Background: Adrenocortical hormones, particularly 11-oxygenated androgens, are pivotal in female reproductive health and fertility. Standardized detection kits and population-specific reference intervals are lacking in China, hindering related clinical applications. Methods: A HPLC-tandem mass spectrometry (HPLC-MS/MS) pipeline was developed, rigorously validated, and applied to simultaneously quantify corticosterone, cortisone, cortisol, 18-OH cortisol, androstenedione (A4), 11β-hydroxyandrostenedione (11-OH A4), dehydroepiandrosterone, and dehydroepiandrosterone sulfate in serum samples from 455 reproductive-aged women (18–45 yrs) in Guangxi, China. Age-dependent concentration trends were analyzed, and reference intervals stratified by age (2.5th to 97.5th percentiles) were established. Correlations with body-composition metrics, ethnicity, and the menstrual cycle were investigated. Results: The HPLC-MS/MS method demonstrated high precision (intra- and inter-assay CVs < 15%), accuracy, and sensitivity. All eight hormones exhibited significant age-related declines (P < 0.001 for seven hormones; P = 0.001 for 11-OH A4). Notably, 11-OH A4 levels were significantly lower in the 35–45-yr (3.05 nmol/L) and 25–34-yr (3.09 nmol/L) age groups than in the 18–24-yr (3.57 nmol/L) age group, whereas no significant difference was observed between the 35–45-yr and 25–34-yr age groups. Weak negative correlations were observed between the body mass index and corticosterone and cortisone levels, whereas ethnicity and the menstrual cycle showed no significant associations with hormone levels. Conclusions We developed an HPLC-MS/MS-based method for simultaneously quantifying eight adrenocortical hormones, including 11-OH A4, and defined age-specific reference intervals for reproductive-aged Chinese women. These findings advance the clinical utility of adrenocortical hormones in diagnosing and managing reproductive disorders.

Hepatocellular carcinoma （HCC） is one of the major malignancies with the heaviest disease burden in China. Many patients have lost the opportunity for radical surgical resection at the time of diagnosis， with locoregional interventional therapy playing an increasingly important role in full-course HCC management. Contrast-enhanced ultrasound （CEUS） enables real-time dynamic assessment of tumor microvascular perfusion and has several practical advantages including bedside availability， no ionizing radiation， and repeatability， and its role has therefore expanded from an adjunctive diagnostic method to the full-course management of precise locoregional diagnosis and treatment for HCC. Before treatment， CEUS can assist in the qualitative diagnosis of lesions， lesion localization， delineation of the viable tumor， and planning of the puncture route， especially for lesions that are poorly visualized on conventional ultrasound. During and after treatment， CEUS can help to detect residual viable tumor， related complications， and local tumor progression， thereby providing a basis for additional ablation， transcatheter arterial chemoembolization， or adjustment of combined treatment strategies. In recent years， the CEUS LI-RADS treatment response assessment system has provided a standardized framework for evaluating response after locoregional therapy， and in addition， the development of unimodal and multimodal fusion imaging techniques has further promoted the standardized application of CEUS in precise locoregional therapy for HCC. As increasing attention is paid to the ablation margin， the goal of response evaluation for local ablation has shifted from “the achievement of imaging-defined complete ablation” to a new treatment paradigm of “no contrast-enhanced imaging， no ablation； no fusion imaging， no curative ablation”. This article reviews the technical advantages， clinical application value， treatment response assessment， fusion imaging strategies， and current limitations of CEUS in locoregional interventional diagnosis and treatment of HCC， in order to provide a reference for the individualized and precise management of HCC.

