[Long-term prescription of benzodiazepines and non-benzodiazepines]. / Langzeitverschreibung von Benzodiazepinen und Non-Benzodiazepinen.

BACKGROUND: The number of persons with a dependence on prescription drugs such as sedatives or tranquilizers in Germany is estimated at between 1.4 and 1.9 million. According to national addiction treatment documentations only very few of them seek help in specialised treatment services. The majority of prescription drug-dependent people use benzodiazepines. This medication is usually prescribed by physicians and according to German guidelines it should be prescribed only for limited, short periods and in low doses. OBJECTIVE: This study aims to determine the extent of the problematic prescription of benzodiazepines and non-benzodiazepines. METHODS: We used prescription data from the Northern Germany Computing Centre for Pharmacies registered between 2005 and 2007. For the German regions of Hamburg, Bremen and Schleswig-Holstein, benzodiazepine prescriptions during an individual prospective period of 12 months were analysed. RESULTS: From July 2005 to June 2006, 294 143 prescriptions of benzodiazepines and non-benzodiazepines were recorded for 78 456 citizens of Hamburg and billed at the expenses of the governmental health insurance funds. In the course of one observed patient year, 51.1% of benzodiazepine prescriptions were in accordance with the German guidelines. 15.6% of the patients were supplied on a long-term basis (0.5-1 DDD during at least 2 months). Prescriptions for women and persons older than 70 years were disproportionately high. Compared with the Federal states of Bremen and Schleswig-Holstein, Hamburg does not show an exceptional position. CONCLUSION: The prescription of benzodiazepines which is not in accordance with the relevant national guidelines is widespread and calls for discussion and education among physicians and pharmacists. Furthermore, professional addiction services should reconsider ways to help and attract prescription drug-dependent people to cover their needs, as their numbers will grow in an aging society.

[Medication dependency and physician's role]. / Zusammenhang zwischen Verschreibungsverhalten der Arzte und Medikamentenabhängigkeit ihrer Patienten.

The administration of benzodiazepines in suicidal, anxious, or agitated patients with depression is common international practice. Nevertheless, the prescription of BZDs is recommended to be limited to a period of a few weeks. There are several epidemiological studies about the situation in Germany, but many questions are still unanswered. The BfArM sought a new method to track prescription of medications with the risk to induce dependency. The present article describes the methodology and the early results of the pilot study. As a new approach, data from a processing center for pharmacies were used; patient-years, a risk scale with six steps, and diazepam-equivalence dose instead of defined daily dose were used for the analysis. About 35% of prescriptions were long-term treatment. Even if several physicians prescribe the medication, the main physician prescribing the medication can identify the risk level of the patient in 80-90% of cases.

Reduction of oxygen delivery during post-ischemic reperfusion protects the isolated guinea pig heart.

OBJECTIVE: To further characterise the influence of oxygen delivery during early reperfusion (first 5 min) in the isolated guinea pig heart, three modes of coronary reperfusion were chosen, differing with respect to reperfusion flow and arterial PO2. METHODS: Isolated working guinea pig hearts underwent ischemia and reperfusion (15 min each). Reperfusion was at constant pressure (Group 1, 60 mmHg, n = 7) or at constant flow (Group 2, 5 ml/min, n = 7) with a PO2 of 600 mmHg. Group 3 (n = 8) was reperfused at 5 ml/min with a PO2 of 300 mmHg for 5 min and a PO2 of 600 mmHg thereafter. Lactate release and oxygen consumption were determined during reperfusion. Glutathione release served to assess myocardial oxidative stress. RESULTS: After ischemia, hearts in Group 1 (mean coronary flow 14.4 +/- 1.1 ml/min during the first 5 min of reperfusion) performed external heart work at 31 +/- 2% of the pre-ischemic level. Performance in Group 2 recovered to 50 +/- 3% and in Group 3 to 68 +/- 3%. Myocardial oxygen consumption during early reperfusion (2nd min) was lowest in Group 3 (1.9 micromol/min) and highest in Group 1 (8.3 micromol/min). No difference in lactate release was observed. Release of glutathione during the first 5 min of reperfusion was 43.8 +/- 7.9 nmol in Group 1, but only 3.6 +/- 0.7 in Group 2 (p < 0.05). CONCLUSIONS: In isolated guinea pig hearts, controlled oxygen delivery during post-ischemic reperfusion by both, reduction of coronary flow and PO2, improves recovery of pump function. The effect is accompanied by less oxidative stress, as indicated by lowered rates of glutathione release.

