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To date no biomarker has been identified bringing together perfect sensitivity and specificity to discriminate between inflammation and infections. Since the 1930s new markers of tissue damage and endothelial damage have been identified but which are incapable of identifying infections in every clinical setting to enable initiation of early antibiotic treatment. In this review the most important classical biomarkers and upcoming new PCR-based approaches are addressed. These markers are highlighted with respect to special clinical settings and to control the success of antibiotic treatment. The issue of discrimination between inflammation and infection is not yet solved. Based on one single biomarker it is impossible to decide whether infection is the reason for the patient's worsening condition but the combination of biomarkers or the integration of new biomarkers may be a meaningful supplement. The measurement of different biomarkers of infection or inflammation is part of the routine in critical care and will be essential in the future. [ABSTRACT FROM AUTHOR]

Sequential and combined therapy for osteoporosis is challenging because of the many options, and difficult because robust fracture data are not available, especially for combination therapies, mostly because the studies are too small. The principle of sequential and combined therapy for osteoporosis is that osteoanabolic therapy (teriparatide [TPTD]), whether sequential or combined, leads to an increase in bone mineral density (BMD), especially in the lumbar spine. The only exception is the sequence of TPTD after denosumab (Dmab), which leads to a loss (transient) of BMD in both the lumbar spine and the hip; for this reason, this sequence should be avoided at all costs. A second principle is that the stronger and longer the antiresorptive pretreatment was, the more delayed and reduced the effect of osteoanabolic therapy (TPTD). A third principle is the need for antiresorptive retreatment after therapies with TPTD and Dmab or their combination to prevent vertebral fractures (Dmab) and maintain bone density (TPTD). An effect of osteoanabolic therapy with TPTD on BMD of the hip is expected only in combination with antiresorptive therapy (bisphosphonates, Dmab). If the antiresorptive therapy is not continued, there is a transient loss in the first months of osteoanabolic monotherapy, the more so the stronger the antiresorptive pretreatment was. [ABSTRACT FROM AUTHOR]