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Michael Tamm

Researcher at University Hospital of Basel

Publications -  473
Citations -  19255

Michael Tamm is an academic researcher from University Hospital of Basel. The author has contributed to research in topics: COPD & Medicine. The author has an hindex of 63, co-authored 439 publications receiving 17529 citations. Previous affiliations of Michael Tamm include University of Basel.

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Effect of procalcitonin-guided treatment on antibiotic use and outcome in lower respiratory tract infections: cluster-randomised, single-blinded intervention trial

TL;DR: Procalcitonin guidance substantially reduced antibiotic use in lower respiratory tract infections and could have important clinical and financial implications in view of the current overuse of antimicrobial therapy in often self-limiting acute respiratory tract infection.
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Procalcitonin guidance of antibiotic therapy in community-acquired pneumonia: a randomized trial.

TL;DR: Procalcitonin guidance substantially reduces antibiotic use in community-acquired pneumonia and may have important clinical and public health implications.
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Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections

TL;DR: In this article, a systematic review included individual patient data from 14 randomised controlled trials with a total of 4211 participants and found no increased risk for all-cause mortality or treatment failure when procalcitonin was used to guide initiation and duration of antibiotic treatment in participants with acute respiratory infections compared to control participants.
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Antibiotic Treatment of Exacerbations of COPD: A Randomized, Controlled Trial Comparing Procalcitonin-Guidance With Standard Therapy

TL;DR: Procalcitonin guidance for exacerbations of COPD offers a sustained advantage over standard therapy in reducing antibiotic use for up to 6 months with a number-needed-to-treat of 3.
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Airway Smooth Muscle Cell Proliferation Is Increased in Asthma

TL;DR: This study shows for the first time that proliferation of ASM cells is increased in patients with asthma and provides evidence for an intrinsic abnormality in the ASM cell in this disease.