scholarly journals Chronic Neck Pain and Whiplash: A Case-Control Study of the Relationship between Acute Whiplash Injuries and Chronic Neck Pain

2006 ◽  
Vol 11 (2) ◽  
pp. 79-83 ◽  
Author(s):  
Michael D Freeman ◽  
Arthur C Croft ◽  
Annette M Rossignol ◽  
Christopher J Centeno ◽  
Whitney L Elkins

The authors undertook a case-control study of chronic neck pain and whiplash injuries in nine states in the United States to determine whether whiplash injuries contributed significantly to the population of individuals with chronic neck and other spine pain.Four hundred nineteen patients and 246 controls were randomly enrolled. Patients were defined as individuals with chronic neck pain, and controls as those with chronic back pain. The two groups were surveyed for cause of chronic pain as well as demographic information. The two groups were compared using an exposure-odds ratio. Forty-five per cent of the patients attributed their pain to a motor vehicle accident. An OR of 4.0 and 2.1 was calculated for men and women, respectively.Based on the results of the present study, it reasonable to infer that a significant proportion of individuals with chronic neck pain in the general population were originally injured in a motor vehicle accident.

2014 ◽  
Vol 1 (4) ◽  
pp. 360-366 ◽  
Author(s):  
Jing-Yuan Wang ◽  
Hong Guo ◽  
Ling Tang ◽  
Jing Meng ◽  
Li-yun Hu

2018 ◽  
Vol 18 (8) ◽  
pp. 1406-1416 ◽  
Author(s):  
Robby De Pauw ◽  
Iris Coppieters ◽  
Tanneke Palmans ◽  
Lieven Danneels ◽  
Mira Meeus ◽  
...  

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Rachael Stovall ◽  
Christine Peloquin ◽  
David Felson ◽  
Tuhina Neogi ◽  
Maureen Dubreuil

Abstract Background Risk of myocardial infarction (MI) is elevated in ankylosing spondylitis and psoriatic arthritis (AS/PsA) compared to the general population. We evaluated the risk of MI related to the use of tumor necrosis factor inhibitor (TNFi) and other therapies in AS/PsA. Methods We conducted a nested case-control study using 1994–2018 data from OptumLabs® Data Warehouse, which includes de-identified medical and pharmacy claims, laboratory results, and enrollment records for commercial and Medicare Advantage enrollees. The database contains longitudinal health information on enrollees and patients, representing a diverse mixture of ages, ethnicities and geographical regions across the United States. Assessing AS/PsA separately, MI cases were matched to 4 controls by sex, age, diagnosis year and insurance type. We evaluated treatment within 6 months prior to MI including NSAIDs (AS referent), disease-modifying anti-rheumatic drug (DMARDs; PsA referent) and TNFi alone or in combinations. We evaluated the relation of treatment categories to MI risk using conditional logistical regression adjusting for confounders. Results Among 26,648 AS subjects, there were 237 MI cases and 894 matched controls. Among 43,734 PsA subjects, there were 404 cases and 1596 controls. In AS, relative to NSAID use, the adjusted odds ratio (aOR) for MI among TNFi only users was 0.85 (95% CI 0.39–1.85) and for DMARD only users was 1.04 (95% CI 0.65–1.68). In PsA, relative to DMARD use, the aOR among TNFi only was 1.09 (95% CI 0.74–1.60). Combination therapies also had no effect. Conclusions Among AS/PsA, no combination of therapies appeared to be protective or harmful with regards to MI. Future studies should capture more AS and PsA patients and include longer term follow up to further investigate this question.


2018 ◽  
Vol 36 (28) ◽  
pp. 2887-2894 ◽  
Author(s):  
Linda D. Mellby ◽  
Andreas P. Nyberg ◽  
Julia S. Johansen ◽  
Christer Wingren ◽  
Børge G. Nordestgaard ◽  
...  

Purpose Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, with a 5-year survival of < 10% because of diffuse symptoms leading to late-stage diagnosis. That survival could increase significantly if localized tumors could be detected early. Therefore, we used multiparametric analysis of blood samples to obtain a novel biomarker signature of early-stage PDAC. The signature was derived from a large patient cohort, including patients with well-defined early-stage (I and II) PDAC. This biomarker signature was validated subsequently in an independent patient cohort. Patients and Methods The biomarker signature was derived from a case-control study, using a Scandinavian cohort, consisting of 16 patients with stage I, 132 patients with stage II, 65 patients with stage III, and 230 patients with stage IV PDAC, and 888 controls. This signature was validated subsequently in an independent case-control cohort in the United States with 15 patients with stage I, 75 patients with stage II, 15 patients with stage III, and 38 patients with stage IV PDAC, and 219 controls. An antibody microarray platform was used to identify the serum biomarker signature associated with early-stage PDAC. Results Using the Scandinavian case-control study, a biomarker signature was created, discriminating samples derived from patients with stage I and II from those from controls with a receiver operating characteristic area under the curve value of 0.96. This signature, consisting of 29 biomarkers, was then validated in an independent case-control study in the United States. The biomarker signature could discriminate patients with stage I and II PDAC from controls in this independent patient cohort with a receiver operating characteristic area under the curve value of 0.96. Conclusion This serum biomarker signature might represent a tenable approach to detecting early-stage, localized PDAC if these findings are supported by a prospective validation study.


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