Anders Erik Astrup Dahm

• Storlien, Torstein & Dahm, Anders Erik A (2023). Behandling av eldre med akutt myelogen leukemi uten allogen stamcelletransplantasjon ved Akershus universitetssykehus. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 143(15). doi: 10.4045/tidsskr.22.0490. Fulltekst i vitenarkiv
• Theocharides, Alexandre; Gisslinger, Heinz; De Stefano, Valerio; Accurso, Vincenzo; Iurlo, Alessandra & Devos, Timothy [Vis alle 18 forfattere av denne artikkelen] (2023). Ruxolitinib in patients with polycythemia vera resistant and/or intolerant to hydroxyurea: European observational study. European Journal of Haematology. ISSN 0902-4441. 112(3), s. 379–391. doi: 10.1111/ejh.14124.
• Hussaini, Parwana; Larsen, Trine-Lise; Ghanima, Waleed & Dahm, Anders Erik A (2023). Risk factors for bleeding in cancer patients treated with conventional dose followed by low-dose apixaban for venous thromboembolism. Thrombosis and Haemostasis. ISSN 0340-6245. doi: 10.1055/a-2188-8773.
• Jervan, Øyvind; Haukeland-Parker, Stacey Marie; Gleditsch, Jostein; Tavoly, Mazdak; Klok, Frederikus A. & Steine, Kjetil [Vis alle 14 forfattere av denne artikkelen] (2023). The Effects of Exercise Training in Patients With Persistent Dyspnea Following Pulmonary Embolism: A Randomized Controlled Trial. Chest. ISSN 0012-3692. 164(4), s. 981–991. doi: 10.1016/j.chest.2023.04.042. Fulltekst i vitenarkiv
• Larsen, Trine-Lise; Svalastoga, Marte; Brekke, Jorunn; Enden, Tone Rønnaug; Frøen, Hege & Garresori, Herish [Vis alle 16 forfattere av denne artikkelen] (2023). Arterial events in cancer patients treated with apixaban for venous thrombosis. Thrombosis Research. ISSN 0049-3848. 228, s. 128–133. doi: 10.1016/j.thromres.2023.05.017.
• Larsen, Trine-Lise; Garresori, Herish; Brekke, Jorunn; Enden, Tone Rønnaug; Frøen, Hege & Jacobsen, Eva-Marie [Vis alle 15 forfattere av denne artikkelen] (2022). Low dose apixaban as secondary prophylaxis of venous thromboembolism in cancer patients – 30 months follow-up. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 20(5), s. 1166–1181. doi: 10.1111/jth.15666. Fulltekst i vitenarkiv Vis sammendrag

  Background There are no data on the effect of low-dose anticoagulation as secondary prophylaxis for venous thromboembolism (VTE) in cancer patients. We assessed the efficacy and safety of low-dose apixaban for 30 months, after initial 6 months of full-dose treatment. Methods We included 298 patients with cancer and any type of VTE in a single arm interventional clinical trial. All patients were treated with full-dose apixaban (5 mg twice daily) for 6 months. Total 196 patients with active cancer after 6 months treatment continued with apixaban 2.5 mg twice daily for another 30 months. The main endpoints were recurrent VTE, major bleeding and clinically relevant non-major bleeding. Results During the 30 months of treatment with low-dose apixaban 14 (7.6%; 95% confidence interval (CI) 4.0%–11.7%) patients experienced recurrent VTE, six (3.1%; 95% CI 1.1%–6.5%) experienced major bleeding and 16 (8.1%, 95% CI: 4.7%–12.8%) experienced clinically relevant non-major bleeding. The incidence rate per person month of recurrent VTE was 0.8% (95% CI 0.41–1.6) at 2–6 months with full-dose apixaban, and 1.0% (95% CI 0.5–1.9) at 7–12 months with low-dose apixaban. The incidence rate of major bleeding was 1.1% (95% CI 0.6–2.0) at 2–6 months, and 0.3% (95% CI 0.1–1.0) at 7–12 months. Between 12 and 36 months the incidence rate of recurrent VTE and major bleedings remained low. Conclusion Dose reduction of apixaban to 2.5 mg twice daily seems safe after 6 months of full-dose treatment. After 12 months the incidence rate of recurrent VTE and major bleeding remained low.

• Dalen, Viktor; Vegsgaard Olsen, Anne-Sofie; Pierre-Jerome, Claude; Geitung, Jonn Terje & Dahm, Anders Erik A (2021). Low diagnostic accuracy and inter-observer agreement on CT and MRI in diagnosis of spinal fractures in multiple myeloma. Hematology Reports. ISSN 2038-8322. 13(3). doi: 10.4081/hr.2021.9037. Fulltekst i vitenarkiv
• Dahm, Anders Erik A (2021). Cancer and Thrombosis: New Treatments, New Challenges. Medical Sciences. ISSN 2076-3271. 9(2), s. 1–11. doi: 10.3390/medsci9020041. Fulltekst i vitenarkiv
• Cui, Xueyan; Tjønnfjord, Geir Erland; Kanse, Sandip; Dahm, Anders Erik A; Iversen, Nina & Myklebust, Christiane Filion [Vis alle 12 forfattere av denne artikkelen] (2021). Tissue factor pathway inhibitor upregulates CXCR7 expression and enhances CXCL12-mediated migration in chronic lymphocytic leukemia. Scientific Reports. ISSN 2045-2322. 11. doi: 10.1038/s41598-021-84695-8. Fulltekst i vitenarkiv
• Berntsen, Christopher Friis; Rootwelt, Pernille & Dahm, Anders Erik A (2021). Bias in animal studies of estrogen effects on cardiovascular disease: A systematic review and meta-analysis. Research and Practice in Thrombosis and Haemostasis (RPTH). ISSN 2475-0379. 5(4), s. 1–11. doi: 10.1002/rth2.12507. Fulltekst i vitenarkiv Vis sammendrag

  Background: Randomized controlled trials on menopausal hormone therapy in humans have not confirmed the benefit of estrogens on cardiovascular disease found in animal studies. Flawed methodology or publication bias in animal studies may explain the dicrepancy. Objectives: The aim of this study was to investigate whether publication of the randomized controlled trials Heart and Estrogen/Progestin Replacement Study and Women's Health Initiative influenced study authors' assessment of research findings (confirmation bias) as well as to investigate publication bias and small-study effects in animal studies of estrogen effects on atherosclerosis. Methods: The data source for this study was PubMed from inception to 2018. We selected animal studies with cardiovascular outcomes comparing 17-β-estradiol, its natural metabolites, or conjugated equine estrogen with control. Qualitative data were extracted on authors' conclusions about estrogen effects on cardiovascular disease, as well as quantitative data for atherosclerosis outcomes. Fixed- and random-effects meta-analyses were used. Publication bias/small-study effects were assessed using funnel plots and Egger's regression. Trim-and-fill plots and extrapolation from Egger's regression were used to adjust for publication bias. The main outcomes and measures were the primary study authors' interpretation of their own results, and estrogen effects on cardiovascular disease in general before and after publication of the Women's health Initiative study (2003). The effects of estrogens on atherosclerosis were measured as standardized mean difference between intervention and control. Results: Of 1925 studies retrieved, 360 were eligible for analyses. Study-specific statements concluded that estrogens were protective against cardiovascular disease in 75% of studies before 2003 and 78% after, but the percentage of general statements about estrogens being cardioprotective changed from 70% to 40%. Meta-analyses showed less atherosclerosis in estrogen-treated animals. Extremely skewed funnel plots and P < .01 in Egger's regression suggested publication bias and/or exaggerated effects in small studies, which was more pronounced after 2002. There was substantial heterogeneity of effects (I 2 = 68%-86%) overall and in all subgroups except cynomolgus monkeys (I 2 = 9%), the only animal subgroup without clear bias. Adjusting for publication bias, overall estimates of estrogen effects on atherosclerosis were close to null effect. Conclusions: We found substantial evidence of publication bias but not of confirmation bias. Publication bias and flawed small studies may partly explain why findings differ between animal studies and clinical trials on the effect of estrogens on cardiovascular disease. Keywords: animals; cardiovascular disease; estrogens; publication bias; systematic review. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. © 2021 The Authors. Research and Practice in Thrombosis and Haemostasis published by Wiley Periodicals LLC on behalf of International Society on Thrombosis and Haemostasis (ISTH)

