[Patients with ICD-10 disorders F3 and F4 in psychiatric and psychosomatic in-patient units - who is treated where? : Allocation features from the PfAD study]. / Patienten mit Störungen nach ICD-10 F3 und F4 in Psychiatrie und Psychosomatik ­ wer wird wo behandelt? : Merkmale der Zuweisung aus der PfAD-Studie.

BACKGROUND: In Germany, in-patient treatment of patients with depressive, neurotic, anxiety, and somatoform disorders (ICD-10 F3, F4) is carried out in different settings in psychiatry and psychosomatics. Which patient characteristics determine referral to one or the other specialty is a crucial question in mental health policy and is a matter of ongoing controversy. However, comparative data on patient populations are widely lacking. METHODS: In the study of Treatment Pathways of Patients with Anxiety and Depression (PfAD study), a total of 320 patients with ICD-10 F3/F4 clinical diagnoses were consecutively recruited from four treatment settings (psychiatric depression ward, psychiatric crisis intervention ward, psychiatric day hospitals, or psychosomatic hospital units; 80 participants per setting) and investigated. RESULTS: In all treatment settings, patients with considerable severity of illness and chronicity were treated. Female gender, higher education, and higher income predicted referral to psychosomatic units; male gender, transfer from another hospital or emergency hospitalization, co-morbidity with a personality disorder, higher general psychiatric co-morbidity, and danger to self at admission predicted referral to psychiatric unit. Patients in psychosomatic units had neither more psychosomatic disorders nor more somatic problems. DISCUSSION: There is considerable overlap between the clientele of psychiatric and psychosomatic units. Referral and allocation appears to be determined by aspects of severity and social status.

An extended convection diffusion model for red blood cell-enhanced transport of thrombocytes and leukocytes.

Transport phenomena of platelets and white blood cells (WBCs) are fundamental to the processes of vascular disease and thrombosis. Unfortunately, the dilute volume occupied by these cells is not amenable to fluid-continuum modeling, and yet the cell count is large enough that modeling each individual cell is impractical for most applications. The most feasible option is to treat them as dilute species governed by convection and diffusion; however, this is further complicated by the role of the red blood cell (RBC) phase on the transport of these cells. We therefore propose an extended convection-diffusion (ECD) model based on the diffusive balance of a fictitious field potential, Psi, that accounts for the gradients of both the dilute phase and the local hematocrit. The ECD model was applied to the flow of blood in a tube and between parallel plates in which a profile for the RBC concentration field was imposed and the resulting platelet concentration field predicted. Compared to prevailing enhanced-diffusion models that dispersed the platelet concentration field, the ECD model was able to simulate a near-wall platelet excess, as observed experimentally. The extension of the ECD model depends only on the ability to prescribe the hematocrit distribution, and therefore may be applied to a wide variety of geometries to investigate platelet-mediated vascular disease and device-related thrombosis.

Monitoring of recombinant hirudin: assessment of a plasma-based ecarin clotting time assay.

Assay conditions of a plasma-based ecarin clotting time (ECT) were evaluated and the precision of the ECT in monitoring plasma levels of r-hirudin assessed. The snake venom enzyme ecarin converts prothrombin to meizothrombin possessing only weak coagulant but strong esterase activity. In r-hirudin containing plasma samples, meizo thrombin is rapidly neutralized by r-hirudin resulting in a dose-dependent prolongation of the clotting times. Among the different assay conditions tested, addition of 50 microliters of ecarin (4 U/ml) to 100 microliters of undiluted citrate-anticoagulated plasma gave optimal results with respect to precision and reproducibility. The measuring range of the ECT performed in this way is about 0.02-5.0 micrograms/ml r-hirudin. In vitro studies performed on r-hirudin-spiked plasma samples of 50 healthy individuals demonstrate remarkably low interindividual differences in r-hirudin responsiveness as indicated by CV-values below 5% and 7% at r-hirudin concentrations between 0-3 micrograms/ml and 4-5 micrograms/ml, respectively. The specificity for r-hirudin of the ECT is further demonstrated by the strong correlation (r = 0.94) between the results of a chromogenic assay and the ECT-measured r-hirudin concentrations obtained on 67 ex vivo blood samples. Depending on the concentration of r-hirudin the ECT is sensitive to plasma levels of prothrombin. In the absence of r-hirudin the critical prothrombin concentration was found to be 20% but increasing to 60% in the presence of 2.0 micrograms/ml r-hirudin. A fibrinogen concentration of 50 mg/dl was found to be the minimal concentration independent of the r-hirudin concentration. The precision of the ECT in measuring plasma levels of r-hirudin is not influenced by treatment with heparin, aprotinin or oral anticoagulants. The data demonstrate that the ECT is a rapid and easily perfor mable clotting assay which allows accurate measurement of r-hirudin plasma levels. ECT-monitored hirudin treatment will help to establish optimal dose regimens that are more efficacious but still as safe as heparin.