Abstract
Bacterial infections with consecutive sepsis have a high incidence in intensive care patients and are often associated with lethal complications. As early diagnosis followed by antibiotic therapy is vital for these patients, sensitive biomarkers indicating sepsis are of fundamental importance for the survival of septic patients. Procalcitonin, which is a protein produced by thyroidal c-cells, has been shown over 20 years to be increased in patients with sepsis. Since then, multiple studies have investigated the role of procalcitonin in patients with sepsis and systemic inflammation. However, the value of procalcitonin in patients with sepsis is still discussed controversial. This review aims to briefly summarize the current literature of procalcitonin and sepsis.
Highlights
As early diagnosis followed by antibiotic therapy is vital for these patients, sensitive biomarkers indicating sepsis are of fundamental importance for the survival of septic patients
This review aims to summarize recent trials on procalcitonin (PCT) in septic patients
The discussed studies have been selected by the personal interest of the authors, with no claim of completeness.History of procalcitonin (PCT) begins with the discovery of the hormone calcitonin (CT) in the early 1960`s by Copp,et al [1] being found in dogs as an adversary to parathormone
Summary
This review aims to summarize recent trials on procalcitonin (PCT) in septic patients. The discussed studies have been selected by the personal interest of the authors, with no claim of completeness.History of procalcitonin (PCT) begins with the discovery of the hormone calcitonin (CT) in the early 1960`s by Copp,et al [1] being found in dogs as an adversary to parathormone. [2]described a precursor protein of calcitonin which was named procalcitonin.The molecular structure of procalcitoninwas firstdescribed in 1981, when it was shown that PCT is a glycoprotein consisting of 116 aminoacids with a weight of 13 kDathat is processed from its own precursor preprocalcitonin[3,4]. Being transcripted from the CALC-1gene located on chromosome 11, PCT is under physiological conditions only produced by thyroidalc-cells, and in small amounts in neuroendocrine cells of the lung and small intestine respectively, where it is processed into its effective hormone calcitonin and stored in cellular vesicles until released in conditions of high serum calcium levels.PCT is nearly not detectable in serum of normocalcaemic patients[5]
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