• Khialani, Deeksha; Vasan, Sowmya; Cushman, Mary; Dahm, Anders Erik A; Sandset, Per Morten & Rossouw, Jacques [Vis alle 7 forfattere av denne artikkelen] (2021). Venous thrombosis with oral postmenopausal hormone therapy: Roles of activated protein C resistance and tissue factor pathway inhibitor. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 19(7), s. 1729–1737. doi: 10.1111/jth.15319.
• Hannevik, Trine-Lise; Brekke, Jorunn; Enden, Tone Rønnaug; Frøen, Hege; Ahmed, Herish & Jacobsen, Eva-Marie [Vis alle 15 forfattere av denne artikkelen] (2020). Thrombosis and bleedings in a cohort of cancer patients treated with apixaban for venous thromboembolism. Thrombosis Research. ISSN 0049-3848. 196, s. 238–244. doi: 10.1016/j.thromres.2020.08.042.
• Berentsen, Sigbjørn; Barcellini, Wilma; D'Sa, Shirley; Randen, Ulla; Tvedt, Tor Henrik Anderson & Fattizzo, Bruno [Vis alle 23 forfattere av denne artikkelen] (2020). Cold agglutinin disease revisited: a multinational, observational study of 232 patients. Blood. ISSN 0006-4971. 136(4), s. 480–488. doi: 10.1182/blood.2020005674.
• Frønæs, Synne Grønvold; Jørgensen, Camilla Tøvik; Dahm, Anders Erik A; Wik, Hilde Skuterud; Gleditsch, Jostein & Raouf, Nezar [Vis alle 9 forfattere av denne artikkelen] (2020). Safety of a strategy combining D-dimer testing and whole-leg ultrasonography to rule out deep vein thrombosis. Blood Advances. ISSN 2473-9529. 4(20), s. 5002–5010. doi: 10.1182/BLOODADVANCES.2020002173. Fulltekst i vitenarkiv
• Frønæs, Synne Grønvold; Dahm, Anders Erik Astrup; Skuterud Wik, Hilde; Jørgensen, Camilla Tøvik; Gleditsch, Jostein & Raouf, Nezar [Vis alle 9 forfattere av denne artikkelen] (2020). Safety and feasibility of rivaroxaban in deferred workup of patients with suspected deep vein thrombosis. Blood Advances. ISSN 2473-9529. 4(11), s. 2468–2476. doi: 10.1182/bloodadvances.2020001556. Fulltekst i vitenarkiv
• Dahm, Anders Erik A; Jacobsen, Eva-Marie; Wik, Hilde Skuterud; Jacobsen, Anne Flem; Mollnes, Tom Eirik & Kanse, Sandip [Vis alle 7 forfattere av denne artikkelen] (2019). Elevated complement C3 and C4 levels are associated with postnatal pregnancy-related venous thrombosis. Thrombosis and Haemostasis. ISSN 0340-6245. 119(9), s. 1481–1488. doi: 10.1055/s-0039-1692426. Fulltekst i vitenarkiv
• Eilertsen, Anette Løken; Dahm, Anders Erik A; Høibraaten, Else; Lofthus, Cathrine Marie; Mowinckel, Marie-Christine & Sandset, Per Morten (2019). Relationship between sex hormone binding globulin and blood coagulation in women on postmenopausal hormone treatment. Blood Coagulation and Fibrinolysis. ISSN 0957-5235. 30(1), s. 17–23. doi: 10.1097/MBC.0000000000000784.
• Frønæs, Synne Grønvold; Wik, Hilde Skuterud; Dahm, Anders Erik A; Jørgensen, Camilla Tøvik; Gleditsch, Jostein & Raouf, Nezar [Vis alle 8 forfattere av denne artikkelen] (2018). Safety of D-dimer testing as a stand-alone test for the exclusion of deep vein thrombosis as compared with other strategies. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 16(12), s. 2471–2481. doi: 10.1111/jth.14314. Fulltekst i vitenarkiv Vis sammendrag

  Background: Several strategies for safely excluding deep vein thrombosis (DVT) while limiting the number of imaging tests have been explored. Objectives: To determine whether D-dimer testing could safely and efficiently exclude DVT as a stand-alone test, and evalu- ate its performance as compared with strategies that incorporate the Wells score and age-adjusted D-dimer. Patients/Methods: We included consecutive outpatients referred with suspected DVT to the Emergency Depart- ment at Østfold Hospital, Norway. STA-Liatest D-Di PLUS D-dimer was analyzed for all patients. Patients with a D-dimer level of ≥ 0.5 lgmL 1 were referred for compression ultrasonography (CUS). In patients with a D-dimer level of < 0.5 lgmL 1 , no further testing was performed and anticoagulation was withheld. Patients were followed for 3 months for venous thromboembolism (VTE). Results: Of the 913 included patients, 298 (33%) had a negative D-dimer result. One hundred and seventy- three patients (18.9%) were diagnosed with DVT at baseline. One of 298 patients had DVT despite having a negative D-dimer result, resulting in a failure rate of 0.3% (95% confidence interval [CI] 0.1–1.9%). Adding the modified Wells score would have yielded a failure rate of 0.0% (95% CI 0.0–1.8%) while necessitating 87 more CUS examinations. Age-adjusted D-dimer as a stand- alone test would have necessitated 80 fewer CUS exami- nations than fixed D-dimer as a stand-alone test, at the cost of a failure rate of 1.6% (95% CI 0.7– 3.4%). Con- clusions: This outcome study shows that a negative high-sensitivity D-dimer result safely excludes DVT in an outpatient population, and necessitates fewer CUS than if used in combination with Wells score. The safety of stand-alone age-adjusted D-dimer needs further assess- ment in prospective outcome studies.

