ObjectiveThis study aims to investigate the action mechanism by which Xiaozheng Zhitong paste （XZP） alleviates bone cancer pain （BCP） by regulating programmed death protein 1 （PD-1）/programmed death-ligand 1 （PD-L1） pathway-induced osteoclast formation. MethodsThirty female C57BL/6 mice were randomly allocated into the following groups （n=6 per group）： normal control group， model group， low‑dose XZP group （31.5 g·kg^-1）， high‑dose XZP group （63 g·kg^-1）， and PD‑1 inhibitor （Niv） group. A bone cancer pain （BCP） model was established by injecting Lewis lung carcinoma cells. Mice in the normal control and model groups received topical application of a blank paste matrix at the wound site. Mice in the low‑ and high‑dose XZP groups were treated with XZP applied topically twice daily. Mice in the Niv group were topically administered the blank paste matrix and additionally received Niv via tail‑vein injection every two days. All interventions were continued for 21 days. During this period， behavioral tests were performed to assess mechanical， motor， and thermal nociceptive sensitivities. After 21 days， all mice were euthanized， and bone tissue from the operated side was collected for sectioning and preservation. Tartrate‑resistant acid phosphatase （TRAP） staining was used to evaluate osteoclast expression in the lesioned bone tissue. Immunohistochemistry was performed to detect the expression of Runt‑related transcription factor 2 （Runx2） in the lesioned bone tissue. Immunofluorescence was employed to assess the expression of PD‑1 and PD‑L1 in the lesioned bone tissue. ResultsCompared with the normal group， the model group showed significantly decreased limb mechanical withdrawal threshold， spontaneous paw flinching， and thermal withdrawal latency （P<0.01）， increased number of osteoclasts in the lesioned bone tissue （P<0.01）， and reduced expression of Runx2 （P<0.01）. Compared with the model group， the BCP mice in the XZP low-dose group， XZP high-dose group， and Niv group exhibited increased limb mechanical withdrawal threshold， movement scores， and thermal withdrawal latency （P<0.01）. The XZP low-dose group showed no significant changes in osteoclast number or Runx2 expression， while the XZP high-dose group and Niv group demonstrated significantly reduced osteoclast numbers （P<0.01） and significantly increased Runx2 expression （P<0.01）. In the lesioned bone tissue of BCP mice， the XZP low-dose group showed no significant decrease in the percentage of PD-1 expression， but a decrease in the percentage of PD-L1 expression （P<0.05）. In contrast， both the XZP high-dose group and the Niv group exhibited significant reductions in the percentages of PD-1 and PD-L1 expression （P<0.01）. ConclusionXZP alleviates the pain of mice with BCP by blocking the PD-1/PD-L1 pathway to inhibit osteoclastogenesis.

