142 research outputs found
Effect of the direct oral anticoagulants rivaroxaban and apixaban on the disposition of calcineurin inhibitors in transplant recipients
No full textCalcineurin inhibitors (CNIs) and direct oral anticoagulants (DOACs) share certain metabolic pathways, but whether DOACs influence CNI exposure has not been assessed.sponsorship: D. Kuypers and J. Maertens have served as consultants to Astellas Pharma and have been on the speaker's bureau for Astellas Pharma. D. Kuypers, J. Maertens, and J. Van Cleemput have received research funding from Astellas Pharma. The remaining authors declare no conflict of interest. (Astellas Pharma)status: Publishe
Apical papillary muscle displacement is a prevalent feature and a phenotypic precursor of apical hypertrophic cardiomyopathy
No full textAIMS: Papillary muscle (PM) abnormalities are considered part of the phenotypic spectrum of hypertrophic cardiomyopathy (HCM). The aim of this study was to evaluate the presence and frequency of PM displacement in different HCM phenotypes. METHODS AND RESULTS: We retrospectively analysed cardiovascular magnetic resonance (CMR) findings in 156 patients (25% females, median age 57 years). Patients were divided into three groups: septal hypertrophy (Sep-HCM, n = 70, 45%), mixed hypertrophy (Mixed-HCM, n = 48, 31%), and apical hypertrophy (Ap-HCM, n = 38, 24%). Fifty-five healthy subjects were enrolled as controls. Apical PM displacement was observed in 13% of controls and 55% of patients, which was most common in the Ap-HCM group, followed by the Mixed-HCM and Sep-HCM groups (respectively: inferomedial PM 92 vs. 65 vs. 13%, P < 0.001; anterolateral PM 61 vs. 40 vs. 9%, P < 0.001). Significant differences in PM displacement were found when comparing healthy controls with patients with Ap- and Mixed-HCM subtypes but not when comparing them with patients with the Sep-HCM subtype. T-wave inversion in the inferior and lateral leads was more frequent in patients with Ap-HCM (100 and 65%, respectively) when compared with Mixed-HCM (89 and 29%, respectively) and Sep-HCM (57 and 17%, respectively; P < 0.001 for both). Eight patients with Ap-HCM had prior CMR examinations because of T-wave inversion [median interval 7 (3-8) years], and in the first CMR study, none showed apical hypertrophy [median apical wall thickness 8 (7-9) mm], while all of them presented with apical PM displacement. CONCLUSION: Apical PM displacement is part of the phenotypic Ap-HCM spectrum and may precede the development of hypertrophy. These observations suggest a potential pathogenetic, mechanical link between apical PM displacement and Ap-HCM.status: Publishe
Ontwikkeling van predictiemodellen voor allogreffevasculopathie in patiënten met een ruilhart
No full textSUMMARY
Cardiac allograft vasculopathy (CAV) is a limiting factor for the long-term survival of heart transplant recipients1,2. CAV is characterized by the development of diffuse concentric fibromuscular intimal hyperplasia in epicardial and smaller intramyocardial arteries along with focal, eccentric atherosclerotic plaques in the larger epicardial arteries3,4. The development of these lesions may lead to the progressive narrowing of the lumen5. According to the response to injury hypothesis of CAV, these lesions are the result of cumulative endothelial injury induced by alloimmune responses as well as non-immunological risk factors such as ischemia-reperfusion injury, viral infections, and metabolic disorders3,6.
Early diagnosis of CAV is essential to implement appropriate prevention and treatment measures. Clinical prediction models of CAV are currently not available and may be useful for non-invasive diagnostic and prognostic purposes. The general aim of this doctoral thesis is to develop diagnostic prediction models for prevalent CAV. The specific central hypothesis of this doctoral thesis is that biomarkers of endothelial homeostasis discriminate between CAV-negative and CAV-positive heart transplant recipients.