ObjectiveTo investigate the mechanism by which Sini San （SNS） treats liver fibrosis through regulating the polarization of intrahepatic Kupffer cells. MethodsSixty SPF-grade male Balb/c mice were randomized into blank control， model， silymarin （0.2 g·kg^-1）， and low-， medium-， and high-dose （2.93， 5.85， 11.70 g·kg^-1， respectively） SNS groups. A mouse model of liver fibrosis was induced by intraperitoneal injection of CCl₄. After 5 weeks of administration， the body mass， liver pathological changes ［Hematoxylin and Eosin （HE）， Masson， and Sirius red staining］， serum biochemical indicators ［alkaline phosphatase （ALP）， aspartate aminotransferase （AST）， and alanine aminotransferase （ALT）］， liver fibrosis markers ［procollagen type Ⅲ （PCⅢ）， laminin （LN）， and hyaluronic acid （HA）］， inflammatory cytokines ［interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and interleukin-10 （IL-10）］， and fibrosis-related proteins ［α-smooth muscle actin （α-SMA）， collagen type Ⅰ （Col Ⅰ）， and collagen type Ⅲ （Col Ⅲ）］ were assessed. A co-culture system of THP-1 cells （M1 macrophages） and human hepatic stellate cells （LX-2） was established. The cell experiment was designed with blank control （LX-2 alone）， model （LX-2 + M1 macrophages）， and low-， medium-， and high-dose SNS （co-culture with 5%， 10%， or 20% SNS-containing serum， respectively） groups. Cell viability， inflammatory cytokines， and macrophage phenotype were examined. Human primary hepatic Kupffer cells were allocated into blank control， M1 （LPS 100 μg·L^-1+IFN-γ 20 μg·L^-1）， M2 （IL-4 20 μg·L^-1+IL-13 20 μg·L^-1）， M1+M2， M1+SNS （supplemented with 10% SNS-containing serum for 2 h after culture under M1 conditions for 24 h）， M2+SNS （supplemented with 10% SNS-containing serum for 2 h after culture under M2 conditions for 24 h）， and M1+M2+SNS groups （supplemented with 10% SNS-containing serum for 2 h after culture under M1+M2 conditions for 24 h）， and the expression of nuclear factor-κB （NF-κB） p65 and signal transducer and activator of transcription 3 （STAT3） at protein and mRNA levels was determined. ResultsCompared with the blank group， the model group exhibited increased serum levels of ALT， AST， ALP， PCⅢ， LN， HA， IL-6， and TNF-α， upregulated protein and mRNA levels of α-SMA， Col Ⅰ， and Col Ⅲ in the liver tissue （P<0.05， P<0.01）， and decreased IL-10 level and STAT3 mRNA level （P<0.05， P<0.01）， accompanied by marked collagen deposition and inflammatory infiltration in the liver. Compared with the model group， all doses of Sini San reversed these alterations （P<0.05， P<0.01）， with the high-dose group showing the most pronounced effects. Cell experiments demonstrated that， compared with the blank control group， the model group had elevated levels of pro-inflammatory cytokines （IL-1β， IL-6， and TNF-α） and upregulated protein and mRNA levels of M1 markers ［cluster of differentiation 86 （CD86， inducible nitric oxide synthase （iNOS）， and monocyte chemoattractant protein-1 （MCP-1）］ （P<0.01）， along with declined level of IL-10 and downregulated expression of M2 markers ［（CD163， CD206， and arginase-1 （Arg-1）］ （P<0.05，P<0.01）. Compared with the model group， treatment with Sini San-containing serum at various concentrations lowered the levels of pro-inflammatory cytokines and expression of M1 markers （P<0.05， P<0.01）， while increasing the IL-10 level and M2 marker expression （P<0.05， P<0.01）. Additionally， Sini San downregulated the mRNA level of NF-κB and upregulated the mRNA level of STAT （P<0.05， P<0.01）. In the experiment with human primary Kupffer cells， compared with the blank group， the M1 group showed increased NF-κB p65 expression （P<0.01） and decreased STAT3 expression （P<0.05）， whereas the M2 group exhibited increased STAT3 expression （P<0.01）. Compared with the respective model groups， Sini San-containing serum reversed the M1-induced overexpression of NF-κB p65 （P<0.05， P<0.01） and further enhanced the M2-induced STAT3 expression （P<0.05， P<0.01）. ConclusionSini San can inhibit the NF-κB p65/STAT3 signaling pathway and repolarize intrahepatic Kupffer cells from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype to attenuate inflammation and suppress hepatic stellate cell activation and collagen deposition， thereby exerting anti-fibrotic effect.

