Plasma tumour necrosis factor alpha (a) concentration is increased in acute Gram negative sepsis, but the effect of chronic infection on plasma concentrations is unknown. A study was carried out in patients with cystic fibrosis to determine the effect of chronic lung infection with Pseudomonas aeruginosa on the plasma concentration of tumour necrosis factor and two other indicators of the inflammatory response, circulating C reactive protein and neutrophil elastase-a, antiproteinase complex (elastase complex). The concentration of immunoreactive tumour necrosis factor in plasma was greater than the upper 95% confidence interval for healthy
Summary:and capillary leak syndrome. Microangiopathy, a characteristic form of EC damage associated with severity of GVHD in recipients of allogeneic bone marrow transplants, has To investigate endothelial cell alterations in BMT recipients developing acute graft-versus-host disease been described earlier by our group 1,2 suggesting that not only the epithelium but also EC may be affected in the (aGVHD) we determined levels of the endothelial cell markers von Willebrand factor (VWF) and thrombomcourse of aGVHD. In these studies, von Willebrand factor (VWF) levels odulin (TM) in 57 patients undergoing BMT. Before conditioning VWF and TM levels did not differ signifiwere used as markers of EC damage. VWF can be synthesized and released by EC and is regarded as an indicator cantly between transplant recipients who later developed no or mild (grade I) aGVHD (group A, alloof EC activation or injury. 3 TM which is localized on the surface of EC plays a crucial role in the activation of the geneic n ؍ 22, autologous n ؍ 7; VWF 136.0 ؎ 44.1%; TM 29.5 ؎ 18.0 ng/ml), and those with moderate or sevnatural anticoagulant protein C. 4 TM, therefore, is an important factor for the maintenance of the antithrombotic ere (grade II or III) aGVHD (group B, n ؍ 28; VWF 142.2 ؎ 37.6%; TM 35.2 ؎ 20.1 ng/ml). A first signifiproperties of EC. A soluble form of TM, which probably represents a degradation product of tissue TM, can be cant rise of both VWF and TM levels was noted after conditioning (day 0) both in group A (VWF measured in plasma and represents a reliable marker of EC damage. 5-8197.0 ؎ 113.3%; P Ͻ 0.001; TM 39.3 ؎ 23.3 ng/ml; P Ͻ 0.01) as well as in group B (VWF 201.7 ؎ 53.3%; P We have now determined VWF and TM levels in the plasma of BMT recipients to evaluate further the possible Ͻ 0.0001; TM 43.5 ؎ 23.5 ng/ml; P Ͻ 0.05). Subgroup analysis of autografted patients revealed no significant association of acute GVHD and endothelial cell injury. increase after conditioning in these patients. At the time of engraftment and onset of aGVHD (day 21), when VWF and TM levels within the groups were signifiPatients, materials and methods cantly elevated as compared with baseline (day −8) levels, group B patients (62.7 ؎ 38.5 ng/ml) had signifiFifty-seven patients (mean age 37.1 Ϯ 10.2 years; range from 16 to 58 years; 25 female, 32 male) suffering from cantly higher (P Ͻ 0.01) TM levels than patients of group A (37.4 ؎ 19.6 ng/ml). This significant elevation hematologic diseases were studied. Diagnoses included AML (n = 18), ALL (n = 9), CML (n = 26), lymphoma (n also persisted at the end of the investigational period (day 28; group B: 56.0 ؎ 37.6 ng/ml; group A:= 2), multiple myeloma (n = 1), and SAA (n = 1). Fifty patients received allogeneic transplants (33 from related, 17 38.2 ؎ 23.7 ng/ml; P Ͻ 0.01). An elevation of endothelial cell markers is found in the course of BMT, particularly from unrelated donors), seven patients autologous transplants. The following conditioning regimens were used: after conditioning and at the...
Twenty seven patients with cystic fibrosis under the age of 12 years and 27 matched patients with asthma were followed up in a prospective study for one year. The isolation rate of non-capsulated strains ofHaemophilus influenzae from cough swabs and sputum specimens taken at routine clinic visits every two months was significantly greater in cystic fibrosis than in asthma. Haemophilus parainfluenzae was equally common in both groups. During exacerbations the isolation rate of H influenzae in cystic fibrosis was significantly greater than at other times, whereas in asthma there was no significant difference.The distribution of biotypes ofH influenzae and H parainfluenzae was similar in the two groups. In cystic fibrosis, biotype I was associated with exacerbations. Biotype V was more common than in previous studies, but was not associated with exacerbations.
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