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Biomedical subjects

R von Känel

Publications and source records attributed to R von Känel.

16 recordsLinked to original sources
PubMed2006

Responsiveness and habituation of soluble ICAM-1 to acute psychosocial stress in men: determinants and effect of stress-hemoconcentration.

We studied the psychophysiology of soluble intercellular adhesion molecule-1 (sICAM-1) in 25 apparently healthy middle-aged men who underwent an acute psychosocial stressor three times with one week apart. Measures of the biological stress response were obtained at week one and three. The magnitude of the sICAM-1 stress response showed no habituation between individual visits. At week one, cognitive stress appraisal independently predicted integrated sICAM-1 area under the curve (AUC) between rest, immediately post-stress, and 45 min and 105 min post-stress (beta=0.67, p=0.012, deltaR(2)=0.41). Diastolic blood pressure AUC (beta=-0.45, p=0.048, deltaR(2)=0.21) and heart rate AUC (beta=0.44, p=0.055, deltaR(2)=0.21) were independent predictors of sICAM-1 AUC at week three. Adjustment for hemoconcentration yielded a decrease in sICAM-1 levels from rest to post-stress (p<0.001). Stress responsiveness of plasma sICAM-1 was predicted by stress perception and hemodynamic reactivity and affected by stress-hemoconcentration but unrelated to cortisol reactivity and not readily adapting to repeated stress.

Acute Disease↗
PubMed2006

[Psychosomatic medicine in primary care].

Patients commonly visit their primary care physician (PCP) because of body symptoms. However, neither the PCP nor his patient can tell immediately whether or not psychosocial factors play a role in the disease manifestation. If this is the case, only a patient-centred approach and basic knowledge in biopsychosocial skills will help the PCP to diagnose and treat his patient appropriately. This article gives a comprehensive overview on how the PCP can approach patients with psychosomatic diseases (i.e. somatic symptoms exacerbated by psychosocial factors, medically unexplained symptoms, functional somatic syndromes, somatic manifestation of psychiatric diseases). Adopting this approach will allow the PCP to be challenged but not overburdened by, on an average, 30-50% of his patients presenting with psychosomatic symptoms.

Humans↗
PubMed2004

Platelet hyperactivity in clinical depression and the beneficial effect of antidepressant drug treatment: how strong is the evidence?

OBJECTIVE: Platelet hyperactivity is thought to contribute to the increased coronary artery disease (CAD) risk in depression. This study reviewed the evidence for hyperactive platelets and for effects of antidepressant drug treatment on platelet 'stickiness' in clinical depression. METHOD: By means of PubMed electronic library search, 34 studies in English were identified (1983-2003) and critically reviewed. RESULTS: In depression, flow cytometry studies allowing detection of subtle platelet activation states consistently found at least one platelet activation marker to be increased, while the bulk of platelet aggregation studies did not suggest increased platelet aggregability. Platelets seem to be more activated in depressed patients with CAD than in depressed individuals without CAD. The selective serotonin reuptake inhibitors normalized platelet hyperactivity in four studies. CONCLUSION: Data on platelet activity in depression are inconclusive. To resolve this issue and its clinical implications, studies in larger sample sizes controlling for confounders of platelet functioning and prospectively designed are needed.

Coronary Disease↗
PubMed2004

Monocyte proinflammatory cytokine release is higher and glucocorticoid sensitivity is lower in middle aged men than in women independent of cardiovascular risk factors.

OBJECTIVE: To investigate whether stimulated monocyte cytokine release and its inhibition by glucocorticoids differs between men and women. DESIGN: In vitro monocyte interleukin 6 (IL-6) and tumour necrosis factor alpha (TNFalpha) release after lipopolysaccharide stimulation were assessed with and without co-incubation with increasing doses of dexamethasone and hydrocortisone separately. Glucocorticoid sensitivity was defined as the amount of a particular glucocorticoid required to inhibit lipopolysaccharide stimulated monocyte cytokine release by 50%. The established cardiovascular risk factors of age, body mass index, number of cigarettes smoked daily, low density cholesterol to high density cholesterol ratio, systolic and diastolic blood pressure, and haemoglobin A1c were used as covariates. SETTING: Aircraft manufacturing plant in southern Germany. PATIENTS: 269 middle aged male and 36 middle aged female employees. RESULTS: Release of monocyte IL-6 and TNFalpha (each p = 0.001) was higher in samples from men than in those from women. Inhibition of lipopolysaccharide stimulated IL-6 and TNFalpha release by either glucocorticoid was less pronounced in samples from men than in those from women (IL-6: dexamethasone p = 0.033, hydrocortisone p = 0.029; TNFalpha: dexamethasone p < 0.001, hydrocortisone p = 0.089). CONCLUSIONS: The finding suggests that proinflammatory activity of circulating monocytes is higher in men than in women independent of cardiovascular risk factors, thereby providing one explanation for the relatively greater coronary risk in men.

