Special Issue:
Challenges and Opportunities in Sepsis
Kristen Anne Salava, MD
Geisinger Medical Center 100 N. Academy Avenue M.C. 21-52 Rheumatology, Danville, PA 17822
Ruchi Patel, DO
Geisinger Medical Center 100 N. Academy Avenue M.C. 21-52 Rheumatology, Danville, PA 17822
Eric Newman, MD
Geisinger Medical Center 100 N. Academy Avenue M.C. 21-52 Rheumatology, Danville, PA 17822
P. Daniel Nicoholas, DO
Geisinger Medical Center 100 N. Academy Avenue M.C. 21-52 Rheumatology, Danville, PA 17822
Dante M. Grassi, PharmD, BCPS
Geisinger Medical Center 100 N. Academy Avenue M.C. 21-52 Rheumatology, Danville, PA 17822
Swana Thomas, PharmD, MPH
Pennsylvania Presbyterian Medical Center 3737 Market Street 11th Fl, Philadelphia, PA 19115
Joseph Chronowski, MBA
Geisinger Medical Center 100 N. Academy Avenue M.C. 21-52 Rheumatology, Danville, PA 17822
David Pugliese, DO
Geisinger Medical Center 100 N. Academy Avenue M.C. 21-52 Rheumatology, Danville, PA 17822
Jonida Cote, DO
Geisinger Medical Center 100 N. Academy Avenue M.C. 21-52 Rheumatology, Danville, PA 17822
Abstract
Objective: To close laboratory screening care gaps via rheumatology-pharmacy co-management in patients starting disease-modifying antirheumatic drugs.
Methods: Laboratory data were obtained from patients who started disease-modifying antirheumatic drugs (DMARDs) during the pre-and post-intervention periods. The intervention consisted of a rheumatology-pharmacy collaborative screening with guideline-driven DMARD protocol for hepatitis B, hepatitis C, and tuberculosis. The care gap closure for patients starting any type of DMARDs such as a conventional synthetic disease-modifying antirheumatic drug (csDMARD), a biologic disease-modifying antirheumatic drug (bDMARD), or a targeted synthetic disease-modifying antirheumatic drug (tsDMARD), was defined as meeting hepatitis screening completion. The care gap closure for patients starting a bDMARD or tsDMARD alone was defined as meeting both the hepatitis and tuberculosis screening completion. The Chi square method was used for the statistical analysis of the data comparing laboratory screening rates of rheumatologists’ pre-intervention versus rheumatologist-pharmacist co-management post-intervention. Post-intervention, subgroup analysis of laboratory screening rates among rheumatologists alone versus rheumatologist-pharmacist co-management was also performed.
Results: During the 30-month period 6/1/2019 to 11/30/2021, hepatitis screening for patients on DMARDs improved from 77% with rheumatologists alone to 82% with co-management post-intervention (P=0.005), whereas hepatitis/tuberculosis screening for patients on bDMARDs/tsDMARDs improved from 75% to 85% respectively (P=0.005). In post-intervention subgroup analysis, hepatitis screening for patients on DMARDs improved from 80% with rheumatologists alone to 95% with co-management(P=0.00), whereas hepatitis/tuberculosis screening for patients on bDMARDs/tsDMARDs improved from 83% to 94% respectively (P=0.033).
Conclusion: By integrating clinical pharmacists into our rheumatology clinic, we significantly improved hepatitis and tuberculosis laboratory screening in our immunosuppressed rheumatic population.
Implications: Rheumatologists can consider integrating clinical pharmacists into their practices to improve patient safety by closing laboratory screening care gaps in the immunosuppressed rheumatic population.
Niclas Stefan Rasmussen
Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.; Copenhagen Research Center for Autoimmune Connective Tissue Diseases – COPEACT, Center for Rheumatology and Spine Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.; Department of Clinical Biochemistry, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Søren Jacobsen
Copenhagen Research Center for Autoimmune Connective Tissue Diseases – COPEACT, Center for Rheumatology and Spine Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.
