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Das diabetische Fußsyndrom (DFS) ist die häufigste Ursache einer Majoramputation in Deutschland. Die meisten Fußläsionen werden durch repetitive Druckbelastung bei diabetischer Polyneuropathie ausgelöst. Die PAVK (periphere arterielle Verschlusskrankheit) verhindert die Wundheilung und ist Hauptrisikofaktor für Amputationen. In diesen Fällen ist die zeitnahe Revaskularisation entscheidend. Der Einsatz von endovaskulären und gefäßchirurgischen Methoden ist abhängig von Verteilungsmuster und Länge der Verschlussprozesse, wobei sich die Techniken ergänzen. Die Wahl des Verfahrens orientiert sich aber auch am perioperativen oder -interventionellen Risiko der häufig alten, multimorbiden Patienten. Das Alter selbst ist kein Ausschlusskriterium, allerdings ergibt sich bei hochbetagten DFS-Patienten häufig die Situation, dass aufgrund zahlreicher Vorbehandlungen keine anatomische oder technische Möglichkeit der Revaskularisation besteht („no option“) oder dass sie für komplexe Eingriffe einfach zu krank sind („too sick“). Multidisziplinäre Zentren, die Revaskularisationen bei DFS anbieten, können in 90 % der Fälle eine Verbesserung der arteriellen Durchblutung erreichen und die Amputationsrate um bis zu 80 % senken. Wegen der hohen Rezidivrate diabetischer Fußläsionen sind Maßnahmen zur Sekundärprophylaxe von herausragender Bedeutung. Dazu gehören regelmäßige Nachuntersuchungen der Füße, die Versorgung mit adäquatem Schuhwerk und Einlagen sowie eine kompetente podologische und orthopädietechnische Betreuung. Chirurgische Korrekturen von Fuß- und Zehendeformitäten zur Vermeidung von Rezidivulzera können die gefäßmedizinischen Ergebnisse langfristig unterstützen.

AbstractThe bone mineral density (BMD) and the associated extracellular status of mineral and acid-base metabolism were evaluated in 11 males, 3–18 years after total gastrectomy (GX). In the lumbar spine, but not in the femoral neck, BMD was decreased in seven, normal in three, and falsely high in one individual. Relative to the limits of normalcy, fasting serum levels of gastrin were low, but normal for calcium, phosphorus, parathyroid hormone, calcitonin and vitamin D, while the level of total alkaline phosphatase was elevated; fasting urine pH and calcium were low, while phosphorus and net acid were high. Regression analyses revealed serum gastrin and phosphorus, and urinary net acid as possible predictors of BMD. It was concluded that over the long-term GX evokes low BMD, but not hyperparathyroidism and deranged vitamin D metabolites. Future studies may focus on gastrin, parathyroid hormone-independent hyperphosphaturia and disturbed acid-base metabolism as indicators of a new extra-cellular equilibrium of minerals.

Summary: The influence of postprandial-like plasma insulin levels on intestinal calcium absorption (CaA) was studied in 9 health men. On separate occasions, they received either an i.v. infusion of 40 mU/m2 minute synthetic human insulin as well as a variable glucose infusion in order to clamp the plasma glucose at the baseline level (=glucose clamp), or insulin- and glucose-free vehicle infusions (=vehicle). During these infusions, an oral load containing 326 mg Ca in the form of Ca chloride was administered and CaA was determined thereafter with a47Ca/85Sr double tracer method. During glucose clamp, mean plasma insulin was 172 ±(1 SEM) 10 as compared to 6±1 μU/ml during vehicle infusions. During the clamp, 3-hour cumulative CaA rose significantly by 14% as compared to vehicle (39.2±2.5 vs. 34.4±2%,P<0.02). At the same time, serum potassium and phosphorus dropped significantly, whereas serum parathyroid hormone (PTH) and 1,25(OH)2D levels were unchanged as compared to vehicle. The urinary excretions of potassium, sodium, and inorganic phosphorus as well as the urinary specific activity of47Ca, dropped significantly during glucose clamp, whereas the urinary excretion of cAMP was unchanged as compared to vehicle. The results suggest that, under the conditions of euglycemic hyper-insulinemic clamp, insulin stimulates CaA of healthy humans in a PTH- and 1,25(OH)2D-independent manner. Insulin may thus possibly be regarded as a factor participating in the regulation of CaA in humans.

Summary: Usingin situ perfusion in the rat, we studied the duodenal bidirectional fluxes (LP, lumen-to-plasma; PL, plasma-to-lumen) and the net absorption of calcium (Ca) at progressive molar citrate: Ca ratios (1∶1, 2.1∶1, 8.5∶1) and three pH levels (pH 5.0, 6.25, 7.0) of the Ca-containing (4 mmol/liter) perfusion solution. Rats perfused with pH-adjusted, citrate-free solutions served as controls. LP-flux and net calcium absorption (net CaA) fell dose-dependently with increasing citrate concentrations. Also, at a given citrate:Ca ratio, LP-flux and net CaA fell with increasing pH of the perfusion solution. PL-fluxes did not change from control values, irrespective of the composition of the perfusion solution. The concomitant serum Ca and parathyroid hormone levels as well as blood pH and bicarbonate, were largely unchanged under any of the citrate-containing perfusion solutions. In conclusion, citrate inhibits duodenal CaA of the rat pH- and dose-dependently, without changing intestinal Ca secretion. This effect is not related to changes in the acid-base status or to suppressed parathyroid gland function of the animals and may be best explained by dose- and pH-dependent intraluminal complex formation between Ca and citrate.

•Investigation of painful and non-painful phantom phenomena in 3,374 unilateral limb amputees•Clinical and demographic variables explained 10.6% of the variance of phantom limb pain•Perceptual variables explained 16.9% of the variance of phantom limb pain•These variables were specific for phantom limb pain and not for residual limb pain