Background: N6-methyladenosine (m6A) modification is implicated in the development of systemic sclerosis-associated pulmonary arterial hypertension (SSc-PAH). This study aimed to identify and characterize m6A-modified gene signatures in SSc-PAH and elucidate their association with immune dysregulation. Methods: Transcriptome expression profiles from Gene Expression Omnibus (GEO) datasets were analyzed to identify differentially expressed genes (DEGs) linked to SSc-PAH. Functional enrichment analysis was performed. Weighted gene co-expression network analysis (WGCNA) was conducted to identify hub genes. m6A target gene expression was assessed via single-sample gene set enrichment analysis (ssGSEA). Feature genes were identified through the application of machine learning algorithms. A nomogram was constructed. Protein-protein interaction (PPI) networks were constructed with GeneMANIA. Immune infiltration was assessed through ssGSEA. Drug-gene interactions were explored using the Drug-Gene Interaction Database (DGIdb). Results: A total of 371 DEGs were identified in SSc-PAH, predominantly enriched in immune- and inflammation-related pathways. WGCNA revealed SSc-PAH-associated modules strongly correlated with immune activation. Integration with validated m6A target genes identified 20 overlapping genes, indicating altered m6A-related transcriptional activity in SSc-PAH. The derived five-gene signature (KRT10, TNFAIP3, PDK4, TLR4, and YES1) exhibited high diagnostic accuracy across multiple cohorts and was closely associated with immune cell infiltration. Conclusions: A five-gene signature was derived from m6A-related targets, which shows reliable diagnostic potential for SSc-PAH and correlates with the immune microenvironment. These findings provide the first integrative transcriptomic evidence connecting m6A-related regulation with immune dysfunction in SScPAH, offering mechanistic insight and potential diagnostic biomarkers.

Pulmonary arterial hypertension (PAH) is a severe pulmonary vascular syndrome characterized by a progressive increase in pulmonary vascular resistance and pulmonary arterial pressure, which may lead to right-heart failure and death. Nutritional deficiencies have been identified in patients with PAH. However, a comprehensive characterization of vitamin deficiencies in patients with PAH and their potential roles remains lacking. Consequently, this review aims to synthesize existing literature on the roles of vitamins in PAH, encompassing the epidemiology of vitamin deficiencies, observational and interventional studies investigating the therapeutic potential of vitamins in patients with PAH, and the molecular mechanisms through which vitamins may influence endothelial dysfunction and pulmonary vascular remodeling.

This study aimed to investigate the role of B7-H3—an immune checkpoint implicated in inflammation and vascular remodeling—in uremic vascular calcification (UVC), particularly its effects on calcium deposition, vascular smooth muscle cell (VSMC) phenotype, and VSMC–macrophage crosstalk. An in vitro UVC model was established using β-glycerophosphate (β-GP) treated human aortic VSMCs (HA-VSMCs). B7-H3 expression was silenced using siRNA. Calcification was assessed by Alizarin Red S staining, ALP activity, and calcium content assays. VSMCs phenotype switching was evaluated by Western blot for contractile and osteogenic markers. Macrophage recruitment, adhesion, and polarization (M1/M2) were assessed using THP-1 cells in co-culture systems and analyzed by qRT-PCR and flow cytometry. The effect of macrophage polarization on VSMCs calcification was investigated in the presence or absence of B7-H3 knockdown. β-GP treatment induced HA-VSMC calcification, osteogenic differentiation, and upregulated B7-H3 expression. Silencing B7-H3 attenuated calcification, restored contractile markers, and reduced osteogenic markers in VSMCs. B7-H3 knockdown also suppressed the recruitment and adhesion of macrophages to HA-VSMCs, inhibited M1 polarization of co-cultured macrophages, and promoted their shift toward the M2 phenotype. Furthermore, silencing B7-H3 mitigated M1 macrophage-induced VSMC calcification and enhanced the protective effects of M2 macrophages. B7-H3 promotes UVC directly by inducing osteogenic transformation of VSMCs and indirectly by enhancing macrophage recruitment and favoring pro-calcific M1 polarization. Thus, targeting B7-H3 may represent a promising therapeutic strategy to mitigate UVC.