[Use of and participation in self-help groups for methadone substitution patients]. / Bedarf und Teilnahmebereitschaft an Selbsthilfegruppen für Substituierte.

To evaluate the importance of self-help groups and the patients' readiness to participate in such groups a sample of 675 methadone patients in Hamburg was asked by means of questionnaires. 43% of the patients had heard of self-help groups. One quarter of them (10% of the whole sample) had participated in self-help groups at some time. The greatest importance of self-help organisations is attached to a representation of the interests of methadone patients to improve their overall situation. Another important purpose of self-help groups is seen in getting help for legal, financial and social problems. Getting in contact with other clients or offering breakfast/lunch, washing clothes or shower facilities etc. is not evaluated as an important task for self-help organisations. Patients who are working on a regular basis and living in stable conditions are less interested in participating in self-help groups. Thus, the participants in self-help groups can hardly benefit from the experiences of the socially better integrated methadone patients.

Maintenance treatment of opiate addicts in Germany with medications containing codeine--results of a follow-up study.

AIMS: Outpatient maintenance treatment of opiate addicts with codeine/dihydrocodeine is a common approach in the treatment of drug addicts in Germany. This study was carried out to assess possible benefits of codeine maintenance in terms of patients' health stabilization, social rehabilitation and drug consumption. DESIGN: Three-year follow-up study. SETTING: Three practices of substituting physicians in large-city areas in Germany. PARTICIPANTS: Of a random sample of 297 people attending for opiate outpatient treatment in 1993, 199 were successfully followed up 3 years later. MEASUREMENTS: Measures of health, living conditions, employment, criminal activities and drug use were collected at baseline and follow-up. The data were based on standardized interviews and medical examinations by the attending doctors as well as on questionnaires from the patients. FINDINGS: Based on a 67%-follow-up rate, after 3 years of codeine maintenance there was improvement in general health and mental problems. The living and working situation remained more or less unchanged and stabilized at a satisfactory level. The same applies to the consumption of drugs. CONCLUSION: The patients' progress shown in this study was comparable to that achieved by methadone maintenance in similar geographical regions. Codeine has a weaker pharmacological effects and our results suggest that codeine maintenance treatment deserves more attention and controlled trials to assess the benefits compared with methadone (or other opioids).

Influence of intact left atrial appendage on hemodynamic parameters of isolated guinea pig heart.

BACKGROUND: In isolated working guinea pig heart preparations using the conventional technique of cannulating the left atrium via the atrial appendage, the resulting cardiac output is often insufficiently low (15-20 ml/min). This is a problem in ischemia reperfusion studies where small absolute differences can be responsible for large relative changes comparing pre- and postischemic values. In an attempt to increase cardiac output, the left atrium was left intact in isolated working guinea pig hearts. The two techniques were compared for hemodynamic parameters and their similarity to the physiological condition. METHODS: The left atrium was cannulated either via the orifices of the pulmonary veins or via an incision in the atrial appendage with its subsequent ligation around the cannula (n = 45-46/group). After 20 min of pressure-volume work cardiac output, heart rate and oxygen partial pressures were measured and myocardial oxygen consumption and cardiac efficiency were calculated. RESULTS: Cardiac output was higher in hearts with intact atrial appendage (64 +/- 2 ml/min) than in hearts with ligated atrial appendage (33 +/- 1 ml/min). Myocardial oxygen consumption (6.1 +/- 0.2 and 8.4 +/- 0.3 micromol/min, resp.) and cardiac efficiency (12.8 +/- 0.6% and 19.9 +/- 0.8%, resp.) were significantly higher in hearts with intact left atrial appendage. CONCLUSIONS: Isolated working guinea pig hearts with an intact left auricle exhibit higher values for important hemodynamic parameters compared to a preparation technique involving ligation of the left auricle.

Taurine protects the heart from neutrophil-induced reperfusion injury.

