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Figure 1: Immature Calcitonin
Medical diagnostics
A 3D cartoon of procalcitonin's parent compound, calcitonin.png
A 3D cartoon of procalcitonin's parent compound, calcitonin

Procalcitonin (PCT) is a peptide precursor of the hormone calcitonin, the latter being involved with calcium homeostasis. It arises once preprocalcitonin is cleaved by endopeptidase.[1] It was first identified by Leonard J. Deftos and Bernard A. Roos in the 1970s.[2] It is composed of 116 amino acids and is produced by parafollicular cells (C cells) of the thyroid and by the neuroendocrine cells of the lung and the intestine.

The level of procalcitonin in the blood stream of healthy individuals is below the limit of detection (0.01 µg/L) of clinical assays.[3] The level of procalcitonin rises in a response to a pro-inflammatory stimulus, especially of bacterial origin. It is therefore often classed as an acute phase reactant.[4]:542 In this case, it is produced mainly by the cells of the lung and the intestine. 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.


Figure 2: Production pathway of PCT and CT in healthy and infected individuals via the induction of CALC-1 gene

PCT is a member of the calcitonin (CT) superfamily of peptides. It is peptide of 116 amino acid with an approximate molecular weight of 14.5 kDa, and its structure can be divided into three sections (see Figure 1):[5] amino terminus (represented by the ball and stick model in Figure 1), immature calcitonin (shown in Figure 1 from PDB as the crystal structure of procalcitonin is not yet available), and calcitonin carboxyl-terminus peptide 1.[5] Under normal physiological conditions, active CT is produced and secreted in the C-cells of the thyroid gland after proteolytic cleavage of PCT, meaning, in a healthy individual, that PCT levels in circulation are very low (<.05 ng/mL).[6] The pathway for production of PCT under normal and inflammatory conditions are shown in Figure 2.[7] During inflammation, LPS, microbial toxin, and inflammatory mediators, such as IL-6 or TNF-α, induce the CALC-1 gene in adipoctyes, but PCT never gets cleaved to produce CT.[7] In a healthy individual, PCT in endocrine cells is produced by CALC-1 by elevated calcium levels, glucocorticoids, CGRP, glucagon, or gastrin, and is cleaved to form CT, which is released to the blood.[7]

PCT is located on the CALC-1 gene on chromosome 11.[5] Bacterial infections induce a universal increase in the CALC-1 gene expression and a release of PCT (>1 μg/mL).[6] Expression of this hormone occurs in a site specific manner.[5] In healthy and non-infected individuals, transcription of PCT only occurs in neuroendocrine tissue, except for the C cells in the thyroid. The formed PCT then undergoes post-translational modifications, resulting in the production small peptides and mature CT by removal of the C-terminal glycine from the immature CT by peptidylglycine α-amidating monooxygenase (PAM).[8] In a microbial infected individual, non-neuroendocrine tissue also secretes PCT by expression of CALC-1. A microbial infection induces a substantial increase in the expression of CALC-1, leading to the production of PCT in all differentiated cell types.[9] The function of PCT synthesized in nonneuroendocrine tissue due to a microbial infection is currently unknown, but, it’s detection aids in the differentiation of inflammatory processes.[5]

Diagnostic Advantages

Due to PCT’s variance between microbial infections and healthy individuals, it has become a marker to improve bacterial infections identification and guide antibiotic therapy.[10] Table 1 is a summary from Schuetz, Albrich, and Mueller, summarizing the current data of selected, relevant studies investigating PCT in different types of infections, where ✓ represents moderate evidence in favor of PCT; ✓✓ is good evidence in favor of PCT; ✓✓✓ is strong evidence in favor of PCT; ~ is evidence in favor or against the use of PCT or still undefined.

Table 1: Diagnostic Summary of Studies Investigating the Therapeutic Advantages of PCT[10]

Infection Type/Setting Study Design PCT Cut-Off (ug/L) PCT Benefit Conclusion References
Abdominal Infections observational 0.25 ~ PCT may help exclude ischemia and necrosis in bowel blockage ,[11][12][13][14]
Arthritis observational 0.1-0.25 PCT differentiates non-infectious (gout) arthritis from true infection ,[15][16][17]
Bacteremic infections observational 0.25 ✓✓ Low PCT levels help rule out microbial infections ,[18][19][20]
Blood stream infection (primary) observational 0.1 ✓✓ PCT differentiates contamination from true infection [21]
Bronchitis RCT 0.1-0. 5 ✓✓✓ PCT reduces antibiotic exposure without adverse outcomes in the ED ,[22][23]
COPD exacerbation RCT 0.1-0. 5 ✓✓✓ PCT reduces antibiotic exposure without adverse outcomes in the ED and hospital ,[22][23][24]
Endocarditis observational 2.3 PCT is an independent predictor with high diagnostic accuracy for acute endocarditis ,[25][26]
Meningitis before-after 0.5 PCT reduces antibiotic exposure during outbreak of viral meningitis ,[27][28][29]
Neutropenia observational 0.1-0.5 PCT is helpful at identifying neutropenic patients with systemic bacterial infection ,[30][31][32]
Pancreatitis observational 0.25-0.5 ~ PCT correlates with severity and extent of infected pancreatitis ,[33][34]
Pneumonia RCT 0.1-0. 5; 80-90% ↓ ✓✓✓ PCT reduces antibiotic without adverse outcomes exposure in the hospital ,[22][23][35][36][37][38]
Postoperative fever observational 0.1-0.5 PCT differentiates non-infectious fever from post-operative infections [39]
Postoperative infections RCT 0.5-1.0; 75-85% ↓ ✓✓ PCT reduces antibiotic exposure without adverse outcomes in the surgical ICU ,[40][41]
Severe sepsis/Shock RCT 0.25-0.5; 80-90% ↓ ✓✓✓ PCT reduces antibiotic exposure without adverse outcomes in the ICU ,[42][43]
Upper respiratory tract infections RCT 0.1-0.25 ✓✓ PCT reduces antibiotic exposure without adverse outcomes in primary care [44]
Urinary tract infections observational 0.25 PCT correlates with severity of urinary tract infections ,[19][45]
Ventilator-associated pneumonia RCT 0.1-0.25 ✓✓ PCT reduces antibiotic exposure without adverse outcomes ,[43][46]

Medical uses


Measurement of procalcitonin can be used as a marker of severe sepsis caused by bacteria and generally grades well with the degree of sepsis,[47] 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.[48] Evidence is emerging that procalcitonin levels can reduce unnecessary antibiotic prescribing to people with lower respiratory tract infections.[49] Currently, procalcitonin assays are widely used in the clinical environment.[50]

A meta-analysis reported a sensitivity of 76% and specificity of 70% for bacteremia.[51]


Given procalcitonin is a blood marker for bacterial infections, evidence shows that it is a useful tool in guiding the initiation and duration of antibiotics in patients with bacterial pneumonia and other acute respiratory infections.[52] The use of procalcitonin guided antibiotic therapy leads to lower mortality, less antibiotic usage, decreased side effects due to antibiotics and promotes good antibiotic stewardship.[52]

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%.[53]


PCT, possibly together with CRP, is used to corroborate the MELD score.[54][55]


Excessive overdose on amphetamine or its analogs can induce systemic inflammation; in a case of amphetamine overdose, sans bacterial infection, significant elevations in procalcitonin were observed.[56]


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