[Scope and limitations of risk-adjusted evaluation of lethality in community-acquired pneumonia using data collected according to section 21 of the German Hospital Reimbursement Law (Krankenhaus-Entgeltgesetz, KHEntG)]. / Möglichkeiten und Grenzen der risikoadjustierten Bewertung der Letalität bei der ambulant erworbenen Pneumonie mithilfe der section 21-Daten des Krankenhaus-Entgeltgesetzes (KHEntG).

INTRODUCTION: Several institutions are currently evaluating whether it is possible to gather valid, risk-adjusted quality indicators from routine billing data according to section 21 of the German Hospital Reimbursement Law (Krankenhaus-Entgeltgesetz, KHEntG). It is hoped that this method will enable hospitals to obtain quality assurance data in an easy and timely fashion. MATERIALS AND METHODS: For analysis, section 21 data according to KHEntG, quality assurance forms, and patients' medical records of the University Medical Center Ulm were evaluated in comparison to state and federal benchmark data from 2006. RESULTS: With regard to the quality indicator "Lethality in community-acquired pneumonia", it is possible to identify those cases that need to be included in quality assurance analysis by using predefined diagnosis lists. Risk adjustment can likewise be done according to the requirements set forth by the Federal Quality Assurance Office (Bundesgeschäftsstelle Qualitätssicherung, BQS), using only those data routinely collected for billing purposes. The results obtained are comparable to state and federal benchmark data. In addition, the analysis shows that the S3 recommendation to measure breathing rate as part of pneumonia risk assessment is not sufficiently being practiced at the moment. CONCLUSIONS: Risk-adjusted quality indicators can be generated from routine billing data according to section 21 KHEntG. Taking the patients' medical records as a reference, these indicators can even be shown to be more valid than those generated from BQS quality assurance data at the University Medical Center Ulm.

Neurotrophin and GDNF expression increases in rat adrenal glands during experimental colitis.

OBJECTIVES: Neurotrophins and GDNF have been recently recognized as important local regulators of inflammatory processes of the gut. RESULTS: We now demonstrate that experimental TNBS-colitis is associated with the increased expression of neurotrophins and GDNF in the adrenal glands. In histological sections of the adrenals from untreated control animals, faint immunolabeling for BDNF, NT-3 and NGF was detectable in the adrenal cortex, with some additional labeling for NGF over the adrenal medulla, whereas GDNF immunolabeling was confined to the adrenal medulla. Induction of TNBS-colitis markedly increased NGF, BDNF, and NT-3 expression within the adrenal cortex after 8 h. NGF declined to basal levels after 7 days. In case of BDNF and NT-3 basal expression levels were reached after 14 days. GDNF expression was robustly upregulated in the adrenal medulla 8 h after induction of colitis and stayed elevated for up to 14 days. CONCLUSION: Together these observations suggest that neurotrophins and GDNF might act as local modulators of components of the HPA-axis during peripheral inflammation.

Protective role of neurotrophins in experimental inflammation of the rat gut.

BACKGROUND & AIMS: Sensory neuropeptides modulate the mucosal response to inflammation in experimental colitis. Because nerve growth factor (NGF) regulates the expression of neuropeptides such as substance P and calcitonin gene-related peptide (CGRP) and is implicated as a link between the nervous system and the immune system in the inflammatory process, we investigated the functional role of NGF and neurotrophin-3 during experimental colitis. METHODS: Immunoneutralizing antibodies specific for NGF and neurotrophin (NT)-3 were used to block their endogenous activity. Mild trinitrobenzene sulfonic acid (TNBS) colitis was induced, and damage scores were assessed after 1 week. Neuropeptide content in the colon and NT messenger RNA (mRNA) expression were determined. RESULTS: The pretreatment with anti-NGF or anti-NT-3 caused a significant 2-3-fold increase in the severity of the experimental inflammation as assessed by a macroscopic damage score, histologic ulceration score, and myeloperoxidase activity in the tissue. CGRP, but not substance P, contents in the colon were significantly reduced by NGF immunoneutralization. NGF mRNA was slightly up-regulated after NGF immunoneutralization, but NT-3 mRNA was unchanged by NT-3 immunoneutralization. CGRP mRNA was not significantly changed after 1 week of colitis by NGF or NT-3 immunoneutralization, whereas beta-preprotachykinin mRNA was up-regulated after immunoneutralization. CONCLUSIONS: These findings suggest a regulatory role for NGF and NT-3 in experimental inflammation of the gut. This effect may be partly caused by the reduction of mucosal CGRP content caused by the NGF blockade.

Calcitonin gene-related peptide mediates the protective effect of sensory nerves in a model of colonic injury.

Recently we demonstrated that sensory denervation with the neurotoxin capsaicin worsened the inflammation in an acute and chronic model of experimental colitis, which suggests a protective role of sensory nerve fibers during gut inflammation. Because we could demonstrate that sensory neuropeptides like Calcitonin gene-related peptide (CGRP) and substance P (SP) are released from sensory nerve fibers during intestinal inflammation, both are strong candidates as mediators for the protective effect of sensory neurons. In this study we investigate the role of CGRP and SP during experimental colitis in the rat by use of receptor antagonists against CGRP (CGRP 8-37, 1 microg/h continuous subcutaneous infusion), SP (RP67580, a NK-1 receptor antagonist, 3 mg/kg i.p.) and an immunoneutralizing CGRP-antibody. A mild colitis was induced by a rectal enema containing trinitrobenzenesulfonic acid. The severity of inflammation increased markedly after 7 days in the CGRP receptor antagonist and CGRP-antibody group compared with the vehicle group as determined by a macroscopic damage score (10.4 +/- 1.2 and 9.6 +/- 1.6 vs. 6.2 +/- 2.1) by a histologic ulceration score (82 +/- 8% and 73 +/- 6% vs. 42 +/- 23%) and by myeloperoxidase activity (19.2 +/- 6.8 and 18.1 +/- 5.9 vs. 8.6 +/- 5.3 U/mg tissue protein), respectively. Treatment with the specific SP receptor antagonist did not significantly alter the severity of colitis at 7 days compared with the control group. These data suggest that CGRP exerts mucosal protection during chronic experimental colitis.