Deficiency of the amino acid taurine is implicated in various pathologic states of the heart. Besides other effects, taurine has been proposed to be an antioxidant. However, its benefit under conditions associated with the generation of reactive oxygen species in the heart has not been clearly demonstrated. To assess the potential of taurine to influence neutrophil-dependent reperfusion injury, a model was developed based on the isolated working guinea pig heart. After an initial work phase, hearts were subjected to 15 min of global ischemia. Reperfusion, in a nonworking mode, was carried out in the absence or presence of homologous neutrophils (PMN) and/or taurine. After 15 min, work was resumed and percentage recovery of function was determined another 20 min later. During the reperfusion phase, coronary venous effluent was collected to quantify release of lactate and glutathione, markers of ischemic challenge and redox-stress, respectively. Furthermore, direct effects of taurine on radical formation were investigated in a chemiluminescence assay. Control hearts without application of PMN or taurine had a postischemic recovery of external heart work (EHW) of 76%, in the presence of taurine (15 mM) recovery was 72%. The application of PMN for merely the first minute of reperfusion led to a significant decrease in recovery to 30%, PMN having no effect without a foregoing ischemia. When taurine was additionally applied during reperfusion, EHW recovered to 60%. Release of lactate and of oxidized glutathione (GSSG) did not differ between the groups. In contrast, effluent concentrations of reduced glutathione (GSH) were considerably elevated by the presence of PMN in the sample and remained high even after PMN-washout. Taurine tended to attenuate this PMN effect. At the 5th and 10th min of reperfusion, GSH release of individual hearts correlated inversely with postischemic recovery of EHW. Surprisingly, taurine, by itself, did not significantly alter glutathione release. However, taurine (15 mM) markedly reduced luminol-dependent chemiluminescence elicited by activated guinea pig PMN as well as by chemically generated hypochlorous acid and hydroxyl radicals, but not superoxide radicals. Our results demonstrate that taurine protects the heart from PMN-induced reperfusion injury and oxidative stress. Because respiratory burst activity of PMN was also significantly reduced in the presence of taurine, the beneficial effect appears to be mediated by antioxidative properties of taurine.

Adenosine and PAF dependent mechanisms lead to myocardial reperfusion injury by neutrophils after brief ischaemia.

OBJECTIVE: The aim was to establish whether polymorphonuclear neutrophils can, by themselves, elicit depression of postischaemic heart function immediately after short periods of ischaemia, and to examine the involvement of endogenous adenosine and platelet activating factor (PAF) in the observed phenomena. METHODS: Isolated buffer perfused guinea pig hearts performing pressure-volume work under standardised conditions were subjected to 15 min of global ischaemia. Constant flow reperfusion (5 ml.min-1) was carried out in the presence or absence of homologous neutrophils (approximately 2000 cells.microliters-1 perfusate). After 15 min of reflow, work was resumed and functional recovery assessed another 20 min later. RESULTS: In hearts perfused only with Krebs-Henseleit buffer, postischaemic heart function recovered to 67(SEM 3)% (n = 13) of the preischaemic value. As early as the first minute of reperfusion, the application of neutrophils already led to a significant decrease in recovery to 39(3)% (n = 12; P < 0.05). Without ischaemia, neutrophils did not have any deleterious effect, recovery of external heart work amounting to 91(4)% (n = 6). Adenosine concentrations measured in the coronary effluent after ischaemia were substantially increased during reperfusion from preischaemic values of < 20 nM to about 800 nM. The adenosine A1 receptor antagonist dipropyl-8-cyclopentyl-xanthine prevented the neutrophil dependent loss of heart function, as did application of the PAF receptor antagonist WEB 2086, recoveries being 60(4)% (n = 6) and 58(8)% (n = 6), respectively. In contrast, the A2 antagonist 3,7-dimethyl-1-propargyl-xanthine tended to worsen the neutrophil induced dysfunction of the heart, recovery amounting to 18(2)% (n = 5). CONCLUSIONS: Even after brief ischaemia, neutrophils introduced into the coronary system can exacerbate reperfusion injury. Adenosine, through its A1 receptor, and PAF appear to play a significant role as mediators of this action.

Stimulation of endothelial adenosine A1 receptors enhances adhesion of neutrophils in the intact guinea pig coronary system.

