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„Klug entscheiden“ ist eine von der Deutschen Gesellschaft für Innere Medizin (DGIM) initiierte Serie, im Rahmen derer diagnostische und therapeutische Positivempfehlungen zusammengefasst werden sollen, die von besonderer medizinischer Bedeutung sind und die wissenschaftlich nachweislich nutzbringend sind, jedoch nach Expertenmeinung häufig nicht fachgerecht erbracht werden. Diese Positivempfehlungen weisen also auf eine Unterversorgung hin. Neben Positivempfehlungen wurden gleichzeitig Negativempfehlungen formuliert, d.h. es wurden diagnostische und therapeutische Empfehlungen herausgearbeitet, die zwar häufig angewandt werden, für die es aus Sicht der Fachgesellschaften aber wenig bzw. keine wissenschaftliche Evidenz gibt, und die somit den Kriterien der Überversorgung entsprechen. Bislang wurden von jeder internistischen Fachgesellschaft je fünf Positiv- und fünf Negativ-Empfehlungen erarbeitet, weitere sind derzeit in Vorbereitung.

The molecular mechanisms mediating mucous cell metaplasia and hypersecretion in the respiratory tract are unknown. Previous work suggests that mucous metaplasia requires the induction of mucin gene expression. We are investigating this possibility by monitoring steady state levels of mucin mRNA in a model of mucous cell metaplasia induced by SO2exposure. Male Sprague Dawley rats were exposed to 400 ppm SO2gas in air for 3h per day, 5 days per week for 0,1,2, or 3 weeks. Sham controls were exposed to air under similar conditions. After 3 weeks, morphological changes were apparent in the epithelium of SO2exposed rats at all levels from the trachea to the distal airways. The epithelial thickness increased, as well as the number and size of glands in the trachea. Epithelial mucous (goblet) cells increased from 0 to 4.5 per rom in the trachea, 0.2 to 6.2 per rom in the main stem bronchi, and 0.2 to 22.7 per rom in the distal airways (mean values obtained for 3-6 tissue blocks per airway level per condition). In parallel experiments, we used SMUC 41, a 950 bp human intestinal cDNA to isolate a human airway cDNA, HAM-1 from a cDNA library constructed in bacteriophage from human bronchial poly A+ RNA. HAM-1 is a 90 bp cDNA encoding a threonine- and proline-rich peptide with 96% homology to the human intestinal cDNA SMUC-41. Next we probed total and poly A+ airway RNA from rats in each exposure condition with SMUC-41 or HAM-1. Blots were then stripped and reprobed with a cDNA encoding beta actin. Densitometry values normalized for the amount of RNA loaded per lane (as determined by actin hybridization intensity) showed that mucin mRNA increased 8-9 fold as a function of SO2exposure. This is consistent with the possibility that mucin gene transcription is induced by SO2exposure, and may represent a primary event in the development of mucous metaplasia and hypersecretion.

Using digoxigenin–UTP‐labelled human HAM‐1(92 bp) or SMUC41(850 bp) cRNA probes, the expression and localization of MUC2gene transcripts were determined by in situhybridization in human nasal tissues obtained as biopsies from 12 patients with cystic fibrosis (CF): all had been part of a gene therapy trial in which CFTRcDNA–liposome complexes had been delivered by topical application to eight and liposome alone to four as a placebo control. For comparison, there were nasal tissues taken at surgical resection from four non‐CF subjects and a further four biopsies taken from normal healthy volunteer controls. Both SMUC41and HAM‐1probes provided a strong signal. MUC2mRNA transcripts were present in serous and mucous acini of submucosal glands, ciliated and basal cells of the surface epithelium, and occasional mononuclear inflammatory cells. The percentages (mean±SEM) of serous and mucous acini showing positivity for MUC2gene expression in the four samples surgically resected from non‐CF subjects were 25·4±5·6 and 26·7±3·3 per cent, respectively. Compared with the non‐CF subjects, the mean percentage of acini showing MUC2gene expression in the four placebo‐treated CF subjects was significantly higher for serous (80·5±12·7 per cent; P<0·05, t‐test), but not for mucous acini (53·1±16·8 per cent; P=0·38). In CF and non‐CF groups, where present, MUC2positivity was strongly expressed and constituted approximately 84 per cent of the cell area in serous acini, whereas it was less obvious and was confined to the perinuclear area of cells in mucous acini. A significantly greater proportion of the surface epithelium was positive for MUC2mRNA transcripts in the CF subjects (89·0, ±1·4 per cent) than in the surgically resected tissues of the four non‐CF subjects (19·4, ±4·0 per cent) (P=0·02). In the eight CFTR‐cDNA‐treated subjects, there was an overall trend to reduction, but no statistically significant alteration of MUC2gene expression. It is concluded that the MUC2gene is expressed at three‐ tofour‐fold higher levels in CF nasal mucosa than in non‐CF nasal tissue and that it is expressed in a variety of cells additional to submucosal mucus‐secreting glands. © 1997 John Wiley & Sons, Ltd.

