To elucidate how unusually large von Willebrand factor (UL-VWF) multimers facilitate thrombus formation, their behavior was analyzed together with that of platelets in living mice deficient in the gene encoding the protease that cleaves UL-VWF, a disintegrin-like and metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13-/-). By crossing ADAMTS13-/- mice with green fluorescent protein-expressing transgenic mice (GFP mice), GFP-ADAMTS13-/- mice were obtained. The dynamics of GFP-expressing platelets were monitored employing intravital confocal fluorescent microscopy. Administration of a vasopressin derivative, DDAVP, a secretagogue of VWF increased the number of platelets adhered to vascular endothelial cells (VECs) on mesentery at sites recognized by an anti-VWF antibody. Some of these platelets were interconnected and aligned as beads on a string. They reached their maximum length at 5 min and were longer in GFP-ADAMTS13-/- mice than in GFP mice (5.3 ± 4.3, N = 6 vs 2.9 ± 2.1 μm, N = 4) (mean±SE). Focal injury of VECs by topical application of FeCl(3) developed longer (25, 3-50 vs 10, 2-25 μm, P < 0.01) (mean, 10th-90th percentile) and more stable (1.3, 0.3-6.3 vs 0.3, 0.2-1.3 s, P < 0.01) connected platelets in GFP-ADAMTS13-/- mice than in GFP mice. This study revealed that ADAMTS13 cleaves platelet-bound UL-VWF multimers, both during their secretion from VECs and after their adherence to injured vascular walls in veins. UL-VWF multimers either being secreted from VECs or circulating in plasma of ADAMTS13-/- mice appeared to facilitate the accumulation of longer and more stable VWF strings with more associated platelets on injured vascular walls.

The purpose of the retrospective study in cancer patients in Poland was to analyze the frequency of anemia and methods of its treatment. An attempt was also made to evaluate the hemoglobin (Hb) levels in relation to patient's performance status (PS) prior to and after anticancer treatment. A total of 999 patients (pts) were enrolled, who were followed for up to six chemotherapy cycles or six evaluation points within a 6-month period. The incidence of anemia at the time of enrollment into the study equaled 31%, and was observed mainly among gynecologic and colorectal cancer pts. After anticancer treatment, anemia was reported in 54% of patients, mainly in gynecologic and lung cancer pts. As many as 71% of patients were anemic at some point of time during the survey, which was most often documented among gynecologic, lung and testicular cancer patients. At the 5th visit more than 50% of patients were anemic. The difference between the mean Hb level at 1st and 6th visit was 1.04 g/dL. However, anemia was treated in only 32% of patients (red blood cell transfusions, 61%; iron supplementation, 33%; while erythropoietic, stimulating proteins in just 6%). Worse PS was observed in anemic pts with lung as well as with head and neck cancer. In Poland the occurrence of anemia in cancer patients is as high as 70%. Anemia in this group of patients is underestimated and undertreated. This calls for more attention of physicians providing medical care to cancer patients.