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Article ; Online: Systemic Lupus Erythematosus-related Lung Disease.

Bendstrup, Elisabeth / Lynn, Evelyn / Troldborg, Anne

Seminars in respiratory and critical care medicine

2024

Abstract: Systemic Lupus Erythematosus (SLE) is a multifaceted, multisystem autoimmune disorder with diverse clinical expressions. While prevalence reports vary widely, pulmonary involvement accounts for significant morbidity and mortality in SLE. This ... ...

Abstract	Systemic Lupus Erythematosus (SLE) is a multifaceted, multisystem autoimmune disorder with diverse clinical expressions. While prevalence reports vary widely, pulmonary involvement accounts for significant morbidity and mortality in SLE. This comprehensive review explores the spectrum of pulmonary disease in SLE, including upper airway manifestations (e.g., laryngeal affection), lower airway conditions (e.g., bronchitis, bronchiolitis, bronchiectasis), parenchymal diseases (e.g., interstitial lung disease, acute lupus pneumonitis, diffuse alveolar hemorrhage), pleural diseases (e.g., serositis, shrinking lung syndrome), and vascular diseases (e.g., pulmonary arterial hypertension, pulmonary embolism, acute reversible hypoxemia syndrome). We discuss diagnostic modalities, treatment strategies, and prognosis for each pulmonary manifestation. With diagnostics remaining a challenge and with the absence of standardized treatment guidelines, we emphasize the need for evidence-based guidelines to optimize patient care and improve outcomes in this complex disease.
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1183617-9
ISSN	1098-9048 ; 1069-3424
ISSN (online)	1098-9048
ISSN	1069-3424
DOI	10.1055/s-0044-1782653
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Article ; Online: Platelets and the Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus or Antiphospholipid Syndrome.

Vils, Signe Risbøl / Troldborg, Anne / Hvas, Anne-Mette / Thiel, Steffen

TH open : companion journal to thrombosis and haemostasis

2023 Volume 7, Issue 2, Page(s) e155–e167

Abstract: ... ...

Abstract	Background
Language	English
Publishing date	2023-06-15
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2901738-5
ISSN	2512-9465 ; 2567-3459
ISSN (online)	2512-9465
ISSN	2567-3459
DOI	10.1055/a-2087-0314
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Article: Systemic Lupus Erythematosus-related Lung Disease

Bendstrup, Elisabeth / Lynn, Evelyn / Troldborg, Anne

Seminars in Respiratory and Critical Care Medicine

(Pulmonary Complications of Connective Tissue Diseases)

2024

Series title	Pulmonary Complications of Connective Tissue Diseases
Abstract	Systemic Lupus Erythematosus (SLE) is a multifaceted, multisystem autoimmune disorder with diverse clinical expressions. While prevalence reports vary widely, pulmonary involvement accounts for significant morbidity and mortality in SLE. This comprehensive review explores the spectrum of pulmonary disease in SLE, including upper airway manifestations (e.g., laryngeal affection), lower airway conditions (e.g., bronchitis, bronchiolitis, bronchiectasis), parenchymal diseases (e.g., interstitial lung disease, acute lupus pneumonitis, diffuse alveolar hemorrhage), pleural diseases (e.g., serositis, shrinking lung syndrome), and vascular diseases (e.g., pulmonary arterial hypertension, pulmonary embolism, acute reversible hypoxemia syndrome). We discuss diagnostic modalities, treatment strategies, and prognosis for each pulmonary manifestation. With diagnostics remaining a challenge and with the absence of standardized treatment guidelines, we emphasize the need for evidence-based guidelines to optimize patient care and improve outcomes in this complex disease.
Keywords	systemic lupus erythematosus ; acute lupus pneumonitis ; alveolar hemorrhage ; pleural effusion ; serositis ; shrinking lung syndrome ; interstitial lung disease ; pulmonary hypertension ; pulmonary embolism
Language	English
Publishing date	2024-03-28
Publisher	Thieme Medical Publishers, Inc.
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	1183617-9
ISSN	1098-9048 ; 1069-3424
ISSN (online)	1098-9048
ISSN	1069-3424
DOI	10.1055/s-0044-1782653
Database	Thieme publisher's database

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Article ; Online: C3dg Quantification by PEG Precipitation and or TRIFMA.

