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Biomedical subjects

J van der Meer

Publications and source records attributed to J van der Meer.

At least 19 recordsLinked to original sources
PubMed1992

Logistical problems in prehospital thrombolysis.

In this study we compared efficacy and safety of prehospital with in-hospital thrombolytic treatment with anistreplase in patients with acute myocardial infarction (AMI). Three-hundred and fifty patients with chest pain were screened for eligibility by the municipal ambulance staff and/or the general practitioner. Patients were included in the absence of contraindications and if the telephone-transmitted ECG showed AMI. In a 6 month period 16 patients (5%) were eligible, but only seven (2%) were randomized. Age over 70 years, duration of chest pain for longer than 4 h and logistic problems were the major factors responsible for the low inclusion rate. The mean time spent at home with and without the ECG procedure was 38 +/- 14 and 14 +/- 8 min, respectively (P less than 0.001). These results demonstrate that in a medium sized town prehospital delivery of intravenous thrombolytic therapy by paramedics and/or the general practitioner is not feasible, leads to unnecessary time delay and may therefore yield no clinical benefits.

Adult↗
PubMed1992

Complement activation and the production of inflammatory mediators during the treatment of severe sepsis in humans.

Sepsis or septic shock is frequently associated with activation of the complement system, coagulation and fibrinolytic changes and the release of several cytokines. In this study we analyzed the relation of complement activation to the inflammatory mediators, hemodynamic and biochemical parameters and severity of illness and outcome in 20 consecutive patients with clinically defined sepsis. Levels of C3a and C3d were elevated in 90% of the patients (median levels 0.19 mg/l and 8.6 mg/l respectively) in comparison to 14% and 42%, respectively of 7 patients with non-septic shock. Levels of C4 were decreased in only 1 of the 20 septic patients. Levels of TNF and IL-6 were elevated in 94% and 100% of the patients, Levels of TNF and IL-6 were elevated in 94% and 100% of the patients, respectively (median levels 122 ng/l and 1300 U/ml) and were clearly interrelated (r = 0.67, p less than 0.01). C3a levels correlated with the APACHE II score (r = 0.57, p less than 0.05) and high C3a levels were associated with fatal outcome (p less than 0.05). C3a was also correlated inversely with mean arterial pressure (r = 0.50, p less than 0.01). Levels of complement C3a and C3d significantly correlated with levels of plasminogen activator inhibitor-1 (PAI) and correlated inversely with AT-III levels. We found no correlation between these complement products and leukocyte counts or lactate levels, nor was there a correlation between C3a or C3d and the cytokines TNF and IL-6. Levels of C3a and C3d did not decrease significantly during the first 24 h of treatment, in contrast to a clear decrease in IL-6 levels in all patients and a decrease in TNF in the surviving patients. TNF levels remained stable or increased in the non-survivors. We conclude that both the complement system and the cytokine system are involved in the pathogenesis of septic shock and may be involved in the development of some of the fatal complications like hypotension and disseminated intravascular coagulation.

Aged↗
PubMed1992

Rheological properties of blood in Raynaud's phenomenon.

Rheological tests were performed in four rigorously defined groups of patients with Raynaud's phenomenon: primary family-related (n = 21), primary family-unrelated (n = 30), 'possible scleroderma' (n = 26), and scleroderma (n = 19). Whole blood and plasma viscosity, and hematocrit were significantly higher in the 'possible scleroderma' group. We conclude that the contribution of central rheological abnormalities in the pathogenesis of Raynaud's phenomenon is limited.

Blood Viscosity↗
PubMed1991

Vascular proliferation as an unusual cause of hemorrhagic diathesis in myelofibrosis.

One year after splenectomy, a patient with myelofibrosis developed spontaneously large hematomas that were not due to coagulation abnormalities or functionally defective platelets. At autopsy, the liver, muscle, and skin showed extramedullary hematopoiesis associated with capillary proliferation and extravasation of blood. These findings indicate that neovascularization can be an additional cause of bleeding in myeloproliferative disorders and might be induced by neoplastic hematopoietic cells.

Aged↗
PubMed1990

Coagulation factor abnormalities as possible thrombotic risk factors after Fontan operations.

Severe thromboembolism occurred in 3 of 37 patients who had undergone Fontan-type operations for correction of congenital heart defects several months to years after the operation. The patients were screened for coagulation factor abnormalities to find out whether known prothrombotic risk factors could explain the high frequency of thromboembolism. 63 abnormalities were found in 24 of the 37 patients. The commonest and most pronounced abnormality was deficiency of protein C, a known risk factor. Concentrations of antithrombin III and factors II and X were significantly lower in protein-C-deficient patients than in those with normal protein C concentrations. These findings suggest that the high thrombotic risk in these patients is caused or at least associated with an imbalance between procoagulant and anticoagulant factors.

Adolescent↗
PubMed1990

Reocclusion three months after successful thrombolytic treatment of acute myocardial infarction with anisoylated plasminogen streptokinase activating complex.