Endothelial homeostasis reflects the balance between endothelial injury and endothelial repair. In chapter 1, we investigated whether biomarkers related to endothelial injury and endothelial repair discriminate between CAV-negative and CAV-positive heart transplant recipients. Fifty-two patients undergoing coronary angiography between 5 and 15 years after heart transplantation were recruited in this study. Flow cytometry was applied to quantify endothelial progenitor cells (EPCs), circulating endothelial cells (CECs), and circulating endothelial microparticles (CEMPs). Cell culture was used for quantification of circulating EPC number and hematopoietic progenitor cell (HPC) number and for analysis of EPC function. EPC number and EPC function did not differ between CAV-negative and CAV-positive patients. In univariable models, age, creatinine, steroid dose, granulocyte colony-forming units, apoptotic CECs, and apoptotic CEMPs discriminated between CAV-positive and CAV-negative patients. The logistic regression model containing apoptotic CECs and apoptotic CEMPs as independent predictors provided high discrimination between CAV- positive and CAV-negative patients (c-statistic 0.812; 95% CI 0.692-0.932). In a logistic regression model with age and creatinine as covariates, apoptotic CECs (p=0.0112) and apoptotic CEMPs (p=0.0141) were independent predictors (c-statistic 0.855; 95% CI 0.756-0.953). These two biomarkers remained independent predictors when steroid dose was introduced in the model. Taken together, the high discriminative ability of apoptotic CECs and apoptotic CEMPs is a solid foundation for the development of clinical prediction models of CAV.
In chapter 2, patients with stable native coronary artery disease (CAD) were compared with heart transplant recipients with CAV. After all, CAV is a particular type of arteriosclerosis with many similarities but also significant differences compared to native CAD. Atherosclerosis in patients with stable native CAD is characterized by the presence of atheromata that contain a lipid core filled with extracellular cholesterol and cellular debris and are covered by a fibrous cap. In contrast, fibromuscular intimal hyperplasia is the most prominent lesion type of CAV and mainly consists of smooth muscle cells and extracellular matrix7. Endothelial injury is assumed to play a key role in the initiation and progression of both native CAD and CAV2,8. In the response-to-injury hypothesis of atherosclerosis of Ross and Glomset, endothelial injury was originally defined as endothelial denudation resulting from focal desquamation of endothelium9,10. Later versions of the response-to-injury hypothesis emphasized endothelial dysfunction rather than denudation8,11. Cellular biomarkers of endothelial injury (CEMPs and CECs) may discriminate between endothelial activation and irreversible endothelial damage. The hypothesis that endothelial injury and circulating platelet microparticles (CPMPs) are distinct in both types of arteriosclerosis was investigated.
The geometric mean of the concentration of CECs (CD45- CD31bright VEGFR-2+) was 2.90-fold (p<0.001) and 2.34-fold (p<0.05) higher in patients with stable native CAD (n=80) and with CAV (n=30), respectively, compared to healthy controls (n=25). No significant difference in total, Annexin V negative, and Annexin V positive (apoptotic) CECs was observed between patients with native CAD and with CAV. The concentration of Annexin V negative CEMPs (CD144+ CD42a-) was 59.2% (p<0.01) higher in transplant recipients with CAV than in native CAD patients but no difference in Annexin V positive CEMPs was observed. The median value of total CD61+ CPMPs in native CAD patients was 69.4% (p<0.001) and 71.6% (p<0.001) lower compared to healthy controls and transplant recipients with CAV, respectively. These differences were even more pronounced when CD42a+CD31+ CPMPs were quantified. In conclusion, the selective increase of Annexin V negative CEMPs and the absence of a difference in Annexin V positive CECs strongly suggest increased endothelial activation but not endothelial apoptosis in CAV-positive patients compared to stable CAD patients. Use of antiplatelet drugs likely underlies the strikingly lower levels of CPMPs in patients with native CAD.
