The cardiovascular toxicity of polystyrene microplastics in rats: based on untargeted metabolomics analysis.

Background: Polystyrene microplastics (PS-MPs) exhibit multi-target, multi-dimensional, chronic, and low toxicity to the cardiovascular system. They enter the bloodstream through the gastrointestinal tract and respiratory system, altering blood parameters and conditions, inducing thrombotic diseases, and damaging myocardial tissue through the promotion of oxidative stress and inflammatory responses in myocardial cells. However, many of the links and mechanisms remain unclear. Methods: In this study, 48 wistar rats were randomly divided into four groups and exposed to different concentrations of PS-MPs: control group (0 mg/kg/d), low dose group (0.5 mg/kg/d), middle dose group (5 mg/kg/d) and high dose group (50 mg/kg/d), with 12 rats in each group. After 90 consecutive days of intragastric administration of PS-MPs, biochemical markers in myocardium, aorta and blood were detected, and HE staining was performed to observe the toxic effects of PS-mps on cardiovascular system. Furthermore, non-targeted metabolomics methods were used to analyze the effect of PS-MPs exposure on the metabolism of cardiovascular system in rats, and to explore its potential molecular mechanism. Results: The results revealed no pathological changes in the heart and aorta following PS-MPs exposure. However, the myocardial enzyme levels in the high dose PS-MPs group of rats showed a significant increase. Moreover, exposure to polystyrene microplastics caused a disorder in lipid metabolism in rats, and led to an increase in indicators of inflammation and oxidative stress in myocardial and aortic tissues, but resulted in a decrease in the level of IL-6. Untargeted metabolomics results showed that metabolites with antioxidant and anti-inflammatory effects, including equol and 4-hydroxybenzoic acid, were significantly upregulated. Conclusion: These results suggest that long-term exposure to high concentrations of PS-MPs may lead to abnormal lipid metabolism and cardiovascular system damage. The mechanism may be related to oxidative stress and inflammatory response. Exogenous antioxidants and changes in own metabolites may have a protective effect on the injury. Therefore, understanding the toxicological mechanism of PS-MPs not only helps to elucidate its pathogenesis, but also provides new ideas for the treatment of chronic diseases.

Cutting Weights of Deep Learning Models for Heart Sound Classification: Introducing a Knowledge Distillation Approach.

Cardiovascular diseases (CVDs) are the number one cause of death worldwide. In recent years, intelligent auxiliary diagnosis of CVDs based on computer audition has become a popular research field, and intelligent diagnosis technology is increasingly mature. Neural networks used to monitor CVDs are becoming more complex, requiring more computing power and memory, and are difficult to deploy in wearable devices. This paper proposes a lightweight model for classifying heart sounds based on knowledge distillation, which can be deployed in wearable devices to monitor the heart sounds of wearers. The network model is designed based on Convolutional Neural Networks (CNNs). Model performance is evaluated by extracting Mel Frequency Cepstral Coefficients (MFCCs) features from the PhysioNet/CinC Challenge 2016 dataset. The experimental results show that knowledge distillation can improve a lightweight network's accuracy, and our model performs well on the test set. Especially, when the knowledge distillation temperature is 7 and the weight α is 0.1, the accuracy is 88.5 %, the recall is 83.8 %, and the specificity is 93.6 %.Clinical relevance- A lightweight model of heart sound classification based on knowledge distillation can be deployed on various hardware devices for timely monitoring and feedback of the physical condition of patients with CVDs for timely provision of medical advice. When the model is deployed on the medical instruments of the hospital, the condition of severe and hospitalised patients can be timely fed back and clinical treatment advice can be provided to the clinicians.

The effects of brominated flame retardants (BFRs) on pro-atherosclerosis mechanisms.

