Risk factors for UPE in malignant oncologic patients.
Risk factors for acute VTE in cancer patients included patient related factors (age,
prior history of VTE and number of chronic medical comorbidities),
cancer related factors (primary site of cancer,
tumor stage and time interval from cancer diagnosis) and treatment related factors (hospitalization,
hormonal and biological therapy,
supportive measures) .
Our study suggested elder patient with adenocarcinoma in advanced stage had high risk for UPE,
which was consistent with previous studies.
Among the independent risk factors revealed in our study,
bed rest or immobilization,
deep vein catheterization,
recent surgery and chemotherapy were also consistent with previous studies.
some risk factors such as physical performance declination and VTE history which were identified in several studies were of no statistical significance in our study.
This might be attributed to inadequate sample size.
some uncertain factors such as gender,
smoke and alcohol intake were not correlated with UPE in our study either.
Comparison of BMI between the two groups demonstrated a P value of 0.0549,
a critical level of statistical significance,
which might due to inadequate sample size or crowd differences.
the conclusions of our study are almost consistent with most current studies .
AVA and UPE in in malignant oncologic patients.
Quantitation of AVA is essential in evaluating the correlation between AVA and related diseases.
CT and MRI are available methods for quantification of AVA .
We measured AVA on high resolution CT images in our study and the results showed TAVA,
VAV/BSA were all statistically different between the UPE group and the control group.
multivariate logistic regression analysis suggested that AATV,
VATV/BMI and VATV/BSA were independent risk factors of UPE.
Every increase of TAVA by 50cm3,
the risk of UPE will increase 45.2%.
Every increase of VAV by 50cm3,
the risk of UPE will increase 95.5%.
Every increase of VATV/BMI by 5 units,
the risk of UPE will increase 126.7%.
Every increase of VATV/BSA by 50 units,
the risk of UPE will increase 67.2%.
The correlation between AVA and the occurrence of VTE has not been reported before as far as we know.
Our study showed no statistical difference in BMI between the two groups (P=0.0549).
As VAV was one of the independent risk factors of UPE,
while BMI was not,
which imply that AVA is more reasonable than BMI in risk prediction of UPE for oncologic patients.
In a study focusing on AVA and arteriosclerosis,
VAV/SAV was reported to be an important indicator for hyperlipemia and arteriosclerosis in obese person independent of BMI .
Our study demonstrated no statistical difference in VAV/SAT between UPE group and the control group,
and no correlation was found between VAV/SAT and UPE in regression analysis (p=0.1971).
It remains to be further studied whether or not VAV/SAT is a risk factor of UPE for patients with oncological malignancy.
3 .AVA and UPE: pathophysiological mechanism.
The pathophysiological mechanism of the correlation between AVA and the occurrence of UPE is still obscure.
The adipokine expression and secretion in AVA has been well documented by several biopsy based histological studies .
AVA functions not only as endocrine organ secreting hormones,
but also as inflammatory tissue secreting cytokines and chemokines .
Researches revealed that obese people have more inflammatory cells and medium than people with normal weight .These cytokines and accumulated inflammatory cells may have multiple impacts on vascular endothelium,
resulting in endothelial damages and dysfunction .
Joint with the hyper coagulating state induced by malignant tumor ,
we assume these factors synergistically increase the risk of thrombosis.
A recent study suggested that immune activation and inflammatory adherence existed throughout the formation of acute VTE.
They hypothesize that VTE is the result of a biological filamentous mesh-like structure formed when circulated allotype antigen cells failed to be effectively and timely cleared in the presence of immune dysfunction .
Relative studies provide new visual angle in the theoretical knowledge of the impact of AVA on the genesis of VTE.
the accurate mechanism still needs further investigations.
Our study is a case-control retrospective study,
and due to relatively small sample size,
conclusions still need to be proved by large scale prospective investigations.
the mechanism of the correlation between AVA and UPE still waits to be elucidated by further clinical and preclinical studies.