Adult↗
PubMed2003

[Changes in blood coagulation in stress and depression--from evolution to gene regulation].

Mental stress and depression are characterized by a hypercoagulable state, which might mediate the increased coronary risk in individuals who feel stressed or depressed. Changes in blood coagulation and fibrinolysis with stress and depression are largely mediated by the sympathetic nervous system via catecholamine and adrenergic receptor activity. Stress might also affect coagulation activity via an influence on the regulation of genes coding for coagulation and fibrinolysis molecules. There is some evidence that non-selective beta-blocking agents decrease hypercoagulability elicited by acute stress. The selective serotonin reuptake inhibitors appear to normalize increased platelet activity in depression. Prospective studies need to show whether there is an association between coagulation abnormalities in stress and depression with hard cardiovascular end-points and whether such an association is favorably affected by therapeutic interventions (e.g., medication, psychotherapy, stress management).

Animals↗
PubMed2002

[Differential diagnosis of chronic pain syndromes of the musculoskeletal system--coding according to ICD-10].

Primary care for patients suffering from chronic pain is regularly provided by either family physicians or inpatient medical wards. A delay in initiating specific pain treatment is associated with poor outcome in terms of pain intensity, work disability and diminished quality of life. We present a diagnostic classification scheme for chronic pain disorders following the biopsychosocial disease model. This classification may help primary care providers initiate appropriate treatment early in the course of chronic pain, and aid in referral of their patients to services familiar with the treatment of chronic pain. Given increasing requests for quality control in health care and for transparency in disease management by health insurance companies, we propose a coding system of chronic non-malignant pain syndromes with the ICD-10.

Adult↗
PubMed2002

[Differential therapy of chronic pain syndromes of the musculoskeletal system in primary health care].

For treatment of chronic non-malignant musculoskeletal pain syndromes to be successful, simultaneous medical and psychosocial interventions are required. We provide different treatment options for chronic pain disorders for the primary care physician who is not a trained psychotherapist. We stress that the physician must adopt a particular therapeutic attitude towards his patient. We further emphasize the elaboration of a biopsychosocial disease model with the patient, cognitive-behavioral interventions, treatment of associated sleep disorders, the use of a rational drug therapy regimen, physical therapy, relaxation techniques, and involvement of the social environment. Such treatment strategies may help primary care physicians to treat their patients suffering from chronic pain more successfully and with greater patient satisfaction.

Chronic Disease↗
PubMed2001

Short-term hyperglycemia induces lymphopenia and lymphocyte subset redistribution.

Alterations in lymphocytes are a common finding in both type I and type II diabetes. Autoimmune phenomena in type I diabetes, the stage of the diabetic disorder and metabolic effects of therapeutic interventions may also affect actual distribution of lymphocyte phenotypes. This study investigated immunological effects specific to standardized hyperglycemia in non-diabetic individuals to exclude immunological changes potentially related to diabetes stage and treatment. 37 subjects (mean age +/- SD 39 +/- 5 years) underwent a sequence-controlled crossover with oral administration of a solution containing either 75 g glucose or artificial sweetener (i.e. placebo). At rest and at two hours, counts of white blood cells (WBC), mixed lymphocytes, mature T-cells (CD3), T-helper cells (CD4), T-suppressor/ cytotoxic cells (CD8), B-cells (CD19), natural killer cells (CD16/CD56), and interleukin-2 receptor bearing peripheral blood mononuclear cells (CD25) were measured by flow cytometry. Subjects showed a significant decrease in WBC, lymphocytes, and all lymphocyte subsets with the OGTT compared with the placebo solution (p < .05 to p < .001). In non-diabetic individuals, short-term hyperglycemia induces immunological changes that may be relevant to explain similar findings in patients with diabetes mellitus. Future studies need to validate these findings and their potential clinical implications in a diabetic population.

Adult↗
PubMed2001

Decrease in the plasma von Willebrand factor concentration following glucose ingestion: the role of insulin sensitivity.

