Die Diagnostik der diabetischen Polyneuropathie und die Prävention sowie die Behandlung des diabetischen Fußsyndroms (DFS) sind ein Fokus der Forschung in der Diabetologie seit mehr als 3 Jahrzehnten. Der Einfluss des Notfallmanagements auf die Prognose von Notfallpatienten mit DFS ist bislang weitestgehend unerforscht. In klinischen Fußbehandlungseinrichtungen werden immer wieder schwere Verläufe bei Patienten mit DFS beobachtet, die eine schnelle und interdisziplinäre Behandlung erfordern. Gelangen Patienten mit einem solchen Notfall nicht in eine spezialisierte Einrichtung, ergibt sich häufig aufgrund der mangelnden Vertrautheit mit den verschleierten Symptomen ein durch Zeitverlust bedingter Gewebe- und ggf. auch Extremitätenverlust. Dieser Artikel trägt dazu bei, auf die speziellen Gegebenheiten aufmerksam zu machen und eine Diskussionsgrundlage für die Erstellung von interdisziplinären „fast tracks“ in der Aufnahmestrategie von Notfallpatienten mit DFS zu bieten.

Fragestellung: Typ 1 Diabetes lässt sich in Übereinstimmung mit den Grundgedanken des Salutogenesemodells (Antonovsky, 1993, 1997, 1998) als chronischer Stressor betrachten. Im Salutogenesemodell wird das Kohärenzgefühl als zentrale Steuerungsfunktion definiert, die die Widerstandsfähigkeit gegenüber Stressoren erhöht und den Einsatz von Bewältigungsressourcen anregt. (Antonovsky, 1997) Studien zum Kohärenzgefühl bei Diabetes mellitus zeigen, dass das Kohärenzgefühl mit der Akzeptanz des Diabetes (Richardson et al., 2001), der emotionalen Bewältigung (Lundman & Norberg, 1993) und diabetesspezifischer Selbstwirksamkeit (Shuk-Man Li, 2007) in Beziehung steht. Allerdings werfen die Befunde die Frage nach dem Zusammenhang zwischen dem Kohärenzgefühl und Bewältigungsressourcen einerseits sowie dem Kohärenzgefühl und diabetesbezogenen Belastungen andererseits auf.

Fragestellung: Im Salutogenesemodell von Antonovsky (1997) wird das Kohärenzgefühl (sense of coherence) als zentrale Steuerungsfunktion definiert, welche die Widerstandsfähigkeit gegenüber Stressoren erhöht und den Einsatz verschiedener Ressourcen und Copingstile anregt. Aufgrund bisheriger Studienergebnisse sind signifikante Zusammenhänge des Kohärenzerlebens mit psychologischen Facetten der Krankheitsverarbeitung, nicht aber mit der Stoffwechseleinstellung gemessen am HbA1c, zu erwarten. Jedoch lässt die Heterogenität des Krankheitsbildes die Annahme zu, dass in Subgruppen des Patientenkollektivs (weibliche Patienten, Patienten ohne Folgeerkrankungen) auch Zusammenhänge zwischen Kohärenzerleben und somatischen Parametern zu finden sind.

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study

Background and Aim: Rapid blood tests for diagnosis of Helicobacter (H.) pylori infection enable to detect antibodies against H. pylori instantly without laboratory equipment. Primary aim: to validate the Helisal (TM) Rapid Whole Blood Test (HRBT) with endoscopic bioptic methods as reference. Secondary aim: to compare the HRBT with ELISA IgG serology. Patients and Methods: The HRBT was performed in 145 consecutive dyspeptic patients (median age 59 years) before undergoing esophagogastroduodenoscopy including biopsies from gastric antrum and corpus. A positive H. pylori status was defined by a positive culture or the combination of a positive rapid urease test and a positive histology, Serum for ELISA IgG testing was available from 92 patients.Results: The H. pylori status was positive in 66% of the patients. The sensitivity of the HRBT resulted at 80%, the specificity at 82%. The sensitivity of the HRBT for a positive ELISA test amounted to 87%, the specificity to 96%.Conclusions: The diagnostic validity of the HRBT is insufficient for clinical application. False test results add up by the general discrepancy between serological and bioptic methods and by diminished sensitivity compared to ELISA serology.

