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Journal Article 2007; 28(6): 832-840 PubMed PMID: 18063922 Citation  Keywords:  Autonomic Nervous System:physiopathology, Cardiovascular Diseases:complications, Depressive Disorder:complications, Humans, Hypothalamo-Hypophyseal System:physiopathology, Inflammation:complications, Pituitary-Adrenal System:physiopathology, Psychology,.   

: Depressive disorders and cardiovascular disease are inter-connected by a whole range of pathophysiological mechanisms. Three biological mechanisms are fundamental: activation of the hypothalamus-hypohysis-adrenal axis with a subsequent increase in sympathetic-adrenal system activity, decrease in vagal tone with a decrease in heart rate variability, and alterations of thrombogenesis with increased platelet aggregability. Behavioural mechanisms and psycho-social factors are also integral to this common pathophysiology. Recently, research has focused mainly on studying various forms of stress, as well as changes and possibilities of influencing the autonomous vegetative system. Temporal aspects of the incidence and development of depressive episodes in relation to cardiovascular disease and subsequent cardiovascular morbidity and mortality are being studied, as well as general mortality risk factors. These findings are important for clinical practice. It is evident that in patients with untreated depressive disorder, the risk of developing cardiovascular disease is significantly higher than in patients suffering from a depressive disorder being treated with anti-depressants. From the data published so far, it may be surmised that depressive disorders in patients with cardiovascular disease may be reliably and safely treated with anti-depressants that act as inhibitors of serotonin re-uptake....

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Journal Article 2007; 28(Suppl 4): 10-11 PubMed PMID: 18030255 Citation  Keywords:  Adult, Aged, Alcohol Drinking:epidemiology, Beer, Biomarkers:blood, Cross-Sectional Studies, Europe:epidemiology, Female, Humans, Inflammation:blood, Male, Middle Aged, Wine,.   

: Anti-inflammatory effects of moderate alcohol consumption have been proposed to explain why moderate alcohol intake lowers coronary heart disease risk. The relationship between overall alcohol, beer or wine consumption and markers of systemic inflammation in three different geographical areas in Europe, was investigated....

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Journal Article 2007; 28(4): 456-462 PubMed PMID: 17693979 Citation  Keywords:  Adult, Case-Control Studies, Cell Nucleus:physiology, Fatigue Syndrome, Chronic:metabolism, Female, Humans, Inflammation:metabolism, Lymphocytes:drug effects, Male, Middle Aged, NF-kappa B:metabolism, Neurasthenia:physiopathology, Oxidative Stress:physiol.   

: There is now some evidence that chronic fatigue syndrome is accompanied by an activation of the inflammatory response system and by increased oxidative and nitrosative stress. Nuclear factor kappa beta (NFkappabeta) is the major upstream, intracellular mechanism which regulates inflammatory and oxidative stress mediators. In order to examine the role of NFkappabeta in the pathophysiology of CFS, this study examines the production of NFkappabeta p50 in unstimulated, 10 ng/mL TNF-alpha (tumor necrosis factor alpha) and 50 ng/mL PMA (phorbolmyristate acetate) stimulated peripheral blood lymphocytes of 18 unmedicated patients with CFS and 18 age-sex matched controls. The unstimulated (F=19.4, df=1/34, p=0.0002), TNF-alpha-(F=14.0, df=1/34, p=0.0009) and PMA-(F=7.9, df=1/34, p=0.008) stimulated production of NFkappabeta were significantly higher in CFS patients than in controls. There were significant and positive correlations between the production of NFkappabeta and the severity of illness as measured with the FibroFatigue scale and with symptoms, such as aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection. The results show that an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiology of CFS and that previous findings on increased oxidative stress and inflammation in CFS may be attributed to an increased production of NFkappabeta. The results suggest that the symptoms of CFS, such as fatigue, muscular tension, depressive symptoms and the feeling of infection reflect a genuine inflammatory response in those patients. It is suggested that CFS patients should be treated with antioxidants, which inhibit the production of NFkappabeta, such as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3 fatty acids....

