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Disease Classification (disease + classification)
Selected AbstractsPotential Advantages and Limitations of Applying the Chronic Kidney Disease Classification to Kidney Transplant RecipientsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2006J. S. Gill The National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) classification of Chronic Kidney Disease (CKD) characterizes patients by their level of kidney function and includes kidney transplant recipients (KTRs). Most KTRs have stage ,3 CKD (estimated glomerular filtration rate <60 mL/min/1.73 m2) and may benefit from aggressive CKD care. Recent modifications to the K/DOQI CKD classification reflect the recognition of KTRs as a unique subset of CKD patients in whom the presentation, progression and implications of CKD may vary from those in nontransplant CKD populations. Currently, there is limited information about how adopting the CKD classification in KTRs will influence clinical management and outcomes. Appropriately designed studies are needed to develop transplant-specific CKD treatment recommendations, and to ensure patient, health provider and payer acceptance of the continued need for aggressive CKD care after transplantation. Education and implementation strategies will be required to ensure appropriate integration of the CKD classification and treatment guidelines into existing posttransplant care programs. The CKD classification thus represents an exciting potential strategy to improve clinical outcomes that should be adopted, further studied and modified to incorporate considerations unique to KTRs. [source] Anti,U3 RNP autoantibodies in systemic sclerosisARTHRITIS & RHEUMATISM, Issue 4 2009Rohit Aggarwal Objective To describe the classification, demographic and clinical features, and survival in anti,U3 RNP autoantibody,positive patients with systemic sclerosis (SSc). Methods Medical records of 108 anti,U3 RNP,positive and 2,471 anti,U3 RNP,negative SSc patients first evaluated during 1985,2003 were reviewed. Anti,U3 RNP antibody was detected by protein and RNA immunoprecipitation. Disease classification, demographic and clinical features, organ system involvement, and survival were compared between the 2 patient groups, by Student's t -test, chi-square analysis, and Mantel-Haenszel test. Results The anti,U3 RNP,positive group had a higher proportion of African American patients (27% versus 5%; P < 0.001) and male patients (29% versus 19%; P = 0.021), and was younger at the time of first physician diagnosis (mean age 42.8 years versus 47.4 years; P = 0.001). The 2 groups had similar proportions of patients with diffuse cutaneous involvement (47% and 45% in those with and those without anti,U3 RNP, respectively). However, among patients with diffuse cutaneous involvement, the mean maximum modified Rodnan skin score was significantly lower in the anti,U3 RNP group (22.3 versus 27.9; P < 0.001). Skeletal muscle involvement was more frequent in anti,U3 RNP,positive patients (25% versus 14%; P = 0.002), as was "intrinsic" pulmonary arterial hypertension (PAH) (31% versus 13%; P < 0.001). The frequency of gastrointestinal involvement, cardiac involvement, pulmonary fibrosis, and "renal crisis" did not differ significantly between the 2 groups. Survival was worse in the anti,U3 RNP,positive group (hazard ratio 1.38 [95% confidence interval 1.05,1.82]). PAH was the most common known cause of death in patients with anti,U3 RNP (30%, versus 10% in the anti,U3 RNP,negative group; P < 0.001). Conclusion The present findings demonstrate that the frequencies of African American race and male sex are greater among SSc patients with anti,U3 RNP antibody than those without, and the former group is younger at SSc diagnosis. Anti,U3 RNP,positive patients have more frequent skeletal muscle involvement and PAH, the latter being the most common cause of death. [source] Unsupervised immunophenotypic profiling of chronic lymphocytic leukemiaCYTOMETRY, Issue 3 2006Luzette K. Habib Abstract Background Proteomics and functional genomics have revolutionized approaches to disease classification. Like proteomics, flow cytometry (FCM) assesses concurrent expression of many proteins, with the advantage of using intact cells that may be differentially selected during analysis. However, FCM has generally been used for incremental marker validation or construction of predictive models based on known patterns, rather than as a tool for unsupervised class discovery. We undertook a retrospective analysis of clinical FCM data to assess the feasibility of a cell-based proteomic approach to FCM by unsupervised cluster analysis. Methods Multicolor FCM data on peripheral blood (PB) and bone marrow (BM) lymphocytes from 140 consecutive patients with B-cell chronic lymphoproliferative disorders (LPDs), including 81 chronic lymphocytic leukemia (CLLs), were studied. Expression was normalized for CD19 totals, and recorded for 10 additional B-cell markers. Data were subjected to hierarchical cluster analysis using complete linkage by Pearson's correlation. Analysis of CLL in PB samples (n = 63) discovered three major clusters. One cluster (14 patients) was skewed toward "atypical" CLL and was characterized by high CD20, CD22, FMC7, and light chain, and low CD23. The remaining two clusters consisted almost entirely (48/49) of cases recorded as typical BCLL. The smaller "typical" BCLL cluster differed from the larger cluster by high CD38 (P = 0.001), low CD20 (P = 0.001), and low CD23 (P = 