In chapter 3, the relation between high density lipoproteins (HDL) and CAV was investigated. The prevalence and the incidence of CAV have been reported to be increased in heart transplant recipients with decreased high density lipoprotein (HDL) cholesterol levels12-15. The association between HDL cholesterol and CAV may reflect causation but might also be due to residual confounding. One such confounding factor is insulin resistance, which is considered to play a role in the pathogenesis of CAV. A triglyceride/HDL cholesterol ratio of greater than 3 has been recognized as a marker of insulin resistance in overweight subjects16 and constituted a risk factor for CAV and major adverse cardiac events in heart transplant recipients17,18.
Remodelling of HDL in heart transplant recipients is significantly affected by a lower activity of cholesterol ester transfer protein, phospholipid transfer protein, and hepatic lipase19,20. Consequently, these patients are characterized by an increased proportion of large HDL particles and reduced pre-ß1-HDL in the presence of normal or even elevated HDL cholesterol levels19,20. These alterations may be partially explained by corticosteroid use21 but may also be potentiated by statin intake22. The modified HDL metabolism and associated compositional changes of HDL particles may lead to an impaired function of these lipoproteins. Reduced HDL function may also occur as a result of ongoing inflammation23.
We hypothesized that HDL function may be impaired in these patients and may discriminate between CAV-positive and CAV-negative patients. Cholesterol efflux capacity of apolipoprotein B-depleted plasma was analysed using a validated assay24. The vasculoprotective function of HDL was studied by means of an EPC migration assay. HDL cholesterol levels were similar in heart transplant patients compared to healthy controls. However, normalized cholesterol efflux and vasculoprotective function were reduced by 24.1% (p<0.001) and by 27.0% (p<0.01), respectively, in heart transplant recipients compared to healthy controls. HDL function was similar in patients with and without cardiac allograft vasculopathy (CAV) and was not related to C-reactive protein (CRP) levels. An interaction effect (p=0.0584) was observed between etiology of heart failure before transplantation and steroid use as factors of HDL cholesterol levels. Lower HDL cholesterol levels occurred in patients with prior ischemic cardiomyopathy not taking steroids. However, HDL function was independent of the etiology of heart failure before transplantation and steroid use. The median C-reactive protein (CRP) level was 2.24-fold (p=0.082) higher in patients with CAV than in patients without CAV. In conclusion, HDL function is impaired in heart transplant recipients but is unrelated to CAV-status.
In chapter 4, the potential of endothelium-enriched microRNAs (miRNAs) as putative biomarkers for the prediction of CAV was investigated. MiRNAs are small, non-coding, single-stranded RNA sequences that regulate gene expression at the post-transcriptional level. Because miRNAs circulate in remarkably stable forms in blood25,26, they have a significant potential as biomarkers. Several reports indicate that miRNAs may play a role in endothelial homeostasis27,28. In this study, a candidate-based approach using circulating levels of endothelium-enriched miRNAs (miR-21-5p, miR-92a-3p, miR-92a-1-5p, miR-126-3p, miR-126-5p) to predict CAV was evaluated. Circulating levels of endothelium-enriched miRNAs (miR-21-5p, miR-92a-3p, miR-92a-1-5p, miR-126-3p, miR-126-5p) were quantified by real-time RT-PCR. The discriminative ability of logistic regression models was quantified using the concordance statistic (c-statistic). Plasma levels of miR-21-5p, miR-92a-3p, miR-126-3p, and miR-126-5p were 1.86-fold (p=NS), 1.91-fold (p<0.05), 1.74-fold (p=0.074), and 1.73-fold (p=0.060) higher, in patients with CAV than in patients without CAV. Recipient age (c-statistic 0.689 (95% CI 0.537-0.842)), serum creatinine (c-statistic 0.703 (95% CI 0.552-0.854)), levels of miR-92a-3p (c-statistic 0.682 (95% CI 0.533-0.831)), and levels of miR-126-5p (c-statistic 0.655 (95% CI 0.502-0.807)) predicted CAV-status in univariable models. In a multivariable logistic regression model with recipient age and creatinine as covariates, miR-126-5p (chi-square=4.374; df=1; p=0.0365), miR-92a-3p (chi-square=6.007; df=1; p=0.0143), and the combination of miR-126-5p and miR-92a-3p (chi square=8.162; df=2; p=0.0169) added significant information. The model with age, creatinine, miR-126-5p and miR-92a-3p as covariables conferred good discrimination between patients without CAV and patients with CAV (c-statistic 0.800 (95% CI 0.674-0.926)). In addition, miR-92a-3p (chi-square=5.454; df=1; p=0.0195) and not miR-126-5p (chi-square=2.037; df=1; p=0.1535) added value in a model with apoptotic CECs and apoptotic CEMPs as predictors (c- statistic0.847 (95% CI 0.740-0.954)). In conclusion, endothelium-enriched miRNAs have predictive ability for CAV beyond clinical predictors.
