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Biomedical subjects

J van de Loo

Publications and source records attributed to J van de Loo.

At least 37 records · Page 2Linked to original sources
PubMed1995

Pulmonary aspergillosis: early diagnosis improves survival.

Bronchoscopy obtaining bronchoalveolar lavage (BAL) fluid and bronchial secretions (BS) and/or high-resolution computed tomography (CT) of the lungs were performed in 33 patients with pulmonary aspergillosis from 1987 to 1992. The sensitivity of BAL fluid or BS for detecting histologically proven fungal disease was 33 and 50%, respectively, whereas positive serologies were only documented in 8% of the cases. CT scans contributed to the early diagnosis of opportunistic fungal pneumonia: characteristic CT signs were found in 16 of 19 episodes. The more frequent use of bronchoscopy and CT scans between 1990 and 1992 compared to 1987-1989 for the differential diagnosis of new pulmonary infiltrates resulted in earlier appropriate treatment. The average introduction of intravenous (i.v.) antifungal therapy after the onset of pneumonia was shifted from 12 to 7 days (p < 0.05). The timely implementation of i.v. antimycotic therapy had a significant impact on survival. Initiation of antifungal treatment later than 10 days after the onset of pneumonia resulted in a mortality of 90%, as opposed to 41% with an earlier start of antimycotics (p < 0.01). The earlier use of appropriate antifungal therapy in the second treatment period improved survival from 33 to 50% (NS). Bronchoscopy and high-resolution CT scans are mutually complementary diagnostic tools and should be performed as early as possible in the course of pneumonia for patients at high risk for aspergillosis.

Adolescent↗
PubMed1995

Immunophenotyping of lymphocytes in bronchoalveolar lavage fluid. A new flow cytometric method vs standard immunoperoxidase technique.

Characterizing lymphocyte subsets in bronchoalveolar lavage fluid (BALF) by flow cytometry (FC) proper gating of the lymphocyte subpopulation being analyzed is crucial. In order to test lymphocyte gate quality for the first time we used a DNA-dye to evaluate plasmamembrane integrity and thus to mark off fluorescent but not DNA-containing particles (eg, debris). A comparative prospective study between this newly developed FC technique and a standard peroxidase anti-peroxidase (PAP) method was performed. Samples of BALF from 50 patients with various pulmonary diseases were examined. After determination of the total cell yield, a differential cell count was performed. Subsequently, the immunophenotype of pan T lymphocyte CD3-, T-helper lymphocyte CD4-, and T-suppressor lymphocyte CD8-positive lymphocyte subsets was assessed with FC as well as with the PAP method. Both methods showed excellent correlation (CD3: r = 0.81; CD4: r = 0.97; CD8: r = 0.96; p < 0.05, respectively). Comparing the mean +/- SEM, FC tends to overestimate CD3+ cells (90.6 +/- 1.0% vs 85.8 +/- 1.3%). For CD4 (45.0 +/- 3.4% vs 44.4 +/- 3.4%) and CD8 (48.1 +/- 3.5% vs 46.7 +/- 3.5%), there was good agreement. In a clinical setting, the reliability of both methods was equivalent, and FC using a DNA-dye to test lymphocyte gate quality offered a rapid and reliable determination of lymphocyte subsets in BAL.

Bronchoalveolar Lavage Fluid↗
PubMed1994

Cytokine response to infection in patients with acute myelogenous leukaemia following intensive chemotherapy.

Septic shock is the major cause of treatment-related death in patients with acute myelogenous leukaemia (AML) undergoing intensive chemotherapy. Interleukins (IL)-1 beta, -6, -8, and tumour necrosis factor alpha (TNF-alpha) have been implicated as mediators of septic shock, with circulating leucocytes being considered a major source for their release. However, plasma cytokine levels of leucocytopenic patients with evolving sepsis have not been studied. We have prospectively measured plasma cytokines during chemotherapy-induced leucocytopenia (< 1 x 10(9)/l) in 50 patients with AML. Cytokine levels in patients with severe sepsis (n = 5) or septic shock (n = 8) were compared to those measured in 13 matched patients with uncomplicated febrile infections. In evolving septic shock, IL-6, IL-8 and TNF-alpha peaked within 48 h of fever onset at levels reported for non-leucocytopenic patients and distinctively higher than during uncomplicated febrile episodes (P < 0.05). Peak concentrations measured within 48 h after onset of fever were related to fatal outcome. IL-1 beta was detected in less than 5% of all samples. Cytokine concentrations were unrelated to leucocyte counts and markers of neutrophil or monocyte activation (elastase and neopterin levels, respectively). We conclude that cytokine release associated with evolving septic shock in patients with AML does not depend on circulating leucocytes.