OBJECTIVE: The primary aim was to determine the action of pathophysiologically relevant adenosine concentrations (0.1-1 microM) on adhesion of neutrophils to coronary endothelium. Further aims were to evaluate the nature and localisation of the adenosine receptor involved, and to assess the effect of endogenous adenosine. METHODS: Adhesion was studied in isolated perfused guinea pig hearts by determining the number of cells emerging in the coronary effluent after intracoronary bolus injections of 600,000 neutrophils prepared from guinea pig or human blood. The system was characterised by the use of the proadhesive stimulus thrombin. RESULTS: A 5 min infusion of adenosine (0.1-0.3 microM) or the A1 receptor agonist N6-cyclopentyladenosine (CPA, 0.01 microM) significantly increased adhesion from about 20% (control) to 30%. This effect was prevented by the A1 receptor antagonist dipropyl-8-cyclopentylxanthine (DPCPX, 0.1 microM). It was not diminished by cessation of adenosine infusion 90 s prior to neutrophil injection. At a higher concentration of adenosine (1 microM), adhesion did not seem to be enhanced. However, coinfusion of the A2 receptor antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 0.1 microM) with 1 microM adenosine unmasked the A1 action, adhesion rising to 39%. Adenosine had a quantitatively identical effect on adhesion of human neutrophils. Total ischaemia of 15 min duration raised adhesion of subsequently applied neutrophils to 35%. This effect was completely blocked by DPCPX, as well as by ischaemic preconditioning (3 x 3 min). Preconditioning raised initial postischaemic coronary effluent adenosine from about 0.8 microM to 1.5 microM. CONCLUSIONS: The findings suggest a bimodal participation of adenosine in the development of postischaemic dysfunction by an endothelium dependent modulation of neutrophil adhesion. Stimulation occurs via endothelial A1 receptors at submicromolar adenosine levels, whereas cardioprotection by adenosine may in part relate to the use of pharmacologically high concentrations of adenosine or enhanced endogenous production after preconditioning.

Results of international and federal German evaluation studies of methadone substitution therapy--an overview. / Resultate internationaler und bundesdeutscher Evaluationsstudien zur Substitutionstherapie mit Methadon--eine Ubersicht.

After a brief historical review results of German evaluation studies are contrasted for the first time with international results concerning the efficiency of methadone treatment of heroin addicts. All studies report a fast and obvious improvement of the patients' physical and psychic well-being. Decrease is observed in drug related criminality as well as in its following consequences such as arrests, trials, and inprisonments. Patients distance themselves from the drug-scene and at the same time increase communication with a drug-free environment. One problem persisting for German methadone-patients is the reintegration into their education or job. As to this only minor improvements have been obtained. Already after a short time patients on a methadone-therapy reduce their illicit use of drugs substantially. Especially the consume of heroin is getting reduced if not totally given up. The use of other drugs such as cocaine, tranquilizers and barbiturates gets reduced. For a number of patients the use of benzodiazepines remains a problem. The time patients stay in methadone-therapies (and to a high degree the success of the therapy itself) depends on a well structured arrangement of the methadone program and on the methadone dosage. Long-term follow-up studies abroad show that after methadone treatment the percentage of patients staying abstinent in the long run is almost the same as after drugfree treatment.

Drug policy and the system of care and treatment in the Federal Republic of Germany.

In this article the absurdity of the prevailing drug policy in the Federal Republic of Germany is shown. The hithero existing system of care and treatment has been determined by the logic of criminalization; moreover, its range and effect was rather small. Instead of at least making corrections to this ineffective and inhuman system, German drug policy continues--despite some promising alternative approaches in some of the federal states--according to the slogan 'more of the same' and propagates the 'war on drugs'. The author, however, pleads for a 'change of paradigm' in drug policy, in which the idea of acceptance, decriminalization, pluralization of offers as well as communication-orientated drug-prevention would play a prominent role.

Adenosine contributes to neutrophil-mediated loss of myocardial function in post-ischemic guinea-pig hearts.

Tissue injury associated with myocardial ischemia is assumed to largely result from the toxic effects of active oxygen species generated by accumulated polymorphonuclear leukocytes (PMNs). Recent reports have indicated that adenosine can interfere with the PMN function in vitro. The potential of adenosine to influence PMN-mediated myocardial tissue injury was assessed using a model of ischemia-reperfusion injury developed in the isolated working guinea-pig heart perfused with homologous PMNs. After an initial work phase, hearts were subjected to 30 min low-flow ischemia (1 ml/min) in the absence and presence of PMNs. Work was resumed after 15 min reperfusion in a non-working mode (Langendorff). Adenosine in the coronary effluent reached a maximum of 0.2 microM during low-flow ischemia. Recoveries of external heart work and cardiac output were reduced from about 80% to about 40% by PMNs. Infusion of adenosine deaminase (ADA, 5 U/ml), theophylline (50 microM) or the selective A1-antagonist dipropyl-8-cyclopentylxanthine (0.1 microM) prevented this effect. Furthermore, application of adenosine (0.1 microM) in combination with PMNs also resulted in a loss of pump function, even in the absence of a direct ischemic stimulus. The data indicate that adenosine contributes to post-ischemic, PMN-mediated damage in the isolated working guinea-pig heart model by a receptor-mediated action.

