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Biomedical subjects

H E Karges

Publications and source records attributed to H E Karges.

34 records · Page 2Linked to original sources
PubMed1983

[Therapy of patients with severe liver insufficiency using antithrombin III and plasma derivatives].

The treatment of three patients suffering from carbon tetrachloride intoxication with antithrombin III and plasma derivatives is reported. In these patients an acute liver failure had been proven, characterized by a disturbed protein synthesis and a severe haemostasis defect. The latter manifested itself by a consumption of platelets, clotting enzymes and the inhibitors antithrombin III and alpha 2-antiplasmin. It was due to an intravascular coagulation leading to disturbances in the microcirculation. This often letal circulus vitiosus could be stopped in these patients by treatment with antithrombin III concentrate combined with low dose heparin and fresh frozen plasma. Clinical improvements are discussed on the basis of the pathophysiology of the liver.

Adult↗
PubMed1982

Additional factor XII (Hageman factor) deficiency in hemophilia A and in von Willebrand syndrome.

Factor XII plasma levels were investigated with several methods in patients with hemophilia A and B and von Willebrand syndrome. There seem to be some families with hemophilia A or von Willebrand syndrome, who have an additional, congenital, partial lack of factor XII (Hageman factor). The mode of inheritance is independent of the other coagulation disorder. Frequently, the first indication of an additional factor XII deficiency is the disproportionate prolongation of the activated partial thromboplastin time (PTT) as regards the factor VIII level. The average factor XII level in patients with hemophilia A and von Willebrand syndrome is significantly lower than in normal subjects or patients with hemophilia B. It cannot be excluded that the frequently low levels of factor XII in patients with severe hemophilia are acquired and probably due to liver cell damage.

Adolescent↗
PubMed1980

Rapid determination of fibronectin by laser nephelometry. Fibronectin concentrations is plasma in human diseases, I.

Fibronectin (Synonyms: cold-insoluble globulin, antigelatin factor) is a cell surface glycoprotein. It has been shown that remarkably large amounts of fibronectin are present in human plasma. Owing to the difficult and expensive radioimmunoassays, only a few reports on the relation of fibronectin and human diseases have so far been published. In this communication a rapid and easily handled immunoassay, using the light scattering effect, is described. The first results on the measurement of fibronectin concentrations in the plasma of patients with chronic active liver diseases are reported.

Antibodies↗
PubMed1976

[Plasminogen estimation as a routine test (author's transl)].

A simple method for the routine determination of plasminogen using the coagulation time is described. 0.2 ml of plasminogen reagent and 0.1 ml of sample plasma, prediluted 1:200, are incubated for 3 minutes at 37 degrees C. 0.05 ml of diluted test thrombin are then added and the coagulation time is measured. It is converted into percent of normal using a standard curve. The test correlates with an immunological method in healthy probands (r = 0.96). Initial measurements in 160 patients show that knowledge of the plasminogen titre may also be of interest outside the problems of haemostasis.

Blood Coagulation Tests↗
PubMed1976

Growth inhibition of human lymphoblastoid Daudi cells in vitro by interferon preparations.

Human interferon (HIF) preparations inhibited the propagation of Daudi cells in stationary suspension cultures, while a control preparation showed no such effect. The growth inhibition (= anticellular) activity of differently pretreated HIF preparations was determined by the reduction of 14C-labelled thymidine (14C-TDR) uptake in a microassay system. These studies demonstrated that the degree of anticellular activity is directly proportional to the antiviral activity of different HIF preparations. These preparations were obtained from peripheral leukocytes (lHIF) or diploid fibroblasts (fHIF). Together with gel chromatography results, and the sensitivity of the anticellular activity to tryptic digestion and heat inactivation, these results suggest that the anticellularly active substance is a protein which is very similar to, or identical with, interferon.

Burkitt Lymphoma↗
PubMed1975

Effect of human leukocyte interferon on vaccinia-and herpes virus-infected cell cultures and monkey corneas.