Introduction and importance: The treatment of a complex calciphylaxis wound with infection continues to be a significant challenge in a clinical situation. Case presentation: We describe a case of an 87-year-old man presented with a nontraumatic painful ulcer on his right heel. Calciphylaxis was diagnosed by the biopsy. Although a serial therapy of sodium thiosulphate, tra-madol hydrochloride, frequent dressing changes, and conventional surgical debridement initiated, the worsening skin wound covered with a necrotic base and blackish eschar was formed. Skin cultures returned positive for the growth of proteus mirabilis. Subsequently, the usage of vacuum sealing drainage appeared to be effective. A complete resolution occurred 12 weeks after vacuum sealing drainage therapy. Clinical discussion: The infected wound due to calciphylaxis is not uncommon. Vacuum sealing drainage tech-nique demonstrated the effective approach to deal with wound infections, especially in the early stage. As the initial measures of wound care, serial debridement and sodium thiosulphate treatment have not slowed down the progress of the disease in this case, the vacuum sealing drainage along with the creative use of topical antibiotic flushing provided the best solution to promote healing of the infected field. Conclusion: This case highlights that vacuum sealing drainage technique could be considered in patients pre-senting with an infected wound involving calciphylaxis.

Objective To investigate how psychological treatment and social support affect patients receiving uremic hemodialysis for social function, anxiety, and depression. Methods The study's participants were 60 hemodialysis patients with uremia who were treated at our hospital between January 2019 and July 2022. Random selection yielded a control group of 30 patients and an observation group of 30 patients. Over the course of a month, both groups were continuously intervened upon, with the observation group receiving psychological intervention combined with social support and the control group receiving regular intervention. Patient satisfaction was measured using the Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36), and anxiety and depression levels were compared using the Anxiety Rating Scale (SAS) and the Depression Rating Scale (SDS). Results Following the intervention compared to pre-intervention levels, both groups' SAS and SDS scores dramatically fell, with the observation group's SAS and SDS scores being significantly lower than the control group's (P<0.05); After the intervention, both groups showed statistically significant increases in PSP scores and decreases in SDSS scores when compared to baseline; Moreover, the observation group's PSP scores were statistically greater than the control group's, and the observation group's SDSS scores were statistically lower than the control group's (P<0.05); Although the SF-36 ratings of the observation group were considerably higher than those of the control group (P<0.05), the SF-36 ratings of both groups were significantly higher than their baseline values after the intervention; Among individuals who got the intervention, satisfaction was significantly higher among those in the observation group (96.67%) than among those in the control group (70.00%). Conclusion In uremic hemodialysis patients, psychological intervention combined with social support can successfully lower anxiety and depression, enhance social function,both of which have significant clinical reference value and improve patients' quality of life and satisfaction with the intervention.

