The Lectin Pathway in Thrombotic Conditions—A Systematic Review

Larsen, Julie Brogaard; Hvas, Christine Lodberg; Hvas, Anne‐Mette

doi:10.1055/s-0038-1654714

Cited by 19 publications

(19 citation statements)

References 144 publications

(278 reference statements)

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“…Mannose‐binding lectin‐deficient individuals are susceptible to other diseases, such as various types of infectious disease, autoimmune disorders, and arterial CVD . These diseases are known to be associated with VTE risk and could thereby counterbalance the potential beneficial effect of MBL deficiency.…”

Section: Discussionmentioning

confidence: 99%

“…Mannose-binding lectin-deficient individuals are susceptible to other diseases, such as various types of infectious disease, autoimmune disorders, and arterial CVD. 35,55 These diseases are known to be associated with VTE risk 40,41,56,57 and could thereby counterbalance the potential beneficial effect of MBL deficiency. Mannosebinding lectin deficiency has been associated with advanced atherosclerosis 58,59 and a higher risk of myocardial infarction, independent of other traditional risk factors.…”

Section: Discussionmentioning

confidence: 99%

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Plasma levels of mannose‐binding lectin and future risk of venous thromboembolism

Liang

Høiland

Ueland

et al. 2019

Journal of Thrombosis and Haemostasis

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Background Animal and observational studies have suggested a pathophysiological role for complement in venous thromboembolism (VTE), but the initiating mechanisms are unknown. Mannose‐binding lectin (MBL) bound to altered host cells leads to activation of the lectin complement pathway, and both high and low MBL levels have been implicated in the pathophysiology of cardiovascular disease. Objectives To investigate the association between plasma MBL levels and future risk of incident VTE. Methods We conducted a nested case‐control study in 417 VTE patients and 849 age‐matched and sex‐matched controls derived from the general population (Tromsø Study). Plasma MBL levels were measured using enzyme‐linked immunosorbent assay. Logistic regression models were used to estimate odds ratio (OR) for VTE across quartiles of plasma MBL levels. Results Subjects with plasma MBL levels in the lowest quartile (<435 ng/mL) had a reduced OR for overall VTE (OR 0.79, 95% confidence interval [CI]: 0.56‐1.10) and for DVT (OR 0.70, 95% CI: 0.47‐1.04) compared to those with MBL in the highest quartile (≥2423 ng/mL) after multivariable adjustments. For VTE, DVT, and pulmonary embolism (PE) the ORs decreased substantially with decreasing time between blood sampling and VTE event. Conclusions Our findings suggest that low plasma MBL levels are associated with reduced risk of VTE, and DVT in particular.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Plasma levels of mannose‐binding lectin and future risk of venous thromboembolism

Liang

Høiland

Ueland

et al. 2019

Journal of Thrombosis and Haemostasis

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“…19,20 These findings have led to investigations of the role of the lectin pathway in a wide range of pro-thrombotic conditions; however, only few studies have investigated associations between sepsisrelated DIC and lectin pathway activation in a clinical setting. 21 Sprong et al found that MBL-deficient children with meningococcal disease had lower DIC scores and milder disease than children with normal MBL expression. 22 In contrast, Zhao et al described higher MBL plasma levels in sepsis patients with DIC than in patients with no DIC.…”

Section: Introductionmentioning

confidence: 99%

Reduced Mannose-Binding Lectin-Associated Serine Protease (MASP)-1 is Associated with Disturbed Coagulation in Septic Shock

et al. 2019

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Background Activation of the complement system is part of the dysregulated immune response in sepsis. The mannose-binding lectin-associated serine proteases (MASP)-1 and -2 activate the lectin pathway of the complement system. Besides, these proteins can activate coagulation in vitro. However, the role of the lectin pathway proteins in the development of sepsis-related disseminated intravascular coagulation (DIC) is only sparsely investigated. Aim This article investigates the association between lectin pathway proteins and coagulation disturbances in septic shock patients. Materials and Methods We included 36 septic shock patients from the intensive care unit, Aarhus University Hospital, Denmark. Blood samples were obtained within 24 hours after admission (day 1), and subsequently on day 2 and day 3. Plasma concentrations of mannose-binding lectin (MBL), H-ficolin, M-ficolin, CL-L1, CL-K1, MASP-1, -2 and -3, MBL-associated proteins of 19 and 44 kDa as well as complement factor C3dg were assessed. Standard coagulation parameters, thrombin generation, thrombin–anti-thrombin (TAT) complex and pro-thrombin fragment 1 + 2 were measured. Sequential Organ Failure Assessment (SOFA) score, DIC score and 30-day mortality were assessed. Results Reduced MASP-1 plasma concentration was associated with DIC score ≥5 (p = 0.02), impaired thrombin generation (p = 0.03) and lower plasma TAT complex levels (p = 0.03). No association was found between lectin pathway proteins and SOFA score or 30-day mortality. Conclusion Reduced MASP-1 concentrations were associated with impaired coagulation in septic shock patients. This indicates that increased MASP-1 activation and consumption is associated with the more severe coagulation disturbances in sepsis and points to a possible role for MASP-1 in sepsis-related DIC.