Ultrasound-guided local ablation therapy for liver tumors has extensive clinical application because of its minimal invasiveness, proven effectiveness, low complication rates, and suitability for repeat treatments. Ultrasound-guided interventional therapy has continuously evolved in terms of the following: technological advancements, from the initial utilization of percutaneous ethanol injection to thermal ablation therapies exemplified by radiofrequency ablation and microwave ablation and presently advancing toward emerging techniques such as irreversible electroporation; imaging methods, from conventional ultrasound guidance to contrast-enhanced ultrasound and fusion imaging for precise guidance and assessment; supplementary strategies, from monotherapy to auxiliary method and synergistic therapy; and innovative treatment concepts, from early-stage small hepatocellular carcinoma to intermediate and even large liver cancers. The development of ultrasound-guided local ablation of liver cancers has progressed from an initial phase of rapid advancement to a mature stage characterized by further enhancements. This article provides a comprehensive overview of the status of technical equipment, treatment processes, efficacy, complications, and challenges encountered in ultrasound-guided local ablation for liver tumors, with the objective of offering valuable insights for interventional ultrasound physicians.

The patient, a 28-year-old male, had experienced splenomegaly for four years with lymphadenopathy for more than two months and presented to the First Affiliated Hospital of the Naval Medical University on October 16th, 2024. On July 31, 2024, he noticed right upper quadrant pain, and an enhanced abdominal CT performed in an external facility revealed splenomegaly with a rounded nodular lesion at the splenic hilum, suggestive of an accessory spleen; in addition to retroperitoneal lymphadenopathy, while tumor marker levels were unremarkable. A complete blood count on August 22nd, 2024, demonstrated leukopenia (2.22×10 9/L), hemoglobin level of 144 g/L, and thrombocytopenia (60×10 9/L). To further elucidate the diagnosis, the patient visit our hematology clinic on August 26th, 2024. His physical examination was normal in general condition, except for a firm palpable spleen 10 cm below the left costal margin, and ultrasonography revealed right thyroid nodule and hepatosplenomegaly. Because of hepatosplenomegaly and retroperitoneal lymphadenopathy, a PET-CT scan was performed. The scan confirmed marked hepatosplenomegaly, multiple enlarged lymph nodes in the retroperitoneal and mesenteric regions with increased metabolic activity, and evidence of elevated bone metabolic activity in the proximal limbs and axial skeleton. Given the possibility of a hematologic lymphoproliferative disorder, a bone marrow biopsy was recommended. On September 12th, 2024, the patient underwent a bone marrow biopsy for evaluations of cell morphology, initial lymphoma immunophenotyping, cytogenetic analysis, and lymphoma-related FISH testing. Flow cytometry, cytogenetic analysis, and FISH results on September 14th, 2024, were unremarkable, manual microscopy of bone marrow morphological evaluation revealed a small population of poorly differentiated lymphocytes; additionally, AI-assisted automated cell scan identified a subset of abnormal cells suspected to be ′Gaucher cells′. Bone marrow pathology indicated a histiocytic neoplasm accompanied by stage 2 myelofibrosis (MF), with tumor cells comprising approximately 70% of the nucleated cells in the marrow, suggesting immunohistochemistry for confirmation. On October 16th, immunohistochemical analysis confirmed the presence of a histiocytic proliferative disorder suspecting Gaucher disease. After admission, the patient initiated enzyme replacement therapy, receiving an initial intravenous dose of 60 U/kg in a weekly basis. On October 31st, 2024, based on enzyme activity assays, genetic testing, and other results, adult Gaucher disease was finally diagnosed. The patient was scheduled for follow-up with stable vital signs, and reduced size of the spleen compared with previous assessments.