Zusammenfassung Hintergrund und Ziel: Blutschnelltests zur Diagnose der Helicobacter-(H.-) pylori -Infektion ermöglichen den Nachweis von Antikörpern gegen H. pylori ohne zeitlichen und apparativen Aufwand. Primäres Ziel: Validierung eines Blutschnelltests, des Helisal™ Rapid Whole Blood Test (HRBT), mit endoskopisch-bioptischen Methoden als Referenz. Sekundäres Ziel: Vergleich des HRBT mit ELISA-IgG-Serologie. Patienten und Methoden: Der HRBT wurde bei 145 konsekutiven Patienten (medianes Alter 59 Jahre) durchgeführt, bevor sie sich wegen Dyspepsie einer Ösophagogastroduodenoskopie mit Antrum- und Korpusbiopsien unterzogen. Ein positiver H.-pylori -Status wurde definiert durch eine positive Kultur oder die Kombination von positivem Ureaseschnelltest mit positiver Histologie. Bei 92 Patienten stand Serum für einen IgG-ELISA-Test zur Verfügung. Ergebnisse: Der H.-pylori -Status war in 66% positiv. Die Sensitivität des HRBT lag bei 80%, die Spezifität bei 82%. Die Sensitivität des HRBT für einen positiven ELISA-Test betrug 87%, die Spezifität 96%. Schlussfolgerungen Die diagnostische Validität des HRBT reicht für die klinische Anwendung nicht aus. Falsche Testergebnisse summieren sich durch die Diskrepanz zwischen serologischen und bioptischen Methoden allgemein und durch eine gegenüber der ELISA-Serologie verminderte Sensitivität.

Helicobacter pylori (H. pylori) causes chronic gastritis of variable activity and distribution. Well established consequences are peptic ulcer disease, gastric cancer and low-grade gastric MALT lymphoma. Cure of the infection is associated with long-term remission of peptic ulcer disease in patients not taking Aspirin or non-steroidal antiinflammatory drugs. Eradication of the bacteria may also bad to complete remission of early stage low-grade gastric MALT lymphoma. it is, however, unclear whether treating the infection will reduce the risk of gastric cancer. Controlled studies on this subject have been started world-wide. Increasing evidence sugggests that H.pylori may also induce autoimmune gastritis with destruction of gastric glands it is still controversial whether H.pylori infection is causally linked to functional dyspepsia. Well designed long-term studies in patients suffering from functional dyspepsla suggest that the benefit of treating the infection is at best marginal There is some evidence to suggest that the infection may protect from gastro-oesophageal reflux disease, especially in patients with a more severe corpus gastritis. Anti-secretory drug treatment deteriorates the severity of corpus gastritis. it remains controversial whether antisecretory drugs also accelerate the development of pre-neoplastic lesions like atrophy. On the other hand, H.pylori renders antisecretory drugs more effective. The H.pylori infected stomach does not adapt to Aspirin. Some preliminary data suggest that curing the infection may reduce the gastrotoxicity of low-dose Aspirin. The rob of H.pylori in the pathogenesis of NSAID associated lesions remains controversial. While one study showed a significant reduction of NSAID induced ulcers following the cure of H.pylori infection, other studies did not indicate any benefit in terms of ulcer healing and ulcer prophylaxis in patients presenting with NSAID induced ulceration. In all patients with H.pylori related diseases, the infection should be treated with one-week triple therapy consisting of a proton pump inhibitor, clarithromycin and amoxicillin or metronidazole.

AIM:To test the hypothesis that 1-week low-dose triple therapy for H. pylori is sufficient for relief from dyspeptic symptoms and healing of duodenal ulcers.METHODS:Fifty-nine out-patients with duodenal ulcers and positive rapid urease test participated in this randomized, double-blind, two-centre study. All patients were treated for 1 week with omeprazole 20 mg b.d., clarithromycin 250 mg b.d. and metronidazole 400 mg b.d. In a double-blind fashion, patients were then randomly treated for another 3 weeks with either omeprazole 20 mg once daily or an identical-looking placebo. Patients were investigated endoscopically before treatment for H. pylori, after 2 weeks and after 4 weeks. H. pylori infection was assessed by a 13C-urea breath test at the time of enrollment and 4 weeks after cessation of any study medication.RESULTS:Fifty-two patients were included in the 'all patients treated' analysis of efficacy. The overall H. pylori cure rate was 96% (95% CI = 87-100%), with no difference between the treatment groups. After 2 weeks duodenal ulcer healing was confirmed in 91% (95% CI = 80-100%) of patients treated with omeprazole and in 76% (95% CI = 60-91%) in the placebo group (P = 0.14). After 4 weeks all ulcers had healed. Relief from dyspeptic symptoms and adverse events (13.8 and 16.7%) did not differ between the treatment groups.CONCLUSIONS:One-week low-dose triple therapy consisting of omeprazole, clarithromycin and metronidazole is a highly effective and well-tolerated approach to the cure of H. pylori infection in patients with a duodenal ulcer. Our data suggest that continuation of antisecretory drug therapy beyond anti-H. pylori therapy is actually excessive regarding relief from dyspeptic symptoms and healing of duodenal ulcers.