Troldborg, Anne / Jensenius, Jens Christian

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2227, Page(s) 43–49

Abstract: Detection of complement activation products can be carried out in a number of ways, and different methods are used in different laboratories. No international standard for measuring complement activation in the clinical setting has been agreed upon.Here ... ...

Abstract	Detection of complement activation products can be carried out in a number of ways, and different methods are used in different laboratories. No international standard for measuring complement activation in the clinical setting has been agreed upon.Here we describe a modified assay for measuring C3dg. The assay is simple, inexpensive and stable. The estimation of C3dg directly reflects complement turnover independently of activation pathway.
MeSH term(s)	Animals ; Biomarkers/analysis ; Biomarkers/blood ; Blood Protein Electrophoresis ; Chemical Precipitation ; Complement Activation/physiology ; Complement C3b/analysis ; Complement C3b/isolation & purification ; Enzyme-Linked Immunosorbent Assay/methods ; Fluorescent Antibody Technique/methods ; Fluoroimmunoassay/methods ; Humans ; Immunoelectrophoresis/methods ; Inflammation/blood ; Inflammation/diagnosis ; Inflammation Mediators/analysis ; Inflammation Mediators/blood ; Peptide Fragments/analysis ; Peptide Fragments/isolation & purification ; Polyethylene Glycols/chemistry ; Rabbits
Chemical Substances	Biomarkers ; Inflammation Mediators ; Peptide Fragments ; complement C3d,g ; Polyethylene Glycol 6000 (30IQX730WE) ; Polyethylene Glycols (3WJQ0SDW1A) ; Complement C3b (80295-43-8)
Language	English
Publishing date	2021-04-13
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1016-9_4
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Article ; Online: Inter-Alpha-Trypsin Inhibitor Heavy Chain 4 (ITIH4) as a Compensatory Protease Inhibitor in Hereditary Angioedema (HAE).

Troldborg, Anne / Godnic-Polai, Zsofia / Cervenak, László / Hansen, Annette G / Farkas, Henriette / Thiel, Steffen

The Journal of allergy and clinical immunology

2024

Abstract: Background: Hereditary angioedema (HAE) is a genetic disorder that manifests as recurrent angioedema attacks, most frequently due to absent or reduced C1 inhibitor (C1-INH) activity. C1-INH is a crucial regulator of enzymatic cascades in the complement, ...

Abstract	Background: Hereditary angioedema (HAE) is a genetic disorder that manifests as recurrent angioedema attacks, most frequently due to absent or reduced C1 inhibitor (C1-INH) activity. C1-INH is a crucial regulator of enzymatic cascades in the complement, fibrinolytic, and contact systems. Inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) is an abundant plasma protease inhibitor that can inhibit enzymes in the proteolytic pathways associated with HAE. Nothing is known about its role in HAE. Objective: Investigate ITIH4 activation in HAE, establish it as a potential biomarker, and explore its involvement in HAE-associated proteolytic pathways. Methods: Specific immunoassays for non-cleaved ITIH4 (Intact ITIH4) and an assay detecting both intact and cleaved ITIH4 (Total ITIH4) were developed. We initially tested serum samples from HAE patients (n=20), ACEI-induced edema patients (ACEI) (n=20), and unknown HAE patients (U-HAE) (n=20). Validation involved an extended cohort of 80 HAE patients (60 type I, 20 type II), including samples taken at attack and quiescent disease periods, as well as 100 healthy controls. Results: In 63% of HAE patients, the Intact ITIH4 assay showed lower signals than the Total ITIH4 assay. This difference was not observed in ACEI and U-HAE patients. Western blotting confirmed cleaved ITIH4 in low-Intact ITIH4 samples. In serum samples lacking intact endogenous ITIH4, we observed immediate cleavage of added recombinant ITIH4 suggesting continuous enzymatic activity in the serum. Confirmatory HAE cohort analysis revealed significantly lower intact ITIH4 levels in both HAE type 1 and type 2 patients compared to controls, with consistently low Intact/Total ITIH4 ratios during clinical HAE attacks. Conclusion: The disease-specific low intact ITIH4 levels highlight its unique nature in HAE. The results suggest that ITIH4 may exhibit compensatory mechanisms in HAE, suggesting its utility as a diagnostic and prognostic biomarker. The variations during quiescent and active disease periods raise intriguing questions about the dynamics of proteolytic pathways in HAE.
Language	English
Publishing date	2024-04-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2024.03.028
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Article: Platelets and the Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus or Antiphospholipid Syndrome