Adult↗
PubMed1994

Fibrinogen and factor VII in the prediction of coronary risk. Results from the PROCAM study in healthy men.

Coronary thrombosis is regarded as the final occlusive event in the progress of coronary heart disease (CHD). Disturbances of the hemostatic system may favor this process and thus may indicate increased risk of myocardial infarction. Coagulation and lipid factors were measured in 2116 healthy male participants of the Prospective Cardiovascular Münster (PROCAM) study. After 6 years of follow-up, 82 coronary events (9 sudden cardiac deaths and 14 fatal and 59 nonfatal myocardial infarctions) were observed. The mean plasma fibrinogen levels of the event and nonevent groups differed by 0.25 g/L (2.88 [SD, 0.68] versus 2.63 [SD, 0.63] g/L, respectively; P = .001). The incidence of coronary events in the upper tertile of the plasma fibrinogen distribution was 2.4-fold higher than in the lower tertile. By multiple logistic function analysis, plasma fibrinogen was found to be an independent risk indicator for CHD (P < .05). Individuals in the high serum low-density lipoprotein (LDL) cholesterol tertile who also showed high plasma fibrinogen concentrations had a 6.1-fold increase in coronary risk. Unexpectedly, individuals with low plasma fibrinogen had a low incidence of coronary events even when serum LDL cholesterol was high. The mean factor VIIc activities in the event and nonevent groups did not differ significantly (112.3% [SD, 19.9] versus 108.4% [SD, 21.6]; P = .09). There was, however, a trend toward higher factor VIIc values when only fatal events were taken into account. Thus, higher levels of plasma fibrinogen markedly increased the predictive power of high serum LDL cholesterol. Low plasma fibrinogen is associated with low coronary risk even when LDL is raised.

Adult↗
PubMed1994

Factor VII-deficient substrate plasmas depleted of protein C raise the sensitivity of the factor VII bio-assay to activated factor VII: an international study.

Plasma from healthy individuals, pregnant women and patients on warfarin were distributed to 3 laboratories supporting major cardiovascular surveys (Northwick Park, Muenster and Houston) for assay of factor VII coagulant activity (VIIc) with their own bio-assays. The mean VIIc in 147 samples agreed to within 1% of standard in Northwick Park and Houston, but was 14% of standard lower in Muenster owing to its more potent standard. In samples with an increased VIIc the Northwick Park assay gave a higher result than the other assays owing to its increased responsiveness to activated factor VII (VIIa). Thus when VIIa concentrations were determined directly with a clotting assay which utilises a soluble recombinant tissue factor, the increase in VIIc with increase in VIIa was considerably greater with the Northwick Park assay than the Muenster assay. This feature of the Northwick Park assay was traced to the virtual absence of protein C in its substrate plasma. Factor Va appears rate-limiting for the coagulant expression of VIIa in test plasma. If the thrombotic response to release of tissue factor is determined by the circulating concentration of VIIa, then the Northwick Park factor VII bio-assay may be preferable to other bio-assays currently employed to estimate risk of acute coronary events.

Adult↗
PubMed1993

[Central sleep apnea syndrome as a cause of impaired wakefulness in multiple myeloma].

Progressive day-time sleepiness developed in a 73-year-old man for 3 years known to have kappa-light-chain myeloma, treated with radio- and chemotherapy. His powers of concentration and intellectual performance were diminished. Neither clinical nor biochemically was there any indication of abnormal water and electrolyte metabolism or hyperviscosity syndrome. The neurological examination was unremarkable. His wife's observation of nocturnal breathing pauses suggested sleep-related abnormal breathing. Polysomnography showed severe central sleep apnoea: an apnoea index of 60/h and blood oxygen saturations as low as 78%. On biphasic positive airway pressure (BIPAP) ventilation by nasal mask at night the apnoea index fell to 6/h and the symptoms improved. During a break in treatment the day-time sleepiness again increased and regressed once again with BIPAP ventilation. There is a 1-5% prevalence of sleep-related impaired breathing among adults. This condition should thus be considered in the differential diagnosis of characteristic day-time sleepiness.