Basic problem and objective of study: The situation of pretherapeutical antimicrobial drug resistance of Helicobacter pylori has therapeutical implications. For this reason the present study was designed to evaluate the frequency of resistance in Germany. Material and methods: A total of 201 H. pylori isolates cultured on the basis of biopsies taken by routine gastroscopies were tested for resistance by E-test. The antibiotics examined were amoxicillin, tetracycline, clarithromycin and metronidazole. For further analysis the last 101 patients were asked for demographical and clinical data that were evaluated for a correlation with metronidazoIe resistance. Results: Pretherapeutical resistance against amoxicillin and tetracycline was not detected. The rate of drug resistance against clarithromycin came to 3% and against metronidazole to 29%. There was a higher incidence of metronidazole resistance in female patients (Odds ratio 1, 71, p = n. s.). Reliable predictors for metronidazole resistance, however, could not be identified. Conclusions: About 30% of H. pylori isolates are pretherapeutically resistant to metronidazole. Resistance to clarithromycin is still rare, but further monitoring remains necessary to detect changes in the community.

BACKGROUND:Previous studies have shown that one-week triple therapy consisting of omeprazole, clarithromycin and amoxycillin may cure Helicobacter pylori infection in the vast majority of patients. The present study was designed to test the hypothesis that a triple therapy with pantoprazole, clarithromycin and amoxycillin cures the infection in > or = 80% of duodenal ulcer patients infected with H. pylori.METHODS:In an open two-centre study, 60 duodenal ulcer patients were treated with pantoprazole 40 mg b.d., clarithromycin 500 mg b.d. and amoxycillin 1 g b.d. for 1 week. During the second week patients received pantoprazole 40 mg once in the morning. We assessed H. pylori infection before treatment and 4 weeks after cessation of the study medication by a rapid urease test, histology after Warthin-Starry stain and a 13C-urea breath test.RESULTS:Sixty patients (42 males, mean age 47.4 years) entered the trial. All patients were infected with H. pylori. One patient was withdrawn from the study because of allergy to penicillin and six patients were protocol violators. H. pylori infection was cured in 47 out of 53 patients who completed the trial according to the protocol (89%; 95% CI: 80-97%) and in 49 of 60 patients included in the trial (82%; 95% CI: 72-92%). Four weeks after the last administration of study drugs, 55 out of 60 ulcers had healed (92%). Twenty-nine patients reported 51 adverse events that were mostly mild to moderate.CONCLUSIONS:One-week triple therapy consisting of pantoprazole, clarithromycin and amoxycillin is a simple and effective approach to the cure of H. pylori infection in patients with duodenal ulcer. In those patients who took the drugs as prescribed the H. pylori cure rate was 89%, with the lower 95% confidence limit being 80%.

BACKGROUND: In healthy subjects, continuous infusions of high dose ranitidine and omeprazole produce high intragastric pH values. AIM: To test the hypothesis that both drugs also maintain high intragastric pH values in patients with bleeding ulcers. PATIENTS AND METHODS: In two parallel studies, 20 patients with bleeding duodenal ulcers and 20 patients with bleeding gastric ulcers were randomly assigned to receive either ranitidine (0.25 mg/kg/hour after a bolus of 50 mg) or omeprazole (8 mg/hour after a bolus of 80 mg) for 24 hours. Intragastric pH was continuously recorded with a glass electrode placed 5 cm below the cardia. RESULTS: Both drugs rapidly raised the intragastric pH above 6. During the second 12 hour period, however, the percentage of time spent below a pH of 6 was 0.15% with omeprazole and 20.1% with ranitidine (p = 0.0015) in patients with duodenal ulcer; in patients with gastric ulcer it was 0.1% with omeprazole and 46.1% with ranitidine (p = 0.002). CONCLUSIONS: Primed infusions of omeprazole after a bolus produced consistently high intragastric pH values in patients with bleeding peptic ulcers, whereas primed infusions with ranitidine were less effective during the second half of a 24 hour treatment course. This loss of effectiveness may be due to tolerance.