Vils, Signe Risbøl / Troldborg, Anne / Hvas, Anne-Mette / Thiel, Steffen

TH Open

2023 Volume 07, Issue 02, Page(s) e155–e167

Abstract: Background: Patients with systemic lupus erythematosus (SLE) have an increased risk of thrombosis even when they do not have antiphospholipid syndrome (APS). Interactions between complement activation and activated platelets have been suggested in SLE ... ...

Abstract	Background: Patients with systemic lupus erythematosus (SLE) have an increased risk of thrombosis even when they do not have antiphospholipid syndrome (APS). Interactions between complement activation and activated platelets have been suggested in SLE and APS and could play a role in the increased thrombosis risk. Objectives: To explore factors potentially related to the prothrombotic pathophysiology in patients with SLE, primary APS, and healthy controls, by investigating lectin pathway proteins (LPPs), complement activation, platelet aggregation, and platelet activation. Methods: This cross-sectional cohort study included 20 SLE patients, 17 primary APS, and 39 healthy controls. Flow cytometry and light transmission aggregometry were used to assess platelet activation and aggregation. Using time-resolved immunofluorometric assays, the plasma concentrations of 11 LPPs and C3dg, reflecting complement activation, were measured. Results: H-ficolin plasma concentrations were higher in SLE and APS patients than in controls ( p = 0.01 and p = 0.03). M-ficolin was lower in SLE than in APS ( p = 0.01) and controls ( p = 0.03). MAp19 was higher in APS patients than in SLE patients ( p = 0.01) and controls ( p < 0.001). In APS patients, MASP-2 and C3dg correlated negatively with platelet activation. Platelet-bound fibrinogen after agonist stimulation and C3dg concentrations correlated negatively with platelet activation. Conclusion: We observed significant differences between SLE and APS patients regarding complement proteins and platelet activation. Particularly the negative correlations between MASP-2 and C3dg with platelet activation only observed in APS patients suggest that interactions between complement activation and platelets differ in SLE and APS.
Keywords	platelets ; complement activation ; lectin ; systemic lupus erythematosus ; antiphospholipid syndrome
Language	English
Publishing date	2023-04-01
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	2901738-5
ISSN	2512-9465 ; 2567-3459
ISSN (online)	2512-9465
ISSN	2567-3459
DOI	10.1055/a-2087-0314
Database	Thieme publisher's database

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Article ; Online: Differentiating between activation via the lectin or the classical complement pathway in patients with systemic lupus erythematosus.

Larsen, Mads Lamm / Troldborg, Anne / Toonen, Erik J M / Hurler, Lisa / Prohaszka, Zoltan / Cervenak, László / Gudmann Hansen, Annette / Thiel, Steffen

Clinical and experimental immunology

2023 Volume 214, Issue 1, Page(s) 18–25

Abstract: Complement activation is a hallmark of systemic lupus erythematosus (SLE) and can proceed through the classical (CP), lectin (LP), or alternative pathway (AP). When managing SLE patients, pathway-specific complement activation is rarely monitored as ... ...

