Category: Overlapping Illnesses

Fungal spores: hazardous to health?

Abstract:

Fungi have long been known to affect human well being in various ways, including disease of essential crop plants, decay of stored foods with possible concomitant production of mycotoxins, superficial and systemic infection of human tissues, and disease associated with immune stimulation such as hypersensitivity pneumonitis and toxic pneumonitis. The spores of a large number of important fungi are less than 5 microm aerodynamic diameter, and therefore are able to enter the lungs. They also may contain significant amounts of mycotoxins. Diseases associated with inhalation of fungal spores include toxic pneumonitis, hypersensitivity pneumonitis, tremors, chronic fatigue syndrome, kidney failure, and cancer.

 

Source: Sorenson WG. Fungal spores: hazardous to health? Environ Health Perspect. 1999 Jun;107 Suppl 3:469-72. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566211/ (Full article)

 

The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity

Abstract:

The authors compared in a group of 118 patients with autoimmune thyroiditis and a positive antibody titre against ovaries the grade of fatigue with the presence of organ specific and non-specific autoantibodies in the peripheral blood stream, antibodies against EBV and CMV, immunoglobulin concentrations, biochemical parameters of the lipid metabolism, glucose tolerance, ion balance and melatonin and serotonin levels. Patients with autoimmune thyroiditis were differentiated according to the degree of fatigue into three groups: 38 with fatigue typical for CFS, 30 with occasional fatigue and 50 without the feeling of fatigue.

Fatigue of the CFS type was characterized by a significantly higher incidence of autoantibodies against the adrenals and a higher cholesterol level. Increased fatigue of the patients was associated with a lower melatonin level, a higher serotonin level and a lower M/S ratio as compared with patients without fatigue. In other indicators no differences were found. Fatigue in CFS could be associated, similarly as in autoimmune endocrinopathies, with impaired immunoendocrine regulation. In autoimmune thyroiditis, regardless of the concomitant presence of fatigue, in addition to antibodies against thyroid peroxidase most frequently antibodies against the ovaries were detected.

 

Source: Sterzl I, Fucíková T, Hrdá P, Matucha P, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitr Lek. 1998 Aug;44(8):456-60. [Article in Czech] http://www.ncbi.nlm.nih.gov/pubmed/10358448

 

Chronic fatigue syndrome

Comment on: Phosphate diabetes in patients with chronic fatigue syndrome. [Postgrad Med J. 1998]

 

Sir, De Lorenzo and colleagues’ report a previously undefined relationship between chronic fatigue syndrome (CFS) and phosphate diabetes. They also report that mean serum phosphate concentration was found to be significantly lower in CFS patients than in control subjects. They explain their findings by the hypothesis that CFS patients have a metabolic defect that is secondary to their chronic underutilisation of skeletal muscle. Another hypothesis can, however, be proposed.

Hypophosphataemia in sepsis has been recently reported to be associated with high levels of tumour necrosis factor-a and interleukin-6.’ However, these inflammatory cytokines are also produced to excess in both CFS patients 3 and hypocortisolaemic subjects.4 De Lorenzo and colleagues’ findings,’ therefore, may simply reflect the hypocortisolism of CFS patients, 5 which is one of the 20 features that CFS shares with Addison’s disease.5

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2431605/pdf/postmedj00143-0063a.pdf

 

Source: Baschetti R. Chronic fatigue syndrome. Postgrad Med J. 1998 Nov;74(877):701. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2431605/ (Full article)

 

Human herpesviruses in chronic fatigue syndrome

Abstract:

We have conducted a double-blind study to assess the possible involvement of the human herpesviruses (HHVs) HHV6, HHV7, Epstein-Barr virus (EBV), and cytomegalovirus in chronic fatigue syndrome (CFS) patients compared to age-, race-, and gender-matched controls.

The CFS patient population was composed of rigorously screened civilian and Persian Gulf War veterans meeting the Centers for Disease Control and Prevention’s CFS case definition criteria. Healthy control civilian and veteran populations had no evidence of CFS or any other exclusionary medical or psychiatric condition. Patient peripheral blood mononuclear cells were analyzed by PCR for the presence of these HHVs.

Using two-tailed Fisher’s exact test analyses, we were unable to ascertain any statistically significant differences between the CFS patient and control populations in terms of the detection of one or more of these viruses. This observation was upheld when the CFS populations were further stratified with regard to the presence or absence of major axis I psychopathology and patient self-reported gradual versus acute onset of disease. In tandem, we performed serological analyses of serum anti-EBV and anti-HHV6 antibody titers and found no significant differences between the CFS and control patients.