BASIC PROBLEM AND OBJECTIVE OF STUDY:The situation of pretherapeutical antimicrobial drug resistance of Helicobacter pylori has therapeutical implications. For this reason the present study was designed to evaluate the frequency of resistance in Germany.MATERIAL AND METHODS:A total of 201 H. pylori isolates cultured on the basis of biopsies taken by routine gastroscopies were tested for resistance by E-test. The antibiotics examined were amoxicillin, tetracycline, clarithromycin and metronidazole. For further analysis the last 101 patients were asked for demographical and clinical data that were evaluated for a correlation with metronidazole resistance.RESULTS:Pretherapeutical resistance against amoxicillin and tetracycline was not detected. The rate of drug resistance against clarithromycin came to 3% and against metronidazole to 29%. There was a higher incidence of metronidazole resistance in female patients (Odds ratio 1.71; p = n.s.). Reliable predictors for metronidazole resistance, however, could not be identified.CONCLUSIONS:About 30% of H. pylori isolates are pretherapeutically resistant to metronidazole. Resistance to clarithromycin is still rare, but further monitoring remains necessary to detect changes in the community.

BACKGROUND: In patients with duodenal ulcer cure of Helicobacter pylori infection resulted in a pronounced decrease in intragastric pH during treatment with omeprazole. AIM: To test the hypothesis that treatment of H pylori adversely affects the pH response to ranitidine. PATIENTS: Eighteen patients with duodenal ulcer who were infected with H pylori were studied. METHODS: Twenty four hour pH recordings were performed during treatment with ranitidine (300 mg) at night before and four to six weeks after cure of H pylori infection. Presence of H pylori was assessed by a rapid urease test, culture, histology, and a 13C urea breath test. Also, the fasting gastrin concentrations were measured before and after treatment for H pylori infection. RESULTS: Cure of H pylori infection resulted in a considerable improvement in both antral and corpus gastritis and a decrease in fasting gastrin concentrations. As a result of the cure the night time intragastric pH during treatment with ranitidine decreased (median pH 6.8 v 5.4; p = 0.007), whereas the acidity during the daytime was not affected. CONCLUSIONS: In patients with duodenal ulcer the intragastric pH during treatment with ranitidine depends on H pylori. However, the loss of effectiveness in altering pH seems to be less pronounced than previously found with omeprazole.

OBJECTIVE:We have previously shown that, in duodenal ulcer patients, pH control by omeprazole is less pronounced after cure of Helicobacter pylori infection. The present study was designed to test the hypothesis that this response to omeprazole persists 1 yr after cure of H. pylori infection.METHODS:In 12 duodenal ulcer patients, intragastric acidity was measured with a glass electrode during treatment with omeprazole (20 mg) once daily before, and 4-6 wk and 1 yr after, cure of H. pylori infection. H. pylori infection was assessed by [13C]urea breath test, culture, histology (Warthin Starry stain), and rapid urease test.RESULTS:Cure of H. pylori infection resulted in a lowered pH during omeprazole treatment. This effect persisted after 1 yr. Median 24-h gastric pH before H. pylori treatment was 5.6; 4-6 wk after cure of the infection it was 2.9 (p = 0.003), and 1 yr after cure of the infection it remained unchanged (pH = 2.5; p = 0.5). Accordingly, twice as much time was spent above pH 3 and pH 4 before H. pylori treatment than 1 or 12 months after cure (percent of time > or = pH 3: 82.7 vs. 49.7 vs. 43.1; percent of time > or = pH 4: 72.7 vs. 38.3 vs. 26.4).CONCLUSION:In duodenal ulcer patients, cure of H. pylori infection resulted in a marked rapid and persistent decrease of the pH increasing effect of omeprazole. Therefore, H. pylori is a determinant of the pH achieved in response to omeprazole treatment in duodenal ulcer patients.