gasoline, gasoline/11% MTBE, and gasoline/15% MTBE, a threshold effect was observed with MTBE-sensitive subjects reporting significantly increased symptoms to gasoline/15% MTBE exposure. Autonomic arousal (heart and respiration rate; end-tidal CO2) in response to odor of chemical mixtures may mediate symptoms for subjects with generalized chemical sensitivities, but not for those whose sensitivities are confined to specific chemicals.

For example, Gulf War veterans with CFS/CS experienced reduced end-tidal CO2 when exposed to diesel fumes, while exposure to MTBE did not produce any psychophysiologic changes in MTBE-sensitive subjects. Controlled olfactory and exposure studies reveal that significant responses can be observed in chemically sensitive subjects even when de-adaptation has not occurred. However, these studies suggest that symptoms are not necessarily accompanied by changes in physiologic arousal. Subject characteristics play a critical role in outcomes.

 

Source: Fiedler N, Kipen HM. Controlled exposures to volatile organic compounds in sensitive groups. Ann N Y Acad Sci. 2001 Mar;933:24-37. http://www.ncbi.nlm.nih.gov/pubmed/12000025

 

Potential mechanisms in chemical intolerance and related conditions

Abstract:

The symptom of chemical intolerance may occur in isolation, but often occurs in conjunction with other chronic symptoms such as pain, fatigue, memory disturbances, etc. This frequent clustering of symptoms in individuals has led to the definition of several chronic multisymptom syndromes, such as multiple chemical sensitivity, fibromyalgia, chronic fatigue syndrome, and Gulf War illnesses. The aggregate research into these syndromes has suggested some unifying mechanisms that contribute to symptomatology. Multiple lines of evidence suggest that there is aberrant function of numerous efferent neural pathways, such as the autonomic nervous system and hypothalamic-pituitary axes, in subsets of individuals with these conditions.

There is perhaps the greatest evidence for abnormal sensory processing in these syndromes, with a low “unpleasantness threshold” for multiple types of sensory stimuli. Psychological and behavioral factors are known to play a significant role in initiating or perpetuating symptoms in some persons with these illnesses. In the field of pain research, the interrelationship between physiologic and psychologic factors in symptom expression has been well studied. Using both established and novel methodologies, studies have suggested that psychologic factors such as hypervigilance and expectancy are playing a relatively minor role in most individuals with fibromyalgia and that clear evidence exists of physiologic amplification of sensory stimuli.

These studies need to be extended to more sensory tasks and to larger numbers of subjects with related conditions. It is of note, though, that existing data on this spectrum of illnesses would suggest that there may be greater psychologic contributions to symptomatology if an illness is defined in part by behavior (e.g., avoidance of chemical exposures) rather than on the basis of symptoms alone.

 

Source: Clauw DJ. Potential mechanisms in chemical intolerance and related conditions.  Ann N Y Acad Sci. 2001 Mar;933:235-53. http://www.ncbi.nlm.nih.gov/pubmed/12000024

 

Mediators of inflammation and their interaction with sleep: relevance for chronic fatigue syndrome and related conditions

Abstract:

In humans, activation of the primary host defense system leads to increased or decreased NREM sleep quality, depending on the degree of early immune activation. Modest elevations of certain inflammatory cytokines are found during experimental sleep loss in humans and, in addition, relatively small elevations of cytokines are seen following commencement of pharmacological treatments with clozapine, a CNS active antipsychotic agent, known to have immunomodulatory properties. Cytokines such as TNF-alpha, its soluble receptors, and IL-6, present in the periphery and the CNS, comprise a link between peripheral immune stimulation and CNS-mediated behaviors and experiences such as sleep, sleepiness, and fatigue. The debilitating fatigue experienced in chronic fatigue syndrome and related diseases may also be related to altered cytokine profiles.

 

Source: Mullington JM, Hinze-Selch D, Pollmächer T. Mediators of inflammation and their interaction with sleep: relevance for chronic fatigue syndrome and related conditions.  Ann N Y Acad Sci. 2001 Mar;933:201-10. http://www.ncbi.nlm.nih.gov/pubmed/12000021

 

Cytokines and chronic fatigue syndrome

Abstract:

Chronic fatigue syndrome (CFS) patients show evidence of immune activation, as demonstrated by increased numbers of activated T lymphocytes, including cytotoxic T cells, as well as elevated levels of circulating cytokines. Nevertheless, immune cell function of CFS patients is poor, with low natural killer cell cytotoxicity (NKCC), poor lymphocyte response to mitogens in culture, and frequent immunoglobulin deficiencies, most often IgG1 and IgG3.

Immune dysfunction in CFS, with predominance of so-called T-helper type 2 and proinflammatory cytokines, can be episodic and associated with either cause or effect of the physiological and psychological function derangement and/or activation of latent viruses or other pathogens. The interplay of these factors can account for the perpetuation of disease with remission/exacerbation cycles. A T-helper type 2 predominance has been seen among Gulf War syndrome patients and this feature may also be present in other related disorders, such as multiple chemical sensitivity. Therapeutic intervention aimed at induction of a more favorable cytokine expression pattern and immune status appears promising.

 

Source: Patarca R. Cytokines and chronic fatigue syndrome.  Ann N Y Acad Sci. 2001 Mar;933:185-200. http://www.ncbi.nlm.nih.gov/pubmed/12000020

 

Brainstem conundrum: the Chiari I malformation

Abstract:

PURPOSE: To describe the Chairi I Malformation in relation to the anatomy of the brain and spinal cord, the common manifestations of the condition, diagnostic considerations, and management for the primary care provider.

DATA SOURCES: Extensive review of the world-wide scientific literature on the condition, supplemented with actual case studies.