Claus Henrik Nielsen
Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Christoffer Tandrup Nielsen
Copenhagen Research Center for Autoimmune Connective Tissue Diseases – COPEACT, Center for Rheumatology and Spine Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Abstract
Background: Generation of galectin-3 binding protein (G3BP)-expressing microvesicles can be induced in-vitro by Toll-like receptor 9 ligation in mononuclear cells. Microvesicles co-expressing G3BP and double-stranded DNA are associated with active lupus nephritis. However, whether the microvesicular G3BP mainly deposits from circulation or is endogenously derived is unknown. In this study, we aim to delineate the origin of G3BP on in-vitro generated microvesicles by using serum as a source of native G3BP.
Methods: G3BP-expressing microvesicles, generated by stimulation of systemic lupus erythematosus patient-derived mononuclear cells with the Toll-like receptor 9-agonist ODN2395, were incubated with normal human serum, heat-inactivated human serum, recombinant human C1q or human albumin. The expression of G3BP by microvesicles was examined by flow cytometry, and the binding of soluble recombinant human C1q to recombinant human G3BP was investigated by ELISA.
Results: Approximately half of the microvesicles released from mononuclear cells expressed G3BP. Surprisingly, the staining was abrogated by incubation of the microvesicles with normal human serum, while incubation with heat-inactivated human serum did not have a similar effect. Reasoning that C1q might be the heat-labile factor blocking access of our G3BP antibody detection system, we incubated microvesicles with recombinant human C1q, which on average inhibited the detectable proportion of G3BP-bearing microvesicles by 87%. Soluble recombinant human C1q bound to immobilized recombinant human G3BP in a dose-dependent manner.
Conclusion: Our data suggest that soluble C1q binds to G3BP on Toll-like receptor 9-induced microvesicles released from systemic lupus erythematosus patient-derived mononuclear cells. This interaction may exarcerbate inflammation in systemic lupus erythematosus but may also serve as a general mechanism for the appropriate clearance of these potentially pathogenic factors.
Thomas F Lansdale III, MD
Deceased, Department of Medicine, Greater Baltimore Medical Center, Johns Hopkins University School of Medicine, Baltimore MD
Geoffrey M. Gratwick, MD
Block and Gratwick PA, Bangor, ME
Samar X. Gupta, MD
Section of Rheumatology, Ann Arbor VA Healthcare System, University of Michigan, Ann Arbor, Michigan,
Stanford M. Shoor
Division of Immunology and Rheumatology, Stanford University School of Medicine, Palo Alto, CA
Cindy Flower, MBBS, DM, FACP
Faculty of Medical Sciences, University of the West Indies, Cave Hill campus
Matthew H. Liang, MD, MPH
Division of Rheumatology, Inflammation and Immunity, Brigham and Women’s Hospital and Section of Rheumatology, Boston VA Healthcare Services, Harvard Medical School, Boston, MA.
Abstract
Mentor has roots in Greek mythology. Its current practitioners have lent their own interpretation and meaning by their actions. We offer the case studies and lived experience of a select group who have never met all the others. Each asked the same questions, they tell the story of how each found their mentor(s), try to be mentors themselves, and what they try to impart to their mentees through the vicissitudes of their professional responsibilities and personal lives over a career.
Céu Tristão Martins Conceição
Psychologist and Psychoanalyst, PhD – Rheumatology Division, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil
Ivone Minhoto Meinão
Rheumatologist, MD, PhD- Rheumatology Division, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil
Sérgio Luís Blay
Professor of Psychiatry and Psychoanalysis, MD, PhD – Department of Psychiatry, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil
Emília Inoue Sato
Professor of Rheumatology MD, PhD – Rheumatology Division, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil
Abstract
Objective: To evaluate the effectiveness in the long-term follow-up of brief group psychoanalytic psychotherapy in improving quality of life, symptoms, coping strategies, anxiety, and depression levels in systemic lupus erythematosus (SLE) patients.