Objective:To investigate the clinical significance of serum 25-hydroxyvitamin D [25(OH)D] level in patients with connective tissue disease (CTD) related-pulmonary arterial hypertension (PAH).Methods:CTD patients with PAH (CTD-PAH) and without PAH (CTD-non-PAH) were colle-cted. All data were analyzed.Results:The serum 25(OH)D in the CTD-PAH group was significantly lower than that in the CTD-non-PAH group [(14±8) ng/ml vs (20±8) ng/ml, t=-5.94, P<0.001]. The 25(OH)D deficiency rate in the CTD-PAH group 86.2%(112/130) was significantly higher than that in the CTD-non-PAH group 57.7% (75/130) ( χ2=26.07, P<0.001), while the insufficiency rate was significantly lower [10.0%(13/130) vs 32.3% (42/130), χ2=19.39, P<0.001]. Serum 25(OH)D levels in the systemic lupus erythematosus (SLE), systemic sclerosis (SSc) associated PAH group were lower than those in the SLE [14(8, 17) ng/ml vs 19(15, 23) ng/ml, Z=-3.66, P<0.001], SSc [11(8, 17) ng/ml vs 24(18, 30) ng/ml, Z=-4.97, P<0.001] without PAH group. The levels of serum 25(OH)D in CTD-PAH youthful group, in the middle age group were lower than that in CTD-non-PAH youthful group [(12±8) ng/ml vs (19±8) ng/ml, t=-4.36, P<0.001] and in the middle age group [(14±7) ng/ml vs (21±8) ng/ml, t=-3.75, P<0.001]. Serum levels of 25(OH)D [ OR (95% CI)=1.100 (1.058, 1.144), P<0.001], uric acid [ OR(95% CI)=0.996(0.993, 0.998), P=0.003], immune globulin (Ig)G [ OR(95% CI)=1.123(1.057, 1.194), P<0.001] were associated with PAH in CTD patients. Serum 25(OH)D was positively correlated with calcium ( r=0.24, P=0.007), while negatively correlated between serum 25(OH)D and IgM ( r=-0.34, P<0.001). Conclusion:The occurrence and development of CTD-PAH may be related to the decrease of 25(OH)D level. Serum 25(OH)D level is associated with PAH in CTD patients.

目的 探讨糖尿病肾病(DN)患者尿液基质金属蛋白酶组织抑制剂2(TIMP-2)、胰岛素样生长因子结合蛋白7(IGFBP7)水平及其临床意义.方法 选取254例DN患者为研究组,另选取同期230例单纯2型糖尿病患者为对照组,比较2组患者临床资料.根据估算肾小球滤过率(eGFR)将DN患者分为Ⅰ期组32例,Ⅱ期组84例,Ⅲ期组90例,Ⅳ期组48例;根据血清肌酐及尿量将DN患者分为AKI组19例和非AKI组235例;比较血清肌酐、尿液TIMP-2、IGFBP7水平在不同组别患者中的差异.采用酶联免疫吸附法检测尿液TIMP-2、IGFBP7水平及尿肌酐水平;采用Pearson检验分析尿液TIMP-2、IGFBP7与相关指标的关系;采用受试者工作特征(ROC)曲线评价尿液TIMP-2、IGFBP7及血清肌酐诊断DN患者发生AKI的效能.结果 研究组血清肌酐、糖化血红蛋白(HbA1c)、血尿酸、尿素氮、尿微量白蛋白、24 h尿蛋白定量、尿β2-微球蛋白水平均高于对照组,血清白蛋白、eGFR水平均低于对照组,差异有统计学意义(P＜0.05).Ⅲ期、Ⅳ期DN患者血清肌酐、尿TIMP-2与尿肌酐的比值(TIMP-2/尿肌酐)、尿IGFBP7与尿肌酐的比值(IGFBP7/尿肌酐)均高于Ⅰ期、Ⅱ期患者,差异有统计学意义(P＜0.05);与非AKI组相比,AKI组患者血清肌酐、尿TIMP-2/尿肌酐、尿IGFBP7/尿肌酐均升高,差异有统计学意义(P＜0.05).尿液TIMP-2、IGFBP7与血清肌酐、HbA1c、血尿酸、尿素氮、尿微量白蛋白、24 h尿蛋白定量、尿β2-微球蛋白均呈正相关(P＜0.05),与血清白蛋白、eGFR均呈负相关(P＜0.05).ROC曲线显示,尿液TIMP-2、IGFBP7、血清肌酐预测DN患者发生 AKI 的曲线下面积(AUC)分别为 0.676(95％CI:0.587～0.756)、0.864(95％CI:0.792～0.918)、0.618(95％CI:0.528～0.703),尿液TIMP-2联合IGFBP7预测DN患者发生AKI的AUC为0.926(95％CI:0.866～0.965).结论 DN 患者尿液TIMP-2、IGFBP7水平随病情加重而呈上升趋势,对DN患者发生AKI有一定的预测价值.