ObjectiveThe paper aims to investigate the mechanism by which Xiaozheng Zhitong paste （XZP） alleviates bone cancer pain （BCP） through regulating the PTEN-induced putative kinase 1 （PINK1）/Parkin-mediated mitophagy-NOD-like receptor protein 3 （NLRP3） inflammasome pathway to suppress microglial pyroptosis. MethodsLipopolysaccharide （LPS） and LPS-adenosine triphosphate （ATP） were used to establish an inflammation and pyroptosis model in microglial cells. The cells were randomly divided into the following groups： control group， LPS group， LPS+low-dose XZP group， LPS+high-dose XZP group， LPS-ATP group， LPS-ATP+low-dose XZP group， LPS-ATP+high-dose XZP group， LPS-ATP+XZP group， and LPS-ATP+XZP+CsA group. Techniques including terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） staining， enzyme-linked immunosorbent assay （ELISA）， Western blot， and confocal fluorescence staining were employed to assess the effects of XZP on microglial apoptosis， inflammatory cytokine release， inflammasome activation， pyroptosis， and mitophagy. ResultsIn vitro experiments showed that compared with the blank group， the LPS group exhibited significantly increased levels of microglial apoptosis and pro-inflammatory factors interleukin （IL）-1β， IL-6， and tumor necrosis factor-α （TNF-α）（P<0.01）， along with significantly upregulated protein expression of inducible nitric oxide synthase （iNOS）， cyclooxygenase-2 （COX-2）， and phosphorylated nuclear factor-κB p65 （p-NF-κB p65） （P<0.01）. Compared with the LPS group， the high-dose LPS-XZP group significantly reduced the level of apoptosis （P<0.01） and the content of the aforementioned pro-inflammatory factors （P<0.01）. Both the low- and high-dose LPS-XZP groups dose-dependently downregulated the protein expression of iNOS， COX-2， and p-NF-κB p65 （P<0.05， P<0.01）. Compared with the blank group， the LPS-ATP group showed significantly upregulated expression of pyroptosis-related proteins， including Caspase-1/pro-Caspase-1， N-terminal fragment of gasdermin D （GSDMD-N）/full-length gasdermin D （GSDMD-F）， NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， IL-1β precursor （pro-IL-1β）， and mature IL-1β （P<0.01）. The levels of pyroptotic factors IL-1β and IL-18 were significantly elevated （P<0.01）， and membrane pore formation and intracellular reactive oxygen species （ROS） levels were significantly increased （P<0.01）. Compared with the LPS-ATP group， both the low- and high-dose LPS-ATP+XZP groups dose-dependently downregulated the expression of the aforementioned pyroptosis-related proteins （P<0.05， P<0.01）. The low-dose LPS-ATP+XZP group reduced IL-1β levels （P<0.01）， while the high-dose group reduced both IL-1β and IL-18 levels （P<0.01） Both the low- and high-dose LPS-ATP+XZP groups dose-dependently reduced membrane pore formation and intracellular ROS production （P<0.01）. Compared with the blank group， the LPS-ATP group showed significantly reduced expression of mitophagy-related proteins PINK1 and Parkin， and a decreased ratio of microtubule-associated protein 1 light chain 3Ⅱ（LC3Ⅱ） to LC3Ⅰ（P<0.01）， while p62 expression was significantly increased （P<0.01）. Mitochondrial ROS levels were significantly enhanced （P<0.01）. Compared with the LPS-ATP group， both the low- and high-dose LPS-ATP+XZP groups dose-dependently reversed the expression of these proteins （P<0.05， P<0.01） and reduced mitochondrial ROS levels （P<0.01）. After treatment with the mitophagy inhibitor cyclosporin A （CsA）， the beneficial effects of XZP on mitochondrial function and its inhibitory effects on pyroptosis-related protein expression were significantly reversed （P<0.05， P<0.01）. ConclusionXZP reduces ROS levels by activating PINK1/Parkin-mediated mitophagy， thereby inhibiting NLRP3 inflammasome activation and microglial pyroptosis， which provides new molecular evidence for the mechanism by which XZP alleviates BCP.

