[Data-driven intensive care: a lack of comprehensive datasets]. / "Data-driven-Intensivmedizin": Mangel an umfassenden Datensätzen.

Intensive care units provide a data-rich environment with the potential to generate datasets in the realm of big data, which could be utilized to train powerful machine learning (ML) models. However, the currently available datasets are too small and exhibit too little diversity due to their limitation to individual hospitals. This lack of extensive and varied datasets is a primary reason for the limited generalizability and resulting low clinical utility of current ML models. Often, these models are based on data from single centers and suffer from poor external validity. There is an urgent need for the development of large-scale, multicentric, and multinational datasets. Ensuring data protection and minimizing re-identification risks pose central challenges in this process. The "Amsterdam University Medical Center database (AmsterdamUMCdb)" and the "Salzburg Intensive Care database (SICdb)" demonstrate that open access datasets are possible in Europe while complying with the data protection regulations of the General Data Protection Regulation (GDPR). Another challenge in building intensive care datasets is the absence of semantic definitions in the source data and the heterogeneity of data formats. Establishing binding industry standards for the semantic definition is crucial to ensure seamless semantic interoperability between datasets.

Cocaine/Levamisole-Induced, Skin-Limited ANCA-Associated Vasculitis with Pyoderma Gangrenosum-like Presentation.

The use of levamisole as the most frequent adulterant of cocaine has merged in previously unknown toxicities, notably a disease entity called cocaine/levamisole-associated autoimmune syndrome (CLAAS). Clinically, CLAAS can manifest with diverse cutaneous and extracutaneous features sharing common laboratory findings (neutropenia, autoantibody patterns). We report the case of a cocaine-abusing female patient with relapsing episodes of painful ulcers, worsening and expanding over a three-year period. The case exhibited all features of a drug-induced, skin-limited, ANCA-associated vasculitis, evolving over time to PG-like findings. In both disease stages, the patient responded well to the cessation of cocaine exposure and systemic glucocorticosteroids. This case demonstrates the continuous nature of cutaneous CLAAS manifestations in a single patient. CLAAS has become a major public health issue in the at-risk group of cocaine users, and clinicians should be alert of this condition when treating cocaine users presenting with single or multiple skin ulcerations.

Critical Illness and Systemic Inflammation Are Key Risk Factors of Severe Acute Kidney Injury in Patients With COVID-19.

INTRODUCTION: Acute kidney injury (AKI) is an important complication in COVID-19, but its precise etiology has not fully been elucidated. Insights into AKI mechanisms may be provided by analyzing the temporal associations of clinical parameters reflecting disease processes and AKI development. METHODS: We performed an observational cohort study of 223 consecutive COVID-19 patients treated at 3 sites of a tertiary care referral center to describe the evolvement of severe AKI (Kidney Disease: Improving Global Outcomes stage 3) and identify conditions promoting its development. Descriptive statistics and explanatory multivariable Cox regression modeling with clinical parameters as time-varying covariates were used to identify risk factors of severe AKI. RESULTS: Severe AKI developed in 70 of 223 patients (31%) with COVID-19, of which 95.7% required kidney replacement therapy. Patients with severe AKI were older, predominantly male, had more comorbidities, and displayed excess mortality. Severe AKI occurred exclusively in intensive care unit patients, and 97.3% of the patients developing severe AKI had respiratory failure. Mechanical ventilation, vasopressor therapy, and inflammatory markers (serum procalcitonin levels and leucocyte count) were independent time-varying risk factors of severe AKI. Increasing inflammatory markers displayed a close temporal association with the development of severe AKI. Sensitivity analysis on risk factors of AKI stage 2 and 3 combined confirmed these findings. CONCLUSION: Severe AKI in COVID-19 was tightly coupled with critical illness and systemic inflammation and was not observed in milder disease courses. These findings suggest that traditional systemic AKI mechanisms rather than kidney-specific processes contribute to severe AKI in COVID-19.

[COVID-19 and acute kidney injury in the intensive care unit]. / COVID-19 und akute Nierenschädigung im Intensivbereich.

Acute kidney injury (AKI) is a frequent and severe complication in coronavirus disease 2019 (COVID-19) patients in the intensive care unit. The development of COVID-19 associated AKI is closely linked to the severity of the disease course. The main risk factor for kidney failure requiring kidney replacement therapy is the necessity for invasive ventilation, whereby the onset of renal failure is often closely associated with the timing of intubation. Additionally, the risk factors for a severe course of COVID-19 have been shown to also be risk factors for renal failure. AKI in COVID-19 shows a high mortality and in some patients leads to chronic kidney disease; however, full recovery of kidney function in survivors who need dialysis is not uncommon. With respect to prevention and treatment of renal failure associated with COVID-19, the same recommendations as for AKI from other causes are valid (Kidney Disease: Improving Global Outcomes, KDIGO bundles). Due to the large numbers of patients in the setting of overwhelmed resources, the availability of extracorporeal renal replacement procedures can become critical, especially since hypercoagulation is frequent in COVID­19. In order to avoid triage situations, in some centers acute peritoneal dialysis was used as an alternative to extracorporeal procedures.

A Yin and Yang in Epithelial Immunology: The Roles of the αE(CD103)ß7 Integrin in T Cells.

The proper function(s) of cell-surface receptors is crucial for the regulation of adaptive immune responses. One such receptor is the αE(CD103)ß7 integrin, whose history in science is closely linked with the evolution of our knowledge of immune regulation. Initially described as a marker of intraepithelial T-lymphocytes, this leukocyte integrin is now seen as a dynamically regulated receptor involved in the functional differentiation of some cytotoxic T cells as well as regulatory T cells, thus presumably contributing to the fine-tuning of immune reactions in epithelial compartments. In this brief overview, we delineate our current view on αE(CD103)ß7 in T-cell-mediated immune responses.