Brominated flame-retardants (BFRs) are environmental endocrine disruptors, comprising several pollutants, which potentially affect the endocrine system and cause dysfunction and disease. Widespread BFR exposure may cause multisystem toxicity, including cardiovascular toxicity in some individuals. Studies have shown that BFRs not only increase heart rate, induce arrhythmia and cardiac hypertrophy, but also cause glycolipid metabolism disorders, vascular endothelial dysfunction, and inflammatory responses, all of which potentially induce pre-pathological changes in atherosclerosis. Experimental data indicated that BFRs disrupt gene expression or signaling pathways, which cause vascular endothelial dysfunction, lipid metabolism-related disease, inflammation, and possibly atherosclerosis. Considerable evidence now suggests that BFR exposure may be a pro-atherosclerotic risk factor. In this study, we reviewed putative BFR effects underpinning pro-atherosclerosis mechanisms, and focused on vascular endothelial cell dysfunction, abnormal lipid metabolism, pro-inflammatory cytokine production and foam cell formation. Consequently, we proposed a scientific basis for preventing atherosclerosis by BFRs and provided concepts for further research.

Effect of Acute Cold Exposure on Energy Metabolism and Activity of Brown Adipose Tissue in Humans: A Systematic Review and Meta-Analysis.

Background: The benefit of cold exposure for humans against obesity has brought the energy metabolism and activity of brown adipose tissue (BAT) induced by cold into focus. But the results are inconsistent. This review is aimed to systematically explore the effect of cold exposure on the activity of BAT and energy metabolism in humans. Methods: We searched relevant papers that were published from 1990 to 2021 and were cited in PubMed Central, Web of science, Embase and Cochrane Library databases to conduct this systematic review and meta-analysis. Energy metabolism, BAT volume, BAT activity and non-esterified fatty acids (NEFA) data reported in eligible researches were extracted. Meta-analysis was applied to combine the mean difference or standard mean difference with their 95% confidence intervals (95%CI). RevMan 5.3 software was used for meta-analysis and evaluating the risk of bias. Stata 16.0 was used for evaluating the publication bias. Results: Ten randomized controlled trials were included in meta-analysis. Compared with human exposed in room temperature at 24°C, the energy expenditure (EE) was increased after acute cold exposure at 16∼19°C (Z = 7.58, p < 0.05, mean different = 188.43kal/d, 95% CI = 139.73-237.13); BAT volume (Z = 2.62, p < 0.05; standard mean different = 0.41, 95% CI = 0.10-0.73); BAT activity (Z = 2.05, p = 0.04, standard mean difference = 1.61, 95% CI = 0.07-3.14) and the intake of BAT NEFA (Z = 2.85, p < 0.05; standard mean different = 0.53, 95% CI = 0.17-0.90) also increased. Conclusion: Acute cold exposure could improve the energy expenditure and BAT activity in adults, which is beneficial for human against obesity.

Apolipoprotein A1-Related Proteins and Reverse Cholesterol Transport in Antiatherosclerosis Therapy: Recent Progress and Future Perspectives.

Hyperlipidemia characterized by abnormal deposition of cholesterol in arteries can cause atherosclerosis and coronary artery occlusion, leading to atherosclerotic coronary heart disease. The body prevents atherosclerosis by reverse cholesterol transport to mobilize and excrete cholesterol and other lipids. Apolipoprotein A1, the major component of high-density lipoprotein, plays a key role in reverse cholesterol transport. Here, we reviewed the role of apolipoprotein A1-targeting molecules in antiatherosclerosis therapy, in particular ATP-binding cassette transporter A1, lecithin-cholesterol acyltransferase, and scavenger receptor class B type 1.

PM2.5 promoted lipid accumulation in macrophage via inhibiting JAK2/STAT3 signaling pathways and aggravating the inflammatory reaction.