ObjectiveTo investigate the effects and underlying mechanisms of Xiaozheng Zhitong Paste （XZP） on bone cancer pain （BCP）. MethodsThirty female BALB/c mice were randomly divided into five groups： a Sham group， a BCP group， a BCP+low-dose XZP group， a BCP+high-dose XZP group， and a BCP+high-dose XZP + protease-activated receptor 2 （PAR2） agonist GB-110 group. BCP mice model was constructed by injecting Lewis lung carcinoma cells into the femoral cavity of the right leg， which was followed by being treated with XZP for 21 d. After 21 d， the mice were sacrificed. Nissl staining was used to evaluate the survival of spinal cord neurons. Immunofluorescence staining was conducted to localize ionized calcium-binding adapter molecule 1 （Iba1） and neuronal nuclear antigen （NeuN） in spinal cord tissue， thereby assessing microglial activation and neuronal survival. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of interleukin-1β （IL-1β）， tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， transforming growth factor-β （TGF-β）， interleukin-4 （IL-4）， and interleukin-10 （IL-10） in spinal cord tissue. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect mRNA expression levels associated with M1/M2 polarization of microglia. Western blot analysis was performed to examine the expression of proteins related to microglial polarization as well as those involved in the PAR2/nuclear factor kappa B （NF-κB）/NOD-like receptor protein 3 （NLRP3） signaling pathway in the spinal cord. ResultsCompared with the Sham group， the spinal cord neurons were damaged， the number of Nissl-positive spinal cord neurons in the spinal cord tissue was significantly reduced （P<0.01）， and the rate of NeuN-positive cells was significantly decreased （P<0.01）. The spinal cord microglia were activated， the inflammatory level of the spinal cord tissue was enhanced， and Iba1 staining was significantly enhanced （P<0.01）. The levels of IL-1β， TNF-α， IL-6， TGF-β， IL-4 and IL-10 were significantly increased （P<0.01）. The mRNA expressions of IL-1β， TNF-α and inducible nitric oxide synthase （iNOS） were significantly increased （P<0.01）， and the expression of PAR2， NLRP3， ASC and NF-κB p65 proteins in the spinal cord tissue of the BCP mice was significantly enhanced （P<0.01）. Compared with the BCP group， high-dose XZP treatment significantly increased the number of Nissl-positive spinal cord neurons in the BCP mice （P<0.01）， significantly enhanced the rate of NeuN-positive cells in the spinal cord tissue， and significantly weakened Iba1 staining （P<0.01）. In addition， the levels of IL-1β， TNF-α， and IL-6 were significantly decreased， while the levels of TGF-β， IL-4， and IL-10 were significantly increased （P<0.05， P<0.01）. The mRNA expression levels of IL-1β， TNF-α， and iNOS were decreased， whereas those of cluster of differentiation 206 （CD206）， arginase-1 （Arg-1）， and YM1/2 were significantly increased （P<0.05， P<0.01）. Low-dose and high-dose XZP treatment significantly decreased the expression of PAR2， NLRP3， ASC， and NF-κB p65 proteins in the spinal cord tissue （P<0.05， P<0.01）. These effects could all be significantly eliminated by the PAR2 agonist GB-110. ConclusionXZP can mitigate BCP in mice， which may be achieved through blocking the activated PAR2/NF-κB/NLRP3 pathway.

ObjectiveThe paper aims to investigate the action mechanism by which the Xiaozheng Zhitong paste （XZP） relieves bone cancer pain （BCP）. MethodsA model of mice with BCP was established by using Lewis tumor cells. The therapeutic effects of XZP， the ferroptosis inhibitor Ferrostatin-1 （Fer-1）， and the nuclear factor erythroid 2-related factor 2 （Nrf2） inhibitor Brusatol （Bru） on BCP were examined. Mice were randomly divided into the Sham operation group， BCP group， BCP+XZP-L group， BCP+XZP-H group， BCP+Fer-1 group， and BCP+XZP-H+Bru group， with six mice in each group. Pain behavior tests were conducted on the mice to assess pain levels. Colorimetric assays were employed to measure ferroptosis-related factors in serum and spinal cord tissue including Fe， malondialdehyde （MDA）， reactive oxygen species （ROS）， and superoxide dismutase （SOD）. Immunofluorescence staining was used to assess ROS production in spinal cord tissue. Transmission electron microscopy was used