Abstract	Complement activation is a hallmark of systemic lupus erythematosus (SLE) and can proceed through the classical (CP), lectin (LP), or alternative pathway (AP). When managing SLE patients, pathway-specific complement activation is rarely monitored as clinical assays are unavailable. In this study, we aim to differentiate between CP- or LP-mediated complement activation in SLE patients by quantifying pathway-specific protein complexes, namely C1s/C1-inhibitor (C1-INH) (CP-specific activation) and MASP-1/C1-INH (LP-specific activation). Levels for both complexes were assessed in 156 SLE patients and 50 controls using two newly developed ELISAs. We investigated whether pathway-specific complement activation was associated with disease activity and lupus nephritis (LN). Disease activity stratification was performed using SLEDAI scores assessed at inclusion. C1s/C1-INH concentrations were significantly increased in active SLE patients (SLEDAI ≥6) when compared with SLE patients with low disease activity (SLEDAI <6, P < 0.01) and correlated with SLEDAI score (r = .29, P < 0.01). In active LN, MASP-1/C1-INH plasma concentrations were significantly increased compared with nonactive LN (P = 0.02). No differences in MASP-1/C1-INH plasma concentrations were observed between active SLE patients and patients with low disease activity (P = 0.11) nor did we observe a significant correlation with disease activity (r = 0.12, P = 0.15). Our data suggest that the CP and the LP are activated in SLE. The CP is activated in active SLE disease, whereas activation of the LP might be more specific to disease manifestations like LN. Our results warrant further research into specific complement pathway activation in SLE patients to potentially improve specific-targeted and tailored-treatment approaches.
MeSH term(s)	Humans ; Complement Pathway, Classical ; Lectins ; Mannose-Binding Protein-Associated Serine Proteases/metabolism ; Lupus Erythematosus, Systemic ; Complement Activation ; Lupus Nephritis/diagnosis
Chemical Substances	Lectins ; Mannose-Binding Protein-Associated Serine Proteases (EC 3.4.21.-)
Language	English
Publishing date	2023-07-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218531-3
ISSN	1365-2249 ; 0009-9104 ; 0964-2536
ISSN (online)	1365-2249
ISSN	0009-9104 ; 0964-2536
DOI	10.1093/cei/uxad070
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Article: Complement Proteins L-Ficolin and M-Ficolin Are Increased in Patients With Axial Spondyloarthritis and Decrease After Tumor Necrosis Factor Inhibitor Treatment.

Mistegaard, Clara Elbæk / Troldborg, Anne / Hansen, Annette / Thiel, Steffen / Jurik, Anne Grethe / Kiil, Rosa M / Christiansen, Alice A / Schiøttz-Christensen, Berit / Hendricks, Oliver / Pedersen, Susanne Juhl / Sørensen, Inge Juul / Østergaard, Mikkel / Loft, Anne Gitte

The Journal of rheumatology

2023

Abstract: Objective: We have previously reported elevated levels of the complement lectin pathway proteins L-ficolin and H-ficolin in patients with axial spondyloarthritis (axSpA) compared with healthy controls. The aim of the present study was to investigate ... ...

Abstract	Objective: We have previously reported elevated levels of the complement lectin pathway proteins L-ficolin and H-ficolin in patients with axial spondyloarthritis (axSpA) compared with healthy controls. The aim of the present study was to investigate these biomarkers in a cross-sectional cohort of patients suffering from low back pain (LBP). Further, we aimed to investigate changes in lectin pathway protein levels after initiation of adalimumab (ADA; a tumor necrosis factor inhibitor) in a longitudinal cohort of patients with axSpA. Methods: Lectin pathway protein levels (mannan-binding lectin [MBL], collectin liver 1, H-ficolin, L-ficolin, M-ficolin, MBL-associated serine protease [MASP]-1, MASP-2, MASP-3, MBL-associated protein 19 [MAp19], and MAp44) in EDTA plasma were determined in 2 well-characterized cohorts: (1) a clinical cross-sectional cohort of patients with LBP, including patients with axSpA (n = 23), patients with unspecific LBP (uLBP) with ≥ 1 SpA features (n = 55), and patients with uLBP without SpA features or magnetic resonance imaging findings suggestive of axSpA (n = 64); and (2) a randomized double-blinded, placebo-controlled trial cohort of patients with axSpA (n = 49) initiating ADA therapy. Lectin pathway protein levels were determined using immunoassays. Results: Plasma levels of L-ficolin and M-ficolin were significantly increased in the cross-sectional cohort of newly diagnosed patients with axSpA compared with clinically relevant controls with uLBP (all Conclusion: L-ficolin and M-ficolin levels are elevated in newly diagnosed patients with axSpA compared with clinically relevant controls. Both L-ficolin and M-ficolin levels decrease significantly after initiating ADA therapy. These findings provide new insights into the inflammatory processes in axSpA and support the involvement of complement in axSpA pathogenesis.
Language	English
Publishing date	2023-09-15
Publishing country	Canada
Document type	Journal Article
ZDB-ID	194928-7
ISSN	1499-2752 ; 0315-162X
ISSN (online)	1499-2752
ISSN	0315-162X
DOI	10.3899/jrheum.2023-0164
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Article ; Online: [Lack of clinical evidence for the use of hydroxychloroquine to treat SARS-CoV-2 infection].