• Kostovski, Emil; Frigato, E; Savikj, Mladen; Dahm, Anders Erik A; Sandset, Per Morten & Mowinckel, Marie-Christine [Vis alle 10 forfattere av denne artikkelen] (2018). Normalization of disrupted clock gene expression in males with tetraplegia: a crossover randomized placebo-controlled trial of melatonin supplementation. Spinal Cord. ISSN 1362-4393. s. 1–8. doi: 10.1038/s41393-018-0176-x. Fulltekst i vitenarkiv
• Panagopoulos, Ioannis; Gorunova, Ludmila; Andersen, Hege Kilen; Bergrem, Astrid; Dahm, Anders Erik A & Andersen, Kristin [Vis alle 8 forfattere av denne artikkelen] (2018). PAN3-PSMA2 fusion resulting from a novel t(7;13)(p14;q12) chromosome translocation in a myelodysplastic syndrome that evolved into acute myeloid leukemia. Experimental hematology and oncology. ISSN 2162-3619. 7(7). doi: 10.1186/s40164-018-0099-4. Fulltekst i vitenarkiv
• Habberstad, Andreas Hanssønn; Tran, Hoa Thi Tuyet; Randen, Ulla; Spetalen, Signe; Dybedal, Ingunn & Tjønnfjord, Geir Erland [Vis alle 7 forfattere av denne artikkelen] (2018). Neutropenia caused by hairy cell leukemia in a patient with myelofibrosis secondary to polycythemia vera: A case report. Journal of Medical Case Reports. ISSN 1752-1947. 12(1). doi: 10.1186/s13256-018-1663-6. Fulltekst i vitenarkiv
• Utne, Kristin Kornelia; Dahm, Anders Erik A; Wik, Hilde Skuterud; Jelsness-Jørgensen, Lars-Petter; Sandset, Per Morten & Ghanima, Waleed Khalid (2018). Rivaroxaban versus warfarin for the prevention of post-thrombotic syndrome. Thrombosis Research. ISSN 0049-3848. 163, s. 6–11. doi: 10.1016/j.thromres.2018.01.013.
• Amundsen, Erik Koldberg; Skadberg, Øyvind; Ghanima, Waleed Khalid; Frønæs, Synne Grønvold; Dahm, Anders Erik A & Tøsdal, Margunn Bye [Vis alle 9 forfattere av denne artikkelen] (2018). D-Dimer: Aldersjusterte beslutningsgrenser ved diagnostikk av venøs tromboembolisme? Klinisk Biokemi i Norden. ISSN 1101-2013. 30(1), s. 26–36.
• Cui, Xue-Yan; Skretting, Grethe; Tinholt, Mari; Stavik, Benedicte; Dahm, Anders Erik A & Sahlberg, Kristine Kleivi [Vis alle 9 forfattere av denne artikkelen] (2017). A novel hypoxia response element regulates oxygen-related repression of tissue factor pathway inhibitor in the breast cancer cell line MCF-7. Thrombosis Research. ISSN 0049-3848. 157, s. 111–116. doi: 10.1016/j.thromres.2017.07.013.
• Prebensen, Christian; Trøseid, Marius; Ueland, Thor; Dahm, Anders Erik A; Sandset, Per Morten & Aaberge, Ingeborg Sundsvalen [Vis alle 10 forfattere av denne artikkelen] (2017). Immune activation and HIV-specific T cell responses are modulated by a cyclooxygenase-2 inhibitor in untreated HIV-infected individuals: An exploratory clinical trial. PLOS ONE. ISSN 1932-6203. 12(5). doi: 10.1371/journal.pone.0176527. Fulltekst i vitenarkiv
• Ali, Huda Omar; Stavik, Benedicte; Myklebust, Christiane Filion; Andersen, Elisabeth; Dahm, Anders Erik A & Iversen, Nina [Vis alle 8 forfattere av denne artikkelen] (2016). Oestrogens downregulate tissue factor pathway inhibitor through oestrogen response elements in the 5′-flanking region. PLOS ONE. ISSN 1932-6203. 11(3). doi: 10.1371/journal.pone.0152114.
• Johnson, Karen C; Aragaki, Aaron; Jackson, Rebecca; Reiner, Alex P; Sandset, Per Morten & Rosing, Jan [Vis alle 14 forfattere av denne artikkelen] (2016). Tissue factor pathway inhibitor, activated protein C resistance, and risk of coronary heart disease due to combined estrogen plus progestin therapy. Arteriosclerosis, Thrombosis and Vascular Biology. ISSN 1079-5642. 36(2), s. 418–424. doi: 10.1161/ATVBAHA.115.306905.
• Cui, Xue-Yan; Tinholt, Mari; Stavik, Benedicte; Dahm, Anders Erik A; Kanse, Sandip & Jin, Yang [Vis alle 11 forfattere av denne artikkelen] (2016). Effect of hypoxia on tissue factor pathway inhibitor expression in breast cancer. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 14(2), s. 387–396. doi: 10.1111/jth.13206.
• Cui, Xueyan; Tinholt, Mari; Stavik, Benedicte; Dahm, Anders Erik A; Kanse, Sandip & Seidl, Sebastian [Vis alle 11 forfattere av denne artikkelen] (2015). Effect of hypoxia on tissue factor pathway inhibitor expression in breast cancer cell lines and tissues. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 13, s. 303–303.
• Iversen, Per Ole; Dahm, Anders Erik A; Skretting, Grethe; Mowinckel, Marie-Christine; Haslestad, Annicke Stranda & Østerud, Bjarne [Vis alle 8 forfattere av denne artikkelen] (2015). Reduced peak, but no diurnal variation, in thrombin generation upon melatonin supplementation in tetraplegia. A randomised, placebo-controlled study. Thrombosis and Haemostasis. ISSN 0340-6245. 114(5), s. 964–968. doi: 10.1160/TH15-05-0396.
• Stiksrud, Birgitte; Nowak, Piotr; Nwosu, Felix Chinweije; Kvale, Dag; Thalme, Anders & Sönnerborg, Anders [Vis alle 15 forfattere av denne artikkelen] (2015). Reduced levels of D-dimer and changes in gut microbiota composition after probiotic intervention in HIV-infected individuals on stable ART. Journal of Acquired Immune Deficiency Syndromes. ISSN 1525-4135. 70(4), s. 329–337. doi: 10.1097/QAI.0000000000000784.
• Kostovski, Emil; Dahm, Anders Erik A; Mowinckel, Marie-Christine; Stranda, Annicke; Skretting, Grethe & Østerud, Bjarne [Vis alle 8 forfattere av denne artikkelen] (2015). Circadian rhythms of hemostatic factors in tetraplegia: a double-blind, randomized, placebo-controlled cross-over study of melatonin. Spinal Cord. ISSN 1362-4393. 53, s. 285–290. doi: 10.1038/sc.2014.243. Fulltekst i vitenarkiv
• Cui, Xueyan; Skretting, Grethe; Dahm, Anders Erik A; Stavik, Benedicte; Iversen, Nina & Sandset, Per Morten (2014). Hypoxia contributes to procoagulant activity of breast cancer cells. Haematologica. ISSN 0390-6078. 99, s. 475–475.
• Tinholt, Mari; Viken, Marte K; Dahm, Anders Erik A; Vollan, Hans Kristian Moen; Sahlberg, Kristine Kleivi & Garred, Øystein [Vis alle 16 forfattere av denne artikkelen] (2014). Increased coagulation activity and genetic polymorphisms in the F5, F10 and EPCR genes are associated with breast cancer: a case-control study. BMC Cancer. ISSN 1471-2407. 14. doi: 10.1186/1471-2407-14-845.
• Kristiansen, Annette; Brandt, Linn; Agoritsas, Thomas; Akl, Elie A.; Berge, Eivind & Bondi, Johan Fridtjof [Vis alle 19 forfattere av denne artikkelen] (2014). Adaptation of trustworthy guidelines developed using the GRADE methodology: a novel five-step process. Chest. ISSN 0012-3692. 146(3), s. 727–734. doi: 10.1378/chest.13-2828. Vis sammendrag

  BACKGROUND: Adaptation of guidelines for use at the national or local level can facilitate their implementation. We developed and evaluated an adaptation process in adherence with standards for trustworthy guidelines and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology, aiming for efficiency and transparency. This article is the first in a series describing our adaptation of Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines for a Norwegian setting. METHODS: Informed by the ADAPTE framework, we developed a five-step adaptation process customized to guidelines developed using GRADE: (1) planning, (2) initial assessment of the recommendations, (3) modification, (4) publication, and (5) evaluation. We developed a taxonomy for describing how and why recommendations from the parent guideline were modified and applied a mixed-methods case study design for evaluation of the process. RESULTS: We published the adapted guideline in November 2013 in a novel multilayered format. The taxonomy for adaptation facilitated transparency of the modification process for both the guideline developers and the end users. We excluded 30 and modified 131 of the 333 original recommendations according to the taxonomy and developed eight new recommendations. Unforeseen obstacles related to acquiring a licensing agreement and procuring a publisher resulted in a 9-month delay. We propose modifications of the adaptation process to overcome these obstacles in the future. CONCLUSIONS: This case study demonstrates the feasibility of a novel guideline adaptation process. Replication is needed to further validate the usefulness of the process in increasing the organizational and methodologic efficiency of guideline adaptation.

• Vartdal, Trond; Fetveit, Arne; Kristiansen, Annette; Brandt, Linn; Halvorsen, Sigrun & Berge, Eivind [Vis alle 9 forfattere av denne artikkelen] (2014). Antitrombotisk behandling og profylakse: - ny generasjon retningslinjer for allmennleger. Utposten. ISSN 0800-5680. 3, s. 41–43.
• Raps, M; Helmerhorst, FM; Fleischer, K; Dahm, Anders Erik A; Rosendaal, FR & Rosing, J [Vis alle 9 forfattere av denne artikkelen] (2013). The effect of different hormonal contraceptives on plasma levels of free protein S and free TFPI. Thrombosis and Haemostasis. ISSN 0340-6245. 109(4), s. 606–613. doi: 10.1160/TH12-10-0771.
• Skretting, Grethe; Iversen, Nina; Myklebust, Christiane Filion; Dahm, Anders Erik A & Sandset, Per Morten (2012). Overexpression of tissue factor pathway inhibitor in CHO-K1 cells results in increased activation of NF-kappa B and apoptosis mediated by a caspase-3 independent pathway. Molecular Biology Reports. ISSN 0301-4851. 39(12), s. 10089–10096. doi: 10.1007/s11033-012-1882-7.
• Dahm, Anders Erik A; Bezemer, Irene D; Bergrem, Astrid; Jacobsen, Anne Flem; Jacobsen, Eva-Marie & Skretting, Grethe [Vis alle 8 forfattere av denne artikkelen] (2012). Candidate gene polymorphisms and the risk for pregnancy-related venous thrombosis. British Journal of Haematology. ISSN 0007-1048. 157(6), s. 753–761. doi: 10.1111/j.1365-2141.2012.09121.x.
• Dahm, Anders Erik A; Eilertsen, Anette Løken; Goeman, Jelle; Olstad, Ole Kristoffer; Øvstebø, Reidun & Kierulf, Peter [Vis alle 9 forfattere av denne artikkelen] (2012). A microarray study on the effect of four hormone therapy regimens on gene transcription in whole blood from healthy postmenopausal women. Thrombosis Research. ISSN 0049-3848. 130(1), s. 45–51. doi: 10.1016/j.thromres.2011.12.009.
• Bergrem, Astrid; Dahm, Anders Erik A; Jacobsen, Anne Flem; Sandvik, Leiv & Sandset, Per Morten (2012). Differential haemostatic risk factors for pregnancy-related deep-vein thrombosis and pulmonary embolism A population-based case-control study. Thrombosis and Haemostasis. ISSN 0340-6245. 108(6), s. 1165–1171. doi: 10.1160/TH12-05-0350.
• Pettersen, Frank Olav; Torheim, Eirik A.; Dahm, Anders Erik A; Aaberge, Ingeborg Sundsvalen; Lind, Andreas & Holm, Malin [Vis alle 10 forfattere av denne artikkelen] (2011). An exploratory trial of cyclooxygenase type 2 inhibitor in HIV-1 infection: Downregulated immune activation and improved T Cell-dependent vaccine responses. Journal of Virology. ISSN 0022-538X. 85(13), s. 6557–6566. doi: 10.1128/JVI.00073-11.
• Bergrem, Astrid; Dahm, Anders Erik A; Jacobsen, Anne Flem; Mowinckel, Marie-Christine; Sandvik, Leiv & Sandset, Per Morten (2011). Resistance to activated protein C is a risk factor for pregnancy-related venous thrombosis in the absence of the F5 rs6025 (factor V Leiden) polymorphism. British Journal of Haematology. ISSN 0007-1048. 154(2), s. 241–247. doi: 10.1111/j.1365-2141.2011.08712.x. Vis sammendrag

