IL-13 gene expression in patients with atopic dermatitis: relation to IgE level and to disease severity

Atopic dermatitis (AD) is a chronic inflammatory skin disease frequently associated with an increased serum IgE level. T helper cells are thought to play an important role in the pathogenesis of AD. It is commonly believed that allergens activate Th2 cells, and it is likely that the cytokines produced by Th2 cells are crucial factors in the induction and maintenance of the disease. IL-13 is one of the cytokines that are produced by Th2 lymphocytes and, like IL-4, it can induce the production of IgE. In order to evaluate its role in the pathogenesis of AD, IL-13 mRNA expression was studied in peripheral blood of patients with different degrees of AD and compared with healthy subjects. Also, we correlated its level of expression with the level of serum IgE and with the severity of the disease. EDTA blood was obtained from 25 patients (divided into three groups ranged from mild to severe AD) and 12 normal subjects as a control group. We examined the blood sample for IL-13 mRNA expression using RNA extraction technique, RT-PCR, PCR amplification using primers specific for IL-13 and beta- actin (as internal control) this is followed by visualization of the expressed bands using gel electrophoresis and DNA marker. Serum IgE level was detected using an ELISA kit. Our results revealed that, IL-13 mRNA is significantly expressed in patients with AD as compared to normal control (P<0.001). IL-13 mRNA shows higher level of expression in severe AD group in comparison with both moderate and mild groups (P = 0.05). Serum levels of IgE showed highly significant increase in patients with AD as compared with the control group (p=0.019), its level is significantly higher in severe AD group versus moderate and mild AD groups (P=0.009 and 0.022, respectively). There is a highly significant positive correlation between serum levels of IgE and the levels of IL-13 mRNA expression in all AD groups (P=0.001). In conclusion, the high level of IL-18 mRNA expression in AD, and its correlation with serum level of IgE and with severity of disease indicates that IL-13 is involved in the pathogenesis of the disease and is an important in vivo IgE inducer.     

Fatigue in rheumatoid arthritis and its relation to interleukin-6 serum level

Patients and methodsThe study included 30 patients with RA diagnosed according to the 2010 ACR-EULAR classification criteria for RA and 15 healthy controls. Patients were included if they were above 18 years and fulfilled a score ?6 over 10 of the 2010 ACR-EULAR classification criteria for RA. Disease activity was assessed using 28 joint disease activity score (DAS28), erythrocytes sedimentation rate (ESR), C-reactive protein (CRP). Fatigue was assessed with the Bristol Rheumatoid Arthritis Fatigue Multidimensional Questionnaire (BRAF-MDQ) and serum IL-6 level was measured in patients and controls.ResultsThe BRAF-MDQ was significantly higher among patients (mean = 50.6 ± 15.2) than controls (mean = 7.8 ± 3.7) (p < 0.001). Patients’ mean IL-6 serum level was 35.05 ± 21.23 pg/ml and 4.72 ± 3.09 pg/ml among control subjects (p < 0.001). DAS 28 ranged between 4.33 and 7.67, mean 1st hour ESR was 43.57 mm and CRP was positive in 76.7% of patients. Significant correlations were found between BRAF-MDQ score and serum IL-6 level (r = 0.947, p < 0.001), ESR (r = 0.509, p < 0.001) as well as CRP positivity (r = 0.411, p = 0.005) in RA patients. Serum IL-6 level correlated with ESR (r = 0.463, p < 0.001) and CRP (r = 0.376, p = 0.01) among patients.ConclusionFatigue is a common symptom and scores higher among RA patients than healthy controls and should be measured in all RA patients with simple fatigue questionnaires matching with different cultures. Fatigue becomes more prominent as serum IL-6 level increases independently of the disease duration and activity.     