Elevated plasma von Willebrand factor (vWF) concentration is thought to be associated with increased prevalence of cardiovascular events in the insulin resistance syndrome. We examined the effects of oral glucose challenge and accompanying metabolic and hemodynamic changes on vWF levels with respect to insulin sensitivity. Forty normotensive and hypertensive subjects (mean age +/- SD, 40 +/- 5 years) underwent a standard oral glucose tolerance test (OGTT). Plasma vWF antigen, glucose, insulin, catecholamines, and hemodynamics were measured at rest, and at 30, 60, 90, and 120 minutes after glucose intake. Insulin sensitivity was determined by the insulin sensitivity index (ISI(0,120)). Resting plasma vWF concentration was associated with screening systolic blood pressure (BP) (r =.43, P =.005). There were time effects for all variables of interest. While vWF antigen (P =.044), epinephrine (P =.003), and diastolic BP (P =.001) decreased after glucose challenge, norepinephrine (P =.009), systolic BP (P =.022), and heart rate (P <.001) increased. Decline in vWF (area under the curve) was associated with decrease in epinephrine (r =.46, P =.004) and with screening systolic BP (r =.45, P =.004). However, neither resting plasma vWF levels nor vWF decrease following glucose ingestion were significantly associated with the ISI(0,120.) The plasma vWF concentration decreases following glucose ingestion. While mechanisms underlying this phenomenon may relate to sympathetic nervous system function, they seem not related to insulin sensitivity. Endothelial dysfunction such as caused by hypertension rather than metabolic dysregulation per se may underlie the elevated plasma vWF concentration found with insulin resistance.

Adult↗
PubMed2001

The hypercoagulable state in sleep apnea is related to comorbid hypertension.

OBJECTIVE: Obstructive sleep apnea (OSA) is associated with increased prevalence of atherosclerotic disease. A hypercoagulable state thought to underly atherosclerosis has been described in both OSA and systemic hypertension. We wondered about the respective contribution of apnea and hypertension to a hypercoagulable state. DESIGN: Eighty-seven subjects with symptoms suggestive of OSA, mean age 47 years (range 32-64 years), underwent polysomnography and blood pressure (BP) screening. OSA was diagnosed when respiratory disturbance index (RDI) > or = 15. Subjects having systolic BP (SBP) > 140 mmHg and/or diastolic BP (DBP) > 90 mmHg were classified as having hypertension. Three hypercoagulability markers were measured: thrombin/antithrombin III complex (TAT), fibrin D-dimer (DD), and von Willebrand factor antigen (vWF:ag). RESULTS: Analysis of variance and multiple linear regression were performed on the following four subject groups: (1) normotensive non-apneics (n = 19), (2) normotensive apneics (n = 38), (3) hypertensive non-apneics (n = 11), and (4) hypertensive apneics (n = 19). OSA (groups 2 and 4) had no significant main effect on hemostasis. Hypertensives (groups 3 and 4) had higher plasma levels of TAT (median/inter-quartile range, 148/59-188 versus 77/53-108 pmol/l; P = 0.009) and of DD (376/265-721 versus 303/190-490 ng/ml; P = 0.040) than normotensives (groups 1 and 2). Across all subjects, SBP was the only significant predictor of TAT (P = 0.001) and of DD (P = 0.004), whereas DBP was the only significant predictor of vWF:ag (P = 0.029). These findings persisted even after controlling for gender, age, body mass index, RDI, mean SaO2, and hematocrit. CONCLUSION: Hypercoagulability in OSA is mediated by comorbid hypertension and might account for high cardiovascular morbidity in OSA in general.

Adult↗
PubMed2000

Effects of sympathetic activation by adrenergic infusions on hemostasis in vivo.

Overactivity of the sympathetic nervous system (SNS) has been related to increased cardiovascular morbidity. Historical reports suggest hastening of blood coagulation following intravenous administration of epinephrine. Given the important role of the hemostatic system in atherosclerosis and thrombosis, it is surprising that short-term adrenergic effects on blood coagulation, fibrinolysis and platelet activity have not been scrutinized closely. To elucidate such effects in vivo, this paper reviews human studies in which alpha- and beta-sympathomimetic agents had been infused. The literature suggests a dose-dependent stimulation of factor VIII clotting activity, von Willebrand factor antigen, tissue-type plasminogen activator, and platelets within a 15- to 40-min infusion of epinephrine. Precise mechanisms underlying hemostatic changes with sympathetic activation remain to some extent speculative. However, there is evidence from adrenoreceptor blockade studies that coagulation and fibrinolysis molecules are released into circulation by stimulation of vascular endothelial beta-adrenoreceptors (most likely beta2-receptors). Combined alpha2- and beta2-adrenoreceptor-related mechanism(s) are responsible for platelet activation. Short-term activation of the SNS effects regular hemostatic activity. While in healthy individuals the hemostatic balance between coagulation and fibrinolysis may be preserved, catecholamine surge may trigger a hypercoagulable state and enhance the odds of overt thrombosis in patients with atherosclerotic disease.

Adrenergic Agonists↗
PubMed2000

Reliability of nocturnal blood pressure dipping.

