Intra-operative ultrasound facilitates the localization of the calcific deposit during arthroscopic treatment of calcifying tendinitis.

PURPOSE: Calcifying tendinitis is a common condition of the shoulder. In many cases, arthroscopic reduction in the deposit is indicated. The localization of the deposit is sometimes challenging and time-consuming. Pre-operative ultrasound (US)-guided needle placement in the deposit and pre-operative US marking of the deposit at the skin with a ballpoint are described and recommended methods to alleviate the procedure without using ionizing radiation by fluoroscopy. METHODS: Intra-operative sonography of the shoulder is introduced as a new method to localize the calcific deposit with high accuracy. After standard arthroscopic buresectomy, the surgeon performs an ultrasound examination under sterile conditions to localize the deposits. A ventral longitudinal US section is recommended, and the upper arm is rotated until the deposit is visible. Subsequently, perpendicular to the skin at the position of the transducer, a needle is introduced under arthroscopic and ultrasound visualization to puncture the deposit. RESULTS: The presence of snow-white crystals at the tip of the needle proves the exact localization. Consecutively, the curettage can be accomplished. Another intra-operative sonography evaluates possible calcific remnants and the tendon structure. CONCLUSION: This new technique may alleviate arthroscopic calcific deposit curettage by visualizing the deposit without using ionizing radiation. Additionally, soft tissue damage due to decreased number of punctures to detect the deposit may be achieved. Both factors may contribute to reduced operation time.

G-455A polymorphism of the fibrinogen beta gene and deep vein thrombosis.

BACKGROUND: Elevated fibrinogen levels have been linked to increased risk for deep venous thrombosis, although it is not clear whether fibrinogen is causal or rather a marker for the presence of other risk factors. A common G/A polymorphism in the gene for the fibrinogen beta-chain (FGB G-455A) is associated with elevated fibrinogen levels. The present study was designed to analyze the role of this genetic marker for deep venous thrombosis. MATERIALS AND METHODS: We performed a case-control study including 307 patients with documented deep venous thrombosis and 316 control subjects. beta-fibrinogen genotypes were determined by allele-specific polymerase chain reaction. RESULTS: GG, GA and AA genotype frequencies were similar among the patients (53.1%, 41.0, 5.9) and controls (51.6%, 42.1, 6.3; P = 0.92). Fibrinogen levels of the patients (median 3.72 g l-1; range 1.93-11.6) did not differ significantly from those of the controls (3.76; 2.17-9.99). Carriers of the homozygous AA genotype had significantly higher fibrinogen levels than noncarriers (patients: 5.32 vs. 3.59; P = 0.024; controls: 6.29 vs. 3.72; P = 0.048). CONCLUSION: Our data suggest that the fibrinogen-elevating FGB G-455A gene polymorphism is not linked to an increased risk for deep venous thrombosis.

[Protection against myocardial ischemia by nisoldipine--an experimental study with valinomycin K-sensitive microelectrodes]. / Myokardiale Ischämieprotektion durch Nisoldipin--eine experimentelle Untersuchung mit Valinomycin-K-sensitiven Mikroelektroden.

It has been shown that dihydropyridines exert a cardioprotective effect during experimental ischemia. This effect is reflected in a reduced K-efflux from the ischemic tissue. Recently we have shown that ischemic K-efflux is largely mediated by ATP-dependent K-channels. Using K-selective microelectrodes we studied the effect of nisoldipine on K-efflux during simulated ischemia (guinea pig papillary muscle immersed in paraffin oil; normal Tyrode solution, HEPES buffered, 100% O2-equilibrated, 37 degrees C). While ischemic K-efflux was Ca-dependent in stimulated preparations, it was independent of extracellular Ca in resting preparations. Our results show that nisoldipine leads to an inhibition of ischemic K-efflux during simulated ischemia. In resting preparations this inhibition is not a direct Ca-antagonistic effect, since withdrawal of extracellular Ca does not inhibit ischemic K-efflux but nisoldipine does. We suggest a direct effect of nisoldipine on the KATP channel which is mainly responsible for ischemic K-loss.