Methods: Prospective, randomized clinical trial including 80 SLE patients divided into two groups: therapy (n=37) and control (n=43), with standard clinical care. Therapy group received weekly therapy for 20 weeks. The assessments were at baseline, after 20 weeks and after 24 months from the end of intervention. Damage and disease activity were assessed by rheumatologists. Self-administered questionnaires were supervised by blind evaluators: quality of life, symptoms, coping strategies, anxiety, and depression. Intent to treat statistical analysis. Comparisons of variance between groups over time (ANOVA repeated measures). P <0.05 significant.
Results: At baseline, both groups were homogeneous. After intervention, therapy group showed significant improvement in most domains of quality of life, symptoms, all domains of anxiety, and depression and several domains of coping strategies. Benefits in quality of life and coping remained at 24 months follow-up. However, the improvement in anxiety, and depression was not maintained. Medications and clinical variables did not change.
Conclusion: This study showed the effectiveness of brief group psychoanalytic psychotherapy in improving quality of life, symptoms and coping strategies in SLE patients even in the long-term follow-up. Depression and anxiety levels reduced at the end of therapy, although, the improvement did not last 24 months.
Nicola Volpi
Department of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy
Abstract
The various Rheumatology/Osteoarthritis Societies (the American College of Rheumatology, the Arthritis Foundation, the European League Against Rheumatism, the National Institute for Health and Care Excellence, the European society for clinical and economic aspects of osteoporosis and osteoarthritis, and the Italian consensus on appropriateness of osteoarthrosis therapies) published specific recommendations for the management of osteoarthrosis affecting hand, hip and knee. These evidence-based guidelines take into account safety and tolerability of pharmacological and non-pharmacological interventions available from the scientific literature as well as the opinions of the clinical specialists to provide complete, clear and transparent recommendations for the management of osteoarthrosis. This article provides an update of the scientific literature for selected treatments of osteoarthrosis focusing on the therapy with symptomatic slow-acting drugs (SYSADOAs) and disease modifying anti-osteoarthrosis drugs (DMOADs) (chondroitin sulfate, glucosamine, diacerein, unsaponifiable soy and avocado extracts). Moreover, the management of osteoarthrosis pain and function, avoidance of adverse events and long-term outcomes by SYSADOAs/DMOADs molecules is considered. Finally, based on the real-world data, the opinion of the various Rheumatology/Osteoarthritis Societies of all over the word is illustrated and discussed also by considering the structure, quality and properties of the SYSADOAs/DMOADs agents used in the treatment of osteoarthrosis. In particular, the results reported in numerous studies are contradictory and not always convincing about the efficacy of chondroitin sulfate and glucosamine as SYSADOAs and DMOADs. The cause of these non-homogeneous results could be due to the use in different studies of chondroitin sulfate and glucosamine preparations of varying quality. It is therefore mandatory to carry out new clinical studies using chondroitin sulfate and glucosamine of pharmaceutical grade or of the best possible quality to ascertain their usefulness as biomolecules in the treatment of osteoarthrosis.
George A Karpouzas, MD
Division of Rheumatology, Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, Torrance, CA, USA
Elizabeth Hernandez, MA
Division of Rheumatology, Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, Torrance, CA, USA
Matthew J Budoff, MD
Division of Cardiology, Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, Torrance, CA, USA
Sarah R Ormseth, PhD
Division of Rheumatology, Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, Torrance, CA, USA
Abstract
Objectives. Underweight patients with rheumatoid arthritis incur greater total and cardiovascular mortality compared to overweight or obese. We explored whether obesity confounded cardiovascular risk estimates and the potential utility of noninvasive coronary atherosclerosis assessment and cardiac damage biomarkers in optimizing risk prediction in obese patients with rheumatoid arthritis.
Methods. We evaluated 150 participants undergoing screening atherosclerosis evaluation with coronary computed tomography angiography and follow-up over 6.0±2.4 years. Framingham 2008 modified general cardiovascular risk score was computed at baseline. Obesity was defined as waist circumference >88 cm in females and >102 cm in males. Serum highly-sensitive cardiac troponin I (hs-cTnI) and leptin were measured at baseline.
