Lene Kristin Brekke1,2, Bjørg-Tilde Svanes Fevang3,4, Andreas P Diamantopoulos3,4, Jörg Assmus3,4, Elisabet Esperø3,4, Clara Gram Gjesdal3,4. 1. From the Hospital for Rheumatic Diseases, Haugesund; Department of Clinical Science, University of Bergen, Bergen; Bergen Group of Epidemiology and Biomarkers in Rheumatic Disease (BEaBIRD), Department of Rheumatology, and Centre for Clinical Research, Haukeland University Hospital, Bergen; Martina Hansens Hospital, Bærum, Norway. lene.kristin.brekke@hsr.as. 2. L.K. Brekke, MD, Hospital for Rheumatic Diseases, and Department of Clinical Science, University of Bergen; B.T. Fevang, MD, PhD, Department of Clinical Science, University of Bergen, and BEaBIRD, Department of Rheumatology, Haukeland University Hospital; A.P. Diamantopoulos, MD, PhD, MPH, Martina Hansens Hospital; J. Assmus, PhD, Centre for Clinical Research, Haukeland University Hospital; E. Esperø, MD, Hospital for Rheumatic Diseases; C. Gram Gjesdal, MD, PhD, Department of Clinical Science, University of Bergen, and BEaBIRD, Department of Rheumatology, Haukeland University Hospital. lene.kristin.brekke@hsr.as. 3. From the Hospital for Rheumatic Diseases, Haugesund; Department of Clinical Science, University of Bergen, Bergen; Bergen Group of Epidemiology and Biomarkers in Rheumatic Disease (BEaBIRD), Department of Rheumatology, and Centre for Clinical Research, Haukeland University Hospital, Bergen; Martina Hansens Hospital, Bærum, Norway. 4. L.K. Brekke, MD, Hospital for Rheumatic Diseases, and Department of Clinical Science, University of Bergen; B.T. Fevang, MD, PhD, Department of Clinical Science, University of Bergen, and BEaBIRD, Department of Rheumatology, Haukeland University Hospital; A.P. Diamantopoulos, MD, PhD, MPH, Martina Hansens Hospital; J. Assmus, PhD, Centre for Clinical Research, Haukeland University Hospital; E. Esperø, MD, Hospital for Rheumatic Diseases; C. Gram Gjesdal, MD, PhD, Department of Clinical Science, University of Bergen, and BEaBIRD, Department of Rheumatology, Haukeland University Hospital.
Abstract
OBJECTIVE: To determine the risk of cancer in a large Norwegian cohort of patients with giant cell arteritis (GCA). METHODS: This is a hospital-based, retrospective, observational cohort study including patients diagnosed with GCA in the Bergen Health Area during 1972-2012. Patients were identified through computerized hospital records using the International Classification of Diseases coding system. Medical records were reviewed. Each patient was randomly assigned population controls matched on age, sex, and geography from the Central Population Registry of Norway. Data on the occurrence of cancer were obtained from the Cancer Registry of Norway. The cumulative risk of malignancy was estimated using Kaplan-Meier methods and potential differences were analyzed using the Gehan-Breslow and log-rank tests. RESULTS: We identified 881 cases with a clinical diagnosis of GCA, of which 792 fulfilled the American College of Rheumatology (ACR) 1990 classification criteria and 528 were biopsy-verified. Cases with no registered cancer prior to GCA diagnosis were included in a time-to-event analysis, with first cancer as the event (n = 767 with clinical GCA diagnosis, 686 fulfilling ACR criteria for GCA, 463 biopsy-verified). These cases were matched with previously cancer-free population controls (n = 1437, 1284, 895, respectively). We found no significant difference in the risk of malignancy after time of diagnosis/matching for GCA patients compared to population controls (p > 0.05). CONCLUSION: In this study of a large and well-characterized cohort of patients with GCA, there was no difference in the risk of malignancy in patients with GCA compared to matched population controls.
OBJECTIVE: To determine the risk of cancer in a large Norwegian cohort of patients with giant cell arteritis (GCA). METHODS: This is a hospital-based, retrospective, observational cohort study including patients diagnosed with GCA in the Bergen Health Area during 1972-2012. Patients were identified through computerized hospital records using the International Classification of Diseases coding system. Medical records were reviewed. Each patient was randomly assigned population controls matched on age, sex, and geography from the Central Population Registry of Norway. Data on the occurrence of cancer were obtained from the Cancer Registry of Norway. The cumulative risk of malignancy was estimated using Kaplan-Meier methods and potential differences were analyzed using the Gehan-Breslow and log-rank tests. RESULTS: We identified 881 cases with a clinical diagnosis of GCA, of which 792 fulfilled the American College of Rheumatology (ACR) 1990 classification criteria and 528 were biopsy-verified. Cases with no registered cancer prior to GCA diagnosis were included in a time-to-event analysis, with first cancer as the event (n = 767 with clinical GCA diagnosis, 686 fulfilling ACR criteria for GCA, 463 biopsy-verified). These cases were matched with previously cancer-free population controls (n = 1437, 1284, 895, respectively). We found no significant difference in the risk of malignancy after time of diagnosis/matching for GCA patients compared to population controls (p > 0.05). CONCLUSION: In this study of a large and well-characterized cohort of patients with GCA, there was no difference in the risk of malignancy in patients with GCA compared to matched population controls.
Authors: Amir Emamifar; Søren Hess; Torkell Ellingsen; Susan Due Kay; Jacob Christian Bang; Oke Gerke; Per Syrak Hansen; Ziba Ahangarani Farahani; Henrik Petersen; Niels Marcussen; Inger Marie Jensen Hansen; Peter Thye Rønn Journal: J Clin Med Date: 2020-12-04 Impact factor: 4.241