The relation between serum erythropoietin level and severity of disease and mortality in patients with chronic heart failure

OBJECTIVE: We evaluated the relation between serum erithropoietin level and the severity of disease and mortality in patients with chronic heart failure (CHF). METHODS: We enrolled 96 CHF patients and 50 age- and sex-matched control subjects. Haemoglobin, haemotocrit, N terminal pro-B type natriuretic peptide (NT-proBNP) and erythropoietin levels and echocardiographic parameters were measured. The patients were contacted 1 year after the evaluations to determine survival. RESULTS: The patients had lower haemoglobin and haematocrit but higher serum erythropoietin and NT-proBNP levels than the control subjects. Serum erythropoietin and NT-proBNP levels increased with worsening functional class. The serum erythropoietin level correlated negatively with left ventricular ejection fraction (r = -0.404, P < 0.001), haemoglobin (r = -0.530, P < 0.001) and haematocrit (r = -0.496, P < 0.001) levels. The patients who died (n = 17) had lower haemoglobin and haematocrit levels and significantly higher erythropoietin and NT-proBNP levels. However, multivariate logistic regression analysis showed that only NT-proBNP level was an independent predictor of mortality (P = 0.002). CONCLUSION: Anaemia and resistance to erythropoietin develop proportionately to disease severity and left ventricular systolic dysfunction in patients with CHF. Although serum erythropoietin level seems related with mortality, this observation needs to be confirmed by studies with more patients and longer follow-up.     

Relationship between skin prick and atopic patch test reactivity to aeroallergens and disease severity in children with atopic dermatitis

BackgroundThe immunological mechanism in aetiology of atopic dermatitis (AD) shows significant differences from other allergic diseases. Allergen inhalation exacerbates AD lesions and AD patients’ complaints decrease in house dust mite (HDM) low level environments, which reveals the importance of inhalant allergens.ObjectiveWe evaluated the skin prick test (SPT) and atopy patch test (APT) positivity rates with aeroallergens and studied the effect of test results, and aimed to determine the value of allergic test reactivity on the clinical characteristics of children with AD.MethodsForty-five children aged 2–15 years with AD were included to study between May 2006 and May 2007 in GATA Haydarpasa Teaching Hospital, Allergy Department. The reactivity to inhalant allergens using SPT and APT was evaluated. The severity of AD, which was assessed with SCORAD, was compared with aeroallergen hypersensitivity.ResultsThe highest positivity of APT was seen against HDM (48.9%). HDM SPT positivity and subjective symptoms score were statistically correlated (P < 0.05). Patients with strong SPT positivity to HDM had a higher total SCORAD score (P < 0.05). Although there was no statistical correlation between HDM APT and SCORAD parameters, APT positive patients had generally higher SCORAD parameters. The statistical significance was only shown between the extent of the disease and strong APT positive reactions to Dermatophagoides pteronyssinus.ConclusionHDM allergens play an important role in determining the clinical severity of AD and strong APT positivity could be more meaningful clinically.     

Staphylococcus aureus in atopic dermatitis: Strain-specific cell wall proteins and skin immunity

Atopic dermatitis (AD) is a common chronic skin disease. The presence of the bacterium Staphylococcus aureus (S. aureus) is frequently detected on skin affected with AD. In this review, we focused on the characteristics of S. aureus strains isolated from AD skin, particularly the proteins on the cell surface that modulates the interactions between Langerhans cell, keratinocyte, and S. aureus. The skin microbiome plays an important role in maintaining homeostasis of the skin, and colonization of S. aureus in AD is considered to be deeply involved in the clinical manifestation and pathogenesis of skin flares. Colonizing S. aureus strains in AD harbor different surface proteins at the strain level, which are indicated as clonal complexes. Moreover, the cell wall proteins of S. aureus affect skin adhesion and induce altered immune responses. S. aureus from AD skin (AD strain) exhibits internalization into keratinocytes and induces imbalanced Th1/Th2 adaptive immune responses via Langerhans cells. AD strain-derived cell wall proteins and secreted virulence factors are expected to represent therapeutic targets. In addition, the microbiome on the AD skin surface is associated with skin immunity; thus, microbiome-based immunotherapy, whose mechanism of action completely differs from that of typical steroid ointments, are expected to be developed in the future.     

Assessment of IL-31 levels and disease severity in children with atopic dermatitis

Introduction and objectives

Atopic dermatitis is a chronic, relapsing, highly pruritic, inflammatory skin disease characterized by typical localization with increasing prevalence of 10–20% in children. Pruritus is one of the major diagnostic criteria of atopic dermatitis and also the main complaint altering quality-of-life of affected patients, inducing and aggravating inflammation. Although pruritus is the absolute symptom of AD, the etiology has not been fully explained yet and current antihistamine therapies are ineffective.The aim of the study was to assess the correlation between IL-31 level and disease severity in patients with atopic dermatitis through Severity SCORing of Atopic Dermatitis (SCORAD) index and the degree of itching assessed subjectively.