  Resistance to activated protein C (aPC) is most commonly due to the F5 rs6025 (factor V Leiden) polymorphism, which increases the risk of venous thrombosis. In the present population-based study of 313 cases and 353 controls, we investigated whether reduced sensitivity to aPC was associated with a history of pregnancy-related venous thrombosis. Calibrated automated thrombography was used to determine the sensitivity to aPC, and normalized aPC sensitivity ratio (n-aPC-sr) was calculated. Pregnant women and women using oral contraceptives and/or anticoagulants were excluded due to the effect on the n-aPC-sr. In women without the F5 rs6025 polymorphism, free tissue factor pathway inhibitor (TFPI), free protein S and protein C activity were associated with n-aPC-sr. Unadjusted odds ratio for venous thrombosis for women with n-aPC-sr in the 4th quartile as compared with n-aPC-sr below the 4th quartile was 2·4 (95% confidence interval 1·7-3·6). Adjusting for free protein S, free TFPI and age did not influence the odds ratios. Also in carriers of the F5 rs6025 polymorphism the risk for venous thrombosis was increased for women with higher n-aPC-sr. Our findings substantiate the importance of the aPC resistant phenotype as a risk factor for pregnancy-related venous thrombosis.

• Kostovski, Emil; Dahm, Anders Erik A; Iversen, Nina; Hjeltnes, Nils; Østerud, Bjarne & Sandset, Per Morten [Vis alle 7 forfattere av denne artikkelen] (2011). Melatonin stimulates release of tissue factor pathway inhibitor from the vascular endothelium. Blood Coagulation and Fibrinolysis. ISSN 0957-5235. 22(4), s. 254–259. doi: 10.1097/MBC.0b013e3283442ce2. Vis sammendrag

  We previously found an association between the circadian variation of free tissue factor pathway inhibitor (TFPI) and melatonin in able-bodied males and in men with complete cervical spinal cord injuries. We therefore examined whether melatonin modifies production and/or secretion of TFPI in endothelial cells. We sampled supernatants from cultures of primary human umbilical vein endothelial cells (HUVECs) and of human coronary artery endothelial cells (HCAECs), that had been exposed to varying doses (0-300 pg/ml) of melatonin for 0.5-24 h. We then measured the protein concentrations of free TFPI, tissue factor and plasminogen activator inhibitor type 1 (PAI-1). We also measured endothelial TFPI, tissue factor and PAI-1 transcripts using quantitative real-time PCR. Melatonin dose dependently increased free TFPI levels about 25-30-fold in supernatants of both HUVEC and HCAEC, and independent of incubation duration. In contrast, TF and PAI-1 remained unaltered upon increasing doses of melatonin. Neither TFPI mRNAs nor tissue factor mRNAs nor PAI-1-mRNAs were changed in cell cultures added melatonin. The ratio of free TFPI in cell supernatants to free TFPI in cell lysates about doubled upon addition of melatonin, indicating that melatonin increased release from intracellular storages of free TFPI or from membrane-bound free TFPI. Our data indicate that melatonin stimulates vascular endothelial cells to secrete TFPI without altering transcription of the TFPI gene. If melatonin increases TFPI release in a similar fashion in vivo as in vitro, this could have potential clinical implications in both prophylaxis and treatment of thromboembolic events.

• Jacobsen, Anne Flem; Dahm, Anders Erik A; Bergrem, Astrid; Jacobsen, Eva-Marie & Sandset, Per Morten (2010). Risk of venous thrombosis in pregnancy among carriers of the factor V Leiden and the prothrombin gene G20210A polymorphisms. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 8(11), s. 2443–2449. doi: 10.1111/j.1538-7836.2010.04038.x. Vis sammendrag

  Background Pregnancy is associated with a ten-fold increased risk of venous thrombosis (VT) with different risk profiles for the ante- and postnatal periods. The purpose of this study was to assess the risk of pregnancy-related VT associated with the factor V Leiden and the prothrombin gene G20210A polymorphisms. Materials and Methods The study comprised 377155 women with 613232 pregnancies at 18 Norwegian hospitals from 1 January 1990 to 31 December 2003. Of total 559 cases with a validated first lifetime diagnosis of VT in pregnancy or within 14 weeks post-partum, and 1229 controls naive for VT, 313 cases and 353 controls donated biological material. Results The odds ratios for venous thrombosis during pregnancy or puerperium were 5.0 (95% CI 3.1 to 8.3) and 9.4 (2.1-42.4) for heterozygous carriers of the factor V Leiden and the prothrombin gene polymorphisms, respectively. All homozygous carriers of the factor V Leiden (n=8) and the prothrombin polymorphism (n=1) developed VT indicating a very high risk of VT. We estimated that pregnancy-related VT occurred in 1.1/1000 non-carriers, in 5.4/1000 heterozygous carriers of factor V Leiden, and in 9.4/1000 heterozygous carriers of the prothrombin polymorphism. To avoid one VT, the number of pregnant women needed to screen for these two polymorphisms and the number needed to be given thromboprophylaxis were 2015 and 157, respectively. Conclusions Although the relative risk for VT during pregnancy and after delivery was increased among carriers of the factor V Leiden and the prothrombin polymorphisms, the overall probability for pregnancy-related VT was low. Trial registration www.clinicaltrials.gov identifier number NCT00856076.

• Sandset, Per Morten; Høibraaten, Else; Eilertsen, Anette Løken & Dahm, Anders Erik A (2009). Mechanisms of thrombosis related to hormone therapy. Thrombosis Research. ISSN 0049-3848. 123, s. S70–S73. doi: 10.1016/S0049-3848(09)70015-5. Vis sammendrag

  Combined oral contraceptives and combined oral postmenopausal hormone therapy are associated with a weak, but clinically significant risk of arterial and venous thrombosis (VT). The effects are related to dose of estrogen and type of progestin. The main effects are increase in markers of activated coagulation, reduction in coagulation inhibitors, and acquired activated protein C resistance. Reduction in tissue factor pathway inhibitor (TFPI) is probably an important mechanism, which predicts activation of coagulation and acquired resistance to activated protein C. Coagulation markers should be used as intermediate or surrogate markers in early pharmacodynamic studies to evaluate the risk associated with new formulations.

