Correlation between 18-fluorodeoxyglucose accumulation in large vessels and serological markers of inflammation in polymyalgia rheumatica: a quantitative PET study.

OBJECTIVE: To quantify 18-fluorodeoxyglucose (FDG) accumulation in large vessels in patients with polymyalgia rheumatica by positron emission tomography (PET), and to compare these data with serological markers of inflammation. METHODS: 13 untreated patients with active polymyalgia rheumatica underwent FDG positron emission tomography; eight were analysed in a second PET when in clinical remission. Six patients with other highly inflammatory conditions served as controls. For quantitative analysis, FDG uptake over nine defined vascular regions, divided by an individual background value, was expressed as a region of interest (ROI) index. These data were compared with the clinical status of the patient and with erythrocyte sedimentation rate (ESR), C reactive protein, haemoglobin, and platelet and leucocyte counts. RESULTS: By visual evaluation, 12 of the 13 patients showed an increased tracer uptake of the aorta or its major branches. By quantitative analysis, FDG uptake was significantly increased in polymyalgia rheumatica. In patients with active disease, the mean ROI index for all vascular regions exceeded that of controls by 70% (mean (SD): 1.58 (0.37) v 0.93 (0.12); p<0.001). In the eight patients who underwent follow up PET, the index declined substantially. In active polymyalgia rheumatica, FDG uptake was significantly correlated with C reactive protein (r = 0.8), ESR (r = 0.79), and platelet counts (r = 0.68). CONCLUSIONS: The observed FDG accumulation in the aorta and its branches and a strong correlation between tracer uptake and markers of inflammation is suggestive of large vessel arteritis. Quantitative ROI analysis appears to be a sensitive tool for detecting such inflammation.

Treatment of advanced rectal cancer in a patient after combined pancreas-kidney transplantation.

BACKGROUND: Organ transplantation is a standard procedure today. Due to immunosuppressive drugs and increasing survival after organ transplantation, patients with transplanted organs carry an increased risk of developing malignant tumours. Accordingly, more patients with malignant tumours after transplantation will be faced by general or oncology surgeons. We report the case of a 48-year-old patient with advanced rectal cancer 6.5 years after pancreas-kidney-transplantation for type I diabetes. METHOD: The patient was treated with neo-adjuvant radio-chemotherapy, followed by low anterior rectal resection with total mesorectal excision. Consecutively, a solitary hepatic metastasis, a solitary pulmonary metastasis and a chest wall metastasis were resected over the course of 13 months. RESULT: The patient eventually died of metastasized cancer 32 months after therapy had been initiated, his organ grafts functioning well until his death. CONCLUSION: Our case report provides evidence that transplantation patients should receive standard oncology treatment, including neo-adjuvant treatment, so long as their general condition and organ graft functions allow us to do so, although a higher degree of morbidity might be encountered.

[Quality standards and their assurance for study centers in the competence network malignant lymphoma]. / Qualitätsstandards und ihre Sicherung für Studienzentralen im Kompetenznetz Maligne Lymphome.

BACKGROUND: The aim of most of the trials of the Competence Network Malignant Lymphoma is to optimize the standard treatment of lymphoma using only registered drugs in the case of medicinal therapies (quality assurance protocols). In contrast to regulatory trials, special regulations for quality assurance protocols are not given by the legislature. However, there is agreement that also for this type of studies the declaration of Helsinki and the Guidelines of the International Conference on Harmonisation (ICH) are relevant. The ICH Guidelines must be formulated to take into account the specific situation of quality assurance protocols and to ensure at the same time efficiency and transparency of these studies. This is the aim of the quality management of the study groups in the Competence Network Malignant Lymphoma. METHOD: The quality assurance measures already established in the study groups are being expanded to a comprehensive quality management concept in agreement with the ICH Guidelines and allowing for the situation of quality assurance protocols. To this end, a working group for quality management (AG-QM) has been set up to define and establish general quality standards for all aspects of planning, executing and evaluating quality assurance protocols in study centers. RESULTS: The AG-QM has developed a system of Standard Operating Procedures (SOPs) reflecting all working procedures of the study centers. Furthermore, evaluation parameters for the quality of trial execution have been identified and the harmonisation of documentation parameters has been initiated. Term definitions are collected and their harmonisation coordinated. CONCLUSIONS: Development of quality standards is the first step of quality management. To ensure the realisation of these standards in practice, the AG-QM will establish quality assurance measures including continuous reevaluation of quality criteria and actualization of quality standards if necessary.

Impact of laparoscopic CO2-insufflation on tumor-associated molecules in cultured colorectal cancer cells.

BACKGROUND: Laparoscopic CO2-insufflation is believed to stimulate proliferation and metastatic potential of gastrointestinal carcinomas. E-cadherin, I-CAM1, I-CAM2, and CD44 are involved into the metastatic process of different cancer cell lines. The current study investigates the influence of CO2-insufflation on the expression of E-cadherin, I-CAM1, I-CAM2, and CD44 in vitro. METHODS: CX-2 and CC531 colon carcinoma cells (human/rat) were exposed to pneumoperitoneal CO2-insufflation. E-cadherin, I-CAM1, I-CAM2, and CD44 were measured 0, 12, 24, 48, and 72 h after CO2-insufflation using flowcytometry. Control groups were exposed to room air. Data were analyzed by the Wilcoxon-Mann-Whitney U-test. RESULTS: Both cell lines showed significant alteration in E-cadherin, I-CAM1, and CD44 expression after CO2 exposure (p <0.05). No significant differences were found regarding I-CAM2 expression. CONCLUSION: The present study demonstrates CO2-insufflation to influence the expression of E-cadherin, I-CAM1 and CD44. Whether these changes increases the metastatic potential of colorectal cancer cells in vivo needs further investigation.

Linkage and allelic association of atopy and markers flanking the IL4-receptor gene.

BACKGROUND: Atopy, a clinical syndrome characterized by heightened IgE responsiveness, is largely determined by genetic factors. The disease may well be heterogeneous but the mode of inheritance is unknown. Several genes have been named which affected IgE responsiveness. However, results are conflicting reflecting heterogeneity and a complicated inheritance pattern of the atopic syndrome. In 1994 linkage of the 5q32 gene region and elevated total IgE levels were reported, leaving the IL4 gene as a prominent candidate. OBJECTIVES: We were interested in a possible involvement of the IL4-receptor gene in the development of atopy. METHODS: We employed sib-pair linkage analysis using highly polymorphic microsatellite markers within and flanking the IL4 receptor gene in atopic families, characterized for specific sensitization to inhalant allergens and elevated total serum IgE. Allele sizes were determined for all microsatellite probes to allow transmission disequilibrium analysis. RESULTS: We found significant sharing of maternal but not paternal alleles in affected sibs from two independent populations, both of which presented enhanced IgE responsiveness. Linkage and maternal inheritance could be confirmed by transmission disequilibrium analysis. CONCLUSIONS: We conclude from our findings that maternal inheritance of a gene in the chromosome 16p12 region increases the risk for enhanced IgE responsiveness. The most prominent candidate in this region is represented by the IL4 receptor gene.