The grey predictive mathematical model based on big data was used for analysis on the effect of Escherichia coli infection on patients with lupus nephritis (LN) in this study. Then, 156 patients diagnosed with LN infections by Wuzhong People’s Hospital’s information system (HIS) from October 30, 2017 to October 30, 2019 were selected as the experimental group, and 89 patients without LN infections were selected as the control group. Besides, the grey theory mathematical model was applied to process the integrated data, and feature analysis was employed to screen out disease-related bio-markers for the diagnosis of LN. The two groups were compared for affected organs, treatment, laboratory indicators, pathogenic bacteria, and recovery status. Multivariate logistic regression was used to analyze the related factors of patients with infections. The results showed that the specificity, sensitivity, and accuracy of the big data diagnosis based on the grey theory mathematical model were 78.9%, 87.6%, and 92.1, respectively; hormones, c-reactive protein, procalcitonin, and the daily antibiotic dose were positively correlated with concurrent infections (P < 0.05); 38 cases of Gram-negative bacteria were screened out, accounting for the largest proportion (37.18%); the effective rate of the experimental group was obviously lower than that of the control group (P < 0.05), suggesting that C-reactive protein (CRP), procalcitonin (PCT), antibiotics, daily dose of hormones, and serum albumin were independent risk factors for LN infection. In conclusion, the grey predictive mathematical model based on big data had high specificity, sensitivity, and accuracy in diagnosing the occurrence of infection in patients with LN; LN infection was mainly respiratory infection, and gram-negative bacteria were the main pathogen. Patients with LN infections showed higher serum creatinine, 24-hour urine protein quantification, CRP, and PCT, and lower serum albumin and recovery effect versus those without LN infections.

Objective:To investigate the clinical effect of far-infrared therapy combined with clopidogrel on thrombosis of autogenous arteriovenous fistula (AVF).Methods:A total of 66 patients who underwent hemodialysis in the hemodialysis center of our hospital from June 2017 to December 2017 were selected and divided into combined group, clopidogrel group and control group according to random number table method, with 22 patients in each group. Patients in the combined group were given the therapy of far-infrared and clopidogrel, while in the clopidogrel group were only treated with clopidogrel. The control group was not treated with far infrared or clopidogrel. After 6 months follow-up, blood flow changes and the incidence of fistula thrombosis were compared in two groups.Results:At the end of follow-up, the patency rate of fistula in the combined group, clopidogrel group and control group were 90.91%(20/22), 77.27%(17/22) and 59.09%(13/22), respectively ( P<0.05). The blood flow of patients in combined group and clopidogrel group after treatment were respectively significantly higher than that before treatment ( P< 0.05). In the control group, there was no significant difference in blood flow before and after treatment ( P>0.05). The index of Hb, plasma albumin and Kt/V in the combined group was significantly higher than that before treatment, while hs-CRP was significantly lower ( P<0.05). The plasma albumin was significantly lower in clopidogrel group after treatment ( P<0.05). The index of serum albumin and Kt/V in the control group were lower than that before treatment ( P<0.05). Conclusions:Therapy of far-infrared combined with clopidogrel may protect AVF via reducing thrombosis.