 

Source: Wallace HL 2nd, Natelson B, Gause W, Hay J. Human herpesviruses in chronic fatigue syndrome. Clin Diagn Lab Immunol. 1999 Mar;6(2):216-23. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC95690/ (Full article)

 

Developing case definitions for symptom-based conditions: the problem of specificity

Symptom-based conditions are postulated organic diseases that are characterized primarily by chronic physical (somatic) symptoms (1, 2). Contemporary conditions associated with multisystem complaints are generally referred to as chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivities, silicone associated atypical rheumatic disease, sick building syndrome, and most recently, Gulf War syndrome (table 1). Possibly related disorders that will not be considered in the following analysis include epidemic neuromyasthenia, hyperventilation syndrome, reactive hypoglycemia, post-lyme disease syndrome, and irritable bowel syndrome (3).

Although the need to consistently define symptombased conditions has been repeatedly emphasized, there has been limited progress in establishing widely accepted diagnostic criteria (1,4). Based on reports in English-language publications, symptom-based conditions were analyzed to determine why it has been difficult to develop case definitions of unique diseases.

You can read the rest of this article here: http://epirev.oxfordjournals.org/content/20/2/148.long

 

Source: Hyams KC. Developing case definitions for symptom-based conditions: the problem of specificity. Epidemiol Rev. 1998;20(2):148-56. http://epirev.oxfordjournals.org/content/20/2/148.long (Full article)

Cytokine dysregulation in the post-Q-fever fatigue syndrome

Abstract:

The post-Q-fever fatigue syndrome (QFS) (inappropriate fatigue, myalgia and arthralgia, night sweats, changes in mood and sleep patterns) follows about 20% of laboratory-proven, acute primary Q-fever cases. Cytokine dysregulation resulting from chronic immune stimulation and modulation by persistence of Coxiella burnetii cells or their antigens is hypothesized.

We studied cytokine release patterns of peripheral blood mononuclear cells (PBMC) stimulated with various ligands in short-term culture, from 18 patients with active QFS, and 27 controls: six with resolving QFS, five who had had acute primary Q-fever without subsequent QFS, eight healthy Q-fever vaccinees and eight healthy subjects without Q-fever antibody. Conditioned media (CM) from PBMC stimulated in short-term culture with Q-fever antigens, PHA or measles antigen (as an unrelated antigen) were assayed for IL-2, IL-4, IL-5, IL-6, IL-10 and IFN gamma by AgEIA, and for IL-1 and TNF alpha/beta by bioassay.

Aberrant cytokine release patterns were observed with PBMC from QFS patients when stimulated with Q-fever antigens: an accentuated release of IL-6 which was significantly [p = 0.01, non-parametric one-way analysis of variance (ANOVA)] in excess of medians for all four control groups. With IL-2, the number of responders in the active QFS group was decreased relative to control groups (Fisher’s exact test, p = 0.01) whereas the number of IFN gamma responders was increased (Fisher’s exact test, p = 0.0008). Significant correlations were observed between concentrations of IL-6 in CM, total symptom scores, and scores for other key symptoms.

Comment in: Fatigue syndromes. [QJM. 1999]

 

Source: Penttila IA, Harris RJ, Storm P, Haynes D, Worswick DA, Marmion BP. Cytokine dysregulation in the post-Q-fever fatigue syndrome. QJM. 1998 Aug;91(8):549-60. http://qjmed.oxfordjournals.org/content/91/8/549.long (Full article)

 

The non-specific environmental syndromes MCS (Multiple Chemical Sensitivity), IEI (Idiopathic Environmental Intolerance) and SBS (Sick Building Syndrome)

Abstract:

This review starts with a clinical description of the most common unspecific environmental diseases, such as Multiple Chemical Sensitivities (MCS), Idiopathic Environmental Intolerances (IEI) and Sick Building Syndrome (SBS). These syndromes are very controversial discussed between scientific medicine and “clinical ecology”. In addition, they have fundamental similarities to Chronic Fatigue Syndrome (CFS) and Fibromyalgia. Finally the spectrum of therapeutic approaches is discussed.

