Effectiveness and cost-effectiveness of an integrated care program for schizophrenia: an analysis of routine data.

In Germany, a regional social health insurance fund provides an integrated care program for patients with schizophrenia (IVS). Based on routine data of the social health insurance, this evaluation examined the effectiveness and cost-effectiveness of the IVS compared to the standard care (control group, CG). The primary outcome was the reduction of psychiatric inpatient treatment (days in hospital), and secondary outcomes were schizophrenia-related inpatient treatment, readmission rates, and costs. To reduce selection bias, a propensity score matching was performed. The matched sample included 752 patients. Mean number of psychiatric and schizophrenia-related hospital days of patients receiving IVS (2.3 ± 6.5, 1.7 ± 5.0) per quarter was reduced, but did not differ statistically significantly from CG (2.7 ± 7.6, 1.9 ± 6.2; p = 0.772, p = 0.352). Statistically significant between-group differences were found in costs per quarter per person caused by outpatient treatment by office-based psychiatrists (IVS: €74.18 ± 42.30, CG: €53.20 ± 47.96; p < 0.001), by psychiatric institutional outpatient departments (IVS: €4.83 ± 29.57, CG: €27.35 ± 76.48; p < 0.001), by medication (IVS: €471.75 ± 493.09, CG: €429.45 ± 532.73; p = 0.015), and by psychiatric outpatient nursing (IVS: €3.52 ± 23.83, CG: €12.67 ± 57.86, p = 0.045). Mean total psychiatric costs per quarter per person in IVS (€1117.49 ± 1662.73) were not significantly lower than in CG (€1180.09 ± 1948.24; p = 0.150). No statistically significant differences in total schizophrenia-related costs per quarter per person were detected between IVS (€979.46 ± 1358.79) and CG (€989.45 ± 1611.47; p = 0.084). The cost-effectiveness analysis showed cost savings of €148.59 per reduced psychiatric and €305.40 per reduced schizophrenia-related hospital day. However, limitations, especially non-inclusion of costs related to management of the IVS and additional home treatment within the IVS, restrict the interpretation of the results. Therefore, the long-term impact of this IVS deserves further evaluation.

Enhanced serotonin transporter function during depression in seasonal affective disorder.

Decreased synaptic serotonin during depressive episodes is a central element of the monoamine hypothesis of depression. The serotonin transporter (5-HTT, SERT) is a key molecule for the control of synaptic serotonin levels. Here we aimed to detect state-related alterations in the efficiency of 5-HTT-mediated inward and outward transport in platelets of drug-free depressed patients suffering from seasonal affective disorder (SAD). 5-HTT turnover rate, a measure for the number of inward transport events per minute, and tyramine-induced, 5-HTT-mediated outward transport were assessed at baseline, after 4 weeks of bright light therapy, and in summer using a case-control design in a consecutive sample of 73 drug-free depressed patients with SAD and 70 nonseasonal healthy controls. Patients were drug-naive or medication-free for at least 6 months prior to study inclusion, females patients were studied in the follicular phase of the menstrual cycle. All participants were genotyped for a 5-HTT-promoter polymorphism (5-HTTLPR) to assess the influence of this polymorphism on 5-HTT parameters. Efficiency of 5-HTT-mediated inward (p=0.014) and outward (p=0.003) transport was enhanced in depressed patients. Both measures normalized toward control levels after therapy and in natural summer remission. Changes in outward transport showed a clear correlation with treatment response (rho=0.421, p=0.001). Changes in inward transport were mediated by changes in 5-HTT transport efficiency rather than affinity or density. 5-HTTLPR was not associated with any of the 5-HTT parameters. In sum, we conclude that the 5-HTT is in a hyperfunctional state during depression in SAD and normalizes after light therapy and in natural summer remission.

Plasma levels of polyunsaturated fatty acids in children with atopic dermatitis and in atopic and nonatopic controls.

BACKGROUND: Atopic dermatitis has been thought to be associated with a disturbance in n-6 polyunsaturated fatty acid (PUFA) metabolism, but randomized trials investigating the clinical efficacy of oral supplementation with gammalinolenic acid have revealed conflicting results. AIM OF THE STUDY: To re-investigate the proposed linkage between PUFA dysregulation and atopic dermatitis. MATERIALS AND METHODS: Plasma levels of linoleic acid (LA), gammalinolenic acid (GLA), dihomogammalinolenic acid (DGLA) and arachidonic acid (AA) were measured using HPLC in 22 children with atopic dermatitis. Patients were subdivided into those with elevated total serum IgE (group A, n = 15, IgE > +1 SD of age-specific normal values) and those with normal IgE (group B, n = 7) and compared with children suffering from allergic rhinitis/asthma (group C, n = 8) and with non-atopic controls (group D, n = 6). RESULTS: GLA levels were significantly lower (p < 0.05) in eczema patients with elevated IgE (A, 0.19 +/- 0.06%) and in atopic controls (C, 0.23 +/- 0.06%) than in eczema patients with low IgE (B, 0.42 +/- 0.19%) and non-atopic controls (D, 0.43 +/- 0.16%). There were no significant differences between groups for LIN, DGLA and AA, except for lower LIN levels in atopic controls. Correlation of individual LA and GLA values showed significantly steeper regression lines in low-IgE responders (B and D, k(x) = 0.058) than in high-IgE responders (A and C, k(x) = 0.012; p < 0.02), suggesting impaired delta-6-desaturase function in the latter. For the study population as a whole, there was a clear negative correlation between total levels of IgE and GLA (r(s) = -0.64) and a moderate negative correlation between total IgE and AA (r(s) = -0.38). CONCLUSIONS: Dysregulation of n-6 PUFA metabolism is neither consistently found in nor specifically associated with atopic dermatitis but rather appears to be associated with IgE production and atopy in general. The finding of decreased GLA levels in eczema patients with elevated total IgE and in children with allergic rhinitis and asthma but not in eczema patients with normal total IgE questions the proposed pathophysiologic role of fatty acid dysregulation in atopic dermatitis.