• van Vliet, Huib AAM; Bertina, Rogier M; Dahm, Anders Erik A; Rosendaal, Frits; Rosing, Jan & Sandset, Per Morten [Vis alle 7 forfattere av denne artikkelen] (2008). Different effects of oral contraceptives containing different progestogens on protein S and Tissue Factor Pathway Inhibitor. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 6(2), s. 346–351. doi: 10.1111/j.1538-7836.2007.02863.x. Vis sammendrag

  Background. Oral contraceptives (OC) containing different types of progestogens induce different sensitivities to activated protein C (APC) measured with the thrombin generation-based APC-resistance test. These differences in APC resistance may be the biological explanation for the differences in thrombotic risk of the various pills. The mechanistic basis of APC resistance observed in OC users is unknown. Our objective was to study the effect of OC on the two main determinants of the APC-resistance test, free protein S and free tissue factor pathway inhibitor (TFPI). Patients/Methods. We measured free protein S and free TFPI in 156 users of various types of OC. Results. Users of desogestrel-containing OC, known to double the risk of thrombosis compared to levonorgestrel-containing OC, had lower free protein S (24 versus 33 U/dL) and TFPI free antigen (2.9 versus 3.6 ng/mL) levels than users of OC containing levonorgestrel. Women using cyproterone acetate-containing OC, known to confer a high thrombotic risk, had the lowest free protein S (19 U/dL) and free TPFI antigen (2.5 ng/mL) levels. Users of OC containing drospirenone had lower free protein S (23 U/dL) and TFPI antigen levels (3.2 ng/mL) than users of levonorgestrelcontaining OC. Low free protein S and low free TFPI antigen levels were associated with an increased resistance to APC, an established risk factor for thrombosis. Conclusions. This study observed that the differences in APC resistance induced by OC containing different progestogens can at least in part be explained by different effects of OC on free protein S and TFPI.

• Dahm, Anders Erik A; Iversen, Per Ole; Hjeltnes, Nils & Sandset, Per Morten (2006). Differences in circadian variations of tissue factor pathway inhibitor type 1 between able-bodied and spinal cord injured. Thrombosis Research. ISSN 0049-3848. 118(2), s. 281–287. Vis sammendrag

  INTRODUCTION: Tissue factor pathway inhibitor type 1 (TFPI) is the physiological inhibitor of the tissue factor pathway of coagulation. TFPI is produced by endothelial cells, and most intravascular TFPI is composed of full-length TFPI associated with the endothelium. Circulating TFPI is mainly truncated and lipoprotein-associated, but a small fraction circulates in a free full-length form. Although hormonal state influences the plasma variation of TFPI between individuals, other factors like temporal variation may be important. Hence, in the current study we aimed at exploring the intra-individual variation with focus on the possible circadian variations of TFPI. MATERIALS AND METHODS: TFPI free and total antigen from 8 able-bodied and 6 tetraplegic men were measured at 12 time points during a 24 h period. RESULTS: TFPI free antigen in the able-bodied exhibited circadian variation with the highest levels ( approximately 20% above mean) from 12:00 to 18:00 h and the lowest levels ( approximately 15% below mean) at 09:00 and 02:00 h. In contrast, TFPI free antigen in the tetraplegic group showed no circadian variation. TFPI total antigen exhibited circadian variation in neither group, but mean TFPI total antigen was lower in the tetraplegic group compared with the able-bodied (80 versus 110 ng/mL, respectively). Notably, even if TFPI total antigen in both groups did not vary according to any specific circadian rhythm, the intra-individual variation was higher than the assay variation. CONCLUSION: TFPI free antigen exhibited circadian variations in able-bodied, but not in tetraplegic subjects and the able-bodied had higher levels of TFPI total antigen than the tetraplegic group.

• Dahm, Anders Erik A; Iversen, Nina; Birkenes, Bård; Ree, Anne Hansen & Sandset, Per Morten (2006). Estrogens, selective estrogen receptor modulators, and a selective estrogen receptor down-regulator inhibit endothelial production of tissue factor pathway inhibitor 1. BMC Cardiovascular Disorders. ISSN 1471-2261. 6. doi: 10.1186/1471-2261-6-40. Vis sammendrag

  Background: Hormone therapy, oral contraceptives, and tamoxifen increase the risk of thrombotic disease. These compounds also reduce plasma content of tissue factor pathway inhibitor-1 (TFPI), which is the physiological inhibitor of the tissue factor pathway of coagulation. The current aim was to study if estrogens and estrogen receptor (ER) modulators may inhibit TFPI production in cultured endothelial cells and, if so, identify possible mechanisms involved. Methods: Human endothelial cell cultures were treated with 17-beta-estradiol (E2), 17-alfa-ethinylestradiol (EE2), tamoxifen, raloxifene, or fulvestrant. Protein levels of TFPI in cell media and cell lysates were measured by an enzyme-linked immunosorbent assay, and TFPI mRNA levels were assessed by quantitative PCR. Expression of ER-alfa was analysed by immunostaining. Results: All compounds (each in a concentration of 10 nM) reduced TFPI in cell medium, by 34% (E2), 21% (EE2), 16% (tamoxifen), and 28% (raloxifene), respectively, with identical inhibitory effects on cellular TFPI levels. Expression of TFPI mRNA was principally unchanged. Treatment with fulvestrant, which was also associated with down-regulation of secreted TFPI (9% with 10 nM and 26% with 1000 nM), abolished the TFPI-inhibiting effect of raloxifene, but not of the other compounds. Notably, the combination of 1000 nM fulvestrant and 10 nM raloxifene increased TFPI secretion, and, conversely, 10 nM of either tamoxifen or raloxifene seemed to partly (tamoxifen) or fully (raloxifene) counteract the inhibitory effect of 1000 nM fulvestrant. The cells did not express the regular nuclear 66 kDa ER-alfa, but instead a 45 kDa ER-alfa, which was not regulated by estrogens or ER modulators. Conclusions: E2, EE2, tamoxifen, raloxifene, and fulvestrant inhibited endothelial production of TFPI by a mechanism apparently independent of TFPI transcription.

• Dahm, Anders Erik A; Osterud, B; Hjeltnes, N; Sandset, PM & Iversen, Per Ole (2006). Opposite circadian rythms in melatonin and tissue factor pathway inhibitor type 1: does daylight affect coagulation? Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 4(8), s. 1840–1842.
• Iversen, Per Ole; Dahm, Anders Erik A & Sandset, Per Morten (2005). Circadian variations within the hemostatic and fibrinolytic systems with emphasis on venous thromboembolism. I Columbus, Frank (Red.), Trends in Chronobiology Research. Nova Science Publishers, Inc.. ISSN 1-59454-482-4. s. 281–297.
• Negaard, Helene; Dahm, Anders Erik A; Sandset, Per Morten; Østenstad, Bjørn & Iversen, Per Ole (2005). Angiogenesis and hemostasis in hematological neoplasias. Current Drug Targets. ISSN 1389-4501. 6, s. 683–699.
• Dahm, Anders Erik A; Andersen, Trine Opstad; Rosendaal, Frits & Sandset, Per Morten (2005). A novel anticoagulant activity assay of tissue factor pathway inhibitor 1 (TFPI). Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 3, s. 651–658. Vis sammendrag

  Tissue factor (TF) pathway inhibitor I (TFPI) is the physiological inhibitor of TF-induced blood coagulation. Circulating blood contains full-length TFPI and TFPI truncated at the C-terminal end. Previous studies have shown that full-length TFPI exerts a stronger anticoagulant effect on diluted prothrombin time (DPT) than truncated TFPI, and it has been suggested that full-length TFPI is biologically more important in vivo. The objective of this study was to develop and validate an assay of TFPI anticoagulant activity. TFPI anticoagulant activity was assayed using a modified DPT assay. Plasmas were incubated in the absence and the presence of TFPI-blocking antibodies. Results were expressed as a ratio with the clotting time in the presence of anti-TFPI as the denominator. The ratio was normalized against a ratio obtained with a reference plasma. The assay was compared with assays of TFPI free antigen, total antigen, and bound TFPI, and TFPI chromogenic substrate activity. We performed all tests in 436 healthy individuals. The normalized TFPI anticoagulant ratio was strongly associated with TFPI free antigen (r = 0.73) but was weakly associated with TFPI chromogenic substrate activity (r = 0.46), TFPI total antigen (r = 0.48), and bound TFPI (r = 0.30). TFPI chromogenic substrate activity was strongly associated with TFPI total antigen (r = 0.73). We have developed a novel assay of TFPI anticoagulant activity in plasma, which may be considered a functional assay of full-length TFPI. Further studies are needed to establish the role of TFPI anticoagulant activity for thrombotic disorders.