Aged↗
PubMed1993

Platelets deficient in glycoprotein IIIb aggregate normally to collagens type I and III but not to collagen type V.

The aggregation of platelets induced by collagens is considered an important step in primary hemostasis. Glycoprotein (GP) IIIb (GPIIIb, GPIV, CD36) has been proposed as a blood platelet receptor for collagen. Platelets from three healthy blood donors were shown to be clearly deficient in GPIIIb. These platelets aggregated normally in response to type I and III collagens. In addition, platelet factor 4, beta-thromboglobulin, and adenosine triphosphate (ATP) secretion in response to type I and III collagens was normal. The findings indicate that GPIIIb is not the major, essential collagen receptor for type I and III collagens. This would explain why all individuals with GPIIIb-deficient platelets examined so far are healthy and, in particular, show no apparent evidence of hemostatic problems. However, in contrast to control platelets, no aggregation and impaired platelet factor 4, beta-thromboglobulin, and ATP secretion was observed in response to type V collagen. Therefore, it is postulated that for type V collagen-induced aggregation both GPIa/IIa and GPIIIb are essential.

Adult↗
PubMed1993

Prothrombin activation fragment 1 + 2 and thrombin antithrombin III complexes in patients with angina pectoris: relation to the presence and severity of coronary atherosclerosis.

Plasma levels of the prothrombin activation fragment 1 + 2 (F 1 + 2) and of thrombin antithrombin III complexes (TAT) were determined in 225 patients with angina pectoris undergoing coronary angiography. Oral anticoagulant therapy was associated with a marked reduction in mean F1 + 2 (0.63 vs 1.62 nmol/l, p < 0.0001) and TAT levels (1.65 vs 2.23 micrograms/l, p < 0.0001). Omitting patients on oral anticoagulants, TAT values showed a positive association with patients' age (r = 0.18; p = 0.01) and were slightly higher in patients with a history of myocardial infarction than in those without (2.47 vs 2.11 micrograms/l; p = 0.06). Both F1 + 2 and TAT levels were increased in patients with angiographically verified coronary atherosclerosis as compared to patients with angina and angiographically normal coronaries (F1 + 2: 1.76 vs 1.36 nmol/l, TAT: 2.35 vs 2.00 micrograms/l; p-values after adjusting for age, sex and past history of myocardial infarction 0.06 and 0.11 respectively). However, no graded relationship between F1 + 2 or TAT values and severity of atherosclerosis was observed. This study provides suggestive evidence that a procoagulant state exists in patients with angina pectoris and coronary atherosclerosis. Its relevance in predicting coronary ischaemic events needs to be studied prospectively.

Adult↗
PubMed1993

[Peripheral arterial occlusive disease--acute intervention and after-care].

Acute ischemia in peripheral arterial occlusive disease due to progressive atherosclerosis is most commonly caused by thrombotic or thromboembolic events. Such a condition is a threat to both the limb and the life of a patient which requires rapid therapeutic decisions based on close cooperation between vascular surgeons, angiologists and radiologists. In complete ischemia with sensomotoric deficit and in suprainguinal occlusions surgical management remains the treatment of choice. Patients with incomplete ischemia and infrainguinal occlusions and patients unfit for major vascular surgery are appropriate candidates for local thrombolysis and percutaneous revascularization procedures. Available data on the main thrombolytic agents fail to show convincing difference between these drugs with regard to their efficacy and safety. Full heparinization is recommended before any definite therapy, after thrombolysis and if necessary after percutaneous transluminal angioplasty (PTA). Antiplatelet drugs should be given before and after reconstructive surgery and PTA and following heparinization after thrombolysis and PTA. In all conditions long-term treatment with antiplatelet drugs is recommended.

Angioplasty, Balloon↗
PubMed1992

Enhancement of spontaneous fibrinolytic activity in diabetic retinopathy.

The fibrinolytic system was studied in 96 patients with type I diabetes mellitus. Patients were grouped according to their degree of retinopathy; 38 patients with no evidence of retinopathy, 28 patients with background retinopathy and 30 patients with proliferative retinopathy. Thirty healthy individuals served as controls. The basal fibrinolytic activity as measured by clot lysis time and t-PA activity was increased in diabetic patients. This was associated with low levels of plasminogen activator inhibitor. Increased levels of D-dimer in diabetic patients further indicate enhanced in vivo fibrinolysis. The increase in fibrinolytic activity was highest in diabetics without retinopathy, and decreased with increasing retinopathy. Endothelial release of t-PA after venous occlusion was not different between controls and all diabetic groups. These findings suggest that in type I diabetics the fibrinolytic system is in an activated state. With worsening of retinopathy this increase in fibrinolytic activity diminishes.

