Az ápolói munkaterhelés és ápolási intenzitás komplex mérésének lehetőségei a magyarországi Ápolástámogató Rendszer kialakításához kapcsolódó fejlesztések keretében

Hazánkban zajlik az ápolástámogató rendszer szoftveres és eszközös fejlesztése, bevezetése, melynek célja a betegbiztonság növelése, a napi ápolási tevékenységek minél szélesebb körű rögzítése. 2022 nyarán több pilot intézményben került a rendszer első verziója tesztelésre, amelyet követően dr. Takács Péter egészségügyi államtitkár felkérte dr. Oláh Andrást az ÁTR ápolásszakmai koordinátori feladatok ellátására és a pilot tapasztalatok alapján a szükség szerinti átdolgozására, fejlesztésére. A folyamat az OKFŐ/ÁKI és PPI, valamint meghatározó ápolásszakmai szervezetek (MESZK; SZK-ÁSZT, MÁE; MÁIE; MÁT) konszenzusos támogatásával valósul meg. A fejlesztés során kiemelt cél, olyan nemzetközi standard, valid skálák, eszközök beépítése, amelyek illeszkednek a későbbi komplex elektronikus ápolási modul fejlesztéséhez. Ennek keretében szükséges egy országosan egységes, nem csak a betegek besorolását, hanem a kapott eredmények elemzését, értékelését és ápolói humán erőforrás tervezésében történő felhasználását is támogató betegosztályozó rendszer bevezetése is. Jelen közlemény célja az ápolási erőforrás-tervező rendszerekkel kapcsolatos rövid összefoglalás, kitérve a német beteg-besorolási rendszerrel kapcsolatos tapasztalatokra, a betegosztályozó rendszerek korlátaira és példákon keresztül bemutatni az ÁTR alkalmazása során használni javasolt finn betegosztályozási rendszer elemeit. The Possibilities of complex measuring of the Nursing Workload and Intensity Part of the Hungarian Electronic Nursing Record’s Developement András OLÁH PhD. Habil, Miklós ZRÍNYI PhD, Noémi FULLÉR, Zoltán BALOGH PhD, Magdolna KÁDÁR PhD, Tünde KIS, Gyula SZEBENI-KOVÁCS SUMMARY The integration of the Hungarian Electronic Nursing Record (ENR) is currently ongoing, its aims are to improve patients’ safety and the broader record of the everyday nursing activities. First version of the the ENR was tested in many institution in the Summer of 2022, then Dr. András Oláh was asked by Dr. Péter Takács Secretary of State for Health to be the coordinator of the Hungarian ENR development process and to improve that based on the pilot experiences. The process was realized with the OKFŐ/ÁKI, PPI and with the consensual support of the major nursing associations (MESZK, SZK-ÁSZT, MÁE, MÁIE, MÁT). Emphasized aim was to install international valid scales and tools which are fitting in to the later complex ENR’s developement. In this framework it is necessary a nationally integrated system which not only classify but also analyze and evaluate correctly the incoming datas. These results may be used to plan nursing human resources and to implement a nursing workload and intensity measurement system. The aim of this study is to give a brief literature review about the nursing resource planning systems, including the experiences about the German patient classification system and the limitations of the patient classification systems. We would like to present on examples how the Finnish patient classification system works what may be part of the Hungarian ENR

IgM antibodies against malondialdehyde and phosphorylcholine in different systemic rheumatic diseases

IgM antibodies against phosphorylcholine (anti-PC) and malondialdehyde (anti-MDA) may have protective properties in cardiovascular and rheumatic diseases. We here compare these antibodies in systemic rheumatic conditions and study their properties. Anti-PC and anti-MDA was measured using ELISA in patients with SLE (374), RA (354), Mixed connective tissue disease (MCTD, 77), Systemic sclerosis (SSc, 331), Sjögren's syndrome (SjS, 324), primary antiphospholipid syndrome (PAPs, 65), undifferentiated connective tissue disease (UCTD, 118) and 515 matched healthy controls (HC). Cardiovascular score (CV) was broadly defined based on clinical disease symptoms. Anti-PC and anti-MDA peptide/protein characterization were compared using a proteomics de novo sequencing approach. anti-MDA and anti-PC were extracted from total IgM. The proportion of Treg cells was determined by flow cytometry. The maximal difference between cases and controls was shown for MCTD: significantly lower IgM Anti-PC but not anti-MDA among patients (median 49.3RU/ml vs 70.4 in healthy controls, p(t-test) = 0.0037). IgM low levels were more prevalent in MCTD, SLE, SjS, SSc and UCTD. IgM anti-PC variable region profiles were different from and more homologous than anti-MDA. Anti-PC but not anti-MDA were significantly negatively correlated with CV in the whole patient group. In contrast to IgM anti-PC, anti-MDA did not promote polarization of Tregs. Taken together, Anti-PC is decreased in MCTD and also in SLE, SjS and SSc but not in other studied diseases. Anti-PC may thus differentiate between these. In contrast, anti-MDA did not show these differences between diseases studied. Anti-PC level is negatively correlated with CV in the patient group cohort. In contrast to anti-PC, anti-MDA did not promote Treg polarization. These findings could have both diagnostic and therapeutic implications, one possibility being active or passive immunization with PC in some rheumatic conditions

