The biomechanical fingerprint of hip and knee osteoarthritis patients during activities of daily living

Background: Osteoarthritis is a highly prevalent disease affecting the hip and knee joint and is characterized by load-mediated pain and decreased quality of life. Dependent on involved joint, patients present antalgic movement compensations, aiming to decrease loading on the involved joint. However, the associated alterations in mechanical loading of the ipsi- and contra-lateral lower limb joints, are less documented. Here, we documented the biomechanical fingerprint of end-stage hip and knee osteoarthritis patients in terms of ipsilateral and contralateral hip and knee loading during walking and stair ambulation. Methods: Three-dimensional motion-analysis was performed in 20 hip, 18 knee osteoarthritis patients and 12 controls during level walking and stair ambulation. Joint contact forces were calculated using a standard musculoskeletal modelling workflow in Opensim. Involved and contralateral hip and knee joint loading was compared against healthy controls using independent t-tests (p &lt; 0.05). Findings: Both hip and knee cohorts significantly decreased loading of the involved joint during gait and stair ambulation. Hip osteoarthritis patients presented no signs of ipsilateral knee nor contralateral leg overloading, during walking and stair ascending. However, knee osteoarthritis patients significantly increased loading at the ipsilateral hip, and contralateral hip and knee joints during stair ambulation compared to controls. Interpretation: The biomechanical fingerprint in knee and hip osteoarthritis patients confirmed antalgic movement strategies to unload the involved leg during gait. Only during stair ambulation in knee osteoarthritis patients, movement adaptations were confirmed that induced unbalanced intra- and inter-limb loading conditions, which are known risk factors for secondary osteoarthritis.</p

The biomechanical fingerprint of hip and knee osteoarthritis patients during activities of daily living

Background: Osteoarthritis is a highly prevalent disease affecting the hip and knee joint and is characterized by load-mediated pain and decreased quality of life. Dependent on involved joint, patients present antalgic movement compensations, aiming to decrease loading on the involved joint. However, the associated alterations in mechanical loading of the ipsi- and contra-lateral lower limb joints, are less documented. Here, we documented the biomechanical fingerprint of end-stage hip and knee osteoarthritis patients in terms of ipsilateral and contralateral hip and knee loading during walking and stair ambulation. Methods: Three-dimensional motion-analysis was performed in 20 hip, 18 knee osteoarthritis patients and 12 controls during level walking and stair ambulation. Joint contact forces were calculated using a standard musculoskeletal modelling workflow in Opensim. Involved and contralateral hip and knee joint loading was compared against healthy controls using independent t-tests (p &lt; 0.05). Findings: Both hip and knee cohorts significantly decreased loading of the involved joint during gait and stair ambulation. Hip osteoarthritis patients presented no signs of ipsilateral knee nor contralateral leg overloading, during walking and stair ascending. However, knee osteoarthritis patients significantly increased loading at the ipsilateral hip, and contralateral hip and knee joints during stair ambulation compared to controls. Interpretation: The biomechanical fingerprint in knee and hip osteoarthritis patients confirmed antalgic movement strategies to unload the involved leg during gait. Only during stair ambulation in knee osteoarthritis patients, movement adaptations were confirmed that induced unbalanced intra- and inter-limb loading conditions, which are known risk factors for secondary osteoarthritis.</p

Gender differences in the use of cardiovascular interventions in HIV-positive persons; the D:A:D Study

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Development and Validation of a Risk Score for Chronic Kidney Disease in HIV Infection Using Prospective Cohort Data from the D:A:D Study

Ristola M. on työryhmien DAD Study Grp ; Royal Free Hosp Clin Cohort ; INSIGHT Study Grp ; SMART Study Grp ; ESPRIT Study Grp jäsen.Background Chronic kidney disease (CKD) is a major health issue for HIV-positive individuals, associated with increased morbidity and mortality. Development and implementation of a risk score model for CKD would allow comparison of the risks and benefits of adding potentially nephrotoxic antiretrovirals to a treatment regimen and would identify those at greatest risk of CKD. The aims of this study were to develop a simple, externally validated, and widely applicable long-term risk score model for CKD in HIV-positive individuals that can guide decision making in clinical practice. Methods and Findings A total of 17,954 HIV-positive individuals from the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study with >= 3 estimated glomerular filtration rate (eGFR) values after 1 January 2004 were included. Baseline was defined as the first eGFR > 60 ml/min/1.73 m2 after 1 January 2004; individuals with exposure to tenofovir, atazanavir, atazanavir/ritonavir, lopinavir/ritonavir, other boosted protease inhibitors before baseline were excluded. CKD was defined as confirmed (>3 mo apart) eGFR In the D:A:D study, 641 individuals developed CKD during 103,185 person-years of follow-up (PYFU; incidence 6.2/1,000 PYFU, 95% CI 5.7-6.7; median follow-up 6.1 y, range 0.3-9.1 y). Older age, intravenous drug use, hepatitis C coinfection, lower baseline eGFR, female gender, lower CD4 count nadir, hypertension, diabetes, and cardiovascular disease (CVD) predicted CKD. The adjusted incidence rate ratios of these nine categorical variables were scaled and summed to create the risk score. The median risk score at baseline was -2 (interquartile range -4 to 2). There was a 1: 393 chance of developing CKD in the next 5 y in the low risk group (risk score = 5, 505 events), respectively. Number needed to harm (NNTH) at 5 y when starting unboosted atazanavir or lopinavir/ritonavir among those with a low risk score was 1,702 (95% CI 1,166-3,367); NNTH was 202 (95% CI 159-278) and 21 (95% CI 19-23), respectively, for those with a medium and high risk score. NNTH was 739 (95% CI 506-1462), 88 (95% CI 69-121), and 9 (95% CI 8-10) for those with a low, medium, and high risk score, respectively, starting tenofovir, atazanavir/ritonavir, or another boosted protease inhibitor. The Royal Free Hospital Clinic Cohort included 2,548 individuals, of whom 94 individuals developed CKD (3.7%) during 18,376 PYFU (median follow-up 7.4 y, range 0.3-12.7 y). Of 2,013 individuals included from the SMART/ESPRIT control arms, 32 individuals developed CKD (1.6%) during 8,452 PYFU (median follow-up 4.1 y, range 0.6-8.1 y). External validation showed that the risk score predicted well in these cohorts. Limitations of this study included limited data on race and no information on proteinuria. Conclusions Both traditional and HIV-related risk factors were predictive of CKD. These factors were used to develop a risk score for CKD in HIV infection, externally validated, that has direct clinical relevance for patients and clinicians to weigh the benefits of certain antiretrovirals against the risk of CKD and to identify those at greatest risk of CKD.Peer reviewe