Adolescent↗
PubMed1992

Rate of fibrinogen breakdown related to coronary patency and bleeding complications in patients with thrombolysis in acute myocardial infarction--results from the PRIMI trial.

Four hundred and one patients with acute myocardial infarction of less than 4 h duration were randomized to receive intravenous thrombolytic treatment with either 80 mg of full length unglycosylated single-chain-urokinase plasminogen activator (INN saruplase) or 1.5 million IU of streptokinase delivered over a 60 min period. Angiographic patency rates were higher at 60 min in saruplase treated patients (71.8% vs 48%; P less than 0.001), but did not differ significantly at 90 min (71.2% vs 63.9%; P = 0.15). Fibrinogen levels dropped markedly in both groups, the decrease being delayed and less pronounced with saruplase. Total fibrin and fibrinogen degradation products and D-dimer values rose earlier and to higher peak values in streptokinase treated patients. In both groups marked plasminogen and alpha 2-antiplasmin consumption was observed. Lower fibrinogen levels, and in particular the faster rate of fibrinogen breakdown, were associated with higher patency rates at 90 min (P less than 0.05). Patients with bleeding complications had lower 'lowest points' and a more rapid decrease in fibrinogen (P less than 0.05). These findings were not related to the drug used. Increased heparin levels at 6 to 12 h were correlated to bleeding complications in streptokinase treated patients. It is concluded that the rate of fibrinogen breakdown during and following thrombolytic treatment for acute myocardial infarction is related to early vessel patency and bleeding complications.

Blood Coagulation Tests↗
PubMed1992

Interleukin-2 followed by fluorouracil and folinic acid in refractory colorectal cancer--results of a clinical phase II study.

In a clinical phase II study, 23 patients with progressive metastatic colorectal cancer and failure after first-line chemotherapy with fluorouracil (5-FU) and folinic acid (FA) were treated with a 5-day continuous infusion of recombinant interleukin-2 (IL-2), 3 x 10(6) cetus U/m2/d, followed after a rest period of 2 days by 5-FU, 600 mg/m2/d, and FA, 300 mg/m2/d over an additional 3 days. After two to four treatment cycles, eight of 22 evaluable patients (36%) revealed antitumor responses, with three partial remissions and five minor responses or stable disease. Side effects consisted most frequently of fever, nausea and vomiting, an elevation of liver enzymes, hypotension, and skin toxicity, and required a 50% reduction of IL-2 dose in 17 of 71 treatment courses (24%). In four of the 23 patients (18%), treatment had to be stopped completely. These data indicate a significant antitumor activity of IL-2 combined with 5-FU/FA therapy in chemotherapy-resistant colorectal cancer. Hence, in spite of a substantial treatment-related toxicity, further studies are warranted to substantiate these findings and to elucidate the underlying mechanisms of the IL-2-5-FU/FA combination therapy.

Adult↗
PubMed1992

[Platelet inhibitors or anticoagulants in prevention after myocardial infarct? The 1991 state of the art].

Recent clinical studies and an indication according to the severity degree provide new insight into the antithrombotic prevention with antiplatelet substances or oral anticoagulants in patients after myocardial infarction. After uncomplicated infarction 0.3-0.5 g acetylsalicylic acid are able to reduce both the reinfarction rate and mortality. Cardiogenic emboli in patients with nonrheumatic atrial fibrillation may be prevented by oral anticoagulants even in reduced dosage (INR 1.5-2.5). Oral anticoagulants in usual dosage may be applied in patients with a complicated course after infarction, i.e. with established intracardial thrombi, with aneurysm or myocardial akinesia, with dilated, large left ventricle or with atrial fibrillation. So far, controlled clinical studies comparing reduced oral anticoagulation and antiplatelet drugs to reduce the reinfarction rate and mortality do not exist. Meanwhile, new anticoagulant drugs, such as hirudins or synthetic thrombin inhibitors are under clinical investigation.

Administration, Oral↗