Results. An interaction between the Framingham risk score and obesity on cardiovascular risk was observed (p=0.032); lower estimates were seen in obese (area under the curve-AUC 0.660, 95% CI 0.487-0.832) vs. non-obese patients (AUC 0.952, 95% CI 0.897-1.007, p=0.002). Likewise, risk estimates were inferior in patients with high (>22.1 ng/ml) vs. low leptin (AUC 0.618, 95% CI 0.393-0.842 vs. 0.874, 95% CI 0.772-0.976, p=0.042). In obese patients, sequential addition of the top highly-sensitive cardiac troponin I tertile values and extensive atherosclerotic plaque (>5 segments) information to a base model including the Framingham risk score alone significantly improved risk estimates, based on changes in net reclassification index (1.093 95% CI 0.517-1.574), integrated discrimination improvement (0.188, 95% CI 0.060-0.526), and AUC (0.179, 95% CI 0.058-0.378, p=0.02). The final, combined model accurately predicted 83.9% of incident cardiovascular events.
Conclusion. Obesity attenuated cardiovascular risk estimate accuracy in patients with rheumatoid arthritis. Risk optimization employing non-invasive assessment of coronary atherosclerosis burden and serum cardiac damage biomarkers may warrant further study.
Amorn Sankhaanuruk, M.D.
Division of Rheumatology, Department of Internal Medicine 1 , Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Nuntana Kasitanon, M.D.
Division of Rheumatology, Department of Internal Medicine 1 , Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Worawit Louthrenoo, M.D.
Division of Rheumatology, Department of Internal Medicine 1 , Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Abstract
Background: Nowadays, we have standard treatment guidelines for lupus nephritis (LN), a substantial proportion of patients have LN flare. The aims here to determine the incidence of LN flare in patients who had renal complete remission (CR) after receiving induction therapy (IT) and to identify factors associated with renal flare after CR in clinical practice.
Methods: Retrospective analysis in a tertiary-level center for the clinical outcomes of patients who had first LN episode, achieved CR (24hr urine protein <0.5 gm/day with normal renal function) within 12 months after received IT and received the maintenance therapy (MT).
Results: Eighty-seven out of 548 patients (96.6% female with mean age 29.5±10.8 years) met the inclusion criteria. During 6.1±3.4 years of observation after CR, 42 (48.3%) patients had LN flare. The incidence ratio of LN flare was 10.9/100 patient-years. The mean time from CR to flare was 3.1 years. Using Cox-regression analysis, induction to remission therapy ≥6 months (OR=0.33, p=0.006), and using statins ≥9 months after reached CR (OR=0.44, p=0.032) had a lower incidence of LN flare, while age at onset of disease ≤20 years had a higher incidence of LN flare.
Conclusion: Despite achieving CR with standard treatment, almost half of the patients had an LN flare within a few years. Young SLE patients had an increased incidence of LN flare, the long period of induction therapy and using statins may retard a flare of the disease.
George A Karpouzas, MD
Division of Rheumatology, Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, Torrance, CA, USA
Sarah R Ormseth, PhD
Division of Rheumatology, Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, Torrance, CA, USA
Elizabeth R Hernandez
Division of Rheumatology, Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, Torrance, CA, USA
Matthew J Budoff, MD
Division of Cardiology, Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, Torrance, CA, USA
Abstract
Methods. The sample included 144 patients with complete biomarker data who underwent plaque evaluation with coronary computed tomography angiography; 95 were re-imaged within 6.9±0.3 years. Presence of >5 segments with plaque or coronary artery calcium >100 constituted extensive disease; lesions rendering >50% stenosis were considered obstructive. The Framingham 2008 cardiovascular risk score was included in all models.
Results. Hs-cTnI added to the cardiovascular risk score increased area-under-the curve (AUC) from 0.710 to 0.729 and improved prediction accuracy for baseline plaque presence [Net Reclassification Improvement =0.538 (95% confidence interval 0.143-0.895)] and Integrated Discrimination Improvement (IDI) =0.035 (0.001-0.128). In contrast, a-b2GPI-IgA did not, and the combination offered no added benefit over hs-cTnI alone. While hs-cTnI alone did not predict plaque progression, a-b2GPI-IgA presence did (p=0.005), especially in patients with >median hs-cTnI (p=0.015). In patients with >median hs-cTnI, adding a-b2GPI-IgA to a cardiovascular risk score model predicting progression from non-extensive/non-obstructive to extensive/obstructive plaque increased AUC from 0.796 to 0.878 and improved model precision [IDI=0.277 (0.011-0.946)].