0.016). These two typical BCLL clusters showed a trend toward a difference in survival (P = 0.1090). Statistically significant cluster stability was demonstrated by expanding the dataset to include BM samples, and by using a method of random sampling with replacement. Conclusions This study supports the concept that unsupervised immunophenotypic profiling of FCM data can yield reproducible subtypes of lymphoma/chronic leukemia. Expanded studies are warranted in the use of FCM as an unsupervised class discovery tool, akin to other proteomic methods, rather than as a validation tool. © 2006 International Society for Analytical Cytology [source] Diabetes classification: grey zones, sound and smoke: Action LADA 1DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 7 2008R. D. G. Leslie Abstract Diseases gain identity from clinical phenotype as well as genetic and environmental aetiology. The definition of type 1 diabetes is clinically exclusive, comprising patients who are considered insulin dependent at diagnosis, whilst the definition of type 2 diabetes is inclusive, only excluding those who are initially insulin dependent. Ketosis-prone diabetes (KPD) and latent autoimmune diabetes in adults (LADA) are each exclusive forms of diabetes which are, at least initially, clinically distinct from type 2 diabetes and type 1 diabetes, and each have a different natural history from these major types of diabetes. KPD can be diagnosed unequivocally as diabetes presenting with the categorical clinical feature, ketoacidosis. In contrast, LADA can be diagnosed by the co-occurrence of three traits, not one of which is categorical or exclusive to the condition: adult-onset non-insulin-requiring diabetes, an islet autoantibody such as glutamic acid decarboxylase autoantibodies (GADA) or cytoplasmic islet cell autoantibodies (ICA), and no need for insulin treatment for several months post-diagnosis. But while some would split diabetes into distinct subtypes, there is a strong case that these subtypes form a continuum of varying severity of immune and metabolic dysfunction modified by genetic and non-genetic factors. This article discusses the nature of disease classification in general, and KPD and LADA in particular, emphasizing the potential value and pitfalls in classifying diabetes and suggesting a need for more research in this area. Copyright © 2008 John Wiley & Sons, Ltd. [source] Purpose and problems of periodontal disease classificationPERIODONTOLOGY 2000, Issue 1 2005Ubele Van Der Velden First page of article [source] 1261: Pathophysiology and classification of uveitisACTA OPHTHALMOLOGICA, Issue 2010AD DICK Purpose This talk will overview the pathophysiology of non-infectious uveitis in relation to recent SUN (standardised uveitis nomenclature) disease classification. Methods The experimental and translational human evidence of autoimmunity and activation of immunity will be discussed. In addition the talk will highlight the pathways and mechanisms of tissue damage that results in sight-threatening disease. Results Traditionally, despite active immune regulatory mechanisms operative within the ocular environment, inflammation still occurs. Activated antigen and non-antigen specific T cells are generated in uveitis. The interplay with innate immunity and in particular cells of myeloid lineage both systemically and within the local environment dictate the severity and extent of pathology we observe. Conclusion The understanding of immune responses during the uveitis open many avenues to potential novel immunotherapies that not only suppress inflammation but attempt to redress immune balance, tolerance and local homeostasis within ocular tissues. [source] Genotypic and phenotypic classification of cancer: How should the impact of the two diagnostic approaches best be balanced?GENES, CHROMOSOMES AND CANCER, Issue 9 2010Petter Brandal Neoplastic tumors are traditionally named based on their differentiation (i.e., which normal cells and tissues they resemble) and bodily site. In recent years, knowledge about the genetic basis of tumorigenesis has grown rapidly, and the new information has in several instances been incorporated into the very definition of cancerous entities. The proper contribution of the diseases' phenotype and genotype to what they are called and how they are delineated from one another has rarely been subjected to explicit reasoning, however, nor is it often made clear whether existing naming practices are founded on ontological or utilitarian grounds. We look at several examples of how the new cytogenetic and molecular genetic understanding of tumorigenesis has impacted oncological nomenclature in a significant manner, but also at counterexamples where no similar change has taken place. In all likelihood, more and more neoplastic diseases will in the future be defined and named based on their pathogenesis rather than their phenotype, not least because effective and specific drug therapies directed against the molecular change at the very heart of oncogenesis will increasingly become available. The fact that this shift in emphasis is primarily guided by utilitarian considerations rather than any perception of acquired genetic changes as somehow being more ontologically "profound" or "important" in tumorigenesis, is as it should be; both the phenotype and the genotype of tumors are key parameters across most of oncology and are likely to be retained as the basis of coexisting disease classifications for as long as we can foresee. © 2010 Wiley-Liss, Inc. [source] | ||||||||||