European journal of clinical investigation
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Eur. J. Clin. Invest. · Apr 1985
Correlation of disease activity in systemic vasculitis with serum C-reactive protein measurement. A prospective study of thirty-eight patients.
In a prospective study over 2 years, serum C-reactive protein (CRP) concentration and erythrocyte sedimentation rate were measured serially in thirty-eight patients with various types of necrotizing systemic vasculitis. The CRP concentration was always elevated in patients with active vasculitis and fell rapidly in association with clinical remission induced by immunosuppression. ⋯ In contrast the sedimentation rate responded more slowly to changes in disease activity and did not necessarily reflect the level of inflammation at a particular time. These results, together with the commercial availability of rapid and precise assays for CRP, indicate that serial measurement of the serum CRP fills the urgent need for an objective index of the activity of the systemic vasculitides and their response to therapy.
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Eur. J. Clin. Invest. · Aug 1983
Abnormal Na+,K+ cotransport function in a group of patients with essential hypertension.
In 50 normotensive controls, the increase in erythrocyte Na+ concentration up to 12.4 +/- 2.0 mmol/l cells (mean +/- SD) ensures half-maximal stimulation of outward Na+,K+ cotransport fluxes. Forty-six out of sixty-five patients with essential hypertension required more than 16 mmol/l cells of internal Na+ concentration to obtain a similar effect, strongly suggesting an abnormal cotransport function. ⋯ Conversely, countertransport fluxes were normal in fourteen hypertensives with abnormal cotransport function. The above results indicate that the total population of patients with essential hypertension is heterogeneous and includes one subgroup of subjects with abnormal Na+,K+ cotransport function, and another with increased Na+,Li+ countertransport fluxes.
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Eur. J. Clin. Invest. · Apr 1982
Human endothelial cell proliferation inhibiting activity in the sera of patients suffering from 'shock' or 'sepsis'.
The response of DNA-synthesis of human endothelial cells to sera derived from twenty-five patients suffering from 'sepsis' or 'shock' was measured by autoradiographic methods. In eight cases a constant decrease in proliferative response was found compared to that of sera from healthy donors. These proliferation values were shown to lie below the '60%-of-control-line'. ⋯ These results correlated well with the clinical state and outcome of patients but not with any of the over sixty clinical, therapeutic, laboratory and post-mortem parameters of investigation. Evidence is presented for a proliferation inhibiting activity in sera of patients in clinically poor states, and some physico-chemical properties of this 'factor' are described. Lethal injury to the cells or an impairment of cellular migration could not be observed within the observation periods used in this study.
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Eur. J. Clin. Invest. · Jun 1981
Effect of angiotensin-II blockade on systemic and hepatic haemodynamics and on the renin-angiotensin-aldosterone system in cirrhosis with ascites.
We have studied the effect of angiotensin-II blockade with saralasin on the cardiovascular and hepatic hemodynamics and on the renin-angiotensin-aldosterone system in fourteen patients with cirrhosis and ascites. Control measurements showed that most of the patients had a low mean arterial pressure, high plasma volume, normal or high cardiac index, low peripheral resistance and high plasma renin activity and aldosterone concentration. The wedged hepatic venous pressure was increased in each patient and the estimated hepatic blood flow was normal in most of them. ⋯ The decrease of the wedged hepatic venous pressure was directly related to the reduction of the mean arterial pressure and also to the control plasma renin activity. Our study indicates that in most patients with cirrhosis, ascites and high plasma renin activity, arterial pressure is maintained by the effect of endogenous angiotensin II on the peripheral vasculature, and we suggest that a pre-existing arterial hypotension secondary to an arteriolar vasodilatation is the cause of renin release in these patients. Our results also show that angiotensin-II blockade is accompanied by a reduction of the post-sinusoidal hepatic vascular resistance.