Recurrent prosthetic valve endocarditis caused by Staphylococcus aureus colonizing skin lesions in severe atopic dermatitis

Infective endocarditis, a serious infection most commonly affecting rheumatic or prosthetic valves, generally occurs after bacteremia. Atopic dermatitis, a very common disease, carries a high prevalence of skin infections, particularly with Staphylococcus aureus. While cutaneous colonization by S. aureus represents an important source of bacteremia, few cases of infective endocarditis arising from the skin lesions of atopic dermatitis have been reported. We describe a patient with recurrent S. aureus prosthetic valve endocarditis developing in this manner.     

Exacerbating factors and disease burden in patients with atopic dermatitis

The number of patients with atopic dermatitis is on the rise worldwide, and Japan is no exception. According to recent estimates of the percentage of patients with atopic dermatitis in Japan by age, the majority of patients are between 20 and 44 years old. Because the peak age of onset of atopic dermatitis is during infancy, many patients may experience prolonged symptoms from infancy to adulthood. A prolonged clinical course also increases the burden of atopic dermatitis on affected patients. Decreased productivity due to work disruptions, reduced daily activity, higher direct medical costs, fatigue, and daytime sleepiness due to sleep disturbances are typical burdens on patients with atopic dermatitis. In order to reduce these burdens, it is necessary to shorten its clinical course and achieve long-term control without relying on medications, possibly by using avoidance or coping measures of aggravating factors. Typical aggravating factors of atopic dermatitis include irritant dermatitis, food allergy in children, sweating, and psychological stress in adults. Food allergy places a heavy burden on the quality of life of affected patients and their families. The effectiveness of educational interventions for sweating and psychological stress is unclear. We must also evaluate the economic burden and cost-effectiveness of interventions on the patient as aggravating factors to be addressed.     

Serum interleukin-23 level in rheumatoid arthritis patients: Relation to disease activity and severity

Aim of the work

The aim of this study was to evaluate interleukin-23 (IL-23) level in the sera of rheumatoid arthritis (RA) patients and to determine its relation with disease activity and severity.

Staphylococcus aureus binds to the N-terminal region of corneodesmosin to adhere to the stratum corneum in atopic dermatitis

Staphylococcus aureus colonizes the skin of the majority of patients with atopic dermatitis (AD), and its presence increases disease severity. Adhesion of S. aureus to corneocytes in the stratum corneum is a key initial event in colonization, but the bacterial and host factors contributing to this process have not been defined. Here, we show that S. aureus interacts with the host protein corneodesmosin. Corneodesmosin is aberrantly displayed on the tips of villus-like projections that occur on the surface of AD corneocytes as a result of low levels of skin humectants known as natural moisturizing factor (NMF). An S. aureus mutant deficient in fibronectin binding protein B (FnBPB) and clumping factor B (ClfB) did not bind to corneodesmosin in vitro. Using surface plasmon resonance, we found that FnBPB and ClfB proteins bound with similar affinities. The S. aureus binding site was localized to the N-terminal glycine–serine-rich region of corneodesmosin. Atomic force microscopy showed that the N-terminal region was present on corneocytes containing low levels of NMF and that blocking it with an antibody inhibited binding of individual S. aureus cells to corneocytes. Finally, we found that S. aureus mutants deficient in FnBPB or ClfB have a reduced ability to adhere to low-NMF corneocytes from patients. In summary, we show that FnBPB and ClfB interact with the accessible N-terminal region of corneodesmosin on AD corneocytes, allowing S. aureus to take advantage of the aberrant display of corneodesmosin that accompanies low NMF in AD. This interaction facilitates the characteristic strong binding of S. aureus to AD corneocytes.