The patient, a 28-year-old male, had experienced splenomegaly for four years with lymphadenopathy for more than two months and presented to the First Affiliated Hospital of the Naval Medical University on October 16th, 2024. On July 31, 2024, he noticed right upper quadrant pain, and an enhanced abdominal CT performed in an external facility revealed splenomegaly with a rounded nodular lesion at the splenic hilum, suggestive of an accessory spleen; in addition to retroperitoneal lymphadenopathy, while tumor marker levels were unremarkable. A complete blood count on August 22nd, 2024, demonstrated leukopenia (2.22×10 9/L), hemoglobin level of 144 g/L, and thrombocytopenia (60×10 9/L). To further elucidate the diagnosis, the patient visit our hematology clinic on August 26th, 2024. His physical examination was normal in general condition, except for a firm palpable spleen 10 cm below the left costal margin, and ultrasonography revealed right thyroid nodule and hepatosplenomegaly. Because of hepatosplenomegaly and retroperitoneal lymphadenopathy, a PET-CT scan was performed. The scan confirmed marked hepatosplenomegaly, multiple enlarged lymph nodes in the retroperitoneal and mesenteric regions with increased metabolic activity, and evidence of elevated bone metabolic activity in the proximal limbs and axial skeleton. Given the possibility of a hematologic lymphoproliferative disorder, a bone marrow biopsy was recommended. On September 12th, 2024, the patient underwent a bone marrow biopsy for evaluations of cell morphology, initial lymphoma immunophenotyping, cytogenetic analysis, and lymphoma-related FISH testing. Flow cytometry, cytogenetic analysis, and FISH results on September 14th, 2024, were unremarkable, manual microscopy of bone marrow morphological evaluation revealed a small population of poorly differentiated lymphocytes; additionally, AI-assisted automated cell scan identified a subset of abnormal cells suspected to be ′Gaucher cells′. Bone marrow pathology indicated a histiocytic neoplasm accompanied by stage 2 myelofibrosis (MF), with tumor cells comprising approximately 70% of the nucleated cells in the marrow, suggesting immunohistochemistry for confirmation. On October 16th, immunohistochemical analysis confirmed the presence of a histiocytic proliferative disorder suspecting Gaucher disease. After admission, the patient initiated enzyme replacement therapy, receiving an initial intravenous dose of 60 U/kg in a weekly basis. On October 31st, 2024, based on enzyme activity assays, genetic testing, and other results, adult Gaucher disease was finally diagnosed. The patient was scheduled for follow-up with stable vital signs, and reduced size of the spleen compared with previous assessments.

AIM: To investigate the relationship between vascular smooth muscle cell (VSMC) injury, organelle stress response and autophagic cell death (autophagy) and ferroptosis induced by the chemical hypoxia inducer cobalt chloride (CoCl2) through the bioinformatics analysis and in vitro cell experimentation. METHODS: The dataset GSE119226 of VSMC treated with cobalt chloride was acquired from the gene expression database (GEO). The R language was used to investigate the relationship between CoCl2 treatment and organelle stress response (Golgi stress, endoplasmic reticulum stress) and two forms of cell death (ferroptosis and autophagic cell death). With primary cultured rat VSMC (rVSMC) and CoCl2-induced anoxia model, the changes in cell viability were detected by CCK-8 method, and reactive oxygen species (ROS) levels were measured using DCFH-DA method. The expression levels of HIF-1α (a key molecule in hypoxia), Golgi stress markers GM130 and p115, endoplasmic reticulum stress markers GRP78 and CHOP, autophagy markers LC3-II / LC3-I and Beclin1, and ferroptosis markers GPx4 and xCT were detected by Western blot. The effect of inducing or inhibiting organelle stress and cell death on the CoCl2-induced cell damage was also observed. RESULTS: Differentially expressed genes analysis of GSE119226 dataset showed that CoCl2 treatment of VSMCs had significant effects on organelle function and stress response, autophagy and ferroptosis-related genes, in which endoplasmic reticulum stress, protein processing in endoplasmic reticulum, regulation of Golgi to plasma membrane protein transport, autophagy / autophagic cell death, and ferroptosis pathways were remarkably enriched. The results of in vitro experiment showed that compared with normal rVSMC, cell viability was significantly decreased after CoCl2 treatment, as well as HIF-1α protein expression and ROS levels in rVSMCs were increased. In rVSMC treated with Co-Cl2, the expression levels of Golgi structural proteins GM130 and p115 (reflecting the occurrence of Golgi stress) were decreased, while the markers GRP78 and CHOP (reflecting the occurrence of endoplasmic reticulum stress) were increased. At the same time, CoCl2 treatment also reduced the expression of autophagy markers LC3-II/LC3-I and Beclin1 (indicating the decrease levels of autophagy), while the expression of ferroptosis markers GPx4 and xCT were decreased (indicating the occurrence of ferroptosis). Compared with CoCl2 treatment group, induced Golgi stress, endoplasmic reticulum stress, or ferroptosis could further reduce cell viability, while inhibition of these processes could improve cell viability. On the other hand, increasing the level of autophagy can improve the cell viability. CONCLUSION: Hypoxia induced by cobalt chloride can lead to VSMC injury. Golgi stress, endoplasmic reticulum stress, ferroptosis, and the reduction of autophagy level play an important role in it. Inhibition of organelle stress response and ferroptosis, or increase of autophagy level can improve VSMC injury caused by cobalt chloride.