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Journal Article 2007; 28(4): 463-469 PubMed PMID: 17693978 Citation  Keywords:  Adult, Case-Control Studies, Cyclooxygenase 2:metabolism, Depression:physiopathology, Fatigue:physiopathology, Fatigue Syndrome, Chronic:enzymology, Female, Humans, Inflammation:metabolism, Lymphocytes:metabolism, Male, Middle Aged, NF-kappa B:metabolism,.   

: Chronic fatigue syndrome (CFS) is a medically unexplained disorder, characterized by profound fatigue, infectious, rheumatological and neuropsychiatric symptoms. There is, however, some evidence that CFS is accompanied by signs of increased oxidative stress and inflammation in the peripheral blood. This paper examines the role of the inducible enzymes cyclo-oxygenase (COX-2) and inducible NO synthase (iNOS) in the pathophysiology of CFS. Toward this end we examined the production of COX-2 and iNOS by peripheral blood lymphocytes (PBMC) in 18 CFS patients and 18 normal volunteers and examined the relationships between those inflammatory markers and the severity of illness as measured by means of the FibroFatigue scale and the production of the transcription factor nuclear factor kappa beta (NFkappabeta). We found that the production of COX-2 and iNOS was significantly higher in CFS patients than in normal controls. There were significant and positive intercorrelations between COX-2, iNOS and NFkappabeta and between COX-2 and iNOS, on the one hand, and the severity of illness, on the other. The production of COX-2 and iNOS by PBMCs was significantly related to aches and pain, muscular tension, fatigue, concentration difficulties, failing memory, sadness and a subjective experience of infection. The results suggest that a) an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiology of CFS; b) the inflammatory response in CFS is driven by the transcription factor NFkappabeta; c) symptoms, such as fatigue, pain, cognitive defects and the subjective feeling of infection, indicates the presence of a genuine inflammatory response in CFS patients; and d) CFS patients may be treated with substances that inhibit the production of COX-2 and iNOS....

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Comparative Study 2007; 28(2): 166-169 PubMed PMID: 17435668 Citation  Keywords:  Adiponectin:blood, Animals, Inflammation:chemically induced, Injections, Intraperitoneal, Lipopolysaccharides, Male, Pituitary Adenylate Cyclase-Activating Polypeptide:administration & dosage, Rats, Rats, Inbred WKY,.   

BACKGROUND: Pituitary adenylate cyclase activating peptide (PACAP 38) is a neuropeptide with anti-inflammatory activity. Vasoactive intestinal peptide (VIP)/PACAP receptors are found in immune cells, endocrine glands and also in adipose tissue. Adiponectin is an adipocyte-derived protein hormone which possesses anti-inflammatory, antidiabetic and antiatherogenic properties. The aim of this study was to examine the influence of PACAP 38 on adiponectin release in basal conditions and during lipopolysaccharide (LPS)-induced acute inflammation.

METHODS: Male Wistar-Kyoto rats were divided into four groups which received intraperitoneal injections of 0.9% NaCl, LPS, PACAP 38 or LPS+PACAP 38, respectively. Serum adiponectin concentrations were measured using an ELISA test.

RESULTS: LPS administration did not change adiponectin concentration; however, PACAP 38 administered alone decreased serum adiponectin concentration after 2 h (p<0.05) and 4 h (p<0.01). In the group that received LPS+PACAP38, compared with LPS alone, no difference in adiponectin concentration was observed.

CONCLUSIONS: We conclude that PACAP 38 may directly modulate adiponectin secretion by adipocytes in basal conditions....

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Journal Article 2006; 27(Suppl 1): 7-16 PubMed PMID: 17261999 Citation  Keywords:  Biomarkers:blood, Dental Amalgam:toxicity, Environmental Pollutants:toxicity, Humans, Hypersensitivity:diagnosis, Inflammation, Lymphocyte Activation, Metals:toxicity, T-Lymphocytes:immunology, Titanium:toxicity,.   

