PubMed · 6783841
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E Ernst. 1981-03-06. [Hyperviscosity syndrome].. https://pubmed.ncbi.nlm.nih.gov/6783841/
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Low socioeconomic status (SES) and psychological stress are associated with increased risk of coronary heart disease, and both may influence haemostatic responses. Von Willebrand factor (vWF), Factor VIII, plasma viscosity, haematocrit, blood viscosity, tissue plasminogen activator (t-PA) and fibrin D-dimer were measured at rest and following stressful tasks in 238 middle-aged British civil servants. SES was defined by grade of employment. Lower SES was associated with higher resting vWF, Factor VIII and plasma viscosity. Psychological stress stimulated increases in haemostatic and rheological factors. Initial stress responses did not vary with SES, but Factor VIII, plasma viscosity and blood viscosity remained more elevated 45 minutes post-stress in lower SES participants. High blood pressure stress reactivity was also associated with greater haemostatic responses. We conclude that lower SES is characterised by more prolonged elevations in procoagulant responses following psychological stress, and that these processes might contribute to increased cardiac risk.
BACKGROUND AND AIMS: There appears little doubt that microvascular ischaemia is involved in Crohn's disease. Studies have consistently demonstrated that the number of blood vessels and the total volume of blood feeding segments of bowel with Crohn's disease are reduced. However, the aetiology of the microvascular ischaemia is yet to be determined. Potential aetiological factors that appear to be disease specific include increased mesenteric platelet aggregation and increased platelet surface expression of P-selectin and GP53. However, there are several other factors known to be raised in active and quiescent disease for which disease specificity is not yet known, including increased submucosal endothelial endothelin-1 receptor expression, increased m RNA expression for several interleukins and cytokines including TNFalpha, increased PAF and thrombomodulin and finally altered cellular adhesion molecule expression. CONCLUSION: Proving cause and effect will always be a difficult task given the self-perpetuating nature of the inflammatory and coagulation cascades and our inability at present to identify persons who subsequently develop Crohn's disease at a point prior to mucosal inflammation. Results to date however, are supportive of each of these factors, alone or in combination playing an integral part in the development of microvascular ischaemia, a pathological process which appears to precede the classic changes which characterize Crohn's disease.
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