BACKGROUND: Abnormal lipid accumulation in macrophages may lead to macrophages foaming, which is the most important pathological process of atherosclerosis. Atmospheric PM2.5 could enter the blood circulation and further affect the lipid metabolism of macrophages. But the underlying mechanism is not unclear. This study was undertaken to clarify the effect of PM2.5 on lipid metabolism in macrophages, and to explore the role of inflammatory reaction and JAK2/STAT3 signaling pathway in this process. METHOD: Macrophages derived from THP-1 cells were exposed to PM2.5 (0,100,200,400 µg/mL) for 6 h and 12 h. STAT3 agonist ColivelinTFA is used to specifically excite STAT3. The survival rate of macrophages was detected by CCK-8. The lipid levels in macrophages were detected by colorimetry. The levels of inflammatory factors secreted by macrophages were detected by ELISA. Q-PCR was used to detect the mRNA expression levels, and Western Blot was used to detect the protein expression levels of JAK2/STAT3 pathway genes. RESULT: The survival rate of macrophages was reduced by PM2.5, and the levels of TG, T-CHO and LDL-C of macrophages exposed to PM2.5 were increased. PM2.5 led to the increasing level of IL-6 and the decreasing level of IL-4, and the JAK2/STAT3 signaling pathway was inhibited by PM2.5. Colivelin TFA significantly decreased the increasing levels of TG, T-CHO and LDL-C levels, and increased the decreasing mRNA levels of IL-4, and LPL induced by PM2.5 (p < 0.05). DISCUSSION: PM2.5 could cause the lipid accumulation of macrophages by inhibiting the JAK2/STAT3 signaling pathway, and inflammatory responses may be involved in this process.

Syncope as the initial presentation of pulmonary embolism in two patients with hepatocellular carcinoma: Two case reports and literature review.

RATIONALE: Pulmonary embolism (PE) has diverse clinical manifestations and syncope might be the first or only symptom of PE. Tumor disease usually presents with symptoms associated with the primary site, however, PE may be the first manifestation of occult tumors. PATIENT CONCERNS: Here, we report 2 patients admitted to our hospital because of syncope. One patient had a chronic hepatitis B history of more than 20 years and the other patient had chronic heavy drinking for many years. Neither patient had been diagnosed with neoplastic disease before admission. DIAGNOSES: Clinical examinations, including laboratory tests and imaging tests upon admission demonstrated PE resulting in syncope. Furthermore, malignant hepatocellular carcinoma (HCC), inferior vena cava, and right atrium tumor thrombus were diagnosed. INTERVENTIONS: Thrombolysis and anti-coagulation therapy were performed immediately after the diagnosis of PE. Twenty-seven HCC patients with PE in 27 articles from 1962 to 2020 in the PubMed database were reviewed. OUTCOMES: The improvement was achieved that no syncope recurred after treatment of PE. The oxygen partial pressure increased and the D-dimer level decreased. The clinical characteristics of 27 HCC patients with PE were summarized and analyzed. LESSONS: It is important for clinicians to be aware that occult carcinoma might be a reason for patients with PE presenting with syncope. If PE cannot be explained by common causes, such as our patient, and HCC should be highly suspected when inferior vena cava and right atrial mass are found on imaging tests.

Higher than recommend dosage of sublingual isosorbide dinitrate for treating angina pectoris: a case report and review of the literature.

Nitrates primarily cause arterial and venous vasodilation effects, which increases coronary artery blood supply, and decreases cardiac preload and afterload by enhancing nitric oxide (NO) levels. The dosage of nitrates used for angina pectoris widely differs among individuals, and therapeutic resistance and tolerance gradually occur. Increasing doses of nitrates are needed to abolish ischemia chest pain onset in patients with angina pectoris, and to obtain satisfactory therapeutic effects. Here, we report the case of a 37-year-old male who was hospitalized six times, from September 2013 to April 2018, with recurrent angina pectoris. Although the patient was implanted with stents, he still presented with chest pain associated with physical efforts. Diagnosis with acute myocardial infarction was based on his ST-segment changes on electrocardiogram (ECG), elevated troponin-T level and coronary angiography. After the stents were implanted, his chest pain had no relief. Following three times of coronary angiography revealed that distal and small branch vessels still had stenosis, but was not required to revascularization. Due to serious headache resulted from sublingual or oral nitroglycerin; he had to take sublingual isosorbide dinitrate, from 20 mg to 150 mg each time, to obtain rapid relief from angina pectoris without doctor's consent. Followed up to April 2019, the patient has continued to take 100-150 mg sublingual isosorbide dinitrate for angina pectoris onset triggered by physical efforts, and has obtained remarkable relief within a few minutes, without blood pressure decrease and other side effects. Higher than recommend dosage of sublingual isosorbide dinitrate might establish better efficacy for angina pectoris in rarely patient.

Association Between D-Dimer Level and In-Hospital Death of Pulmonary Embolism Patients.