The central hypothesis at the start of this doctoral thesis was that biomarkers of endothelial homeostasis discriminate between CAV-negative and CAV-positive heart transplant recipients. The validity of this hypothesis has been convincingly demonstrated. The refinement and validation of these models in a larger follow-up study may lead to a clinically useful model that can be applied for monitoring heart transplant recipients.
REFERENCES
1. Stehlik, J., Edwards, L.B., Kucheryavaya, A.Y., Benden, C., Christie, J.D., Dobbels, F., Kirk, R., Rahmel, A.O. ,Hertz, M.I. The Registry of the International Society for Heart and Lung Transplantation: Twenty-eighth Adult Heart Transplant Report--2011. J Heart Lung Transplant 30, 1078-1094 (2011).
2. Schmauss, D. ,Weis, M. Cardiac allograft vasculopathy: recent developments. Circulation 117, 2131-2141 (2008).
3. Vassalli, G., Gallino, A., Weis, M., von Scheidt, W., Kappenberger, L., von Segesser, L.K. ,Goy, J.J. Alloimmunity and nonimmunologic risk factors in cardiac allograft vasculopathy. Eur Heart J 24, 1180-1188 (2003).
4. Rahmani, M., Cruz, R.P., Granville, D.J. ,McManus, B.M. Allograft vasculopathy versus atherosclerosis. Circ Res 99, 801-815 (2006).
5. Kapadia, S.R., Nissen, S.E. ,Tuzcu, E.M. Impact of intravascular ultrasound in understanding transplant coronary artery disease. Curr Opin Cardiol 14, 140-150 (1999).
6. Ross, R. The pathogenesis of atherosclerosis--an update. N Engl J Med 314, 488-500 (1986).
7. Lu, W.H., Palatnik, K., Fishbein, G.A., Lai, C., Levi, D.S., Perens, G., Alejos, J., Kobashigawa, J. ,Fishbein, M.C. Diverse morphologic manifestations of cardiac allograft vasculopathy: a pathologic study of 64 allograft hearts. J Heart Lung Transplant 30, 1044-1050 (2011).
8. Ross, R. Atherosclerosis--an inflammatory disease. N Engl J Med 340, 115-126. (1999).
9. Ross, R. ,Glomset, J.A. Atherosclerosis and the arterial smooth muscle cell: Proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis. Science 180, 1332-1339 (1973).
10. Ross, R. ,Glomset, J.A. The pathogenesis of atherosclerosis (first of two parts). N Engl J Med 295, 369-377 (1976).
11. Ross, R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 362, 801-809. (1993).
12. Parameshwar, J., Foote, J., Sharples, L., Wallwork, J., Large, S. ,Schofield, P. Lipids, lipoprotein (a) and coronary artery disease in patients following cardiac transplantation. Transpl Int 9, 481-485 (1996).