ObjectiveTo explore the influence of excessive weight gain during pregnancy in pre-pregnancy overweight and obese women on pregnancy outcomes and neonatal conditions， and to provide scientific evidence for formulating weight management strategies before and during pregnancy and prevent adverse pregnancy outcomes. MethodsClinical data of 2 172 parturients collected from a community in Huangpu District from 2017 to 2021 were retrospectively analyzed， and they were divided into pre-pregnancy overweight and obesity group （n=530）， normal pre-pregnancy weight group（n=937）， and underweight pre-pregnancy group（n=705） according to maternal precursor body mass index （BMI）. Based on their weight gain during pregnancy，the parturient were divided into moderate gestational weight gain （MGWG） group and excessive gestational weight gain （EGWG） group. Meanwhile， the pregnancy and neonatal outcomes such as postpartum hemorrhage， puerperal infection， placental abruption， premature rupture of membranes， mode of delivery， premature birth， stillbirth， fetal distress， admission to the intensive care unit （ICU）， macrosomia， and Apgar score， were recorded. Then the differences in pregnancy and neonatal outcomes between groups were compared. The effects of pre-pregnancy BMI and gestational weight gain on pregnancy outcomes and neonatal conditions was retrospectively analyzed. ResultsThe pre-pregnancy overweight and obese group had higher proportions of placental abruption， premature rupture of membranes， cesarean section， premature birth， fetal distress， and macrosomia compared to the normal pre-pregnancy weight group and the underweight pre-pregnancy group， with Apgar scores lower than the normal pre-pregnancy weight group and the underweight pre-pregnancy group （all P<0.05）. The EGWG group had higher proportions of postpartum hemorrhage， placental abruption， premature rupture of membranes， cesarean section， premature birth， fetal distress， admission to the ICU， and macrosomia than the MGWG group （all P<0.05）. In the pre-pregnancy overweight and obese group， the EGWG group had higher proportions of placental abruption， premature rupture of membranes， premature birth， fetal distress， admission to the ICU， and macrosomia than the MGWG group， with lower Apgar scores than the MGWG group （all P<0.05）. In the normal pre-pregnancy weight group， the EGWG group had higher proportions of placental abruption， premature rupture of membranes， premature birth， fetal distress， admission to the ICU， and macrosomia than the MGWG group （all P<0.05）. In the pre-pregnancy overweight and obese group， the EGWG group had higher proportions of premature rupture of membranes， cesarean section， premature birth， fetal distress， and macrosomia than the EGWG group in the normal pre-pregnancy weight group（all P<0.05）. Logistic regression analysis showed that EGWG in pre-pregnancy overweight and obese women was a risk factor for placental abruption （OR=2.971， 95%CI： 1.098‒8.042）， premature rupture of membranes （OR=4.662， 95%CI： 2.798‒7.770）， cesarean delivery （OR=1.375，95%CI： 1.260‒2.541）， premature birth （OR=4.249， 95%CI： 2.384‒7.573）， fetal distress （OR=3.238， 95%CI： 1.589‒6.598）， admission to the ICU （OR=3.010， 95%CI： 1.265‒7.164）， and macrosomia （OR=5.437， 95%CI： 3.392‒8.716） （all P<0.05）. ConclusionExcessive gestational weight gain in pre-pregnancy overweight and obese women is a risk factors for placental abruption， premature rupture of membranes， cesarean section， premature birth， fetal distress， admission to the ICU， and macrosomia.