To investigate whether D-dimer level could predict pulmonary embolism (PE) severity and in-hospital death, a total of 272 patients with PE were divided into a survival group (n = 249) and a death group (n = 23). Comparisons of patient characteristics between the 2 groups were performed using Mann-Whitney U test. Significant variables in univariate analysis were entered into multivariate logistic regression analysis. Receiver operating characteristic (ROC) curve analysis was performed to determine the predictive value of D-dimer level alone or together with the simplified Pulmonary Embolism Severity Index (sPESI) for in-hospital death. Results showed that patients in the death group were significantly more likely to have hypotension (P = 0.008), tachycardia (P = 0.000), elevated D-dimer level (P = 0.003), and a higher sPESI (P = 0.002) than those in the survival group. Multivariable logistic regression analysis showed that D-dimer level was an independent predictor of in-hospital death (OR = 1.07; 95% CI, 1.003-1.143; P = 0.041). ROC curve analysis showed that when D-dimer level was 3.175 ng/ml, predicted death sensitivity and specificity were 0.913 and 0.357, respectively; and when combined with sPESI, specificity (0.838) and area under the curve (0.740) were increased. Thus, D-dimer level is associated with in-hospital death due to PE; and the combination with sPESI can improve the prediction level.

Combination of D-dimer and simplified pulmonary embolism severity index to improve prediction of hospital death in patients with acute pulmonary embolism.

OBJECTIVE: To investigate whether the combination of D-dimer and simplified pulmonary embolism severity index (sPESI) could improve prediction of in-hospital death from pulmonary embolism (PE). METHODS: Patients with PE (n = 272) were divided into a surviving group (n = 249) and an in-hospital death group (n = 23). RESULTS: Compared with surviving patients, patients who died in hospital had significantly higher rates of hypotension and tachycardia, reduced SaO2 levels, elevated D-dimer and troponin T levels, higher sPESI scores, and were more likely to be classified as high risk. Elevated D-dimer levels and high sPESI scores were significantly associated with in-hospital death. Using thresholds for D-dimer and sPESI of 3.175 ng/mL and 1.5, respectively, the specificity for prediction of in-hospital death was 0.357 and 0.414, respectively, and the area under the receiver operating characteristic curve (AUC) was 0.665 and 0.668, respectively. When D-dimer and sPESI were considered together, the specificity for prediction of in-hospital death increased to 0.838 and the AUC increased to 0.74. CONCLUSIONS: D-dimer and sPESI were associated with in-hospital death from PE. Considering D-dimer levels together with sPESI can significantly improve the specificity of predicting in-hospital death for patients with PE.

Rivaroxaban treatment for young patients with pulmonary embolism (Review).

Pulmonary embolism (PE) is a serious, life-threatening condition that affects young populations (>18 and <50 years old, according to most literature reviews) with improved recognition of its clinical manifestations and the widespread use of sensitive imaging techniques, PE is increasingly diagnosed in younger patients. At present, there is limited understanding of the clinical features and adequate anticoagulant treatment options for this population. Most studies to date have yet to demonstrate significant differences in PE pathophysiology or symptoms between young and elderly patients. Although the overall incidence of PE is lower in young populations compared with elderly patients, important risk factors also apply for young patients. Hereditary thrombophilia is common and is a major cause of PE in younger patients. Immobilization, trauma, obesity, smoking and infection are also becoming increasingly frequent in young patients with PE. Among female patients, oral contraceptive use, pregnancy and postpartum status are predominant risk factors underlying PE. Rivaroxaban is a direct oral anticoagulant with a rapid onset of action that is associated with less drug-drug interactions compared with other therapies. Because the drug is administered at fixed doses with no requirement for routine coagulation monitoring, it is becoming an attractive option for anticoagulation treatment in young patients with PE. Therefore, the present literature review focuses on the clinical characteristics of PE and rivaroxaban therapy in younger patients.

Identification of foam cell biomarkers by microarray analysis.

