Agreement of multislice CT angiography and MR angiography in assessing the degree of carotid artery stenosis in consideration of different methods of postprocessing.

OBJECTIVE: We investigated the agreement of multislice computed tomography angiography (CTA) and magnetic resonance angiography (MRA) in the quantitative measurement of carotid artery stenosis. The dependency of the agreement of the chosen postprocessing procedures was also investigated. METHODS: Fifty consecutive symptomatic patients were included in this study. In all patients, a CTA was performed with a 16-slice CT scanner. Within 30 days, the extracranial vessels were examined using a combined time-of-flight and contrast-enhanced MRA. The CT data sets were used to calculate the degree of stenosis according to the North American Symptomatic Carotid Endarterectomy Trial, European Carotid Surgery Trial, and Common Carotid methods by means of the 1-mm thick, transverse raw data (RD), a sagittal maximum-intensity projection reconstruction, and sagittal multiplanar reconstruction. In addition, a semiautomated analysis was done using a specialized postprocessing software. For all combinations of postprocessing procedures and methods of calculating the degree of stenosis, the correlation coefficient and the agreement based on Bland/Altman plots were calculated. RESULTS: Eleven of the 100 primarily included carotid arteries could not be evaluated. The correlation coefficients for all combinations were comparable and lied in the interval between 0.932 and 0.787. The best correlation was found for the combination of RD/sagittal multiplanar reconstruction and ECST method. The evaluation of the agreement gave a systematic overestimation of CTA between 1.9% and 10.7% with a 95% confidence interval between +/-26.7% and +/-43.3%. With the semiautomated postprocessing software, additional 33 vessels could not be evaluated. The agreement of the calculated degrees of stenoses was worse than that of the planar procedures. CONCLUSIONS: CTA and MRA had a feasible agreement in measuring the degree of stenosis of the carotid arteries. The best result could be obtained for the evaluation of the RD and the NASCET method. In this case one has to take into account a systematic overestimation of CTA of 1.9%. The combination with an additional reconstructive postprocessing procedure did not improve the result but might be useful for the radiologist to identify the location of the closest narrowing.

Diagnosis of hepatic veno-occlusive disease by plasminogen activator inhibitor-1 plasma antigen levels: a prospective analysis in 350 allogeneic hematopoietic stem cell recipients.

BACKGROUND: Veno-occlusive disease (VOD) is one of the most serious complications following allogeneic hematopoietic stem cell transplantation (HSCT) and is associated with a high mortality. We conducted a large trial in order to investigate the value of plasminogen activator inhibitor-1 (PAI-1) plasma antigen levels in VOD patients as PAI-1 has been described as a possible diagnostic marker of VOD. METHODS: In all, 350 stem cell recipients were included in our study. PAI-1 levels were analyzed prior to conditioning therapy and then weekly until eight weeks after HSCT. Transplantation-related complications (TRC) including VOD, microangiopathic hemolytic anemia (MAHA), and graft-versus-host disease (GVHD) were recorded weekly throughout the study. RESULTS: Maximum PAI-1 antigen levels were increased in all patients with VOD (n=15; mean 248 ng/ml; 95% CI 183-314 ng/ml). Maximum PAI-1 levels above 120 ng/ml showed a sensitivity of 100% and a specificity of 30.6% for VOD after HSCT. CONCLUSION: Our study underlines that maximum PAI-1 plasma antigen levels not exceeding 120 ng/ml have a strong negative predictive value in the diagnosis of VOD and thus represent a helpful non-invasive tool for exclusion of VOD after HSCT.

Factor XIII activity levels in patients with allogeneic haematopoietic stem cell transplantation and acute graft-versus-host disease of the gut.

Severe graft-versus-host disease (GvHD) of the gut clinically resembles Crohn's disease and ulcerative colitis. As low plasma levels of factor XIII (FXIII) have been described in chronic inflammatory bowel disease (CIBD) and as beneficial effects of FXIII concentrates in CIBD have been reported, we studied the FXIII plasma activity levels in patients undergoing allogeneic stem cell transplantation (SCT). In 20 of 22 patients with an uncomplicated course of SCT, FXIII stayed within the normal range (median 102 iu/dl, range 74-122), but was significantly reduced with the lowest FXIII levels on d 0 and 7 (d 0: median 83 iu/dl, range 55-165, d 7: median 83, range 70-101). In 20 of 22 patients with histologically proven GvHD of the gut, FXIII levels far below the normal range were observed (median 50, range 21-87) with a strong correlation between FXIII activity levels and degree of GvHD (r = -0.908; P < 0.001). We conclude that FXIII is consumed in patients with GvHD of the gut. As FXIII plays a a crucial role in haemostasis and wound healing, a study on the potential benefit of FXIII substitution in patients with severe GvHD of the gut might be rewarding.

Analgesic profile of peroral and topical ketoprofen upon low pH-induced muscle pain.

Topical analgesics are widely marketed for treatment of muscle and joint pain. We have recently developed a model of muscle pain and have used this model to evaluate the efficacy of commercially available topical and peroral ketoprofen in order to evaluate the time- and dose-dependence of analgesia. In the present study, we examined the dose- (0, 50, and 100 mg) and time-dependence (hourly to 8 h) of commercially available peroral and topical ketoprofen. In order to achieve infusion times of 8 h (and thus study the time course of analgesic action), we adapted the model of low pH-induced muscle pain in humans to these requirements by applying the infusions continuously for 10 min every hour for 8 h. We found that the 10 min infusion produced reliable and consistent pain levels that were reproducible over the 8 h of the study. The study was performed double-blind, randomized, and with a 1-week interval between each of five different sessions (cross-over). Altogether six volunteers underwent intramuscular infusions of isotonic phosphate-buffered saline solution of pH 5.2; during each 8 h session the infusion was switched on eight times with a duration of 10 min at 50 min intervals (there was no infusion during the 50 min interval). The intramuscular infusion of low pH phosphate buffer induced a localized dull-aching or stinging muscle pain sensation; the flow rate of the pH infusion was individually adjusted to induce pain of a magnitude of 20% on a visual analogue scale (ranging from "no pain" (0%) to "unbearable pain" (100%)). Twenty minutes after starting the infusion the volunteers received a capsule with either a placebo or 50 or 100 mg ketoprofen perorally and, in addition, either placebo gel or 50 or 100 mg of a 2.5% commercial ketoprofen gel was applied topically to the skin. One of the sessions included a placebo gel and an oral placebo. The intensity of the recurrent pain stimulus was significantly reduced by 59% following administration of 100 mg peroral ketoprofen within the first 3 h (P<0.03, Wilcoxon test); this analgesia lasted up to the sixth hour of the experimental protocol. Oral ketoprofen (50 mg) was less effective and reduced the pain intensity by 45% (P<0.05) from only the second to the third hour. In contrast, pain reduction after topical ketoprofen application was not of the same magnitude but appeared to be faster to develop (with a maximum effect within 1 h) on average. The maximum pain suppression with 100 mg topical 2.5% ketoprofen gel was by 51% (significant with P<0.03), while 50 mg topical ketoprofen produced a non-significant reduction of 29%. The apparent analgesia was rapid to develop but transient and pain ratings increased back to baseline values within 3 h for the 100 mg dose and within 2 h for the 50 mg dose. This data suggests that topical application of commercial gel-based systems does not provide long-lasting analgesia in the muscle when compared to perorally-dosed ketoprofen. In addition, the data show that even doses of 100 mg peroral ketoprofen do not provide complete relief of muscle pain.