AIM:To observe the effect of icariin-astragaloside Ⅳ-puerarin mixture(Yin-Huang-Ge mixture,YHG)on cognitive function and ferroptosis amino acid metabolism pathway in hepcidin(HAMP)knockout APPswe/PS1dE9(APP/PS1 HAMP-/-)mice.METHODS:The mice were divided into 7 groups:negative control(C57BL/6 mice)group,APP/PS1 group,APP/PS1 HAMP-/-group,APP/PS1+YHG group,APP/PS1 HAMP-/-+YHG group,APP/PS1+de-ferasirox(DFX)group,and APP/PS1 HAMP-/-+DFX group,with 6 mice in each group.The YHG and DFX were adminis-tered intragastrically,while the mice in C57 group,APP/PS1 group and APP/PS1 HAMP-/-group were given intragastric administration of distilled water,once a day for 2 months.The iron content in mouse brain tissues was detected by tissue iron kit.The morphological changes of the mitochondria in hippocampal neurons were observed by transmission electron microscopy.Morris water maze was used to detect the learning and memory ability of the mice.The content of neuronal nu-clear antigen(NeuN)in mouse brain tissues was detected by immunofluorescence staining.The expression of glutathione(GSH)in mouse brain tissues was detected by biochemical kit.The expression levels of glutamate-cysteine ligase catalytic subunit(GCLC)and glutamatase 2(GLS2)in mouse brain tissues were detected by Western blot.RESULTS:Compared with C57BL/6 mice,the brain iron content of APP/PS1 mice was significantly increased(P＜0.01),the mitochondria were seriously damaged,the learning and memory ability was significantly decreased(P＜0.05),the brain neurons were seri-ously damaged(P＜0.01),and the expression levels of GSH,GCLC and GLS2 were significantly decreased(P＜0.01).Compared with APP/PS1 mice,the brain iron content of APP/PS1 HAMP-/-mice was significantly increased(P＜0.01),the mitochondria were seriously damaged,the learning and memory ability was significantly decreased(P＜0.05),the brain neurons were seriously damaged(P＜0.01),and the expression levels of GSH,GCLC and GLS2 were significantly decreased(P＜0.05).After treatment with YHG and DFX,the brain iron content was significantly decreased(P＜0.01),the mitochondrial damage was alleviated,the learning and memory ability was significantly increased(P＜0.05),the brain neuron damage was alleviated(P＜0.01),and the expression levels of GSH,GCLC and GLS2 were significantly increased(P＜0.05).CONCLUSION:The YHG can improve the cognitive function of APP/PS1 HAMP-/-mice,and its mechanism may be related to the regulation of ferroptosis amino acid metabolism and the enhancement of antioxidant capacity.

Objective To explore the relationship between serum soluble cell surface differentiation antigen 40 ligand(sCD40L),a disintegrin-like and metalloproteinase with thrombospondin type-1 motif 13(ADAMTS13)levels and postoperative lower extremity deep vein thrombosis(DVT)formation in elderly pa-tients with hip fractures.Methods A total of 192 elderly patients with hip fractures who visited the hospital from June 2022 to June 2023 were selected and separated into non DVT group(120 cases)and DVT group(72 cases)based on whether they experienced lower extremity DVT after surgery.Enzyme-linked immunosorbent assay was applied to detect serum sCD40L and ADAMTS13 levels in each group.Pearson method was applied to analyze the correlation between serum sCD40L and ADAMTS13 levels in patients.Multivariate Logistic re-gression model was applied to analyze the factors affecting postoperative lower extremity DVT in elderly pa-tients with hip fractures.Receiver operating characteristic(ROC)curve was applied to evaluate the predictive value of serum sCD40L and ADAMTS13 levels for postoperative lower extremity DVT in elderly patients with hip fractures.Results There were statistically significant differences in the proportion of hyperlipidemia and the time from fracture to surgery between the two groups(P＜0.05).Compared with the non DVT group,the serum sCD40L level in the DVT group increased(P＜0.05)and the ADAMTS13 level decreased(P＜0.05).Pearson method results showed that the serum sCD40L level was negatively correlated with ADAMTS13 level in patients(r=-0.457,P＜0.001).Multivariate Logistic regression model analysis showed that hyperlipi-demia,long time from fracture to surgery,increased level of serum sCD40L were risk factors for postoperative lower extremity DVT in elderly patients with hip fractures(P＜0.05),and the increased level of serum AD-AMTS13 was a protective factor for postoperative lower extremity DVT in patients with hip fractures(P＜0.05).The area under the curve of the combined prediction of serum sCD40L and ADAMTS13 for postopera-tive lower extremity DVT in elderly patients with hip fractures was 0.812,which was larger than that of sCD40L and ADAMTS13 alone(P＜0.05).Conclusion Serum sCD40L level increases and ADAMTS13 level decreases in elderly patients with hip fracture who had lower extremity DVT after surgery,the two could re-flect the risk of DVT and have predictive value for the occurrence of lower extremity DVT in elderly patients with hip fracture.