BACKGROUND: Increasing evidence documents the fact that individuals whose blood pressure drops or 'dips' relatively little at night have a higher risk of numerous cardiovascular illnesses. OBJECTIVE: To examine the reliability of various measures of nocturnal blood pressure dipping. METHODS: This study examined 17 individuals with ambulatory blood pressure monitoring on three 24 h recordings while they pursued a schedule similar to that of in-patients on a clinical research unit. Nocturnal dipping of blood pressure was scored three ways: as the drop in blood pressure between 10 p.m. and 6 a.m. ('clocktime'), as the drop in blood pressure tailored to each individual's reported bedtime ('bedtime'), and as the drop in blood pressure accompanying polysomnographically verified sleep ('sleeptime'). RESULTS: Adequate reliability was obtained for all three measures of dipping. There was, in general, a significant correlation across testing occasions (P<0.05). The correlation coefficient ranged from 0.5 to 0.8, depending on which criterion of dipping was selected and whether the endpoint was systolic blood pressure, diastolic blood pressure, or mean arterial blood pressure. CONCLUSIONS: The reliability of systolic blood pressure dipping was somewhat lower than that of diastolic or mean arterial blood pressure dipping. Dipping appears to be a reliable construct. While no one definition of dipping was demonstrably better than another, the most sensible definition of dipping would allow some adjustment for defining 'night' on the basis of each individual's idiosyncratic bed time.

Adult↗
PubMed1998

[Splenic infarct in heterozygote sickle cell trait (Hb AS)].

We present a carrier of the sickle cell trait who developed a serious splenic infarction. An antecedent hypoxaemic event and a blood coagulation disorder were ruled out. The observation shows that the sickle cell trait can represent a risk factor for a life-threatening thrombotic event, even in the absence of a predisposing condition.

Adult↗
PubMed1992

Factor XII clotting activity and antigen levels in patients with thromboembolic disease.

Individuals with severe factor XII (FXII) deficiency may be prone to thromboembolic disease and this thrombophilic state may be due to insufficient contact activation dependent fibrinolysis. According to our previous study (Thromb Haemostas 1991; 65: 117-121), however, heterozygous FXII deficiency is not a strong prethrombotic risk factor, only one out of 45 obligatory or possible heterozygotes having sustained a thrombotic event. In the present study, FXII clotting activity (FXII:C) and antigen concentration (FXII:AG) were measured in 200 patients having suffered from idiopathic thromboembolism and compared with the values in 200 healthy controls. Mean FXII levels were not significantly different in thrombophilic patients and controls, and subnormal FXII values were not more frequently encountered in patients than in controls. Specific FXII activity, i.e. the ratio of FXII:C to FXII:AG, showed considerable variation in each of the two groups, but patients and controls had a similar distribution of specific FXII activity. Variations in specific FXII activity were not explained by differences in beta 2-glycoprotein I levels. In conclusion, heterozygous FXII deficiency is not a strong prethrombotic risk factor and subnormal FXII values are not more common in thrombophilic patients than in healthy individuals.

Adolescent↗
PubMedDate not supplied

Effects of psychological stress and psychiatric disorders on blood coagulation and fibrinolysis: a biobehavioral pathway to coronary artery disease?

OBJECTIVE: A hypercoagulable state before overt thrombosis resulting from an imbalance between the coagulation and fibrinolysis systems is related to cardiovascular disease progression and acute coronary syndromes. Psychological stressors and depressive and anxiety disorders also are associated with coronary artery disease. This review explores whether changes in blood coagulation, anticoagulant, and fibrinolytic activity may constitute psychobiological pathways that link psychological factors with coronary syndromes. METHODS: Literature on coagulation, anticoagulation, and fibrinolysis measures in conjunction with psychological factors (mental stress, psychosocial strain, and psychiatric disorders) was identified by MEDLINE search back to 1966 and through checking the bibliographies of these sources. Sixty-eight articles were critically reviewed. RESULTS: In healthy subjects, acute mental stress simultaneously activates coagulation (ie, fibrinogen or von Willebrand factor) and fibrinolysis (ie, tissue-type plasminogen activator) within a physiological range. In patients with atherosclerosis and impaired endothelial anticoagulant function, however, procoagulant responses to acute stressors may outweigh anticoagulant mechanisms and thereby promote a hypercoagulable state. Chronic psychosocial stressors (job strain or low socioeconomic status) are related to a hypercoagulable state reflected by increased procoagulant molecules (ie, fibrinogen or coagulation factor VII) and by reduced fibrinolytic capacity. There is also some evidence that points to hypercoagulability in depression. CONCLUSIONS: Different categories of psychological measures to varying extent are associated with characteristic patterns of coagulation and fibrinolysis activity. Associations between psychological factors and several coagulation and fibrinolysis variables related to atherosclerosis provide a plausible biobehavioral link to coronary artery disease.

Anxiety Disorders↗