: Environmental factors are recognized as a cause of the increasing frequency of allergic and autoimmune diseases. In addition to external pollutants, metal ions released from dental restorations or from other body implants might trigger inflammation in susceptible subjects. In humans, genes governing metal-induced inflammation and autoimmunity are not yet known. In clinical praxis, metal-sensitive patients will present various symptoms ranging from oral mucosal changes and skin disease to excessive fatigue and autoimmune diseases. Since genetic markers of genetic susceptibility in man are not known, one has to rely on the phenototypic markers. Such biomarkers might be certain detoxification enzymes but also the presence of metal-specific memory cells in the blood. With the increasing use of metal implants in medicine and dentistry, it is important to have a proper tool for the diagnosis of metal allergy in susceptible subjects. After nickel, gold is now the second most common sensitizer. In addition to patch test, an in vitro blood test, an optimized commercially available lymphocyte transformation test (MELISA) is discussed. Both tests were used for the diagnosis of metal allergy in a selected group of 15 patients who suffered from clinical metal sensitivity in addition to other health problems. The concordance of the two tests was good but MELISA detected more metal allergies than patch test. The removal of incompatible dental material (RID) resulted in long-term health improvement in the majority of patients. We postulate that in vivo, metal ions activate T-cells, initiating systemic inflammation, which, through cytokines, affects the brain and hypothalamus-pituitary-adrenal axis. We postulate that in vivo metal ions will activate T-cells starting systemic inflammation which, through cytokines affect the brain and hypothalamus-pituitary-adrenal (HPA) axis. The treatment and rehabilitation of metal sensitive patients is based on a firm understanding and recognition of individual susceptibility. RID has to be done done with extreme caution and according to standard working protocol. If performed properly, this treatment can result in decreased systemic inflammation and improved health in sensitized patients....

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Introductory Journal Article 2006; 27(Suppl 1): 5-6 PubMed PMID: 17261995 Citation  Keywords:  Dental Amalgam:adverse effects, Humans, Hypersensitivity, Immune System:drug effects, Inflammation, Metals:adverse effects, Neurosecretory Systems:drug effects,.   

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Journal Article 2006; 27(4): 453-458 PubMed PMID: 16892000 Citation  Keywords:  Adolescent, Biomarkers:blood, Blood Glucose, C-Reactive Protein:metabolism, Child, Child, Preschool, Cholesterol, HDL:blood, Cholesterol, LDL:blood, Diabetes Mellitus, Type 2:epidemiology, Female, Fibrinogen:metabolism, Humans, Inflammation:epidemiology, .   

BACKGROUND: There is growing evidence that low-grade systemic inflammation is closely involved in the pathogenesis of type 2 diabetes.

OBJECTIVE: The aim of this study was to investigate the relationship between serum inflammatory markers and selected parameters known as risk factors of type 2 diabetes in obese children and adolescents.

SUBJECTS AND METHODS: Fasting levels of C-reactive protein (CRP), fibrinogen (FB) interleukin-6 (IL-6), interleukin 1-beta (IL-1beta), glucose, insulin, total, HDL and LDL cholesterol, triglycerides, white blood cell count (WBC) and fasting glucose to insulin ratio (FGIR) were measured in 281 obese children and adolescents. Pearson's correlation was used for assessing the relationship between inflammatory markers and selected clinical parameters.

RESULTS: Inflammatory markers correlated significantly with insulin resistance indices, HbA1c, lipid profile, hypertension, positive family history of type 2 diabetes, low physical fitness, and mixed high-fat and high-carbohydrate diet.

CONCLUSIONS: Serum inflammatory markers were significantly correlated with most factors implicated in the development of type 2 diabetes. These data provide additional support for previously reported in adults relationship between subclinical inflammation and the risk of type 2 diabetes....

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