Atopic dermatitis (AD) is a chronic inflammatory skin disorder, affecting 15 to 20% of children (1, 2). During disease flares, patients experience painful inflamed skin lesions accompanied by intense itch. Epidermal barrier dysfunction, increased type 2 immune responses, and recurrent skin infections are features of AD (3). The most common cause of infection is Staphylococcus aureus. This bacterium colonizes the skin of the majority of AD patients (4, 5). Isolates representing several S. aureus lineages are recovered from AD skin; however, strains from the clonal complex 1 (CC1) lineage are the most frequently isolated (6–9). The burden of S. aureus on lesional and nonlesional skin correlates with severity of the disease (10, 11). S. aureus directly influences pathogenesis, and several factors produced by the bacterium increase inflammation and exacerbate AD symptoms, including staphylococcal superantigen B and delta-toxin (12–15).Despite the clear association between S. aureus colonization and AD disease severity (11), the bacterial and host factor determinants underlying colonization are poorly understood (16). Adhesion is a critical early step in the colonization process. S. aureus adheres to corneocytes in the stratum corneum of AD skin (6, 17, 18). We previously found that clumping factor B (ClfB), a cell wall-anchored protein displayed on the surface of S. aureus, can mediate adhesion to corneocytes from AD patients (6). ClfB also binds to the alpha chain of fibrinogen and to the cornified envelope proteins loricrin and cytokeratin 10 (K10) in desquamated nasal epithelial cells (19–21). To date, ClfB is the only bacterial factor known to promote adherence to corneocytes in AD. However, a ClfB-deficient mutant retained the ability to bind to corneocytes (6), suggesting that additional bacterial factors are at play.Filaggrin deficiency is common in patients with established AD and is either genetic or caused by down-regulation of gene expression by Th-2–type cytokines (22–24). Filaggrin deficiency causes epidermal barrier defects and a loss of the hygroscopic filaggrin breakdown products that normally contribute to the natural moisturizing factor (NMF) in corneocytes (25). NMF comprises a collection of humectants, including filaggrin breakdown products urocanic acid and pyrrolidone acid, along with urea, citrate, lactate acid, and sugars, and is responsible for regulating hydration in the skin (26). Low-NMF levels are associated with a loss of hydration, increased disease severity, and abnormal corneocyte morphology (27). We showed recently that S. aureus binds more strongly to low-NMF AD corneocytes than to corneocytes with normal levels of NMF (18).Corneocytes with low NMF have very different surface topography when compared with corneocytes with normal levels of NMF (27). Aberrant “villus-like” projections (VPs) protrude from the surface of low-NMF corneocytes (18, 27). The protein corneodesmosin (CDSN) is confined to the cell–cell junctions between corneocytes in healthy skin, where homophilic interactions between the CDSN proteins on adjacent cells facilitate cell–cell cohesion (28). In AD patients, however, CDSN decorates the tips of the VPs on low-NMF corneocytes (27).This study aimed to elucidate a key component of S. aureus colonization by identifying the molecular determinants of adherence to AD corneocytes. We recognized that the occurrence of VPs on low-NMF corneocytes presents a different colonization surface to the bacterium and postulated that the accessibility of CDSN on the tips of VPs could influence pathogen adherence. We show that S. aureus can interact with CDSN and identify the S. aureus proteins promoting adherence to this host protein. We use single-cell and single-molecule atomic force microscopy (AFM), surface plasmon resonance (SPR), and ex vivo bacterial adherence studies with patient corneocytes to characterize this interaction. This study expands the repertoire of ligands for S. aureus and, crucially, links bacterial interactions with a host protein (CDSN) to binding to corneocytes taken from patients. Thus, our findings provide insights into the adhesion process and develop our understanding of the mechanisms underlying colonization of the skin of AD patients by S. aureus.     

Risk factors for sexual dysfunction in Egyptian patients with rheumatoid arthritis and its relation to disease activity

Aim of the work

To assess risk factors for sexual dysfunction in married rheumatoid arthritis (RA) patients.

Preventing Staphylococcus aureus bacteremia and sepsis in patients with Staphylococcus aureus colonization of intravascular catheters: a retrospective multicenter study and meta-analysis