• Visser, MC; Hylckama Vlieg, Astrid; Tans, Guido; Rosing, Jan; Dahm, Anders Erik A & Sandset, Per Morten [Vis alle 8 forfattere av denne artikkelen] (2005). Determinants of the APTT- and ETP-based APC sensitivity tests. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 3(7), s. 1488–1494. Vis sammendrag

  Background: A reduced sensitivity for activated protein C (APC) is associated with an increased risk of venous thrombosis even in the absence of the factor (F)V Leiden mutation. This risk has been demonstrated with two APC sensitivity tests, which quantify the effects of APC on the activated partial thromboplastin time (APTT) and the endogenous thrombin potential (ETP), respectively. Objectives: We examined determinants of both APC sensitivity tests in the control group of the Leiden Thrombophilia Study (LETS). Methods: Multiple linear regression analysis was performed with normalized APC-SR(APTT) or APC-SR(ETP) as dependent variable and putative determinants [levels of FII, FV, FVII, FVIII, FIX, FX, FXI, FXII, FXIII A subunit, FXIII B subunit, protein S total, protein S free, protein C, tissue factor pathway inhibitor (TFPI) total, TFPI free, antithrombin and fibrinogen] as independent variables. Results and conclusions: The major determinant of the APTT-based test was FVIII level, followed by FII level. The ETP-based test was influenced most by free protein S and free TFPI levels. In both tests FXa formation plays a major role, as the effect of FVIII and TFPI on the tests seems to be executed via FXa. The ETP-based test was also strongly influenced by oral contraceptive use, even when we adjusted for all the clotting factors listed above. This means that the effect of oral contraceptives on the ETP-based test is not fully explained by the changes of coagulation factor levels investigated in this study, and that the molecular basis of acquired APC resistance during use of oral contraceptives remains to be established.

• Dahm, Anders Erik A; Vlieg, Astrid van Hylckama; Bendz, Bjørn; Rosendaal, Frits; Bertina, Rogier M. & Sandset, Per Morten (2003). Low levels of tissue factor pathway inhibitor (TFPI) increase the risk of venous thrombosis. Blood. ISSN 0006-4971. 101(11), s. 4387–4392. Vis sammendrag

  There is now strong experimental evidence that tissue factor pathway inhibitor (TFPI) is a critical inhibitor to modulate tissue factor induced coagulation, but the role of TFPI as a risk factor for thrombosis is yet to be to be determined. This study investigated the role of low TFPI levels for the development of deep vein thrombosis (DVT). We determined TFPI activity and TFPI free and total antigen levels in the subjects enrolled in the Leiden Thrombophilia Study, which is a large population-based case-control study of 474 patients and 474 controls. The odds ratio (OR) for DVT in subjects who had TFPI free antigen levels below the 10(th) percentile in the controls, as compared with those who had TFPI free antigen levels above this cut-off, was 1.7 (95% confidence interval [CI], 1.1-2.6). The ORs for low TFPI activity and low total antigen were also mildly increased. Using the 5(th) percentile as a cut-off, the ORs were 2.1 (95% CI 1.1-4.1) for both TFPI free and total antigen. Exogenous female hormones had a profound lowering effect on TFPI levels with lower levels in oral contraceptive (OC) users than in premenopausal non-users, who again had lower levels than postmenopausal women and men. These results indicate that low levels of TFPI, especially low TFPI free and total antigen in plasma, is a risk factor for DVT.

• Dahm, Anders Erik A & Brørs, Odd (2002). Phenytoin toxicity caused by interaction with ticlopidin. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 37, s. 4–9.
• Blomhoff, Svein; Jacobsen, M.B.; Spetalen, S.; Dahm, Anders Erik A & Malt, Ulrik Fredrik (2000). Perceptual hyperreactivity to auditory stimuli in patients with Irritabel Bowel Syndrome. Scandinavian Journal of Gastroenterology. ISSN 0036-5521. 35, s. 583–589.

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• Jervan, Øyvind; Haukeland-Parker, Stacey Marie; Gleditsch, Jostein; Tavoly, Mazdak; Klok, Frederikus A. & Steine, Kjetil [Vis alle 14 forfattere av denne artikkelen] (2023). Rehabilitation to improve exercise capacity and quality of life after pulmonary embolism.
• Larsen, Trine-Lise; Ghanima, Waleed; Sandset, Per Morten; Frøen, Hege; Jacobsen, Eva-Marie & Torfoss, Dag [Vis alle 7 forfattere av denne artikkelen] (2023). Faktor Xa-hemmere til forebygging og behandling av venøs tromboembolisme ved kreft. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 143(1). doi: 10.4045/tidsskr.22.0228. Fulltekst i vitenarkiv
• Larsen, Trine-Lise; Garresori, Herish; Brekke, Jorunn; Enden, Tone Rønnaug; Frøen, Hege & Jacobsen, Eva-Marie [Vis alle 15 forfattere av denne artikkelen] (2022). “Low dose apixaban as secondary prophylaxis of venous thromboembolism in cancer patients - 30 months follow-up”: Reply. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 20(8), s. 1937–1939. doi: 10.1111/jth.15774.
• Dahm, Anders Erik A & Sandset, Per Morten (2021). Tissue factor pathway inhibitor and bleeding tendency: can hormonal state explain the differences? Blood Advances. ISSN 2473-9529. 5(11), s. 2516–2517. doi: 10.1182/BLOODADVANCES.2021004651. Fulltekst i vitenarkiv
• Cui, Xueyan; Tjønnfjord, Geir Erland; Kanse, Sandip; Iversen, Nina; Dahm, Anders Erik A & Myklebust, Christiane Filion [Vis alle 11 forfattere av denne artikkelen] (2019). Tissue factor pathway inhibitor enhances transendothelial migration of chronic lymphocytic leukemia cells trhough CXCL12/CXCR7 chemotaxis. Research and Practice in Thrombosis and Haemostasis (RPTH). ISSN 2475-0379. 3.
• Dahm, Anders Erik Astrup & Hannevik, Trine-Lise (2019). Forebygging av venøs tromboembolisme ved kreft - hvilke pasienter kan DOAK være relevante for? . BestPractice Nordic. ISSN 1902-7583.
• Sandset, Per Morten & Dahm, Anders Erik Astrup (2019). Is venous thromboembolism a problem in patients with cancer in palliative care? The Lancet Haematology. ISSN 2352-3026. doi: 10.1016/S2352-3026(18)30218-7.
• Cui, Xueyan; Skretting, Grethe; Tinholt, Mari; Stavik, Benedicte; Dahm, Anders Erik A & Kanse, Sandip [Vis alle 8 forfattere av denne artikkelen] (2017). A novel hypoxia response element regulates oxygen-related repression of tissue factor pathway inhibitor in breast cancer. Research and Practice in Thrombosis and Haemostasis (RPTH). ISSN 2475-0379. 1, s. 395–395.
• Dahm, Anders Erik A; Jacobsen, Eva-Marie; Jacobsen, Anne Flem; Skuterud Wik, Hilde & Sandset, Per Morten (2017). High complement C3 increases the risk for postnatal venous thrombosis.
• Dahm, Anders Erik A & Ghanima, Waleed Khalid (2017). Nye direktevirkende antikoagulasjonsmidler til kreftpasienter? Tidsskrift for Den norske legeforening. ISSN 0029-2001. 137(3), s. 171–172. doi: 10.4045/tidsskr.17.0008.
• Utne, Kristin Kornelia; Wik, Hilde Skuterud; Jelsness-Jørgensen, Lars-Petter; Sandset, Per Morten; Dahm, Anders Erik A & Tavoly, Mazdak [Vis alle 7 forfattere av denne artikkelen] (2017). Rivaroxaban Reduces the Rate of Post-Thrombotic Syndrome After DVT - a Cross-Sectional Study Comparing Rivaroxaban to Warfarin.
• Dahm, Anders Erik A; Tiscia, Gianluca; Holmgren, Asbjørn; Jacobsen, Anne Flem; Skretting, Grethe & Grandone, E. [Vis alle 7 forfattere av denne artikkelen] (2015). Genetic variations in the annexin A5 gene and the risk of pregnancy-related venous thrombosis. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 13(3), s. 409–413. doi: 10.1111/jth.12817.
• Stiksrud, Birgitte; Nowak, Piotr; Kvale, Dag; Thalme, Anders; Birkeland, Stein-Erik & Dahm, Anders Erik A [Vis alle 8 forfattere av denne artikkelen] (2014). Reduced D-dimer levels and inflammation markers after probiotic supplement in HIV-infected on ART.
• Jacobsen, Eva-Marie; Dahm, Anders Erik A; Vartdal, Trond & Sandset, Per Morten (2014). Antikoagulasjon ved venøs trombose og indremedisinsk sykdom. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 134(9), s. 924–924.
• Kristiansen, Annette; Brandt, Linn; Berge, Eivind; Dahm, Anders Erik A; Halvorsen, Sigrun & Sandset, Per Morten [Vis alle 7 forfattere av denne artikkelen] (2014). Nye retningslinjer for antitrombotisk behandling og tromboseprofylakse. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 134(9), s. 921–922. doi: 10.4045/tidsskr.13.1582. Vis sammendrag

  Nye retningslinjer med 250 anbefalinger for antitrombotisk behandling og tromboseprofylakse er nå tilgjengelig på nett. Retningslinjene fra Norsk selskap for trombose og hemostase imøtekommer nye standarder for troverdige retningslinjer og benytter seg av innovative teknologiske løsninger.