Renal fibrosis is a critical process underlying the development progression of chronic kidney disease to end-stage renal disease, which has intrigued much attention. This study aimed to investigate the role of Sphingosine kinase 1 (SphK1) on epithelial-mesenchymal transition (EMT) in renal fibrosis and the potential regulatory mechanisms. In the present study, unilateral ureteral obstruction (UUO)-induced mouse renal fibrosis model was established. HE and Masson staining were employed to detect the pathological change and fibrous deposition in renal tissues respectively. Moreover, the expression of SphK1, EMT relative proteins including E-cadherin (E-cad), N-cadherin (N-cad) and vimentin as well as fibrosis marker protein α-smooth muscle actin (α-SMA) were measured by immunohistochemistry and Western blot, respectively. In vitro, SphK1 silencing was generated in TGF-β induced human renal tubular epithelial HK-2 cells. Immunofluorescence staining was applied to examine the expression of α-SMA, then the levels of EMT relative proteins and NF-κB signaling were measured using Western blot. The results revealed that notably tubulointerstitial damage and fibrous deposition were detected in the UUO mouse renal tissues. The expression level of E-cad and SphK1 were decreased coupled with an increase of N-cad, vimentin and α-SMA expression. Furthermore, after knockdown of SphK1 in TGF-β induced HK-2 cells, the E-cad expression was up-regulated while N-cad, vimentin and α-SMA expression were down-regulated remarkably. In addition, the expression levels of phospho-NF-κB p65 (p-NF-κB p65) and p-IκB-α were lowered significantly following SphK1 silencing. These findings indicated that the inhibition of SphK1 protected renal tubular epithelial cells against renal fibrosis, by contribution to decrease the EMT via blocking the NF-κB signaling. Therefore, SphK1 may serve as a therapeutic target in the future.

This study aimed to report a unique case of primary adrenal insufficiency that was accompanied by painful gynecomastia, which was resolved by treatment with prednisone. Enlargement of the left breast with continuous weakness and generalized nausea in a male was discovered 3 months before admission. Magnetic resonance imaging of the brain was normal 1 month before presentation. A physical examination revealed that the diameter of the left breast was 5 cm and the height was 3 cm. Laboratory investigations revealed hyponatremia, with a low serum cortisol level and an elevated prolactin level. Hyperprolactinemia was suspected because of adrenal deficiency that was directly or indirectly associated with increased prolactin levels. Thus, a diagnosis of hyperprolactinemia was confirmed. Ultrasonography of the left breast showed glandular tissue hyperplasia. In the present study, treating adrenal insufficiency with prednisone relieved both gynecomastia and hyponatremia. However, gynecomastia regression and hyponatremia resolution were observed when prednisone was stopped. Gynecomastia completely resolved by re-administering prednisone. Therefore, treating the underlying disease is essential so that prednisone can be given in a timely manner.