BACKGROUND: Lipid infiltration and inflammatory response run through the occurrence of atherosclerosis. Differentiation into macrophages and foam cell formation are the key steps of AS. Aim of this study was that the differential gene expression between foam cells and macrophages was analyzed to search the key links of foam cell generation, so as to explore the pathogenesis of atherosclerosis and provide targets for the early screening and prevention of coronary artery disease (CAD). METHODS: The gene expression profiles of GSE9874 were downloaded from Gene Expression Omnibus (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9874) on GPL96 [HG-U133A] Affymetrix Human Genome U133. A total of 22,383 genes were analyzed for differentially expression genes (DEGs) by Bayes package. GO enrichment analysis and KEGG pathway analysis for DEGs were performed using KOBAS 3.0 software (Peking University, Beijing, China). STRING software (STRING 10.0; European Molecular Biology Laboratory, Heidelberg, Germany) was used to analyze the protein-protein interaction (PPI) of DEGs. RESULTS: A total of 167 DEGs between macrophages and foam cells were identified. Compared with macrophages, 102 genes were significantly upregulated and 65 genes were significantly downregulated (P < 0.01, fold-change > 1) in foam cells. DEGs were mainly enrich in 'sterol biosynthetic and metabolic process', 'cholesterol metabolic and biosynthetic process' by GO enrichment analysis. The results of KEGG pathway analysis showed all differential genes are involved in biological processes through 143 KEGG pathways. A PPI network of the DEGs was constructed and 10 outstanding genes of the PPI network was identified by using Cytoscape, which include HMGCR, SREBF2, LDLR, HMGCS1, FDFT1, LPL, DHCR24, SQLE, ABCA1 and FDPS. CONCLUSION: Lipid metabolism related genes and molecular pathways were the key to the transformation of macrophages into foam cells. Therefore, lipid metabolism disorder is the key to turn macrophages into foam cells, which plays a major role in CAD.

Congenital unilateral proximal radioulnar synostosis: A surgical case report.

RATIONALE: Congenital proximal radioulnar synostosis is a rare genetic malformation of the upper limb. This deformity, which is found mainly in preschool-aged children, has no recognized diagnosis and treatment. Current diagnostic methods cannot effectively assess both bone structure and soft tissue abnormalities, and most surgical treatments introduce complications and do not prevent recurrence. More work is needed; therefore, to address the diagnosis and treatment of this disease. PATIENT CONCERNS: An 8-year-old male patient was hospitalized in our department. He reported deformity and limited motion in his right elbow for the past 2 years. He denied a traumatic or family history of bony malformation. The chief complaint at the time of the hospitalization was the limitation in forearm rotation. DIAGNOSIS: Digital radiography of the right elbow joint showed proximal radioulnar synostosis and a valgus deformity. A 3-dimensional computed tomography scan further showed proximal ulna and radius dysplasia as well as anterior dislocation of the radius head. The patient was diagnosed with congenital right proximal radioulnar synostosis. INTERVENTIONS: Surgical procedures included arthrolysis of the right proximal radioulnar joint, osteotomy of the proximal radius, internal fixation with Kirschner wires, and reconstruction of the annular ligament. The right elbow was immobilized in plaster in a flexion and supination position for 2 weeks. OUTCOMES: Recurrence of the right proximal radioulnar synostosis was observed during the 6-month follow-up, but the rotation function of the patient's forearm was significantly improved. LESSONS: The findings from this case suggest that we should carefully monitor all patients younger than 6 years old who report long-term issues with forearm rotation. This case also highlights the need to assess soft tissue and epiphysis abnormalities in addition to bone assessments via digital radiography and 3-dimensional computed tomography. We suggest that surgery should not be performed until the proximal radius epiphysis has closed. Not all cases require surgical treatment, but when surgery is needed, a suitable method should be selected according to the individual needs of the patient. Any surgery performed should treat both the bony malformations and soft tissue abnormalities to maximize the therapeutic effect and reduce complications during and after surgery.

Current status of rivaroxaban in elderly patients with pulmonary embolism (Review).