to observe the ultrastructure of mitochondria in lumbar spinal cord tissue. Quantitative real-time polymerase chain reaction （Real-time PCR） was employed to detect mRNA expression of Nrf2， heme oxygenase-1 （HO-1）， glutathione peroxidase 4 （GPX4）， and solute carrier family 7 member 11 （SLC7A11） in spinal cord neuron tissue. The protein expression of Nrf2， HO-1， GPX4， and SLC7A11 in spinal cord neurons was measured by Western blot. ResultsCompared with the Sham group， mice in the BCP group exhibited significantly reduced limb usage scores， mechanical foot withdrawal thresholds， and thermal foot withdrawal thresholds （P<0.01）. Serum and lumbar spinal cord tissue levels of Fe， MDA， and reactive oxygen species （ROS） were significantly elevated （P<0.05）， while superoxide dismutase （SOD） levels were significantly decreased （P<0.05）. Lumbar spinal cord mitochondrial structural damage was observed， and mRNA and protein expression of Nrf2， HO-1， GPX4， and SLC7A11 were significantly downregulated （P<0.01）. Compared with the BCP group， both low- and high-dose XZP groups improved the aforementioned pain behavioral indicators （P<0.05，P<0.01）， reduced ferroptosis-related biomarkers including Fe， MDA， and ROS levels （P<0.05）， increased SOD levels （P<0.05，P<0.01）， alleviated mitochondrial damage， and upregulated Nrf2， HO-1， GPX4， SLC7A11 mRNA and protein expression （P<0.05，P<0.01）. The high-dose XZP group exhibited comparable efficacy to Fer-1 in alleviating pain and inhibiting ferroptosis. Following Bru administration， XZP's effects on pain behavioral indicators， regulation of ferroptosis-related markers， mitochondrial structural protection， and activation of the Nrf2/HO-1/GPX4/SLC7A11 pathway were significantly reversed （P<0.05，P<0.01）. ConclusionExternal application of XZP alleviates pain symptoms in BCP mice by activating the Nrf2/HO-1/GPX4/SLC7A11 pathway， thereby inhibiting ferroptosis and neuronal damage in spinal cord neurons.

Cancer pain is one of the most common complications in patients with malignant tumors， severely affecting their quality of life. Its pathogenesis involves complex interactions among the tumor microenvironment， peripheral sensitization， and central sensitization. The tumor microenvironment initiates peripheral pain sensitization by secreting algogenic mediators， activating ion channels and related receptor signaling pathways， driving abnormal osteoclast activation， and mediating neuro-immune crosstalk. Persistent nociceptive input further triggers increased excitability of central neurons， activation of glial cells， and neuroinflammatory cascade reactions， ultimately leading to central pain sensitization. Although traditional opioid drugs can alleviate pain to some extent， they still have many limitations， such as incomplete analgesia， drug tolerance， and adverse reactions. In recent years， traditional Chinese medicine （TCM） compounds have made continuous progress in the treatment of cancer pain. Studies have shown that they can not only effectively relieve cancer pain and reduce the dosage of opioids but also significantly improve patients' quality of life. TCM treatment of cancer pain follows the principle of syndrome differentiation and treatment. Based on this， targeted therapeutic principles have been proposed， including promoting blood circulation， removing stasis， regulating Qi， and unblocking collaterals； tonifying the kidney， replenishing essence， warming Yang， and dispersing cold， activating blood， resolving phlegm， detoxifying， and dispersing nodules， as well as strengthening the body， replenishing deficiency， and harmonizing Qi and blood. Modern research indicates that TCM compounds can exert synergistic effects through multiple pathways， inhibiting inflammatory responses， regulating nerve conduction， intervening in bone metabolism and related gene expression， thereby producing anti-inflammatory and bone-protective effects to achieve the goal of alleviating cancer pain. This article systematically elaborates on the pathogenesis of cancer pain， the clinical application of TCM in treating cancer pain， and its related mechanisms of action， aiming to provide a theoretical basis and new strategies for the integration of TCM into comprehensive cancer pain management.