Postischemic dysfunction of the heart induced by small numbers of neutrophils via formation of hypochlorous acid.

The role of polymorphonuclear neutrophils (PMN) in the injury of the heart following ischemia and reperfusion is still controversial. The aim of this study was to investigate whether small numbers of PMN may cause myocardial dysfunction in an isolated system, how the resulting loss of function can be characterized and whether the formation of hypochlorous acid (HOCl) can be responsible for the PMN-mediated effect. Isolated working guinea pig hearts were subjected to a 90% reduction of coronary flow for 30 min, with or without intracoronary infusion of homologous PMN (approximately 1-2 x 10(5) cells/min, i.e. about 5-10% of normal blood count). This ischemia was followed by a 15 min reflow period in a non-working ("Langendorff") mode before work was resumed. In hearts perfused only with buffer, post-hypoxic heart function recovered to 75-80% of the initial value. Inclusion of unstimulated PMN did not further attenuate cardiac function. However, cardiac output was decreased to 42% of the initial value, provided thrombin (0.3 U/ml) and H2O2 (10(-5) M) were also present, and the retained PMN (about 10% of those infused) were additionally stimulated during reflow by application of FMLP (10(-6) M for 1 min). In these instances, coronary flow at any time of the experiment and release of lactate or purines during ischemia and reflow did not differ significantly between hearts perfused with or without PMN. There was no substantial release of myoglobin in controls and in PMN-treated hearts. Inotropic stimulation of the hearts with noradrenaline or exogenous Ca2+ caused a sustained increase in contractile force. However, the response was significantly reduced in PMN-perfused hearts in comparison to control hearts. The myocardial contents of high-energy phosphates with and without inotropic stimulation proved to be identical irrespective of whether experiments had been performed in the absence or presence of PMN. A similar loss of myocardial function as mediated by PMN could be produced by infusing chemically generated hypochlorous acid (HOCl, 5 x 10(-7) M for 10 min). Strikingly, that portion of the infused HOCl which actually reacted with cardiac tissue was comparable to the amount shown to be generated by stimulating 10(6) PMN retained in the coronary system (about 7 nmoles). Supplementing the perfusate with the scavengers L-methionine (10(-4) M) or uric acid (5 x 10(-4) M) prevented the attenuation of heart function provoked by PMN. The results indicate that small numbers of PMN, sufficiently activated, can depress cardiac function after 30 min of ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)

[Possible significance of free oxygen radicals for reperfusion injury]. / Mögliche Bedeutung von Sauerstoffradikalen für den Reperfusionsschaden.

Enhanced formation of radicals during post-ischemic reperfusion, foremost of superoxide (O2-) and hydroxyl (OH) radicals, has been directly and indirectly demonstrated in a number of tissues. However, the close chemical interrelationship of O2- and OH with other non-radical oxidants, such as hydrogen peroxide (H2O2) and hypochlorous acid (HOCl), makes it prudent to speak of reactive oxygen metabolites in conjunction with cell and organ dysfunction incurred by reperfusion. In the case of the heart, evidence for the causal involvement of such reactive molecular species includes (1) the increased formation of lipid peroxides, (2) the ability to mimic all facets of reperfusion injury (arrhythmias, contractile and vascular dysfunction, infarct extension) by exogenously applying reactive oxygen species, and (3) the propensity of a great variety of antioxidative and radical scavenging measures to afford cardioprotection during reperfusion. Potential sources of reactive oxygen metabolites in the reperfused heart are the mitochondrial redox-chain, endothelial enzymes such as cyclooxygenase, monoaminooxidase, NO-synthase and xanthine oxidase, and formed blood constituents (platelets, monocytes, granulocytes). According to our own results, adenosine, endogenously formed in the heart during ischemia, rapidly enhances adhesion of granulocytes introduced into the coronary system at reperfusion. Furthermore, small numbers of these cells suffice to induce contractile dysfunction in an isolated guinea pig heart model of ischemia-reperfusion injury, the major mediator of damage being HOCl. The striking disparity between the enormous volume of experimental data supporting involvement of reactive oxygen metabolites in reperfusion damage and the virtual lack of clinical-therapeutic regimens employing anti-oxidative measures is largely due to a still rudimentary knowledge of the homeostatic control of formation and removal of radicals and oxidants. In particular, the inability to correctly assess the individual time-course and extent of oxidative stress seems to be a major problem. Also, confounding issues such as compartmentation of radical formation as opposed to radical scavenging and the unwitting down-regulation of endogenous protective systems (e.g., of uric acid in the course of inhibiting xanthine oxidase) need to be resolved. On the other hand, we have been able to demonstrate protection by ACE inhibitors elicited via endothelially produced nitric oxide (a scavenger of O2- and OH) in the isolated heart. Thus, enhancement of endogenous protection may offer a perspective for mitigating against reperfusion damage.