Pretreatment of human fibroblast cultures with human leukocyte interferon (HIF, 1,000 IU/ml) resulted in a 24-h delay of virus replication after infection with vaccinia virus and herpes simplex virus type 1 and type 2. Additional HIF treatment 24 h after infection effectively lowered the maximum yield of viral infectivity. Equal results were obtained in simian cells with 3,000 IU of HIF per ml. The spread of two cell-bound herpesviruses, varicella zoster virus and Medical Lake macaque herpesvirus, was inhibited by 2,000 IU of HIF per ml in human fibroblasts and Vero cells, respectively. Varicella zoster virus infectivity was notably reduced by HIF, whereas the latter system showed a low sensitivity. To study the effect of HIF in the infected cornea, keratitis was induced experimentally in both eyes of 12 rhesus monkeys and 12 African green monkeys by inoculation with vaccinia virus and herpes simplex virus, respectively. In each monkey one eye served as a control for the full cycle of disease. In the other eye HIF treatment was initiated prophylactically 15 h before or simultaneously with the challenge virus infection or 6 to 20 h postinfectionally or therapeutically after onset of the disease, and the treatment was continued for 2 to 7 days. Prophylactic and simultaneous administration equally resulted in inhibition of both vaccinia and herpes keratitis. Postinfectional and therapeutic administration of interferon moderated the course of keratitis slightly and shortened the period of virus shedding.

Animals↗
PubMedDate not supplied

Activation of the coagulation cascade in falciparum malaria.

The incidence and progression of coagulation abnormalities were studied in 52 patients with acute falciparum malaria. The patients were prospectively divided into 3 groups; severe (parasitaemia greater than or equal to 5% or vital organ dysfunction), 12 patients; moderate (parasitaemia 1%- less than 5% without complications), 16 patients; and mild (parasitaemia less than 1%), 24 patients. No case died or developed clinical evidence of disseminated intravascular coagulation. Conventional indices of coagulation (prothrombin time, partial thromboplastin time, fibrinogen, fibrin degradation products) were usually within the normal range but reduced plasma concentrations of antithrombin III (AT-III) levels were noted in all groups, and the incidence was significantly higher in patients with severe and moderate malaria (83% and 81%) compared with the mild group (37%; P less than 0.005). Depletion of AT-III was associated with thrombocytopenia, decreased AT-III activity and elevated plasma concentrations of thrombin-antithrombin III complexes (P less than 0.01), confirming activation of the coagulation cascade and increased clotting factor consumption. AT-III levels returned to normal coincident with clinical improvement. Activation of coagulation is a common and sensitive measure of disease activity in acute falciparum malaria. It is not a specific feature, nor is there evidence to suggest it has a primary pathological role in severe infections.

Adolescent↗
PubMedDate not supplied

Polymorphonuclear leucocyte elastase in Plasmodium falciparum malaria.

Sixty-one patients with falciparum malaria were studied prospectively to determine the plasma concentrations of the lysosomal proteinase, polymorphonuclear leucocyte elastase (PMN-elastase) and their relationship to disease severity. The patients were divided into 3 groups; severe (parasitaemia > 5%) or vital organ dysfunction (n = 23), moderate (parasitaemia 1%-5% without complications) (n = 15), and mild (parasitaemia < 1%) (n = 23). The mean plasma PMN-elastase level in 10 healthy Thai volunteers was 49.5 (SD = 21.6) ng/ml (range 33-65 ng/ml). Plasma PMN-elastase concentrations on admission were elevated (> 2 x SD above normal) in all patients with severe malaria and were above 100 ng/ml in 86.6% and 65% of the moderately severe and mild patients respectively. PMN-elastase levels during the first 3 hospital days were significantly higher in severe malaria compared with the other 2 groups (P = < 0.001-0.013). The levels decreased as the patients became afebrile and aparasitaemic. Admission plasma concentrations of PMN-elastase correlated directly with bilirubin (rs = 0.50, P < 0.001), serum glutamic oxalacetic transaminase (rs = 0.54, P0.001), parasite count (rs = 0.62, P < 0.001), blood urea nitrogen (rs = 0.54, P < 0.001) and inversely with antithrombin III activity (rs = 0.54, P < 0.001) and the platelet count (rs = 0.58, P < 0.001). Polymorphonuclear leucocyte activation may contribute to the pathogenesis of severe malaria.

Acute Kidney Injury↗