Pain， as one of the most common symptoms in cancer patients， seriously affects the survival quality of patients. The three-step pain relief program currently used in clinical practice cannot completely relieve pain in cancer patients and is accompanied by many problems. From the perspective of Jueyin syndrome in traditional Chinese medicine （TCM）， this paper believed that the core pathogenesis of cancer pain was declined healthy Qi and cold and heat in complexity， and used Wumeiwan as the main formula with modification according to syndrome for clearing the upper， warming the lower part of the body， and harmonizing the cold and heat. It can regulate the pathological environment of deficiency， cold， stasis， toxicity， and heat， and restore the physiological function of Yang transforming Qi while Yin constituting form， so as to prevent， relieve， and even eliminate cancer pain， having achieved good clinical efficacy. It can not only help cancer patients relieve pain， but also control tumor and eliminate tumor， achieving a dual benefit of pain relief and tumor suppression. It gives full play to the characteristics and advantages of syndrome differentiation and treatment in TCM， and expands the scope of ZHANG Zhongjing's treatment for Jueyin syndrome， which provides ideas for the clinical diagnosis and treatment of cancer pain from the perspective of deficiency-excess in complexity and cold and heat in complexity.

Objective:To investigate the gait characteristics of patients with early Parkinson′s disease (PD) under cognitive dual task, and to provide sensitive kinematic indicators for the early diagnosis, timely treatment and reasonable rehabilitation of PD.Methods:A total of 62 outpatients and inpatients with early non-tremor Parkinson′s disease in Shijingshan Branch of Beijing Chaoyang Hospital Affiliated to Capital Medical University from September 2021 to August 2023 were selected as experimental group (PD group), and 62 healthy controls with comparable age composition ratio were selected as control group. The baseline data, Montreal Cognitive Assessment Scale scores, and the gait assessment scores of the motor part of the Unified Parkinson′s Disease Rating Scale were compared between the 2 groups. The wearable gait analysis device was used to collect the gait parameters of the 2 groups of subjects under single task and dual task, and the foot kinematic characteristics of the patients with early PD were quantified. Independent sample t test and Mann-Whitney U test were used to analyze the gait parameters of the 2 groups. The statistically significant variables were included in Logistic regression analysis to explore the association between gait parameters and PD. Finally, the diagnostic value of the variables was estimated by receiver operating characteristic (ROC) curve analysis. Results:Gait spatio-temporal parameters (per gait cycle): (1) The gait speed of the PD group was slower than that of the control group [(1.01±0.12) m/s vs (1.22±0.18) m/s, t=-7.526] during single task walking. The bipedal support time in the PD group was significantly longer than that in the control group [(0.29±0.05) s vs (0.22±0.06) s, t=6.659]. The differences were both statistically significant (both P<0.001). (2) During dual-task walking, PD patients showed slower gait speed [(0.88±0.11) m/s vs (1.19±0.16) m/s, t=-12.158, P<0.001]. The bipedal support time in the PD group was longer than that in the control group [(0.36±0.05) s vs (0.22±0.05) s, t=12.828, P<0.001]. PD patients had shorter stride length [(109.20±6.21) cm vs (112.77±5.87) cm, t=-3.203, P=0.010]. Stride frequency in the PD group was higher than that in the control group [(114.45±7.10) steps/min vs (110.87±7.16) steps/min, t=2.724, P=0.020]. The single leg support time was longer than that of the control group [(0.49±0.12) s vs (0.45±0.06) s, t=2.643, P=0.020] , and the differences were statistically significant. Gait kinematics parameters: (1) During single task walking, the maximum angle of foot movement in the sagittal plane in the PD group was smaller than that in the control group (17.19°±2.37° vs 19.71°±2.92°, t=-4.691, P<0.001). The minimum angle of movement in the sagittal plane was smaller than that in the control group (-67.08°±4.63° vs -70.10°±3.94°, t=0.395, P=0.001). The minimum horizontal angle of the foot during exercise in the PD group was lower than that in the control group (9.08°±4.02° vs 11.80°±3.60°, t=-3.461, P<0.001). The minimum angle of the foot coronal plane in the PD group was smaller than that in the control group (-10.55°±2.87° vs -12.04°±2.31°, t=2.831, P=0.030; the negative sign only represents the movement direction). The touch angle of the foot in the PD group was significantly lower than that in the control group (11.14°±2.78° vs 12.78°±3.57°, t=-2.779, P=0.030). (2) During dual-task walking, the maximum sagittal angle (15.44°±2.54° vs 18.99°±2.71°, t=-6.673, P<0.05), the minimum angle of sagittal plane (-65.68°±4.73° vs -70.02°±4.04°, t=-4.747, P<0.001; the negative sign only represents the direction of movement), the minimum coronal movement angle (-11.15°± 2.99° vs -13.18°±2.50°, t=3.642, P=0.020), the touch angle (11.01°±3.10° vs 12.83°±4.01°, t=-2.438, P=0.010), the minimum horizontal angle (8.83°±4.04° vs 11.83°±3.63°, t=-3.776, P<0.001), and the change of the angle from the ground (-65.00°±3.54° vs -67.06°±3.61°, t=3.133, P<0.001) in the PD group were all smaller than that in the control group. The differences were all statistically significant. Logistic regression analysis showed that step frequency was positively correlated with PD ( OR=1.124,95% CI 1.040-1.201, P=0.001), minimum angle of coronal plane was positively correlated with PD ( OR=1.501, 95% CI 1.040-2.151, P=0.030). Stride length was negatively correlated with PD ( OR=0.902, 95% CI 0.830-0.978, P=0.010). ROC curve was used to evaluate the diagnostic value of step frequency, stride length and minimum angle of coronal plane. For step frequency, when the maximum Youden index was 0.880, the best cut-off value to distinguish the PD group from the control group was 115.000, the sensitivity was 0.577, the specificity was 0.710, and the area under the curve was 0.656. For the minimum coronal angle, when the maximum Youden index was 0.251, the best cut-off value was -12.575, the sensitivity was 0.728, the specificity was 0.531, and the area under the curve was 0.670. For stride length, when the maximum Youden index was 0, the best cut-off value was 100.91, the sensitivity was 0.950, the specificity was 0.050, and the area under the curve was 0.300. Conclusions:Some gait parameters such as step frequency and minimum angle of coronal plane can be used as kinematic markers to reflect the gait characteristics of early PD, which may be helpful in tracking and evaluating the gait disorder characteristics of early PD patients and predicting the risk of PD. Some gait parameters of PD patients are significantly different from those of healthy people during cognitive-motor dual-task walking.

New drug discovery is under growing pressure to satisfy the demand from a wide range of domains, especially from the pharmaceutical industry and healthcare services. Assessment of drug efficacy and safety prior to human clinical trials is a crucial part of drug development, which deserves greater emphasis to reduce the cost and time in drug discovery. Recent advances in microfabrication and tissue engineering have given rise to organ-on-a-chip, an in vitro model capable of recapitulating human organ functions in vivo and providing insight into disease pathophysiology, which offers a potential alternative to animal models for more efficient pre-clinical screening of drug candidates. In this review, we first give a snapshot of general considerations for organ-on-a-chip device design. Then, we comprehensively review the recent advances in organ-on-a-chip for drug screening. Finally, we summarize some key challenges of the progress in this field and discuss future prospects of organ-on-a-chip development. Overall, this review highlights the new avenue that organ-on-a-chip opens for drug development, therapeutic innovation, and precision medicine.