[Are the radical scavenging properties of ACE inhibitors with sulfhydryl groups in therapeutically effective concentrations of quantitative significance?]. / Sind Radikalfänger-Eigenschaften von ACE-Inhibitoren mit Sulfhydrylgruppen bei therapeutisch wirksamen Konzentrationen von quantitativer Bedeutung?

The chemiluminescence reaction elicited from luminol in the presence of hydroxyl radicals was concentration-dependently suppressed by captopril, indicating efficacious radical scavenging. As to be expected, ACE inhibitors lacking free sulfhydryl groups (ramipril, enalapril) were inactive. However, the endogenous scavenger and anti-oxidant uric acid proved to be far superior to captopril, when concentrations of both were compared that are realized in vivo. A substantial augmentation of endogenous scavenging ability during therapy with captopril thus seems unlikely. In a model of standardized myocardial hypoxia (isolated working heart of the guinea pig with 30 min low flow perfusion) captopril, ramiprilat and uric acid equally improved post-hypoxic heart function. There was no cardioprotective action of captopril in excess of that accountable for by inhibition of ACE. It seems possible that ACE (kininase II) inhibitors exert cardioprotection via elevated tissue levels of kinins: bradykinin also improved heart performance after low flow perfusion and bradykinin-induced coronary dilatation was markedly enhanced in the presence of ramiprilate, reflecting attenuated degradation by endothelial kininase II.

Cardiovascular reactions and respiratory events during platelet activating factor-induced shock.

The platelet activating factor (PAF), a low molecular phospholipid, plays an important role in inflammation, anaphylaxis, and shock state development. In the isolated perfused guinea pig heart, PAF induces a decrease in coronary flow and cardiac contractility and atrioventricular conduction disturbances. Furthermore, PAF mediates a powerful bronchoconstrictory action causing a severe impairment in respiratory function. In the present study an attempt was made to separate cardiac from respiratory events during PAF-induced shock in vivo. PAF was injected intravenously (0.1-10 micrograms/kg) into anesthetized guinea pigs ventilated with room air or 100% oxygen. Administration of 10 micrograms/kg PAF was uniformly lethal: already within 2 min, cardiac output decreased by 60% and end-diastolic left ventricular pressure increased markedly indicating cardiac failure. ECG recordings showed signs of acute myocardial ischemia. Arrhythmias occurred in terms of atrioventricular conduction delay. Blood pressure initially increased, then declined continuously to below baseline within 10 min. All animals died within 25 min. Ventilation with room air was paralleled by development of severe hypoxia. However, under ventilation with 100% oxygen a dissociation between PAF-mediated cardiac and respiratory effects occurred. It is concluded that the PAF-induced shock is primarily based on direct cardiac damage. Furthermore, the ECG signs of ischemia are most likely due to coronary spasms.

[Therapy of bladder cancer. Value of transurethral resection--treatment results]. / Die Therapie des Harnblasenkarzinoms. Stellung der transurethralen Resektion--Behandlungsergebnisse.

The significance of carcinomas of the bladder is shown on the basis of epidemiological data. A survey is given of the numbers of operations using various methods over the last 24 years; in our institution TuTuR is mainly used. A report is given on the indications, procedure and possibilities of complications, showing the limits of the method. Problems of radical operations, which make supravesical derivation of the urine necessary, are discussed. Our therapeutic results are presented in the form of mortality curves. The unfavourable therapeutic results cause us to pose the question once again whether, in the light of modern intensive medicine, greater radicality might not be recommendable.