INTRODUCTION Pheochromocytoma is a rare catecholamine-producing tumor with the primary presentations, both of intermittent fever and nonoliguric acute renal failure. Only several articles were retrieved with the rare presentation of fever. However, no case characterized by both of fever and acute renal failure has been retrieved. CASE REPORT A 66-year-old man sought medical help for intermittent fever. The onset was often sudden with the normal temperature rising to 40°C. The high fever always sustained for several hours and then declined to normal. A review of the past medical history revealed a hypertension over 3 years. His blood pressure (BP) was under good control by orally taking 5 mg amlodipine daily. On initial examination, he had an elevated BP of 230/120 mmHg, temperature of 38.5°C. Physical examination showed a heart rate of 103–125 beats/min in sinus rhythm. The remainder of physical examination yielded no abnormalities. On admission, urine dipstick showed a reaction for protein 3+. Laboratory data revealed both an elevated C-reactive protein (CRP) level of 26.3 (normal range [NR] 0–3) mg/L and a marked leukocytosis (leukocyte count 21.24 [NR 4–10] × 109/L, 86% [NR 40–75%]). Besides, a serum creatinine (Scr) level elevated to 198.1 (NR 59–104) µmol/L and blood urea nitrogen (BUN) to 9.4 (NR 2.9–8.2) mmol/L. Subsequently, the patient was referred to our department. Although procalcitonin was normal (NR <0.1 ng/ml), an infectious disease consultant suggested that an infection was coming. The antibiotics of intravenous piperacillin-tazobactam and levofloxacin were then started. However, he had intermittent fever with the same intensity. A marked increasing BP in a previously stable state was noted. Thus, a single dose of labetalol hydrochloride was administered intravenously. After a few minutes, he became hypotensive with a BP dropped to 80/60 mmHg and even unrecorded later. In view of hypotension, labetalol was discontinued. High-dose of intravenous fluid was required to maintain mean arterial pressure. When hypotension was corrected, his BP remained high. A subsequent morning Scr level was elevated to 325.6 µmol/L and BUN raised to 11.03 mmol/L. The level of serum cystatin C was enhanced to 1.66 (NR 0.55–1.14) mg/L. Repeated urine specimen revealed a reaction for protein 3+ and a few of hyaline casts. However, the urine output was normal (2000 ml/day). Based on the clinical presentations above, pheochromocytoma was highly suspect. However, urine (24 h) vanillylmandelic acid level was 14.3 (NR 9.6–49.5) µmol/24 h. Subsequently, abdominal computed tomography confirmed a solid heterogeneous mass in the left adrenal gland [Figure 1]. As the diagnosis of pheochromocytoma was considered, the more traditionally used prazosin was commenced. In the ward, the Scr level rose to a peak of 474 µmol/L. Following the usage of prazosin, the levels of Scr and BUN surprisingly began to fall and returned to baseline after 2 days [Table 1]. Subsequently, laparoscopic excision of the left adrenal tumor was undertaken uneventful. The pathological examination confirmed the diagnosis of pheochromocytoma. Postoperatively, the patient became symptom-free with normal temperature. At present, the patient remained asymptomatic with normal renal function and his BP was under good control.Figure 1: Abdominal computed tomography showed a large tumor about 7.7 cm × 6.4 cm × 8.0 cm (white arrow) at the left adrenal gland.Table 1: Data of Scr and BUNDISCUSSION Pheochromocytoma is a catecholamine-producing tumor.[1] Clinical manifestations of pheochromocytoma are highly variable. The diagnosis is clinically challenging with the atypical symptoms. Less frequent clinical manifestation includes fever of unknown origin. High fever with leukocytosis and raised CRP strongly indicated that infection was occurring. The site of infection was considered more likely in the left adrenal gland in this case. In fact, the exact mechanism of fever in patients with pheochromocytoma is unclear. Presumably, it may due to catecholamine overproduction caused by pheochromocytoma that finally led to an increase in inflammatory cytokines. The previous study demonstrated that pheochromocytoma presenting with fever was associated with elevated cytokine of interleukin-6.[2] Ultimately, the patient, in this case, achieved fever remission through the adrenalectomy. It is therefore of utmost importance, to look for an undiscovered pheochromocytoma in a case presenting with fever. Early diagnosis and prompt management are crucial. The patient in our case was at risk for the appearance of nonoliguric acute renal failure. The prominent signs of renal injury in this patient were the increase in Scr and BUN, persistent proteinuria, and a few of hyaline casts. It is unknown what triggered his acute presentation and subsequent deterioration of renal function. Probably, acute renal failure in pheochromocytoma may be due to hypertensive injury, hypoperfusion, acute tubular necrosis following hypotension, and drugs. Although the exact cause was difficult to determine, the excessive catecholamine, either directly or indirectly, played a part in causing acute renal failure. A massive catecholamine release during the procedure manifested itself as a hypertensive crisis, which produced severe vasoconstriction and thereby provoked ischemia of the patient's kidney. The insults ultimately resulted in the serious clinical condition of nonoliguric acute renal failure. Retrospectively, renal failure is uncommon in benign hypertension. However, our patient progressed from benign to malignant hypertension, renal failure commonly supervened. Second, it was probably that renal failure developed as a consequence of the hypotension. In this case, the hypertension was controlled by administration of labetalol, but an episode of hypotension developed. There may be a decrease in renal blood flow secondary to hypotension. The tendency of the patient was to present prerenal azotemia. Moreover, partial necrosis of renal tubular epithelium may be present. Finally, acute renal failure may develop with the full indicated dose of levofloxacin. Levofloxacin is a third-generation fluorinated quinolone antibiotic and the active levo stereoisomer of loxacin. It has one of the most adverse reaction profiles.[3] Levofloxacin is a dangerous drug in patients with renal dysfunction. In this report, pheochromocytoma crisis with nonoliguric acute renal failure was preoperatively controlled by the treatment of α1-adrenergic receptor blocking agent. In clinic, the diagnosis of pheochromocytoma requires a high degree of clinical suspicion. Pheochromocytoma must be considered as a part of the differential diagnosis complicated with both of fever and acute renal failure. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