Acute pulmonary embolism (PE) occurs with a high incidence rate in elderly patients, demonstrating complex clinical manifestations, as well as a difficult anticoagulant treatment strategy. Currently, there is limited understanding of the selection criteria for anticoagulant treatment in elderly patients with PE. In fact, the vitamin K antagonist warfarin, a commonly prescribed anticoagulant, has multiple disadvantages, including a narrow therapeutic range, unpredictable pharmacokinetics, multiple food and drug interactions and genetic polymorphisms resulting in poor response to this therapy; therefore, routine laboratory monitoring is required. Most elderly patients with PE fail to adhere to the treatment regimen or even discontinue it, and clinicians are equally hesitant to initiate oral anticoagulants in elderly patients with PE. This leads to a dilemma regarding the use of anticoagulation therapies and a worse prognosis for the patients. Rivaroxaban, a direct Xa factor inhibitor, has demonstrated considerable practical and clinical advantages, exhibits fast-start action pharmacokinetic and pharmacodynamic characteristics, and has an enhanced predictable anticoagulant effect with fewer drug-drug interactions. Based on randomized controlled trials and real-world clinical practice, rivaroxaban has also been recognized as a safe and effective anticoagulant, and these advantages have improved the therapeutic compliance of elderly patients with PE. Thus, this review focused on the current status of rivaroxaban treatment for elderly patients with PE, and described its significance in changing the current anticoagulation treatment regimens for patients. It is expected that rivaroxaban will become a good choice for the treatment of PE in elderly patients.

Successful treatment of amniotic fluid embolism complicated by disseminated intravascular coagulation with rivaroxaban: A case report.

RATIONALE: An amniotic fluid embolism (AFE) is a rare, lethal syndrome that is commonly associated with disseminated intravascular coagulation (DIC). Anticoagulation therapy is the most important strategy to inhibit excessive activation of the coagulation cascade in patients with AFE and DIC. At present, treatment of AFE with rivaroxaban has not been reported. PATIENT CONCERNS: We report a 37-year-old woman (gravida 2, para 1) at 39 weeks' gestation with irregular contractions of the uterus was admitted to the obstetrical department. Ten minutes after the spontaneous rupture of the membranes, the patient complained of dyspnea and dysphoria and exhibited cyanosis of her lips. The patient's blood pressure decreased and heart rate increased rapidly, and 2100 mL of unclotted blood flowed from her vagina within 1 hour. Her platelet count dropped to 21 × 10/L, and the results from routine coagulation tests, and D-dimer and fibrin degradation product tests were obviously abnormal. DIAGNOSES: According to the current research consensus, AFE with DIC should be considered immediately when sudden cardiovascular collapse occurs around the time of labor and delivery, followed by the development of coagulopathy and hemorrhage. INTERVENTIONS: In addition, the variety of supportive treatments, rivaroxaban was used in anticoagulant therapy. OUTCOMES: At follow-up 30 and 60 days, there were no complaints of discomfort or abnormal laboratory assays. The patient recovered completely. LESSONS: This case highlights that rivaroxaban, as a direct inhibitor of activated factor Xa, demonstrates a good therapeutic efficacy for treating AFE with DIC.

Considerations for routine coagulation monitoring with rivaroxaban: A case report and review of the literature.

BACKGROUND: Rivaroxaban is a non-vitamin K antagonist oral anticoagulant that does not require coagulation monitoring based on current recommendations. Our goal is to explore whether routine coagulation monitoring should not be required for all patients receiving oral rivaroxaban, what relationship between routine coagulation abnormalities and bleeding, and how to deal with the above clinical situations through our case and review of the literature. CASE SUMMARY: We report a 67-year-old woman with a history of atrial fibrillation who presented to the hospital with worsening dyspnea and cough. Based on electrocardiogram, venous compression ultrasonography, and computed tomography pulmonary angiography, the diagnosis of atrial fibrillation, deep venous thrombosis, and acute pulmonary embolism was confirmed. Her coagulation assays and renal function were normal on admission; she was not underweight, did not have a history of hemorrhagic disease, and her CHA2DS2-VAS, HAS-BLED, and simplified Pulmonary Embolism Severity Index scores were 3, 0, and 0, respectively. Oral rivaroxaban (15 mg twice daily) was administered. The following day, she presented gastrointestinal and gum bleeding, combined with coagulation abnormalities. Following cessation of rivaroxaban, her bleeding stopped and tests improved over the next 2 d. Rivaroxaban was begun again 3 d after recovery. However, she again presented with gastrointestinal and gum bleeding and the abnormal tests, and the therapy was discontinued. At 30-d follow-up after discharge, she presented normal coagulation tests without bleeding. CONCLUSION: Although current guidelines recommend that using non-vitamin K antagonist oral anticoagulants including rivaroxaban do not require coagulation monitoring, a small number of patients may develop routine coagulation test changes and bleeding during rivaroxaban therapy, especially in the elderly. Clinicians should pay attention to these patients and further obtain evidence in practice.