Using digoxigenin–UTP-labelled human HAM-1 (92 bp) or SMUC41 (850 bp) cRNA probes, the expression and localization of MUC2 gene transcripts were determined by in situ hybridization in human nasal tissues obtained as biopsies from 12 patients with cystic fibrosis (CF): all had been part of a gene therapy trial in which CFTR cDNA–liposome complexes had been delivered by topical application to eight and liposome alone to four as a placebo control. For comparison, there were nasal tissues taken at surgical resection from four non-CF subjects and a further four biopsies taken from normal healthy volunteer controls. Both SMUC41 and HAM-1 probes provided a strong signal. MUC2 mRNA transcripts were present in serous and mucous acini of submucosal glands, ciliated and basal cells of the surface epithelium, and occasional mononuclear inflammatory cells. The percentages (mean±SEM) of serous and mucous acini showing positivity for MUC2 gene expression in the four samples surgically resected from non-CF subjects were 25·4±5·6 and 26·7±3·3 per cent, respectively. Compared with the non-CF subjects, the mean percentage of acini showing MUC2 gene expression in the four placebo-treated CF subjects was significantly higher for serous (80·5±12·7 per cent; P&lt;0·05, t-test), but not for mucous acini (53·1±16·8 per cent; P=0·38). In CF and non-CF groups, where present, MUC2 positivity was strongly expressed and constituted approximately 84 per cent of the cell area in serous acini, whereas it was less obvious and was confined to the perinuclear area of cells in mucous acini. A significantly greater proportion of the surface epithelium was positive for MUC2 mRNA transcripts in the CF subjects (89·0, ±1·4 per cent) than in the surgically resected tissues of the four non-CF subjects (19·4, ±4·0 per cent) (P=0·02). In the eight CFTR-cDNA-treated subjects, there was an overall trend to reduction, but no statistically significant alteration of MUC2 gene expression. It is concluded that the MUC2 gene is expressed at three- tofour-fold higher levels in CF nasal mucosa than in non-CF nasal tissue and that it is expressed in a variety of cells additional to submucosal mucus-secreting glands. © 1997 John Wiley & Sons, Ltd.

The significance of neuron-specific enolase (NSE) in the diagnosis and treatment monitoring of lung cancer was investigated in comparison with such established tumour markers as carcinoembryonic antigen (CEA), tissue polypeptide antigen (TPA), ferritin and calcitonin. We determined the serum concentrations of these tumour markers in 25 patients with small cell lung cancer (SCLC), 30 patients with non small cell lung cancer (NSCLC), and 38 patients with benign pulmonary diseases (BPD). In 14 patients with lung cancer, it was possible to follow up the behaviour of the tumour markers under treatment for up to 16 months. Calcitonin proved to have a surprisingly low sensitivity for SCLC. The utility of TPA and of ferritin was restricted, although the sensitivity was comparably high, by the high rate of false positive results. For NSCLC, CEA proved to be the best tumour marker. At present, NSE appears to be the tumour marker with the greatest specificity and sensitivity for SCLC. Its determination in the diagnosis, treatment and follow-up of SCLC makes good sense.

ABSTRACTSpondylodiscitis caused by Campylobacterspecies is a rare disease which is most often caused by Campylobacter fetus. We report a case of culture-negative spondylodiscitis and a psoas abscess due to Campylobacter jejuniin a 68-year-old woman, as revealed by 16S rRNA gene and Campylobacter-specific PCRs from biopsied tissue.