OBJECTIVE: To evaluate effectiveness of proximal femur bionic nail (PFBN) in treatment of intertrochanteric fractures in the elderly compared to the proximal femoral nail antirotation (PFNA). METHODS: A retrospective analysis was made on 48 geriatric patients with intertrochanteric fractures, who met the selection criteria and were admitted between January 2020 and December 2022. Among them, 24 cases were treated with PFBN fixation after fracture reduction (PFBN group), and 24 cases were treated with PFNA fixation (PFNA group). There was no significant difference in baseline data such as age, gender, cause of injury, side and type of fracture, time from injury to operation, and preoperative mobility score, American Society of Anesthesiologists (ASA) score, Alzheimer's disease degree scoring, self-care ability score, osteoporosis degree (T value), and combined medical diseases between the two groups ( P>0.05). The operation time, intraoperative blood loss, number of blood transfusions, transfusion volume, length of hospital stay, occurrence of complications, weight-bearing time after operation, and postoperative visual analogue scale (VAS) score, walking ability score, mobility score, self-care ability score were recorded and compared between the two groups. And the radiographic assessment of fracture reduction quality and postoperative stability, and fracture healing time were recorded. RESULTS: The operations in both groups were successfully completed. All patients were followed up 6-15 months with an average time of 9.8 months in PFBN group and 9.6 months in PFNA group. The operation time was significantly longer in PFBN group than in PFNA group ( P<0.05), but there was no significant difference in intraoperative blood loss, number of blood transfusions, transfusion volume, length of hospital stay, change in activity ability score, and change in self-care ability score between the two groups ( P>0.05). The weight-bearing time after operation was significantly shorter in PFBN group than in PFNA group ( P<0.05), and the postoperative VAS score and walking ability score were significantly better in PFBN group than in PFNA group ( P<0.05). Radiographic assessment showed no significant difference in fracture reduction scores and postoperative stability scores between the two groups ( P>0.05). All fractures healed and there was no significant difference in fracture healing time between the two groups ( P>0.05). The incidence of complications was significantly lower in PFBN group (16.7%, 4/24) than in PFNA group (45.8%, 11/24) ( P<0.05). CONCLUSION Compared with PFNA, PFBN in the treatment of elderly intertrochanteric fractures can effectively relieve postoperative pain, shorten bed time, reduce the risk of complications, and facilitate the recovery of patients' hip joint function and walking ability.
Humans ; Aged ; Retrospective Studies ; Fracture Fixation, Intramedullary ; Bionics ; Blood Loss, Surgical ; Treatment Outcome ; Bone Nails ; Hip Fractures/surgery* ; Femur

To evaluate the psychological symptoms of patients with Crohn disease (CD), and to explore the risk factors affecting quality of life (QOL) in CD patients, 50 adult patients with CD, and 50 healthy controls were enrolled. Psychological questionnaires including self-rating anxiety scale (SAS), self-rating depression scale (SDS), the inflammatory bowel disease questionnaire (IBDQ) and the short form-36 health survey (SF-36) were completed. The results showed both the SAS (40.3±8.5 VS 37.6±7.0) and the SDS (47.1±11.1 VS 41.8±9.6) in CD patients were significantly higher than those in the healthy controls ( t=5.4, P<0.05; t=10.6, P<0.05). The IBDQ scores revealed the physical symptoms scores were 49.50±7.62, systemic symptoms scores 23.92±5.07, emotional functions scores 57.13±15.62, and social function scores 22.15±9.08 in CD active phase. However, the above scores were 60.12±4.01, 26.24±3.97, 67.34±15.17, and 25.44±2.03 respectively in the remission phase. Four subscale items of IBDQ in CD active phase were significant lower than those in the remission phase (all P<0.05). The subscale items of SF-36 scores (PF, RP, BP, GH, VT, SF, RE, MH) in CD patients were significant lower than those in healthy controls (all P<0.05). The SF-36 items scores of PF,RP and MH in the remission phase were significant higher than those in the active phase (all P<0.05). The SF-36 items scores of GH and VT in patients with malnutrition were significant lower than those with nutrition (both P<0.05). Multivariate regression analysis showed that disease status and nutritional risk ( P<0.05) significantly affected the patients' IBDQ scores. Factors including sex, age, marital status, education background, medical insurance, use of biologicals, surgery treatment had little influence on the total score of IBDQ ( P>0.05). Psychological conseling and treatment in the active phase may improve QOL of CD patients.