Procalcitonin As A Marker In The Systemic Inflammatory Response

Severe infection and sepsis are frequent causes of morbidity and mortality in intensive care units. Infection and sepsis are accompanied by clinical signs and changes in laboratory analysis, as well as changes in body temperature, leukocytosis and tachycardia. However, these signs and symptoms of systemic inflammation (SIRS) may have an infectious or non-infectious etiology. They are not specific or sensitive to sepsis. A similar inflammatory response can be seen in patients with pancreatitis, severe trauma and burns without infectious complications. Sometimes it is difficult to distinguish patients with systemic infection, organ dysfunction and "shock" from other patients with the same clinical symptoms and laboratory findings that do not have infection. Bacteriological evidence of the infection may not develop at the same time as the clinical symptoms of sepsis. Positive bacteriological tests may result from contamination and similarly negative tests do not necessarily exclude sepsis. Since this symptomatology and laboratory analysis are not sufficiently sensitive or specific, an initial marker that identifies the infection as a cause of the systemic inflammatory response is necessary. Recently the measure of procalcitonin has been proposed as that marker. The Procalcitonin is normally produced in thyroid C cells and is the precursor of calcitonin. A specific protease converts procalcitonin to calcitonin , katacalcin and a terminal N residue. Under normal conditions all the Procalcitonin is converted and nothing reaches the bloodstream, therefore, procalcitonin levels are undetectable (<0.1ng / ml) in a healthy person. During a severe infection with systemic manifestations the levels can increase up to 100 ng / ml. These increases in procalcitonin do not produce an increase in calcitonin because the half-life of this is 10 minutes while that of procalcitonin is 25-30 hours in the serum.In the presence of severe and generalized bacterial, parasitic or mycotic infections with systemic manifestations, and procalcitonin levels increase. In severe viral infections or inflammatory reactions of non-infectious origin, procalcitonin does not increase or shows only a moderate increase. Procalcitonin was approved by the FDA in January 2005. It has not been evaluated by the Technology Assessment Center (TEC) of the BCBS Association. <a id="