Maryam Zulfiqar1, Fares Qeadan2, Asad Ikram1, Mudassir Farooqui3, Sarah P Richardson1, Christopher S Calder1, Syed A Quadri4, Puja Mathur1, Corey Ford1, Santiago O Gutierrez5, Enrique Liera5, Harry Snow2, Joel N Gonzalez1, Atif Zafar6. 1. Department of Neurology, University of New Mexico, Albuquerque, New Mexico. 2. Clinical and Translational Science Center, University of New Mexico, Albuquerque, New Mexico. 3. Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma. 4. Department of Neurosurgery, California Institute of Neurosciences, Thousand Oaks, California. 5. Department of Neurology, University of Iowa Hospitals and Clinic, Iowa City, Iowa. 6. Department of Neurology, University of New Mexico, Albuquerque, New Mexico. Electronic address: azafar@salud.unm.edu.
Abstract
BACKGROUND: To identify the vascular risk factors associated with the occurrence of intracerebral hemorrhage (ICH) in Multiple Sclerosis (MS) patients. METHODS: This is an observational, retrospective cohort study using the nationwide electronic medical records (EMR) database. Patients with the diagnosis of MS were extracted from inpatient and outpatient EMR using the international classification of diseases, ninth/tenth revisions, clinical modification codes. We excluded patients younger than 18 years, and those where gender was not specified. Patients were further stratified based on their demographics, risk factors, medications, and comorbidities. Tobacco, diabetes, hypertension, and alcohol were the predicting variables; antiplatelet medication, and anticoagulant agents were the primary exposures for the development of ICH. A validated diagnosis code algorithm defined the diagnosis of ICH. Multivariable logistic regression models were utilized to assess the risk of ICH in MS patients. RESULTS: Of the total 57,099 MS patients (women: 75%, n = 41,517), 107 (.19%) sustained an ICH. Age (OR = 2.74, CI = 1.13-6.62), use of anticoagulants (OR = 2.15, 95% CI = 1.30-3.56, P = .0028), and history of tobacco exposure (OR = 2.44, CI = 1.37-4.36, P = .0025) were associated with increased risk of ICH. Use of antiplatelet and disease-modifying drugs (DMDs) showed a protective trend against ICH. CONCLUSIONS: Tobacco exposure and anticoagulant use were strongly associated with increased risk of ICH in patients with MS. There might be a protective effect that antiplatelet and DMDs have in the pathophysiology of this disease. Further prospective investigations are warranted to establish these associations.
BACKGROUND: To identify the vascular risk factors associated with the occurrence of intracerebral hemorrhage (ICH) in Multiple Sclerosis (MS) patients. METHODS: This is an observational, retrospective cohort study using the nationwide electronic medical records (EMR) database. Patients with the diagnosis of MS were extracted from inpatient and outpatient EMR using the international classification of diseases, ninth/tenth revisions, clinical modification codes. We excluded patients younger than 18 years, and those where gender was not specified. Patients were further stratified based on their demographics, risk factors, medications, and comorbidities. Tobacco, diabetes, hypertension, and alcohol were the predicting variables; antiplatelet medication, and anticoagulant agents were the primary exposures for the development of ICH. A validated diagnosis code algorithm defined the diagnosis of ICH. Multivariable logistic regression models were utilized to assess the risk of ICH in MSpatients. RESULTS: Of the total 57,099 MSpatients (women: 75%, n = 41,517), 107 (.19%) sustained an ICH. Age (OR = 2.74, CI = 1.13-6.62), use of anticoagulants (OR = 2.15, 95% CI = 1.30-3.56, P = .0028), and history of tobacco exposure (OR = 2.44, CI = 1.37-4.36, P = .0025) were associated with increased risk of ICH. Use of antiplatelet and disease-modifying drugs (DMDs) showed a protective trend against ICH. CONCLUSIONS:Tobacco exposure and anticoagulant use were strongly associated with increased risk of ICH in patients with MS. There might be a protective effect that antiplatelet and DMDs have in the pathophysiology of this disease. Further prospective investigations are warranted to establish these associations.