CONCLUSIONS: The adult Chairi I Malformation is an insidious congenital brainstem anomaly that consists of caudal displacement of the cerebellar tonsils, brainstem and fourth ventricle into the upper cervical space, resulting in overcrowding of the posterior fossa.

IMPLICATIONS FOR PRACTICE: Due to the vague, and often ambiguous presenting symptoms of Chiari I Malformation, many patients are misdiagnosed with conditions such as multiple sclerosis, fibromyalgia, chronic fatigue syndrome, or psychiatric disorders. Patients frequently experience symptoms months to years prior to accurate diagnosis and often incur irreversible neurologic deficits.

 

Source: Mueller D. Brainstem conundrum: the Chiari I malformation. J Am Acad Nurse Pract. 2001 Apr;13(4):154-9. http://www.ncbi.nlm.nih.gov/pubmed/11930527

 

Dynamics of chronic active herpesvirus-6 infection in patients with chronic fatigue syndrome: data acquisition for computer modeling

Abstract:

Ten adult patients with persistent active HHV-6 variant A infection and clinical chronic fatigue syndrome (CFS) were studied over a period of 24 months after initial clinical diagnosis. CFS was diagnosed according to IIIP-revised CDC-criteria as defined by the CFS Expert Advisory Group to the German Federal Ministry of Health in 1994. Changes in HHV-6 antibody titer, viral DNA load, peripheral blood T lymphocytes and subpopulations, as well as CD4/CD8 cell ratio and cell death (apoptosis) were monitored. Data were collected for comparison with respective changes in acute HHV-6 infection and as a basis for future computer simulation studies.

The results showed variable but slightly elevated numbers of HHV-6 DNA copies in the blood of patients with CFS, while PBL (peripheral blood lymphocyte) apoptosis rates were clearly increased. CD4/CD8 cell ratios varied from below 1 up to values as seen in autoimmune disorders. Contrary to acute HHV-6 infection, T lymphocytes do not exhibit the usual response to HHV-6, that is elevation of mature and immature populations suggesting a certain degree of unresponsiveness.

The data suggest that persistent low-dose stimulation by HHV-6 may favor imbalanced immune response rather than overt immune deficiency. This hypothesis requires confirmation through additional functional studies.

 

Source: Krueger GR, Koch B, Hoffmann A, Rojo J, Brandt ME, Wang G, Buja LM. Dynamics of chronic active herpesvirus-6 infection in patients with chronic fatigue syndrome: data acquisition for computer modeling. In Vivo. 2001 Nov-Dec;15(6):461-5. http://www.ncbi.nlm.nih.gov/pubmed/11887330

 

Defining and managing chronic fatigue syndrome

Abstract:

Objectives: Objectives of this evidence report are to summarize research evidence regarding the case definitions, prevalence, natural history and therapy of chronic fatigue syndrome (CFS).

Search Strategy: English and non-English citations were identified through July 2000 from four electronic bibliographic databases (MEDLINE, The Cochrane Library, PsycINFO, EMBASE), CFS Internet sites, the Journal of Chronic Fatigue Syndrome, references of pertinent articles, textbooks, and experts. The electronic search was updated through October 2000 using PubMed; experts identified relevant citations up to January 2001.

Selection Criteria: Published and unpublished studies that were conducted after 1980 and that involved adults with CFS were reviewed.

Data Collection and Analysis: Two reviewers (physician, psychometrician, research methodologist, and/or nurse) independently abstracted data from the selected studies. Data were synthesized descriptively, emphasizing the quality and methodologic design of studies. Meta-analyses were not done because of marked heterogeneity of study designs.

Main Results: There are four well-recognized case definitions of CFS, and the Centers for Disease Control and Prevention (CDC) is spearheading the development of a fifth. Definitions, developed primarily by expert knowledge and consensus, have evolved over time. A few comparative research studies support the concept of a condition, characterized by prolonged fatigue and impaired ability to function, which is captured by the case definitions. The superiority of one case definition over another is not well established. The validity of any definition is difficult to establish because there are no clear biologic markers for CFS, and no effective treatments specific only to CFS have been identified.

Findings from surveys show that the prevalence of CFS in community populations is probably less than 1% and in primary care populations less than 3%. The reliability of these estimates is limited, because surveys used different case definitions and varied assessment and reporting methods, and sometimes had poor response rates.

Precise estimates of recovery, improvement, and/or relapse from CFS are not possible because there are few natural history studies and those that are available have involved selected referral populations or have used varying case definitions and followup methods.

 

Source: Mulrow CD, Ramirez G, Cornell JE, Allsup K. Defining and managing chronic fatigue syndrome. Evid Rep Technol Assess (Summ). 2001 Sep;(42):1-4. http://www.ncbi.nlm.nih.gov/books/NBK33797/ (Full article)

 

Assessing attitudes toward new names for chronic fatigue syndrome

Abstract:

A questionnaire was distributed at the American Association of Chronic Fatigue Syndrome’s biannual convention in Washington in January 2001 as well as through various Internet Web sites and listserves during early February and March of 2001. The sample consisted of 432 respondents. Most respondents (86%) indicated they wanted a name change, although more patients than scientists were in favor of this change. It was also apparent that the patients and physicians were clearly split between adopting a name such as myalgic encephalopathy versus one such as neuro-endocrine immune disorder. Also, among those respondents who selected either of these two choices for a new name, less than 30% of them supported the other name. Although the majority of respondents feel the name should be changed at this time, this survey suggests there are different stakeholders involved in the name-change process, each with strong and sometimes disparate feelings about changing the name.

 

Source: Jason LA, Eisele H, Taylor RR. Assessing attitudes toward new names for chronic fatigue syndrome. Eval Health Prof. 2001 Dec;24(4):424-35. http://www.ncbi.nlm.nih.gov/pubmed/11817200