Conclusion. High hs-cTnI significantly improved prediction of baseline plaque presence and may trigger an initial non-invasive coronary atherosclerosis evaluation. A-b2GPI-IgA presence may justify a follow-up interrogation in patients with non-extensive, non-obstructive plaque at baseline.
Wen Liu
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Department of Neuroscience, Uppsala University, Uppsala, Sweden
Mark Gonn
Unit of Internal Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden
Susanna von Holst
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Jessada Thutkawkorapin
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Xiang Jiao
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Jan Björk2
Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Gastroenterology section, medical unit Gastroenterology, Rheumatology and Dermatology, Karolinska University hospital, Stockholm, Sweden
Ann-Sofie Backman
Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden: Gastroenterology section, medical unit Gastroenterology, Rheumatology and Dermatology, Karolinska University hospital, Stockholm, Sweden
Kristina Lagerstedt-Robinson
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Genetics, Karolinska University Hospital, Stockholm, Sweden
Annika Lindblom
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Genetics, Karolinska University Hospital, Stockholm, Sweden
Abstract
Colorectal cancer (CRC) is a multifactorial disease, where both the environment and genetics play a role. It is estimated that approximately 35% of CRCs have a potentially identifiable genetic cause. Well-known and highly penetrant genetic causes make up less than 5% of all CRC, and leave many families not explained by known predisposing genes/mutations. Low penetrant alleles have also been thought to modify the risk of CRC. Linkage studies have been successful in discovering and localizing highly penetrant genes in CRC and risk loci has become possible to discover performing genome wide association studies (GWAS).
In this study we have analyzed families with CRC where individuals with CRC as well as individuals with premalignant lesions, adenomas, were codes as affected. In total 600 individuals in 121 families were included in the study.
In total three genomic regions were found with suggestive linkage located at 4p16.3, 6p24.3 and 10p14. These regions were further studied using sequencing analysis and association studies using haplotypes.
Anokhi Saklecha, BS
Division of Rheumatology, Allergy and Immunology University of California, San Diego, USA
Chelsey J. F. Smith, MD
Division of Rheumatology, Allergy and Immunology University of California, San Diego, USA
Abstract
Active lupus nephritis poses severe maternal and fetal risks in pregnant patients. Management in pregnancy is challenging and limited by lack of pregnancy-safe medication options. Preeclampsia is an associated maternal risk that shares many clinical features with lupus nephritis, often making it difficult to identify the primary disease process. In this report, we present a case of severe preeclampsia superimposed on active lupus nephritis in a 25-year-old pregnant female. We highlight the risks and management options for lupus nephritis in pregnancy, the overlaps in presentation between lupus nephritis and preeclampsia, and techniques to clinically distinguish between the two.
Thomas P. Olenginski, MD
Geisinger Department of Rheumatology, Danville, PA, USA
Abstract
Background: In 2008, Geisinger Rheumatology established a Fracture Liaison Service (FLS) termed HiROC (High-Risk Osteoporosis Clinic). Inpatient HiROC teams integrated with outpatient HiROC clinics.
Aim: We review the history of Geisinger HiROC, performance and lessons learned. We examine this: In a high-risk, post-fracture, drug-indicated patient without treatment contraindications, was patient treated? If a patient chose followup with Geisinger primary care physician (PCP), was that patient treated?
Results: Four Geisinger HiROC analyses are presented: 2008-2011; 2013-2015;2016; and 2017-2018. HiROC treatment rates are 80 %, 75.4 %, 74 %, and 72 %, respectively. Geisinger PCP treatment rates are 32.2 %, 13.8 %, and 14 %. (PCP data from 2017-2018 not included) 2008-2011 analysis included 888 patients, mean age 76.1, 77.6 % women and 22.4 % men. Mean 25-OH Vit. D was 25.6. Hip fractures represented 58.2 % of cohort and vertebral fractures (VF) 11.6 %. At discharge, 44.3 % went to Rehab, 31.5 % to Nursing Home (NH) and 24 % home. Six- month mortality was 14.7 % and HiROC followup 51.5 %.