13. Valantine, H., Rickenbacker, P., Kemna, M., Hunt, S., Chen, Y.D., Reaven, G. ,Stinson, E.B. Metabolic abnormalities characteristic of dysmetabolic syndrome predict the development of transplant coronary artery disease: a prospective study. Circulation 103, 2144-2152 (2001).
14. Cooke, G.E., Eaton, G.M., Whitby, G., Kennedy, R.A., Binkley, P.F., Moeschberger, M.L. ,Leier, C.V. Plasma atherogenic markers in congestive heart failure and posttransplant (heart) patients. J Am Coll Cardiol 36, 509-516 (2000).
15. Sanchez-Gomez, J.M., Martinez-Dolz, L., Sanchez-Lazaro, I., Almenar, L., Sanchez-Lacuesta, E., Munoz-Giner, B., Portoles, M., Rivera, M., Valera-Roman, A., Gonzalez-Juanatey, J.R., Tejada-Ponce, D., Aguero, J., Buendia, F. ,Salvador, A. Influence of metabolic syndrome on development of cardiac allograft vasculopathy in the transplanted heart. Transplantation 93, 106-111 (2012).
16. McLaughlin, T., Abbasi, F., Cheal, K., Chu, J., Lamendola, C. ,Reaven, G. Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med 139, 802-809 (2003).
17. Biadi, O., Potena, L., Fearon, W.F., Luikart, H.I., Yeung, A., Ferrara, R., Hunt, S.A., Mocarski, E.S. ,Valantine, H.A. Interplay between systemic inflammation and markers of insulin resistance in cardiovascular prognosis after heart transplantation. J Heart Lung Transplant 26, 324-330 (2007).
18. Raichlin, E.R., McConnell, J.P., Lerman, A., Kremers, W.K., Edwards, B.S., Kushwaha, S.S., Clavell, A.L., Rodeheffer, R.J. ,Frantz, R.P. Systemic inflammation and metabolic syndrome in cardiac allograft vasculopathy. J Heart Lung Transplant 26, 826-833 (2007).
19. Atger, V., Leclerc, T., Cambillau, M., Guillemain, R., Marti, C., Moatti, N. ,Girard, A. Elevated high density lipoprotein concentrations in heart transplant recipients are related to impaired plasma cholesteryl ester transfer and hepatic lipase activity. Atherosclerosis 103, 29-41 (1993).
20. Sviridov, D., Chin-Dusting, J., Nestel, P., Kingwell, B., Hoang, A., Olchawa, B., Starr, J. ,Dart, A. Elevated HDL cholesterol is functionally ineffective in cardiac transplant recipients: evidence for impaired reverse cholesterol transport. Transplantation 81, 361-366 (2006).
21. Stamler, J.S., Vaughan, D.E. ,Loscalzo, J. Immunosuppressive therapy and lipoprotein abnormalities after cardiac transplantation. Am J Cardiol 68, 389-391 (1991).
22. Yamashita, S., Tsubakio-Yamamoto, K., Ohama, T., Nakagawa-Toyama, Y. ,Nishida, M. Molecular mechanisms of HDL-cholesterol elevation by statins and its effects on HDL functions. J Atheroscler Thromb 17, 436-451 (2010).
23. Fisher, E.A., Feig, J.E., Hewing, B., Hazen, S.L. ,Smith, J.D. High-density lipoprotein function, dysfunction, and reverse cholesterol transport. Arterioscler Thromb Vasc Biol 32, 2813-2820 (2012).
24. Khera, A.V., Cuchel, M., de la Llera-Moya, M., Rodrigues, A., Burke, M.F., Jafri, K., French, B.C., Phillips, J.A., Mucksavage, M.L., Wilensky, R.L., Mohler, E.R., Rothblat, G.H. ,Rader, D.J. Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. N Engl J Med 364, 127-135 (2011).