Two previous studies in tertiary care hospitals identified Staphylococcus aureus colonization of intravascular (IV) catheters as a strong predictor of subsequent S. aureus bacteremia (SAB), even in the absence of clinical signs of systemic infection. Bacteremia was effectively prevented by timely antibiotic therapy. We conducted this study to corroborate the validity of these findings in non-university hospitals.Using the laboratory information management systems of the clinical microbiology departments in 6 Dutch hospitals, we identified patients who had IV catheters from which S. aureus was cultured between January 1, 2003, and December 31, 2008. Patients with demonstrated SAB between 7 days before catheter removal and 24 hours after catheter removal were excluded. We extracted clinical and demographic patient data from the patients' medical records. The primary risk factor was initiation of anti-staphylococcal antibiotic therapy within 24 hours, and the primary endpoint was SAB >24 hours after IV catheter removal. Subsequently, we performed a systematic review and meta-analysis of all observational studies evaluating the effect of antibiotic therapy for S. aureus IV catheter tip colonization.In the current study, 18 of the 192 included patients developed subsequent SAB, which was associated with not receiving antibiotic therapy within 24 hours (odds ratio [OR], 4.2; 95% confidence interval [CI], 1.1-15.6) and with documented exit-site infection (OR, 3.3; 95% CI, 1.2-9.3). When we combined these results with results of a previous study in a university hospital, a third risk factor was also associated with subsequent SAB, namely corticosteroid therapy (OR, 2.9; 95% CI, 1.3-6.3). We identified 3 other studies, in addition to the present study, in a systematic review. In the meta-analysis of these studies, antibiotic therapy yielded an absolute risk reduction of 13.6% for subsequent SAB. The number needed to treat to prevent 1 episode of SAB was 7.4.We conclude that early initiation of antibiotic therapy for IV catheters colonized with S. aureus prevents subsequent SAB.     

乙型肝炎相关慢加急性肝衰竭患者血清白细胞介素1受体拮抗剂与疾病严重程度的关系

目的探讨乙型肝炎相关慢加急性肝衰竭(HBV-ACLF)患者外周血白细胞介素(IL)1受体拮抗剂(IL-1Ra)与患者疾病严重程度的关系。方法选取福州市传染病医院2013年10月-2015年1月就诊的31例HBV-ACLF患者为研究对象,另选取同期28例急性乙型肝炎(AHB)和30例慢性乙型肝炎(CHB)患者作为对照。用Q-Plex法检测外周血IL-1Ra、IL-1β、IL-6、IL-4、IL-10、肿瘤坏死因子(TNF)α、干扰素(IFN)γ等细胞因子浓度,并检测各组肝功能、凝血功能等,将血清IL-1Ra等细胞因子浓度与患者肝功能、MELD评分及HBV DNA等进行相关分析。多组间比较采用Kruskal-wallis H检验,进一步两两比较采用Mann-Whitney U检验;计数资料采用χ2检验;相关分析采用Spearman秩相关。结果 IL-1Ra、IL-1Ra/IL-1β在3组之间的差异均有统计学意义(P值均0.05),其中HBV-ACLF组IL-1Ra水平[186.46(162.68~512.90)pg/ml]显著高于CHB组[70.47(47.07~92.47)pg/ml]和AHB组[143.69(117.75~208.54)pg/ml],差异均有统计学意义(Z=6.300,P0.001;Z=2.505,P=0.012);而HBV-ACLF患者IL-1Ra与IL-1β比值[2.92(2.20~4.74)]较AHB组[4.54(2.75~6.05)]低,但较CHB患者[2.49(1.50~2.50)]高,差异均有统计学意义(Z=1.966,P=0.048;Z=2.682,P0.001)。HBV-ACLF组IL-1β、IL-6、TNFα水平显著高于其他2组(P值均0.01)。血清IL-1Ra与TBil、MELD评分均呈负相关(r值分别为-0.506、-0.818,P值均0.01),与凝血酶原活动度(PTA)呈正相关(r=0.475,P=0.007)。结论 IL-1Ra与反映HBV-ACLF严重程度的指标TBil、MELD评分呈负相关,与PTA呈正相关,IL-1ra在HBV-ACLF发病过程中可能起重要作用。     