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“…However, data are controversial as some studies show an association of cardiovascular (CV) manifestations with MBL deficiency in the general population but others found no such link [37][38][39] . This controversy has also recently been summarized by Larsen et al 40 . In addition, an association of deficiency of complement MBL with reduced mortality in patients with MCI undergoing percutaneous coronary intervention 41 as well as with smaller cerebral infarcts and a favorable outcome 42 has been described previously.…”

mentioning

confidence: 78%

No association of complement mannose-binding lectin deficiency with cardiovascular disease in patients with Systemic Lupus Erythematosus

Kieninger-Gräfitsch

Vogt

Ribi

et al. 2020

Sci Rep

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Cardiovascular (CV) morbidity is the major cause of death in patients with Systemic LupusErythematosus (SLE). Previous studies on mannose-binding lectin (MBL) gene polymorphisms in SLE patients suggest that low levels of complement MBL are associated with cardiovascular disease (CVD). However, as large studies on MBL deficiency based on resulting MBL plasma concentrations are lacking, the aim of our study was to analyze the association of MBL concentrations with CVD in SLE patients. Plasma MBL levels SLE patients included in the Swiss SLE Cohort Study were quantified by ELISA. Five different CV organ manifestations were documented. Of 373 included patients (85.5% female) 62 patients had at least one CV manifestation. Patients with MBL deficiency (levels below 500 ng/ml or 1000 ng/ml) had no significantly increased frequency of CVD (19.4% vs. 15.2%, P = 0.3 or 17.7% vs. 15.7%, P = 0.7). After adjustment for traditional CV risk factors, MBL levels and positive antiphospholipid serology (APL+) a significant association of CVD with age, hypertension, disease duration and APL+ was demonstrated. In our study of a large cohort of patients with SLE, we could not confirm previous studies suggesting MBL deficiency to be associated with an increased risk for CVD.Systemic lupus erythematosus (SLE) is an idiopathic, chronic and highly heterogeneous inflammatory disorder, driven by an immune response against self-antigens. The prevalence generally ranges from 20 to 70 per 100.000 1 and affects both sexes of any age but predominates in women of childbearing age 2 with a male-to-female ratio of about 9:1 3 .The etiology of SLE is multifactorial and the complexity of different factors (genetic, hormonal, immunological and environmental) matches the diversity of clinical manifestations in SLE patients 4 . Associated with the presence of immune complexes, ongoing complement system activation leads to inflammation and consumption of complement proteins 5 . This chronic inflammatory state predisposes SLE patients to premature cardiovascular disease (CVD) and infections.Premature CVD, mostly related to accelerated atherosclerosis 6 , is acknowledged as the major cause of death in SLE patients, regardless of the time after diagnosis 7,8 , resulting in a bimodal mortality curve, first described by Urowitz et al. in the 1970s 9 . The 5-year survival after diagnosis nowadays exceeds 90% 10-12 , but this survival rate has not improved since the 1980s.The prevalence of ischemic heart disease in SLE patients is estimated to be between 3.8 and 16% 13-18 , a 10-fold higher prevalence compared to the general population 19 . Moreover, the risk of myocardial infarction in young

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The Lectin Pathway in Thrombotic Conditions—A Systematic Review

Cited by 19 publications

References 144 publications

Plasma levels of mannose‐binding lectin and future risk of venous thromboembolism

Plasma levels of mannose‐binding lectin and future risk of venous thromboembolism

Reduced Mannose-Binding Lectin-Associated Serine Protease (MASP)-1 is Associated with Disturbed Coagulation in Septic Shock

No association of complement mannose-binding lectin deficiency with cardiovascular disease in patients with Systemic Lupus Erythematosus

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