Objective: In his original series of 129 surgically treated acetabular fractures, Letournel did not operate on patients older than 60 years. Almost 30 years later, he still emphasized that no patients with reduced bone quality should be operated on. The aim of the study was to analyze epidemiologic characteristics and treatment modes for today's cohort of elderly patients with acetabular fractures. Design: Retrospective analysis. Setting: Multicenter registry/Level I trauma center. Patients: Three thousand seven hundred ninety-three patients who had sustained a fracture of the acetabulum. Intervention: Operative and nonoperative treatment of acetabular fractures. Main Outcome Measurements: Epidemiologic characteristics, treatment mode, in-hospital mortality, rate of secondary hip arthroplasty, and quality of life indicated by EQ-5D score. Results: For the multicenter registry, more than 50% of all patients with acetabular fractures had an age of 60 years or over. The age peak was found at 75–80 years. Fifty percent of the elderly patients were treated surgically. The in-hospital mortality was significantly higher in elderly patients than patients younger than 60 years. In our Level I trauma center, surgical treatment by open reduction and internal fixation did not influence in-hospital mortality or quality of life of elderly patients with acetabular fractures. Conclusions: Today, elderly persons represent the dominant cohort among patients with fractures of the acetabulum. Fifty-five years after the publication of Letournel's original case series, data indicate that currently, surgical treatment is a common and necessary option in the therapy of acetabular fractures in elderly patients. Level of Evidence: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.

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A BS TRACT: Background: Coding and noncoding repeat expansions are an important cause of neurodegenerative diseases.Objective: This study determined the clinical and genetic features of a large German family that has been followed for almost 2 decades with an autosomal dominantly inherited spinocerebellar ataxia (SCA) and independent co-occurrence of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Methods: We carried out clinical examinations and telephone interviews, reviewed medical records, and performed magnetic resonance imaging and positron emission tomography scans of all available family members. Comprehensive genetic investigations included linkage analysis, short-read genome sequencing, longread sequencing, repeat-primed polymerase chain reaction, and Southern blotting. Results: The family comprises 118 members across seven generations, 30 of whom were definitely and five possibly affected. In this family, two different pathogenic mutations were found, a heterozygous repeat expansion in C9ORF72 in four patients with ALS/FTD and a heterozygous repeat expansion in DAB1 in at least nine patients with SCA, leading to a diagnosis of DAB1related ataxia (ATX-DAB1; SCA37). One patient was affected by ALS and SCA and carried both repeat expansions. The repeat in DAB1 had the same configuration but was larger than those previously described ([ATTTT] ≈75 [ATTTC] ≈40-100 [ATTTT] ≈415 ). Clinical features in patients with SCA included spinocerebellar symptoms, sometimes accompanied by additional ophthalmoplegia, vertical nystagmus, tremor, sensory deficits, and dystonia. After several decades, some of these patients suffered from cognitive decline and one from additional nonprogressive lower motor neuron affection. Conclusion:We demonstrate genetic and clinical findings during an 18-year period in a unique family carrying two different pathogenic repeat expansions, providing

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IntroductionCommunity-acquired pneumonia (CAP) and acute exacerbations of chronic obstructive pulmonary disease (AECOPD) result in high morbidity, mortality, and socio-economic burden. The usage of easily accessible biomarkers informing on disease entity, severity, prognosis, and pathophysiological endotypes is limited in clinical practice. Here, we have analyzed selected plasma markers for their value in differential diagnosis and severity grading in a clinical cohort.MethodsA pilot cohort of hospitalized patients suffering from CAP (n = 27), AECOPD (n = 10), and healthy subjects (n = 22) were characterized clinically. Clinical scores (PSI, CURB, CRB65, GOLD I-IV, and GOLD ABCD) were obtained, and interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-2-receptor (IL-2R), lipopolysaccharide-binding protein (LBP), resistin, thrombospondin-1 (TSP-1), lactotransferrin (LTF), neutrophil gelatinase-associated lipocalin (NGAL), neutrophil-elastase-2 (ELA2), hepatocyte growth factor (HGF), soluble Fas (sFas), as well as TNF-related apoptosis-inducing ligand (TRAIL) were measured in plasma.ResultsIn CAP patients and healthy volunteers, we found significantly different levels of ELA2, HGF, IL-2R, IL-6, IL-8, LBP, resistin, LTF, and TRAIL. The panel of LBP, sFas, and TRAIL could discriminate between uncomplicated and severe CAP. AECOPD patients showed significantly different levels of LTF and TRAIL compared to healthy subjects. Ensemble feature selection revealed that CAP and AECOPD can be discriminated by IL-6, resistin, together with IL-2R. These factors even allow the differentiation between COPD patients suffering from an exacerbation or pneumonia.DiscussionTaken together, we identified immune mediators in patient plasma that provide information on differential diagnosis and disease severity and can therefore serve as biomarkers. Further studies are required for validation in bigger cohorts.