重组人降钙素原蛋白

CALCA

Calcitonin

Secreted.

Sepsis: Measurement of procalcitonin can be used as a marker of severe sepsis caused by bacteria and generally grades well with the degree of sepsis, although levels of procalcitonin in the blood are very low. PCT has the greatest sensitivity (85%) and specificity (91%) for differentiating patients with systemic inflammatory response syndrome (SIRS) from those with sepsis, when compared with IL-2, IL-6, IL-8, CRP and TNF-alpha. Evidence is emerging that procalcitonin levels can reduce unnecessary antibiotic prescribing to people with lower respiratory tract infections. Currently, procalcitonin assays are widely used in the clinical environment.
Pneumonia: Procalcitonin levels may be useful to distinguish bacterial infections from nonbacterial infections. This may help guide antibiotic use, which can help save on cost and drug resistance.
Kidney disease: Patients with chronic kidney disease and end-stage renal disease are at higher risk for infections, and procalcitonin has been studied in these populations, who often have higher levels. Procalcitonin can be dialyzed, and so levels are dependent upon when patients receive hemodialysis. While there is no formally accepted cutoff value for patients undergoing HD, using a value of greater or equal to 0.5 ng/mL yielded a sensitivity of 97-98% and a specificity of 70-96%.
Hepatitis: PCT, possibly together with CRP, is used to corroborate the MELD score.

Belongs to the calcitonin family.

The level of procalcitonin in the blood stream of healthy individuals is below the limit of detection (0.01 µg/L) of clinical assays. The level of procalcitonin rises in a response to a proinflammatory stimulus, especially of bacterial origin. It does not rise significantly with viral or non-infectious inflammations. With the derangements that a severe infection with an associated systemic response brings, the blood levels of procalcitonin may rise to 100 µg/L. In serum, procalcitonin has a half-life of 25 to 30 hours. Remarkably the high procalcitonin levels produced during infections are not followed by a parallel increase in calcitonin or a decrease in serum calcium levels.