• Tinholt, Mari; Viken, MK; Borresen-Dale, AL; Kristensen, V; Karesen, R & Schlichting, E [Vis alle 12 forfattere av denne artikkelen] (2013). The link between the hemostatic system and cancer: A genotype-phenotype study in breast cancer patients. Thrombosis Research. ISSN 0049-3848. 131, s. S75–S76.
• Bergrem, Astrid; Dahm, Anders Erik A; Jacobsen, Anne Flem; Sandvik, Leiv & Sandset, Per Morten (2013). Differential risk factors for pregnancy-related deep vein thrombosis and pulmonary embolism - Results from a population-based case-control study. Thrombosis Research. ISSN 0049-3848. 131, s. S75–S75.
• Skretting, Grethe; Iversen, Nina; Myklebust, Christiane Filion; Dahm, Anders Erik A & Sandset, Per Morten (2012). Apoptosis in CHO-K1 cells overexpressing TFPI involves both intrinsic and extrinsic pathways additional to induced activation of NF-kappa B. Thrombosis Research. ISSN 0049-3848. 129, s. S192–S192.
• Bergrem, Astrid; Dahm, Anders Erik A; Jacobsen, Anne Flem; Sandvik, Leiv & Sandset, Per Morten (2012). Differential risk factors for pregnancy related deep vein thrombosis and pulmonary embolism' results from a population-based case-control study. Thrombosis Research. ISSN 0049-3848. 130, s. S122–S123. doi: 10.1016/j.thromres.2012.08.059.
• Dahm, Anders Erik A; Eilertsen, Anette Løken; Goeman, J.; Olstad, Ole Kristoffer; Øvstebø, Reidun & Kierulf, Peter [Vis alle 9 forfattere av denne artikkelen] (2011). A microarray study on the effect of four hormone therapy regimens on gene transcription in leucocytes from healthy postmenopausal women. Thrombosis Research. ISSN 0049-3848. 127, s. S124–S124.
• Bergrem, Astrid; Dahm, Anders Erik A; Jacobsen, Anne Flem; Mowinckel, Marie-Christine; Sandvik, Leiv & Sandset, Per Morten (2011). Reduced sensitivity to activated protein C in the absence of the factor V Leiden polymorphism is a risk factor for pregnancy related venous thrombosis. Thrombosis Research. ISSN 0049-3848. 127, s. S127–S127.
• Dahm, Anders Erik A; Bezemer, ID; Sandset, Per Morten & Rosendaal, Frits (2010). Interaction between tissue factor pathway inhibitor and factor V levels on the risk of venous thrombosis. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 8(5), s. 1130–1132. doi: 10.1111/j.1538-7836.2010.03805.x.
• Dahm, Anders Erik A; Bezemer, Irene D; Bergrem, Astrid; Jacobsen, Anne Flem; Jacobsen, Eva-Marie & Skretting, Grethe [Vis alle 8 forfattere av denne artikkelen] (2010). Candidate Gene Polymorphisms and the Risk for Pregnancy Related Venous Thrombosis. Blood. ISSN 0006-4971. 116(21), s. 1708–1709.
• Dahm, Anders Erik A; Sandset, Per Morten & Rosendaal, Frits (2008). The association between protein S levels and anticoagulant activity of tissue factor pathway inhibitor type 1. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 6, s. 393–395. doi: 10.1111/j.1538-7836.2007.02859.x.
• Negaard, Helene FS; Eilertsen, Anette Løken; Dahm, Anders Erik A; Iversen, Per Ole; Østenstad, Bjørn & Sandset, Per Morten (2006). Decreased lung cancer survival with hormone replacement therapy – Due to decreased tissue factor pathway inhibitor level? Journal of Clinical Oncology. ISSN 0732-183X. 24(17), s. 2683–2684.
• Dahm, Anders Erik A; Andersen, Trine Opstad; Rosendaal, Frits & Sandset, Per Morten (2004). A novel assay for tissue factor pathway inhibitor (TFPI) anticoagulant activity in plasma. Vis sammendrag

  Introduction. Several studies have shown that full-length free TFPI is a much stronger anticoagulant in diluted prothrombin time (dPT) assays than truncated and lipoprotein associated TFPI. Although it has been suggested that TFPI anticoagulant activity is of importance for the effect of TFPI in vivo, no assays have so far been standardized to assay TFPI anticoagulant activity in patient samples. Aims. To develop an assay measuring the anticoagulant properties of TFPI and study the relationship between the TFPI anticoagulant activity and TFPI free antigen and TFPI total antigen. Materials and Methods. TFPI anticoagulant assay: 32 µL of plasma was first incubated for 5 min with either 8 µL TBS or anti-TFPI immunoglobulin, which completely blocked TFPI activity. Then, 30 µL recombinant, relipidated tissue factor (Innovin®) at 1/200 fold dilution was added and incubated for 3 min. Clotting was initiated by the addition of 30 µL CaCl2 (35 mM). Results were expressed as a ratio, with clotting times in the absence of anti-TFPI as the denominator (a value of 1.0 indicating no TFPI anticoagulant activity). This ratio was normalized against the ratio obtained with reference plasma within each run to minimize day-to-day variation in clotting times. After normalization, high ratios reflect little functional TFPI anticoagulant, whereas low ratios reflect high activity. TFPI antigen assays: TFPI free and total antigen were assayed with commercial kits from Stago, of which TFPI free antigen is specific for circulating full-length TFPI. Study population: Control subjects (n=436) of the Leiden Thrombophila Study (LETS). Results. Mean TFPI anticoagulant ratio was 0.97 (SD 0.0062, range 0.82-1.15). The assay coefficient of variation was 2.8% between days and from 0.6% to 1.5% within days. The regression coefficient (B) for TFPI free antigen, with TFPI anticoagulant ratio as dependent variable, was -100·10-4 (95% confidence interval �110·10-4 to �90·10-4), which means that an increase in TFPI free antigen of 10 ng/mL is consistent with a decrease of TFPI anticoagulant ratio of 0.10. The correlation coefficient (r) was 0.67. B for TFPI total antigen was -20·10-4 (�23·10-4 to �16·10-4) with r=0.47. Conclusions. A novel and reproducible assay for detection of TFPI anticoagulant activity in plasma has been developed. TFPI anticoagulant ratio was much stronger associated with free antigen than with TFPI total antigen, which supports the hypothesis that free TFPI is biologically relevant in vivo.

• Dahm, Anders Erik A; Høibraaten, Else; Morrissey, Jim; Andersen, Trine Opstad & Sandset, Per Morten (2004). The influence of hormone replacement therapy (HRT) on the factor VIIa/antithrombin (FVIIa/AT) complex. Vis sammendrag

  Introduction. In a recent randomised, double-blind, placebo-controlled trial on the effects of oral hormone replacement therapy (HRT)(Høibraaten et al,Thromb Haemost 2001; 85, 775-81), we found that combined 17-&#946;- estradiol (2 mg) and norethisterone acetate (1 mg) induced a reduction in activated factor VIIa (FVIIa) by median 17-23%, but with no decrease in total FVII concentration. Free tissue factor pathway inhibitor (TFPI) decreased by 29-30%, whereas antithrombin (AT) decreased by 8-9%. Recently it has been shown that AT may inhibit FVIIa bound to tissue factor (TF), building a FVIIa/AT complex, which is then released from TF, and may potentially be a marker of TF activated coagulation. Aims. To investigate whether the reduction in FVIIa on HRT, but not in the total FVII concentration, can be explained by AT induced inactivation of FVIIa and the formation of FVIIa/AT complexes, and also to investigate whether FVIIa/AT covariates with markers of activated coagulation. Materials and methods. Patients were 140 post-menopausal women with a history of venous thrombosis who were randomized to receive HRT (n=71) or placebo (n=69). This study reports data at baseline and after 3 months. FVIIa/AT complexes were assayed with an ELISA developed by Dr. Jim Morrissey. Results. At baseline FVIIa/AT was median 160 pM (25th, 75th percentiles 102, 219) in placebo patients and 167 pM (103, 254) in the HRT group. Median relative changes from baseline to 3 months in placebo and HRT treated patients were: FVIIa/AT +5.1% and -8.9% (ns), respectively, FVII antigen +2.4% and -7.5% (ns), respectively, and FVIIa +7,9% and -14,9% (p<0.001). Simple linear regression within the HRT group with prothrombin fragments 1+2 (F1+2) showed that an increase in the relative change in FVIIa/AT was weakly associated to the increase in F1+2 from baseline to 3 months.