Syncope as the initial presentation of pulmonary embolism in a young adult with testicular tumor: A case report and literature review.

RATIONALE: Venous thrombus embolism (VTE) includes deep-vein thrombosis (DVT) and pulmonary embolism (PE) which may be an initial symptom for patients with cancer. PE has diverse clinical manifestations and is a rare complication of testicular tumor (TT). PATIENT CONCERNS: Here, we report a 21-year-old man admitted to our hospital due to syncope. DIAGNOSES: Clinical examinations upon admission demonstrated PE resulting in syncope. Further, a malignant TT, liver metastasis, and inferior vena cava (IVC) thrombosis were diagnosed. INTERVENTIONS: Low molecular heparin was administered immediately after PE was diagnosed. OUTCOMES: The patient suffered from cardiac arrest on hospitalization. LESSONS: Physicians should consider the possibility of TT when a young male patient presents with syncope and is diagnosed with PE that cannot be explained by a common cause. Treatment for TT and PE should be performed as early as possible to improve the prognosis of patients combine with TT and PE.

Routine coagulation test abnormalities caused by rivaroxaban: A case report.

RATIONALE: Rivaroxaban is a non-vitamin K antagonist oral anticoagulant. Current recommendations state that coagulation monitoring is not required, and neither the dose nor dosing interval requires adjustment in response to changes in coagulation parameters when rivaroxaban is used for approved indications. Guidelines mainly discuss the indications for rivaroxaban and non-vitamin K antagonist oral anticoagulants in general; they offer less guidance regarding how to use these medications in specific clinical situations to bridge the gulf between guidelines and clinical practice. PATIENT CONCERNS: An 88-year-old man with a long history of atrial fibrillation presented to the hospital with worsening dyspnea and chest pain. Significantly, he had an estimated glomerular filtration rate of 46.7 mL/min. He was prescribed oral rivaroxaban 20 mg once daily. After 7 days, the patient complained of maroon colored stools. DIAGNOSIS: Laboratory investigations revealed that the patient's prothrombin time (PT) and activated partial thromboplastin time (aPTT) were elevated. Rivaroxaban induced gastrointestinal bleeding was suspected. INTERVENTIONS: Rivaroxaban was discontinued and routine coagulation tests were monitored daily. OUTCOMES: Two days following the discontinuation of the drug, the bleeding was controlled and hemoglobin was normal, but the PT and aPTT remained abnormal. On the third day after discontinuing rivaroxaban, the patient experienced sudden syncope and pulselessness and expired. LESSONS: This case indicates that in real-world situations, a small number of patients may develop changes in both PT and aPTT during rivaroxaban therapy. Therefore, coagulation monitoring should be considered in patients with risk factors for bleeding, such as elderly patients with renal insufficiency.

Nephrotic syndrome with acute pulmonary embolism in young adults: Two case reports.

INTRODUCTION: Pulmonary embolism (PE) is often misdiagnosed, or the diagnosis is delayed because of its diverse clinical manifestations, it may even remain asymptomatic until sudden death. Most risk factors are not associated with young people, and there is a paucity of literature regarding PE in children and young adults. CASE PRESENTATION: Patient 1 who died was diagnosed with nephrotic syndrome more than 10 years before. He presented to a clinic with gradually worsening dyspnea, which was initially misdiagnosed as myocarditis. Patient 2 presented with sudden shortness of breath after treatment for nephrotic syndrome. His PE was quickly diagnosed, allowing prompt initiation of anticoagulant therapy. At follow-up 30 days after hospital discharge, his symptoms had disappeared, and his abnormal laboratory results had returned to almost normal. CONCLUSION: The diagnosis and treatment of the above 2 patients suggest that the possible occurrence of PE in a young person with nephrotic syndrome should not be ignored. The early diagnosis and delayed diagnosis will have different clinical outcomes.