25. Suarez, Y., Fernandez-Hernando, C., Yu, J., Gerber, S.A., Harrison, K.D., Pober, J.S., Iruela-Arispe, M.L., Merkenschlager, M. ,Sessa, W.C. Dicer-dependent endothelial microRNAs are necessary for postnatal angiogenesis. Proc Natl Acad Sci U S A 105, 14082-14087 (2008).
26. Kuehbacher, A., Urbich, C., Zeiher, A.M. ,Dimmeler, S. Role of Dicer and Drosha for endothelial microRNA expression and angiogenesis. Circ Res 101, 59-68 (2007).
27. Scott, E., Loya, K., Mountford, J., Milligan, G. ,Baker, A.H. MicroRNA regulation of endothelial homeostasis and commitment-implications for vascular regeneration strategies using stem cell therapies. Free Radic Biol Med 64, 52-60 (2013).
28. Yamakuchi, M. MicroRNAs in Vascular Biology. Int J Vasc Med 2012, 794898 (2012).status: Publishe
Late-onset visceral presentation with cardiomyopathy and without neurological symptoms of adult Sanfilippo A syndrome
No full textSanfilippo A syndrome, mucopolysaccharidosis type IIIA, is caused by a deficiency of heparan sulphamidase activity, and usually presents in childhood with neurodegeneration leading to death in teenage years. Visceral symptoms are limited to coarsening and diarrhea. We now describe an adult patient who presented with cardiomyopathy. At age 45 years she had hypertension, and the next year she developed a progressively worsening cardiomyopathy with prominent apical hypertrophy and atrial fibrillation. At age 53, she had severe concentric hypertrophic nonobstructive cardiomyopathy in both ventricles. There was no coarsening of features. Neurologic function, skeleton, cornea, liver, and spleen were normal. Percutaneous endomyocardial biopsy showed ballooned cardiomyocytes with storage vacuoles, containing acid mucopolysaccharides. Leucocytes, uterus, and brain biopsy did not show this storage material. There was a slight increase in total urine mucopolysaccharides, with an increased proportion of heparan sulfates. Heparan sulphamidase activity was deficient in leukocytes and heparan sulphamidase protein and activity were reduced in cultured fibroblasts. No mutations were identified after sequencing of the heparan sulphamidase gene at the cDNA and the genomic level. This new clinical presentation expands the clinical spectrum of Sanfilippo A syndrome to include a primary visceral presentation of cardiomyopathy without neurologic symptoms in the adult. The late onset may be related to the residual heparan sulphamidase activity. The genetic basis of this new variant is still unclear. Physicians evaluating adults must remain aware of possible new adult presentations of storage conditions.Van Hove, Johan L. K. ; Wevers, Ron A. ; Van Cleemput, Johan ; Moerman, Philippe ; Sciot, Raf ; Matthijs, Gert ; Schollen, Els ; De Jong, Jan G. N. ; Carey, William F. ; Muller, Viv ; Nicholls, Cath ; Perkins, Kelly ; Hopwood, John J
De electieve endovasculaire behandeling van het abdominale aorta aneurysma (AAA)
No full textxvii, 165 p.ill
Belgian population norms for the EQ-5D-5L, 2018
No full textPurpose. Health-related quality of life outcomes are increasingly used to monitor population health and health inequalities and to assess the (cost-) effectiveness of health interventions. The EQ-5D-5L has been included in the Belgian Health Interview Survey, providing a new source of population-based self-perceived health status information. This study aims to estimate Belgian population norms for the EQ-5D-5L by sex, age, and region and to analyze its association with educational attainment.
Methods. The BHIS 2018 provided EQ-5D-5L data for a nationally representative sample of the Belgian population. The dimension scores and index values were analyzed using logistic and linear regressions, respectively, accounting for the survey design.