• Dahm, Anders Erik A; Andersen, Trine Opstad; Rosendaal, Frits & Sandset, Per Morten (2004). A novel assay for tissue factor pathway inhibitor (TFPI) anticoagulant activity in plasma. Vis sammendrag

  Introduction. Several studies have shown that full-length free TFPI is a much stronger anticoagulant in diluted prothrombin time (dPT) assays than truncated and lipoprotein associated TFPI. Although it has been suggested that TFPI anticoagulant activity is of importance for the effect of TFPI in vivo, no assays have so far been established and validated to assay TFPI anticoagulant activity in patient samples. Aims. To develop and validate an assay of TFPI anticoagulant activity and study the relationship between TFPI anticoagulant activity and TFPI free and total antigen and TFPI chromogenic substrate activity. Materials and Methods. TFPI anticoagulant assay: 32 µL of plasma was first incubated for 5 min with either 8 µL TBS or anti-TFPI immunoglobulin, which completely blocked TFPI activity. Then, 30 µL recombinant, relipidated tissue factor (Innovin®) at 1/200 fold dilution was added and incubated for 3 min. Clotting was initiated by the addition of 30 µL CaCl2 (35 mM). Results were expressed as a ratio, with clotting times in the presence of anti-TFPI as the denominator. This ratio was normalized against the ratio obtained with a reference plasma within each run to minimize day to day variation in clotting times. After normalization, high ratios reflect high functional TFPI anticoagulant activity, whereas low ratios reflect low activity. TFPI antigen assays: TFPI free and total antigen were assayed with commercial kits from Stago, France. TFPI free antigen is specific for circulating full-length TFPI, whereas TFPI total antigen detects both full-length and truncated forms of TFPI. Study population: Control subjects (n=436) of the Leiden Thrombophila Study (LETS). Results. Mean TFPI anticoagulant ratio was 1.03 (SD 0.0066, range 0.87-1.22). The assay coefficient of variation was 2.8% between days and from 0.6% to 1.5% within days. Linear regression showed that the n-TFPIac ratio was strongly associated to the levels of TFPI free antigen, but weakly associated to bound TFPI (table 1). Conclusions. We have established a novel and reproducible assay for detection of TFPI anticoagulant activity in plasma. TFPI anticoagulant ratio was strongly associated to free antigen, and may be considered an activity assay of full-length TFPI in plasma. Table 1 - The association of normalized TFPI anticoagulant ratio to other TFPI assays TFPI assay Normalized TFPI anticoagulant ratio- b (95% CI) Correlation coefficient- r TFPI free antigen 0.049 (0.044 to 0.053) 0.73 Total TFPI 0.033 (0.027 to 0.038) 0.48 TFPI chrom. subst. activity 0.031 (0.025 to 0.037) 0.46 Bound TFPI 0.020 (0.014 to 0.026) 0.30 Standardized regression coefficient (b), 95% confidence interval (CI) and correlation coefficient (r). (b) shows the change in n-TFPIac ratio per increase of one standard deviation in the TFPI assay studied.

• Dahm, Anders Erik A; Andersen, Trine Opstad; Rosendaal, Frits & Sandset, Per Morten (2004). Biological relevance of a new TFPÌ anticoagulant activity assay of full-length TFPI. Vis sammendrag

  Introduction: We have recently shown that low TFPI is a weak risk factor for deep vein thrombosis (DVT)(Dahm et al Blood 2003;101;4387-92). Plasma contains free, full-length TFPI (FL-TFPI) and truncated and lipoprotein associated TFPI. Since free, FL-TFPI has a much stronger ability to prolong clotting time in diluted prothrombin time (dPT) assay than other types of TFPI, it has been suggested that FL-TFPI biologically plays a more important role than other forms of TFPI. Aims: To determine the fraction of free, FL-TFPI in plasma and to determine the role of TFPI anticoagulant activity in the prevention of DVT. Materials and Methods: Normalized TFPI Anticoagulant Activity (n-TFPIac) Ratio was assayed using a dPT assay after incubation of plasma in the absence and the presence of neutralizing anti-TFPI antibodies. Results were expressed as a ratio with dPT in the presence of anti-TFPI as the denominator. The ratio was normalized against a ratio obtained with a reference plasma within each run. TFPI chromogenic substrate (TFPIcs) activity assay was determined by the quantification of residual TF/FVIIa catalytic activity after the incubation of diluted plasma (containing TFPI) with TF, FVIIa, and FXa. TFPI antigen assays: TFPI free antigen (full-length TFPI) and TFPI total antigen (full-length + truncated TFPI) were assayed with commercial kits from Stago, France. Bound TFPI was calculated as the difference between TFPI total antigen and TFPI free antigen. Study population: Individuals included in The Leiden Thrombophila Study (LETS), which is a case-control study of 474 patients with DVT and 474 controls. 363 controls and 362 cases were available for the OR calculations and 473 controls for the estimation of the fraction of free, FL-TFPI. Statistics: The fraction of free, FL-TFPI was calculated by dividing TFPI free antigen by TFPI total antigen. Odds ratios (OR) for DVT were calculated for individuals with TFPI values below the 10th percentile as compared with those above. Results: The fraction of free, FL-TFPI in plasma was 19%, but with large variations due to hormonal state (table 1). Normalized TFPIac ratio below the 10th percentile gave an OR of 1.5 (95% CI 0.97-2.4) for DVT, which was comparable to the ORs obtained with other TFPI assays. Individuals with low TFPI in both activity assays had an OR of 5.9 (95% CI 1.7-20) for DVT (table 2). Conclusion: Approximately 20% of TFPI in plasma was free, FL-TFPI. Low n-TFPIac ratio was a weak risk factor for DVT, but was not a stronger risk factor than low TFPI in the other assays. However, combined low n-TFPIac ratio and low TFPIcs activity seemed to be a strong risk factor for DVT. Table 1. Mean (95% CI) plasma fraction of TFPI free antigen in controls OC users (n=54) OC nonusers (n=99) Postmenopausal women (n=89) Men (n=201) All (n=473) TFPI Free Antigen/TFPI total TFPI antigen 0.125 (0.115-0.135) 0.175 (0.165-0.184) 0.197 (0.186-0.208) 0.206 (0.199-0.209) 0.187 (0.182-0.192) Table 2. OR (95% CI) for DVT for different TFPI parameters below the 10th percentile nTFPIac ratio TFPI free antigen TFPI total antigen TFPIcs activity Bound TFPI n-TFPIac ratio + TFPIcs activity 1.5 (0.97-2.4) 1.3 (0.83-2.1) 1.3 (0.85-2.1) 1.2 (0.75-1.9) 1.4 (0.90-2.2) 5.9 (1.7-20)

• Dahm, Anders Erik A; Vlieg, Astrid van Hylckama; Bendz, Bjørn; Rosendaal, Frits; Bertina, Rogier M. & Sandset, Per Morten (2002). Tissue factor pathway inhibitor (TFPI) and risk of deep venous thrombosis (DVT).
• Dahm, Anders Erik A; Vlieg, Astrid van Hylckama; Bendz, Bjørn; Rosendaal, Frits; Bertina, Rogier M. & Sandset, Per Morten (2002). Low levels of tissue factor pathway inhibitor (TFPI) increase the risk of venous thrombosis.
• Dahm, Anders Erik A; Andersen, Trine Opstad; Rosendaal, Frits; Bertina, Rogier M. & Sandset, Per Morten (2002). Tissue factor pathway inhibitor (TFPI) and the risk of deep venous thrombosis (DVT).
• Dahm, Anders Erik A; Vlieg, Astrid van Hylckama; Bendz, Bjørn; Rosendaal, Frits; Bertina, Rogier M. & Sandset, Per Morten (2002). Low levels of tissue factor pathway inhibitor (TFPI) increase the risk of venous thrombosis.
• Dahm, Anders Erik A (2002). Low levels of tissue factor pathway inhibitor (TFPI) increase the risk of venous thrombosis.
• Dahm, Anders Erik A (2002). Low levels of tissue factor pathway inhibitor (TFPI) increase the risk of venous thrombosis.
• Dahm, Anders Erik A (2002). Low levels of tissue factor pathway inhibitor (TFPI) increase the risk of venous thrombosis.

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