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Query: UMLS:C0149871 (
deep vein thrombosis
)
12,364
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Thalidomide has antiangiogenic properties and was found to be effective in patients with multiple myeloma (MM) when used in the setting of posttransplantation relapse. We have now analyzed risk factors associated with development of
deep vein thrombosis
(
DVT
) in a cohort of 535 patients treated with thalidomide with cytotoxic chemotherapy (VAD [vincristine/doxorubicin/dexamethasone], CAD [cyclophosphamide/doxorubicin/dexamethasone], DCEP [dexamethasone/cyclophosphamide/etoposide/cisplatin], or DT-PACE [dexamethasone/thalidomide/cisplatin/doxorubicin/cyclophosphamide/etoposide] or without cytotoxic chemotherapy (thalidomide and dexamethasone only). A total of 82 patients developed
DVT
, and the frequency was affected by a number of baseline characteristics. On multivariate analysis, the combination of thalidomide with chemotherapy including doxorubicin was associated with the highest odds ratio (OR) for
DVT
(4.3; P < or = 0.001); in addition, newly diagnosed disease (OR, 2.5; P = 0.001) and chromosome 11 abnormality (OR, 1.8; P = 0.048) were also independent predictors for
DVT
. With a median follow-up of 2.9 years, survival was inferior in patients with chromosome 13 abnormalities (P = 0.001), age > 60 years (P = 0.001),
lactate dehydrogenase
level > or = 190 IU/L (P = 0.002), and creatinine level > or = 2 mg/dL (P < 0.001). However, the development of
DVT
did not adversely affect survival when examined as a time-dependent variable and adjusted for standard risk features (hazard ratio, 0.8; P = 0.162).
...
PMID:Thalidomide and deep vein thrombosis in multiple myeloma: risk factors and effect on survival. 1283 52
Venous thromboembolism (VTE) constitutes a common cause of hospital-related morbidity and mortality, with the proverbial clinical feature of
deep venous thrombosis
(
DVT
). Endothelial cell injury and dysfunction comprise the critical contributor for the development of
DVT
. Lipoxin A4 (LXA4) fulfills pleiotropic roles in injury repair. However, its role in
DVT
remains poorly elucidated. In the present study, LXA4 supplementation dampened H
2
O
2
-evoked cytotoxic injury in human umbilical vein endothelial cells (HUVECs) by increasing cell viability, suppressing cell apoptosis and caspase-3 activity. Moreover, treatment with LXA4 afforded cytoprotective effects against oxidative stress damage in response to H
2
O
2
by abrogating ROS,
lactate dehydrogenase
(
LDH
) and MDA leakage, and elevating anti-oxidant SOD levels. Notably, LXA4 administration attenuated pro-vasoconstriction factor endothelin-1(ET-1) expression in HUVECs exposed to H
2
O
2
, but enhanced the productions of vasodilatation factor NO and prostacyclin (PGI2). Simultaneously, H
2
O
2
-induced high expression of pro-thrombotic Von Willebrand Factor (vWF) was also inhibited by LXA4. Mechanism analysis substantiated that LXA4 further augmented activation of the Nrf2-HO-1 pathway. Nevertheless, blocking this signaling via si-Nrf2 transfection or HO-1 antagonist ZnPP both reversed LXA4-mediated effects against oxidative stress injury and thrombotic potential. Cessation of the LXA4 receptor pathway by its inhibitor Boc2 not only counteracted LXA4-evoked activation of the Nrf2-HO-1, but also reversed LXA4-mediated anti-oxidative stress and thrombosis-related factor expression. Accordingly, this study suggests that LXA4 may ameliorate vascular endothelial cell oxidative stress injury and subsequent thrombotic response via LXA4 receptor-dependent activation of the Nrf2-HO-1 signaling, implying a promising strategy for
DVT
and its complication.
...
PMID:Lipoxin A4 restores oxidative stress-induced vascular endothelial cell injury and thrombosis-related factor expression by its receptor-mediated activation of Nrf2-HO-1 axis. 3105 86