Troldborg, Anne / Bartels, Lars Erik / Deleuran, Bent

Ugeskrift for laeger

2019 Volume 182, Issue 20

Abstract: The severity of COVID-19 disease has led to an urgent need for the discovery of new treatments. Thus, global stocks of hydroxychloroquine (HCQ) have been put under pressure with a study of 26 patients treated with HCQ during their infection with SARS-CoV- ...

Abstract	The severity of COVID-19 disease has led to an urgent need for the discovery of new treatments. Thus, global stocks of hydroxychloroquine (HCQ) have been put under pressure with a study of 26 patients treated with HCQ during their infection with SARS-CoV-2. Despite the study's lack of quality, several countries' medicines agencies subsequently issued guidelines for the use of HCQ for COVID-19. This review aims to elucidate potential mechanisms, which make HCQ treatment interesting in the fight against SARS-CoV-2 infection, as well as the current evidence for clinical use of HCQ to treat COVID-19.
MeSH term(s)	Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; Betacoronavirus ; Coronavirus Infections/drug therapy ; Humans ; Hydroxychloroquine/pharmacology ; Hydroxychloroquine/therapeutic use ; Pandemics ; Pneumonia, Viral/drug therapy
Chemical Substances	Antiviral Agents ; Hydroxychloroquine (4QWG6N8QKH)
Keywords	covid19
Language	Danish
Publishing date	2019-09-04
Publishing country	Denmark
Document type	Journal Article ; Review
ZDB-ID	124102-3
ISSN	1603-6824 ; 0041-5782
ISSN (online)	1603-6824
ISSN	0041-5782
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Article ; Online: [Sjögren's syndrome].

Jensen, Marie Louise Næstholt / Troldborg, Anne Margrethe / Pfeiffer-Jensen, Mogens / Deleuran, Bent

Ugeskrift for laeger

2021 Volume 183, Issue 31

Abstract: Sjögren's syndrome (SS) is a common autoimmune disease with a prevalence of 1%. SS affects primarily women between the age of 30 and 50 years. The classic manifestations are sicca symptoms, musculoskeletal pain and fatigue but the disease can affect all ... ...

Abstract	Sjögren's syndrome (SS) is a common autoimmune disease with a prevalence of 1%. SS affects primarily women between the age of 30 and 50 years. The classic manifestations are sicca symptoms, musculoskeletal pain and fatigue but the disease can affect all organs. SS is associated with the antibody anti-SSA antibodies. The patients have a 15-20 times higher risk of lymphoma and an increased risk of spontaneous abortion and AV-block in life-born children. In this review, we share the diagnostic process and risk stratification and outline the treatments available from private practice.
MeSH term(s)	Adult ; Child ; Fatigue ; Female ; Humans ; Middle Aged ; Prevalence ; Sjogren's Syndrome/complications ; Sjogren's Syndrome/diagnosis ; Sjogren's Syndrome/drug therapy
Language	Danish
Publishing date	2021-08-11
Publishing country	Denmark
Document type	Journal Article ; Review
ZDB-ID	124102-3
ISSN	1603-6824 ; 0041-5782
ISSN (online)	1603-6824
ISSN	0041-5782
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