{'fraction_non_alphanumeric': 0.060770975056689346, 'fraction_numerical': 0.023582766439909298, 'mean_word_length': 4.835978835978836, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Clinical significance of plasminogen activator inhibitor-1 (PAI-1) in the early development of HSCT-associated thrombotic complications.].

OBJECTIVE
To illustrate the early alteration of plasminogen activator inhibitor-1 (PAI-1) in the recipients of hematopoietic stem cell transplantation (HSCT) and explore its clinical significance in transplantation-associated thrombotic complications.


METHODS
Ninety-five patients undergoing HSCT were enrolled in this study. PAI-1 level and other hemostatic parameters were measured by enzyme linked immunosorbent assay (ELISA) in platelet poor plasma samples from patients on conditioning therapy and then weekly until four weeks after HSCT.


RESULTS
Significant increase in PAI-1 was detected after conditioning treatment, followed by a diminution in the very week on transplantation (week 0), then increased with in time after transplantation. According to the occurrence of transplant-associated complications, patients were classified into four groups: thrombus group \[veno-occlusive disease (VOD) (n = 5), thrombotic microangiopathy (TMA) n = 1\], aGVHD group (n = 29), infection group (n = 19) and non-complication group (n = 41). One of 30 patients (3.3%) was diagnosed as thrombus in the auto-HSCT group, while five of 65 patients (7.7%) did in the allo-HSCT group. PAI-1 level of thrombotic patients was significantly increased compared with non-thrombotic subjects, and the patients without thrombotic complications have higher PAI-1 level in the allo-HSCT group than in auto-HSCT group. All the patients with complications presented with significantly increased PAI-1 compared with those with no complications (P < 0.05). The six patients with thrombotic complications showed extremely elevated PAI-1 \[(62.8 +/- 7.5) microg/L\] compared with that of aGVHD patients \[(45.1 +/- 9.1) microg/L\] or infection patients \[(50.0 +/- 11.2) microg/L\] post-HSCT (P < 0.05).


CONCLUSION
The increase in plasma PAI-1 may be a specific mark for transplantation-associated thrombotic complications. Increased PAI-1 reflects the development of thrombotic complications. Extreme elevation of PAI-1 contributes to the early diagonsis of VOD and TMA after HSCT.