Standardization procedure for flow cytometry data harmonization in prospective multicenter studies

One of the most challenging objective for clinical cytometry in prospective multicenter immunomonitoring trials is to compare frequencies, absolute numbers of leukocyte populations and further the mean fluorescence intensities of cell markers, especially when the data are generated from different instruments. Here, we describe an innovative standardization workflow to compare all data to carry out any large-scale, prospective multicentric flow cytometry analysis whatever the duration, the number or type of instruments required for the realization of such project

Machine learning identifies a common signature for anti-SSA/Ro60 antibody expression across autoimmune diseases

Anti-Ro autoantibodies are among the most frequently detected extractable nuclear antigen autoantibodies, mainly associated with primary Sjögren's syndrome (pSS), systemic lupus erythematosus (SLE) and undifferentiated connective tissue disease (UCTD). Is there a common signature to all patients expressing anti-Ro60 autoantibodies regardless of their disease phenotype?Using high-throughput multi-omics data collected within the cross-sectional cohort from the PRECISESADS IMI project (genetic, epigenomic, transcriptomic, combined with flow cytometric data, multiplexed cytokines, classical serology and clinical data), we assessed by machine learning the integrated molecular profiling of 520 anti-Ro60-positive (anti-Ro60+ ) compared to 511 anti-Ro60-negative (anti-Ro60- ) patients with pSS, SLE and UCTD, and 279 healthy controls (HCs).The selected features for RNA-Seq, DNA methylation and GWAS data allowed a clear separation between anti-Ro60+ and anti-Ro60- patients. The different features selected by machine learning from the anti-Ro60+ patients constitute specific signatures when compared to anti-Ro60- patients and HCs. Remarkably, the transcript z-score of three genes (ATP10A, MX1 and PARP14), presenting an overexpression associated with a hypomethylation and genetic variation, and independently identified by the Boruta algorithm, was clearly higher in anti-Ro60+ patients compared to anti-Ro60- patients in all the diseases. We demonstrate that these signatures, enriched in interferon stimulated genes, were also found in anti-Ro60+ patients with rheumatoid arthritis and systemic sclerosis and remained stable over time and not influenced by treatment.Anti-Ro60+ patients present a specific inflammatory signature regardless of their disease suggesting that a dual therapeutic approach targeting both Ro-associated RNAs and anti-Ro60 autoantibodies should be considered

Association of Combined Anti-Ro52/TRIM21 and Anti-Ro60/SSA Antibodies With Increased Sjögren Disease Severity Through Interferon Pathway Activation