Results. More than half of respondents reported problems of pain/discomfort, while over a quarter reported problems of anxiety/depression. The average index value was 0.84. Women reported more problems on all dimensions, but particularly on anxiety/depression and pain/discomfort, resulting in significantly lower index values. Problems with mobility, self-care, and usual activities showed a sharp increase after the age of 80 years. Consequently, index values decreased significantly by age. Lower education was associated with a higher prevalence of problems for all dimensions except anxiety/depression and with a significantly lower index value.
Conclusion. This paper presents the first nationally representative Belgian population norms using the EQ-5D-5L. Inclusion of the EQ-5D in future surveys will allow monitoring over time of self-reported health, disease burden, and health inequalities
The ‘Self’ as Barrier for Self-Management Technologies in Healthcare?
No full textSelf-management technologies are promising in healthcare. In the name of patient empowerment, they can address an important challenge: how to meet an increasing demand for care without additional resources. We designed and evaluated the PICASSO-Tx system: a technology solution to support transplant patients and their self-management of diet, physical activity and medication adherences. In a field study, 19 patients used the system for two weeks at home. We discovered that although we intended patients to become actors in the management of their own health, they saw themselves rather as a subject, leaving the active role for caregivers. In this paper, we describe how patients expected their data to be shared with others, how they perceived the system as a tool for monitoring by caregivers, and what expectations towards these caregivers this perception brings. Furthermore, we discuss the barriers we encountered caused by the ‘self’ and conclude with design recommendations for self-management technologies in healthcare related to these expectations, perceptions, and barriers.sponsorship: The research described is part of the PICASSO-Tx project, funded by Bijzonder Onderzoeksfonds KU Leuven (OT project OT13/101). We would like to thank Sabina De Geest, Thierry Troosters, Patrick De Maziere, Pieter Philippaerts, Dirk Kuypers, Frederik Nevens, Johan Vanhaecke, Geert Verleden, Lieven Dupont, Diethard Monbaliu, Jacques Pirenne, Dirk Van Raemdonck, Johan Van Cleemput, Robin Vos, Annette De Vito Dabbs, John Hughes, and Bernard Vrijens. (Bijzonder Onderzoeksfonds KU Leuven (OT project)|OT13/101)status: Publishe
Assessing cancer patients’ quality of life and supportive care needs: Translation-revalidation of the CARES in Flemish and exhaustive evaluation of concurrent validity
No full textThe prevalence of cancer increases every year, leading to a growing population of patients and survivors in need for care. To achieve good quality care, a patient-centered approach is essential. Correct and timely detection of needs throughout the different stages of the care trajectory is crucial and can be supported by the use of screening and assessment in a stepped-care approach. The Cancer Rehabilitation Evaluation System (CARES) is a valuable and comprehensive quality of life and needs assessment instrument. For use in Flemish research and clinical practice, the CARES tool was translated for the Dutch-speaking part of Belgium (Flanders) from its original English format. This protocol paper describes the translation and revalidation of this Flemish CARES version.After forward-backward translation of the CARES into Flemish we aim to recruit 150 adult cancer patients with a primary cancer diagnosis (stage I, II or III) for validation. In this study with a combination of qualitative and a quantitative approach, qualitative data will be collected through focus groups and supplemented by two phases of quantitative data collection: i) an initial patient survey containing questions on socio-demographic and medical data, the CARES and seven concurrent instruments; and ii) a second survey administered after 1 week containing the CARES and supplementary questions to explore their impressions on the content and the feasibility of the CARES.With this extensive data collection process, psychometric validity of the Flemish CARES can be tested thoroughly using classical test theory. Internal consistency of summary scales, test-retest reliability, content validity, construct validity, concurrent validity and feasibility of the instrument will be examined. If the Flemish CARES version is found reliable, valid and feasible, it will be used in future research and clinical practice. Comprehensive assessment with the CARES in a stepped-care approach can facilitate timely identification of cancer patients' psychosocial concerns and care needs so it can contribute to efficient provision of patient-centered quality care.ClinicalTrials.gov: NCT02282696 (July 16, 2014)
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