老年帕金森病患者血尿酸水平及其与认知功能的关系

目的 探讨老年帕金森病(PD)患者血尿酸水平与认知功能的关系,并对相关因素进行分析.方法 回顾性分析60例老年PD患者的病历资料,选择性别、年龄相匹配的60例健康体检者作为对照,记录性别、年龄、病程、Hoehn&Yahr分期(H-Y分期)、尿酸、简易智能量表(MMSE)评分,并进行比较和相关性分析.结果 老年PD组血浆尿酸水平[(262±53)μmol/L]明显低于对照组[(332±45)μmol/L],差异有统计学意义(t=-6.724,P＜0.001).PD组男性血浆尿酸水平[(271±48)μmol/L]均值略高于女性水平[(254±39)μmol/L],但差异无统计学意义(t=3.282,P=0.058).PD组男性血浆尿酸水平明显低于对照组男性尿酸水平[(353±62)μmol/L],差异有统计学意义(t=-5.625,P＜0.001).PD组女性血浆尿酸水平低于对照组女性尿酸水平[(294±59)/μmol/L],差异有统计学意义(t=-4.721,P=0.012).老年PD各亚组间血尿酸水平无显著差异,但与对照组比较差异均有统计学意义(F=22,039,P＜0,01).老年PD组血尿酸水平与病程长短无明显相关性(r=0.961,P＞0,05).老年PD患者存在认知功能障碍,其MMSE评分与H-Y分期(r=-0.577,P=0.019)、年龄(r=-0.333,P=0.034)呈负相关,与血尿酸水平呈正相关(r=0.789,P=0.000),与病程(r=-0.333,P=0.027)、体质指数(BMI)(t=-0.410,P=0.115)无相关性.结论 老年PD患者血尿酸水平降低,低尿酸水平可能与老年PD患者的认知功能障碍有关.

Abstract：

Objective To explore the relationship between uric acid (UA) level and cognitive function in elderly patients with Parkinson,s disease (PD) and analyze the cognition related factors.Methods The clinical data of 60 elderly PD cases in our hospital from 2001 to 2009 were retrospectively analyzed. The 60 healthy people receiving medical examination in our hospital and matched by gender and age, were as control group. The information including gender, age, illness duration, Hoehn & Yahr stage (H-Y stage), serum UA level and Mini-Mental State Examination (MMSE) scale were recorded. Results The serum UA level was significantly lower in PD group than in control group [(262±53) μmol/L vs. (332±45) μmol/L, t=-6.724, P＜0.001]. In PD group, the serum UA level was slightly higher in males than in females [(271 ±48) μmol/L vs.(254±39) μmol/L, t=3. 282, P=0. 058]. The serum UA level was significantly lower in male PD patients than in male controls [(353± 62) μmol/L, t=- 5. 625, P＜0. 001], and was lower in female PD patients than in female controls [( 294 ± 59) μmol/L, t = - 4. 721, P = 0. 012]. There were no significant differences in serum UA level among different H-Y stage subgroups (P＞0. 05), but the serum UA level was lower in different H-Y stage subgroups than in control group (F=22. 039, P＜0. 01 ). There was no correlation between the UA level and the illness duration (r=0. 961, P＞0.05).The MMSE score had significant difference between elderly PD group and control group (t= -3. 168,P＜0. 001). In PD patients, the MMSE score was positively correlated with serum UA level (r=0. 789, P= 0. 000), and was negatively correlated with H-Y stage (r= - 0. 577, P = 0. 019 ), age (r= -0. 333, P=0. 034), but was not correlated with illness duration (r= -0. 333, P=0. 207) and BMI (t=- 0. 410, P= 0. 115). Conclusions The level of serum UA is lower in elderly patients with PD than in normal controls. There is correlation between the serum UA level and cognitive impairment. Lower serum UA level predicts worse cognitive scores.     

血清Irisin水平与冠状动脉病变严重程度的相关性

目的 探讨冠心病患者血清鸢尾素(Irisin,一种肌肉因子)水平与冠状动脉病变严重程度的相关性。方法 连续入选于西京医院诊断为冠心病的患者249例,其中稳定型心绞痛(SAP)30例、不稳定型心绞痛(UAP)76例、急性心肌梗死(AMI)143例,收集一般临床资料。采用ELISA方法检测空腹血清Irisin水平,并将研究对象分为低Irisin组(Irisin≤2.3μg/ml)和高Irisin(Irisin>2.3μg/ml)组,比较两组受试者冠脉病变严重程度,分析血清Irisin浓度和冠脉病变严重程度的相关性。结果 低Irisin组和高Irisin组相比,具有男性比例高、高肌钙蛋白I(Tn I)、高CK-MB、高肌红蛋白和低左室射血分数(LVEF)的临床特点(均P<0.05),且冠脉病变严重程度(平均病变支数,Gensini评分)显著性加重(P<0.05,P<0.01);多元逐步回归分析显示,病变血管支数和Gensini评分是影响血清Irisin水平的独立因素(P<0.01);Gensini评分和血清Irisin水平呈负相关(r=-0.183,P<0.01)。结论 冠心病患者血清Irisin浓度与冠脉病变程度具有一定的相关性。