The biologic diagnosis of primary Sjögren disease (SjD) mainly relies on anti-Ro60/SSA antibodies, whereas the significance of anti-Ro52/TRIM21 antibodies currently remains unclear. The aim of this study was to characterize the clinical, serological, biologic, transcriptomic, and interferon profiles of patients with SjD according to their anti-Ro52/TRIM21 antibody status.Patients with SjD from the European PRECISESADS (n = 376) and the Brittany Diagnostic Suspicion of primitive Sjögren's Syndrome (DIApSS); (n = 146) cohorts were divided into four groups: double negative (Ro52-/Ro60-), isolated anti-Ro52/TRIM21 positive (Ro52+), isolated anti-Ro60/SSA positive (Ro60+), and double-positive (Ro52+/Ro60+) patients. Clinical information; EULAR Sjögren Syndrome Disease Activity Index, a score representing systemic activity; and biologic markers associated with disease severity were evaluated. Transcriptome data obtained from whole blood by RNA sequencing and type I and II interferon signatures were analyzed for PRECISESADS patients.In the DIApSS cohort, Ro52+/Ro60+ patients showed significantly more parotidomegaly (33.3% vs 0%-11%) along with higher β2-microglobulin (P = 0.0002), total immunoglobulin (P < 0.0001), and erythrocyte sedimentation rate levels (P = 0.002) as well as rheumatoid factor (RF) positivity (66.2% vs 20.8%-25%) compared to other groups. The PRECISESADS cohort corroborated these observations, with increased arthritis (P = 0.046), inflammation (P = 0.005), hypergammaglobulinemia (P < 0.0001), positive RF (P < 0.0001), leukopenia (P = 0.004), and lymphopenia (P = 0.009) in Ro52+/Ro60+ patients. Cumulative EULAR Sjögren Syndrome Disease Activity Index results further confirmed these disparities (P = 0.002). Transcriptome analysis linked anti-Ro52/TRIM21 antibody positivity to interferon pathway activation as an underlying cause for these clinical correlations.These results suggest that the combination of anti-Ro52/TRIM21 and anti-Ro60/SSA antibodies is associated with a clinical, biologic, and transcriptional profile linked to greater disease severity in SjD through the potentiation of the interferon pathway activation by anti-Ro52/TRIM21 antibodies

Integrative Analysis Reveals a Molecular Stratification of Systemic Autoimmune Diseases

Clinical heterogeneity, a hallmark of systemic autoimmune diseases (SADs) impedes early diagnosis and effective treatment, issues that may be addressed if patients could be grouped into a molecular defined stratification.With the aim of reclassifying SADs independently of the clinical diagnoses, unsupervised clustering of integrated whole blood transcriptome and methylome cross-sectional data of 955 patients with 7 SADs and 267 healthy controls was undertaken. In addition, an inception cohort was prospectively followed for 6 and 14 months to validate the results and analyze if cluster assignment changed or not with time.Four clusters were identified and validated. Three were pathological representing 'inflammatory', 'lymphoid', and 'interferon' patterns each including all diagnoses and defined by genetic, clinical, serological, and cellular features. A fourth cluster with no specific molecular pattern associated with low activity, and accumulated also healthy controls. A longitudinal and independent inception cohort showed a relapse-remission pattern, where patients remained in their pathological cluster, moving only to the healthy one, thus showing that with time, the molecular clusters remain stable and that single pathogenic molecular signatures characterize each individual patient.Patients with SADs can be jointly stratified into three stable disease clusters with specific molecular patterns differentiating different molecular disease mechanisms. These results have important implications for future clinical trials and the study of therapy non-responsiveness marking a paradigm shift in our view of SADs

Interferon and B-cell Signatures Inform Precision Medicine in Lupus Nephritis

Introduction: Current therapeutic management of lupus nephritis (LN) fails to induce long-term remission in over 50% of patients, highlighting the urgent need for additional options. Methods: We analyzed differentially expressed genes (DEGs) in peripheral blood from patients with active LN (n = 41) and active nonrenal lupus (n = 62) versus healthy controls (HCs) (n = 497) from the European PRECISESADS project (NTC02890121), and dysregulated gene modules in a discovery (n = 26) and a replication (n = 15) set of active LN cases. Results: Replicated gene modules qualified for correlation analyses with serologic markers, and regulatory network and druggability analysis. Unsupervised coexpression network analysis revealed 20 dysregulated gene modules and stratified the active LN population into 3 distinct subgroups. These subgroups were characterized by low, intermediate, and high interferon (IFN) signatures, with differential dysregulation of the “B cell” and “plasma cells/Ig” modules. Drugs annotated to the IFN network included CC-motif chemokine receptor 1 (CCR1) inhibitors, programmed death-ligand 1 (PD-L1) inhibitors, and irinotecan; whereas the anti-CD38 daratumumab and proteasome inhibitor bortezomib showed potential for counteracting the “plasma cells/Ig” signature. In silico analysis demonstrated the low-IFN subgroup to benefit from calcineurin inhibition and the intermediate-IFN subgroup from B-cell targeted therapies. High-IFN patients exhibited greater anticipated response to anifrolumab whereas daratumumab appeared beneficial to the intermediate-IFN and high-IFN subgroups. Conclusion: IFN upregulation and B and plasma cell gene dysregulation patterns revealed 3 subgroups of LN, which may not necessarily represent distinct disease phenotypes but rather phases of the inflammatory processes during a renal flare, providing a conceptual framework for precision medicine in LN. © 2024 International Society of Nephrolog