Thirty consecutive patients with acute myocardial infarction (AMI) were treated with anisoylated plasminogen streptokinase activating complex (APSAC) within 4 hours after onset of symptoms. After 1.5 and 48 hours, patency of the infarct-related vessel and the quantitative degree of residual diameter stenosis were studied by selective coronary angiography. Ventriculograms were made to determine the global left ventricular ejection fraction. Patients showing patency at 48 hours were reevaluated angiographically after 3 months. At 1.5 and 48 hours after APSAC administration patent vessels were demonstrated in 65 and 69% of patients, respectively. Mean residual stenosis decreased significantly from 56 +/- 11% at 1.5 hours to 46 +/- 13% at 48 hours (p less than 0.01). Patients not responding to thrombolytic therapy showed significant deterioration of the left ventricular function during the first 48 hours after AMI. Side effects were minor and mainly associated with invasive procedures. Despite adequate oral anticoagulation, angiographically documented reocclusion at 3 months amounted to 28%. Reocclusion, however, was neither associated with clinically documented reinfarction, nor with a decrease in the left ventricular ejection fraction. Our study shows that APSAC is an effective thrombolytic agent in AMI but that late reocclusion may occur. Oral anticoagulants appear to be less effective in the prevention of reocclusion in the treatment regimen after thrombolysis.

Adult↗
PubMed1990

A systemic non-lytic state and local thrombolytic failure of anistreplase (anisoylated plasminogen streptokinase activator complex, APSAC) in acute myocardial infarction.

The relation between coronary thrombolysis and coagulation variables after administration of anistreplase (anisoylated plasminogen streptokinase activator complex, APSAC) was studied in patients with an acute myocardial infarction. Fifty eight consecutive patients with acute myocardial infarction were given 30 U of anistreplase intravenously within 4 hours of the onset of symptoms. A fall in the plasma concentration fibrinogen to less than 1.0 g/l 90 minutes after administration of anistreplase was considered to reflect a systemic lytic state. Coronary angiography was performed 48 hours after thrombolytic treatment. The overall patency rate was 74% (43/58). Patency rates were significantly different in patients with a systemic lytic (83% (43/52)) and a systemic non-lytic state (0% (0/6)). The absence of a systemic lytic state after anistreplase administration seemed to be highly predictive of the failure of coronary thrombolysis. Coagulation studies showed evidence of inhibition of anistreplase induced fibrinolytic activity which may explain the failure of thrombolytic treatment in patients with evidence of a systemic non-lytic state.

Adult↗
PubMed1990

The periarteriolar lymphocyte sheath in immunodeficiency T- or B-lymphocyte area?

T- and B-lymphocyte populations in peripheral lymphoid tissues occur in distinct compartments (e.g., the periarteriolar lymphocyte sheath of the splenic white pulp is a T-cell area). The authors report on two patients with severe combined immunodeficiency (SCID) and one patient with immunodeficiency after anti-T-cell treatment for rejection of a heart transplant, in which the area surrounding the central arteriole in spleen white pulp was well-populated despite T-cell deficiency (documented by, for example, severe depletion of lymph node paracortex). Immunologic phenotyping showed the B-lymphoid lineage of lymphocytes at this location. The framework in the periarteriolar area consisted of follicular dendritic cells, which are typical framework components of B-cell areas. We conclude that assessment of only conventional histopathology of the spleen in these patients leads to erroneous conclusions about the type of immunodeficiency and that immunologic phenotyping is required to document the exact nature of the deficiency.

Adult↗
PubMed1990

Disappearance of renin-induced proteinuria by an ACE-inhibitor: a case report.

A 55-year-old man developed renovascular hypertension that was characterized by high plasma renin activity. This was accompanied by nephrotic range proteinuria. Treatment with nifedipine and furosemide lowered the blood pressure to normal values, but proteinuria persisted. However, treatment with an ACE-inhibitor brought resolution of the proteinuria, suggesting a role for angiotensin II in urinary protein loss.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Linoleic-acid-enriched diet: long-term effects on serum lipoprotein and apolipoprotein concentrations and insulin sensitivity in noninsulin-dependent diabetic patients.

Long-term (30 wk) effects on serum lipoproteins and insulin sensitivity of two diets, one with a low polyunsaturated to saturated fat ratio (P:S 0.3) and one with a P:S of 1.0, were compared in 14 patients with noninsulin-dependent diabetes mellitus (NIDDM) in a crossover study. Total and LDL-cholesterol levels declined by 7.6% (p less than 0.01) and 9.8% (p less than 0.01), respectively, during the high P:S diet. VLDL-, HDL2-, and HDL3-cholesterol; triacylglycerol; and apolipoprotein A1, A2, and B levels were not affected by the change in P:S. Despite a modest increase of insulin-mediated glucose disposal at physiologic insulinemia during the high P:S diet, no influence was seen on glycemic control, and on blood glucose, plasma insulin, and C peptide responses to mixed meals. In conclusion, a linoleic-enriched diet in patients with NIDD causes a less atherogenic lipoprotein profile but does not influence glycemic control and carbohydrate tolerance.

Adult↗
PubMed1988

Is the antiproteinuric effect of dipyridamole hemodynamically mediated?

We studied the acute antiproteinuric and renal hemodynamic effect of dipyridamole 30-60 mg intravenously in 13 salt-depleted patients with the nephrotic syndrome of different etiology. Whereas mean arterial pressure did not change, a small fall in glomerular filtration rate with a concomitant fall in filtration fraction and a decrease in urinary protein loss occurred. The fall in filtration fraction was positively correlated with the fall in proteinuria. This suggests that the antiproteinuric effect of dipyridamole is at least partly due to an efferent vasodilation with a fall in intraglomerular capillary pressure.

Dipyridamole↗
PubMed1987

Hypothyroidism leads to more small-sized platelets in circulation.

The effect of induced hypothyroidism on platelet count and platelet volume distribution was studied in twelve athyreotic patients. After a two weeks withdrawal of triiodothyronine supplementation, platelet count and the ratio between platelet and red cell count were increased in all patients. Furthermore, mean platelet volume was declined and platelet distribution width was risen. Thus, hypothyroidism appears to increase the number of circulating platelets, especially the smaller ones.

Adult↗