2013-2015 analysis included 1279 patients with mean age of 77.8 and 74 % women, 26 % men. Hip fractures were seen in 67.6 % and VF in 6.6 % and mean 25-OH Vit. D was 25.8. Patients chose HiROC 42.6 %, 37 % HiROC patients were lost to followup, and 6 month mortality was 16 %. GHP insured 27.4 % and within GHP-insured patients, HiROC treated 74.7 % versus 19.7 % by Geisinger PCP. In 2016, we reported 380 patients, mean age 78, 69 % women, 31 % men. Hip fractures accounted for 74.5 %, VF 6.6 %, with mean 25-OH Vit.D 25.8 and 17 % six month mortality. Patients chose HiROC 46 % of time.
2017-2018 analysis included 740 patients, mean age 78, with 89 % women and 11 % men. Hip fractures accounted for 78 % and VF 6.6 %. HiROC was chosen by 45 % patients and 6-month mortality was 14 %.
Conclusions: Geisinger HiROC treated high-risk, post-fractured, drug indicated patients 72 – 80 % of time, far superior to Geisinger PCP rates of 13.8 – 32.2 %.
George A Karpouzas
Division of Rheumatology, Harbor-UCLA Medical Center and The Lundquist Institute, Torrance, CA, USA
Nicoletta Ronda
Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 43124 Parma, Italy
Matthew J Budoff
Division of Cardiology, Harbor-UCLA Medical Center and The Lundquist Institute, Torrance, CA, USA
Sarah R Ormseth
Division of Rheumatology, Harbor-UCLA Medical Center and The Lundquist Institute, Torrance, CA, USA
Abstract
Methods. Coronary artery calcium, number of coronary plaques, and extensive ( 5 plaques) or obstructive (>50% stenosis) disease was evaluated with computed tomography angiography in 150 patients at baseline and 101 patients 6.9±0.4 years later. Cardiovascular events were recorded. Oxidized LDL was measured with monoclonal antibody E06. Serum cholesterol loading capacity on macrophages was measured as intracellular cholesterol content with a fluorometric assay.
Results. Abdominal obesity was not associated with per-patient number of coronary plaques or coronary artery calcium score at baseline. Low LDLc positively associated with number of plaques (b 2.13 [95% confidence interval 1.03 to 3.22]), likelihood of extensive or obstructive plaque (odds ratio 6.58, 95% confidence interval [1.63 to 26.46]), and log-transformed CAC (b 1.90 [0.89 to 2.91]) exclusively in nonobese patients (p-for-interaction <0.001, 0.061, and 0.001 respectively). Low LDLc associated with increased likelihood of >median oxidized LDL and higher ratio of cholesterol loading capacity to LDLc in nonobese patients (p-for-interaction 0.041 and 0.001 respectively). Abdominal obesity negatively associated with likelihood of plaque stenosis progression (odds ratio 0.19 [0.07 to 0.54]). Low LDLc associated with greater likelihood of per-segment plaque formation (OR 4.68 [2.26 to 9.66]) and increased stenotic severity (odds ratio 5.35 [1.62 to 17.67]) only in nonobese patients (p-for-interaction 0.002 and 0.040 respectively). Abdominal obesity was not linked to cardiovascular risk (Hazard Ratio 1.57, 95% confidence interval [0.66-3.73]). Low LDLc associated with higher cardiovascular risk in nonobese (Hazard Ratio 7.94 [1.52 to 41.36]) but not obese patients (p-for-interaction=0.017).
Conclusion. Abdominal obesity was not linked to plaque progression or cardiovascular risk in RA. Only in nonobese patients, low LDLc associated with higher atherosclerosis burden, plaque progression and cardiovascular risk. This may reflect higher oxidation and macrophage cholesterol loading capacity of LDL when LDLc is <70mg/dl.