 

Source: Csef H. The non-specific environmental syndromes MCS (Multiple Chemical Sensitivity), IEI (Idiopathic Environmental Intolerance) and SBS (Sick Building Syndrome). Fortschr Med. 1998 Nov 30;116(33):18-20, 22, 24. [Article in German] http://www.ncbi.nlm.nih.gov/pubmed/9889460

 

Changes in immune parameters seen in Gulf War veterans but not in civilians with chronic fatigue syndrome

Abstract:

The purpose of this study was to evaluate immune function through the assessment of lymphocyte subpopulations (total T cells, major histocompatibility complex [MHC] I- and II-restricted T cells, B cells, NK cells, MHC II-restricted T-cell-derived naive and memory cells, and several MHC I-restricted T-cell activation markers) and the measurement of cytokine gene expression (interleukin 2 [IL-2], IL-4, IL-6, IL-10, IL-12, gamma interferon [IFN-gamma], and tumor necrosis factor alpha [TNF-alpha]) from peripheral blood lymphocytes.

Subjects included two groups of patients meeting published case definitions for chronic fatigue syndrome (CFS)-a group of veterans who developed their illness following their return home from participating in the Gulf War and a group of nonveterans who developed the illness sporadically. Case control comparison groups were comprised of healthy Gulf War veterans and nonveterans, respectively.

We found no significant difference for any of the immune variables in the nonveteran population. In contrast, veterans with CFS had significantly more total T cells and MHC II+ T cells and a significantly higher percentage of these lymphocyte subpopulations, as well as a significantly lower percentage of NK cells, than the respective controls.

In addition, veterans with CFS had significantly higher levels of IL-2, IL-10, IFN-gamma, and TNF-alpha than the controls. These data do not support the hypothesis of immune dysfunction in the genesis of CFS for sporadic cases of CFS but do suggest that service in the Persian Gulf is associated with an altered immune status in veterans who returned with severe fatiguing illness.

 

Source: Zhang Q, Zhou XD, Denny T, Ottenweller JE, Lange G, LaManca JJ, Lavietes MH, Pollet C, Gause WC, Natelson BH. Changes in immune parameters seen in Gulf War veterans but not in civilians with chronic fatigue syndrome. Clin Diagn Lab Immunol. 1999 Jan;6(1):6-13. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC95652/ (Full article)

 

Medical evaluation of Persian Gulf veterans with fatigue and/or chemical sensitivity

Abstract:

The purpose of this study was to determine if Gulf War veterans with complaints of severe fatigue and/or chemical sensitivity (n = 72) fulfill case definitions for chronic fatigue syndrome (CFS) and/or multiple chemical sensitivity (MCS) and to compare the characteristics of those veterans who received a diagnosis of CFS (n = 24) to a group of non-veterans diagnosed with CFS (n = 95).

Thirty-three veterans received a diagnosis of CFS with 14 having MCS concurrently; an additional six had MCS but did not fulfill a case definition for CFS. The group of fatigued veterans receiving a diagnosis of CFS was comprised of significantly fewer women and fewer Caucasians than the civilian group, and significantly fewer veterans reported a sudden onset to their illness.

Veterans with CFS had a milder form of the illness than their civilian counterparts based on medical examiner assessment of the severity of the symptoms, reported days of reduced activity, and ability to work. Since CFS in veterans seems less severe than that seen in civilians, the prognosis for recovery of veterans with this disorder may be better.

 

Source: Pollet C, Natelson BH, Lange G, Tiersky L, DeLuca J, Policastro T, Desai P, Ottenweller JE, Korn L, Fiedler N, Kipen H. Medical evaluation of Persian Gulf veterans with fatigue and/or chemical sensitivity. J Med. 1998;29(3-4):101-13. http://www.ncbi.nlm.nih.gov/pubmed/9865452

 

Autonomic neuropathies

Abstract:

A limited autonomic neuropathy may underlie some unusual clinical syndromes, including the postural tachycardia syndrome, pseudo-obstruction syndrome, heat intolerance, and perhaps chronic fatigue syndrome. Antibodies to autonomic structures are common in diabetes, but their specificity is unknown. The presence of autonomic failure worsens prognosis in the diabetic state. Some autonomic neuropathies are treatable. Familial amyloid polyneuropathy may respond to liver transplantation. There are anecdotal reports of acute panautonomic neuropathy responding to intravenous gamma globulin. Orthostatic hypotension may respond to erythropoietin or midodrine.

 

Source: Low PA. Autonomic neuropathies. Curr Opin Neurol. 1998 Oct;11(5):531-7. http://www.ncbi.nlm.nih.gov/pubmed/9848003