目的 探讨采用丹参酮ⅡA磺酸钠注射液治疗过敏性紫癜对患者紫癜消退及肾受累的影响.方法 选取2013年8月至2014年10月已确诊为过敏性紫癜的患者68例,每组34例.采用随机数字表将患者分为实验组和对照组,每组34例.对照组给予常规治疗,实验组在常规治疗的基础上加静脉滴注丹参酮ⅡA磺酸钠注射液.观察两组过敏性紫癜患者紫癜消退情况及肾脏受累情况.结果 入院时两组各有6例为肾型紫癜,基础肾受累率相当(P＞0.05);入院后新发肾脏受累实验组2例(5.88％),对照组9例(26.47％),新发肾脏受累率实验组明显低于对照组,差异有统计学意义(P＜0.05).且治疗后实验组原6例肾型紫癜患者肾脏损害减轻,逐渐转为镜下血尿;而对照组原6例肾型紫癜的肾脏损害几乎无改善.结论 在常规治疗基础上加用丹参酮ⅡA磺酸钠注射液治疗过敏性紫癜,可降低患者的肾脏受累率,改善肾脏损害程度.

目的:探讨超声引导肾穿刺活检对弥漫性肾病的诊断价值。方法:对26例可疑弥漫性肾病患者超声引导下肾穿刺活检进行回顾性分析。结果:所有病例均获得病理学诊断。结论:超声引导下肾穿刺活检对弥漫性肾病的诊断、治疗及预后判断具有重要意义。

目的:探讨血清胱抑素C水平与脑梗死的关系。方法:以100例住院非脑血管病患者为对照组,104例脑梗死患者为观察组,测定血清胱抑素C水平。结果:观察组和对照组血清胱抑素C水平分别为(1.38±0.47)mg/L和(1.10±0.26)mg/L,两组比较差异有统计学意义(P<0.05)。结论:血清胱抑素C水平升高是脑梗死的危险因素之一。

目的 探讨脑钠肽(BNP)水平和心力衰竭(HF)严重程度的关系及临床应用.方法 选择2008年4月～2010年3月住院治疗的心力衰竭患者120例,正常对照组30例,用ADVIA Centauf BNP测定法定量测定血浆脑钠肽水平.对各级心功能组和正常对照组的血浆脑钠肽水平进行比较.结果 HF组总体血浆BNP水平明显高于对照组(P<0.01),NYHA Ⅰ、Ⅱ、Ⅲ、Ⅳ级组间血浆BNP依次递增(P<0.01).结论 血浆BNP浓度与心功能分级呈正相关,血浆BNP的浓度变化对心力衰竭的诊断、严重程度的判断有重婴价值.

目的探讨血浆脑钠肽(BNP)与CA125在不同严重程度的慢性心力衰竭(CHF)患者中的水平及其相关性。方法 65例临床确诊为慢性心力衰竭并按照纽约心脏学会(NYHA)分级区分其心衰程度的患者作为研究对象,选取20例健康体检人员作为对照组;采用ADVIACentaurBNP测定法定量测定血浆BNP水平,采用化学免疫发光法定量测定CA125水平;将两组的BNP及CA125值进行比较,做相关性分析。结果 CHF组血浆BNP与CA125水平在心功能Ⅱ级与Ⅲ级、Ⅲ级与Ⅳ级之间比较,差异有统计学意义(P<0.01),并且各组间与对照组间差异有统计学意义(P均<0.05),BNP或CA125水平与左室射血分数LVEF呈负相关(r值分别是-0.90和-0.61,P<0.05)。结论血浆BNP与CA125值在左室功能不全的患者中升高并与NYHA分级有明显的相关性,BNP与CA125值可作为诊断心力衰竭的筛选指标,并可用于指导心力衰竭的治疗。