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Partial Thromboplastin Time

Anatomy and Physiology · NLM MeSH · updated 2026-10-31 · version 1

Citations verified against PubMedNot yet clinician-reviewed9 referencesApproximately 4 min read

The time required for the appearance of fibrin strands following the mixing of plasma with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides).

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 3 complete abstracts (628 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

The time required for the appearance of fibrin strands following the mixing of plasma with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of blood coagulation. It is used as a screening test and to monitor heparin therapy.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Activated Partial Thromboplastin Time; Thromboplastin Time, Partial; Kaolin-Cephalin Coagulation Time; Coagulation Time, Kaolin-Cephalin; Kaolin Cephalin Coagulation Time; Coagulation Time, Cephalin-Kaolin; Coagulation Time, Cephalin Kaolin; Cephalin-Kaolin Coagulation Time.

Where it fits in the MeSH classification

Broader topics
Blood Coagulation Tests; Blood Physiological Phenomena
See also
Blood Coagulation

Related concepts

  • Fibrin
  • Plasma
  • Blood Coagulation
  • Heparin

Research landscape

PubMed indexes 7,762 records tagged with the MeSH heading “Partial Thromboplastin Time” (counts retrieved 2026-10-31). 1,019 of them (13.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,973 records.

Reviews account for 438 records (5.6%) and meta-analyses for 25. Randomized controlled trials number 447 (5.8%) as a share of all records on the topic.

PubMed records by publication periodthrough 1999: 2,973 records; 2000-2009: 1,703 records; 2010-2019: 2,067 records; 2020 onward: 1,019 records2,973through 19991,7032000-20092,0672010-20191,0192020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19992,973
2000-20091,703
2010-20192,067
2020 onward1,019
Share of records by publication typeReviews: 5.6 percent; Meta-analyses: 0.3 percent; Randomized controlled trials: 5.8 percentReviews5.6% (438)Meta-analyses0.3% (25)Randomized controlled trials5.8% (447)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 7,762 PubMed records
TypeRecordsShare
Reviews4385.6%
Meta-analyses250.3%
Randomized controlled trials4475.8%

Method: PubMed query "Partial Thromboplastin Time"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.

Reading the evidence in anatomy and physiology

Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Point-of-care testing for emergency assessment of coagulation in patients treated with direct oral anticoagulants
Ebner M, Birschmann I, Peter A, Spencer C, Härtig F, Kuhn J, et al.
2017Research article
Design not recorded in structured metadata
53cc by
PMID 28196509 · DOI · PMC5309971
Influence of factor XII deficiency on activated partial thromboplastin time (aPTT) in critically ill patients
Bachler M, Niederwanger C, Hell T, Höfer J, Gerstmeyr D, Schenk B, et al.
2019Research article
Design not recorded in structured metadata
46cc by
PMID 31124034 · DOI · PMC6744379
Diabetes mellitus is associated with shortened activated partial thromboplastin time and increased fibrinogen values
Zhao Y, Zhang J, Zhang J, Wu J
2011Research article
Design not recorded in structured metadata
40cc by
PMID 21297995 · DOI · PMC3030587

Point-of-care testing for emergency assessment of coagulation in patients treated with direct oral anticoagulants [1]

Research article Ebner M, Birschmann I, Peter A, Spencer C, Härtig F, Kuhn J, et al. · · 2017 · cited 53 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundPoint-of-care testing (POCT) of coagulation has been proven to be of great value in accelerating emergency treatment.
Closing excerpt
Retrospectively registered on 18 February 2015.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (245 words)

BackgroundPoint-of-care testing (POCT) of coagulation has been proven to be of great value in accelerating emergency treatment. Specific POCT for direct oral anticoagulants (DOAC) is not available, but the effects of DOAC on established POCT have been described. We aimed to determine the diagnostic accuracy of Hemochron® Signature coagulation POCT to qualitatively rule out relevant concentrations of apixaban, rivaroxaban, and dabigatran in real-life patients.MethodsWe enrolled 68 patients receiving apixaban, rivaroxaban, or dabigatran and obtained blood samples at six pre-specified time points. Coagulation testing was performed using prothrombin time/international normalized ratio (PT/INR), activated partial thromboplastin time (aPTT), and activated clotting time (ACT+ and ACT-low range) POCT cards. For comparison, laboratory-based assays of diluted thrombin time (Hemoclot) and anti-Xa activity were conducted. DOAC concentrations were determined by liquid chromatography-tandem mass spectrometry.ResultsFour hundred and three samples were collected. POCT results of PT/INR and ACT+ correlated with both rivaroxaban and dabigatran concentrations. Insufficient correlation was found for apixaban. Rivaroxaban concentrations at 95% specificity at PT/INR POCT ≤1.0 and ≤1.1 and ACT+ POCT ≤120 and ≤130 s. Dabigatran concentrations at 95% specificity at PT/INR POCT ≤1.1 and ≤1.2 and ACT+ POCT ≤100 s.ConclusionsHemochron® Signature POCT can be a fast and reliable alternative for guiding emergency treatment during rivaroxaban and dabigatran therapy. It allows the rapid identification of a relevant fraction of patients that can be treated immediately without the need to await the results of much slower laboratory-based coagulation tests.Trial registrationUnique identifier, NCT02371070 . Retrospectively registered on 18 February 2015.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28196509 · DOI · PMC5309971

Influence of factor XII deficiency on activated partial thromboplastin time (aPTT) in critically ill patients [2]

Research article Bachler M, Niederwanger C, Hell T, Höfer J, Gerstmeyr D, Schenk B, et al. · · 2019 · cited 46 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
FXII deficiency results in spontaneous prolongation of activated partial thromboplastin time (aPTT), which is widely used to monitor thromboprophylaxis.
Closing excerpt
Those patients received insufficient thromboembolic prophylaxis.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (239 words)

FXII deficiency results in spontaneous prolongation of activated partial thromboplastin time (aPTT), which is widely used to monitor thromboprophylaxis. Misinterpretation of spontaneously prolonged aPTT may result in omission of thromboembolic treatment or even unnecessary transfusion of blood products. This retrospective analysis was performed to calculate a threshold level of FXII resulting in aPTT prolongation. 79 critically ill patients with spontaneous prolongation of aPTT were included. A correlation analysis and a ROC curve for aPTT prolongation predicted by FXII level were created to find the FXII threshold level. Prolongation of aPTT was associated with disease severity. A significant inverse proportionality between FXII and aPTT was seen. A ROC curve for aPTT prolongation, predicted by FXII level (AUC 0.85; CI 0.76-0.93), revealed a FXII threshold level of 42.5%. Of our patients 50.6% experienced a FXII deficiency, in 80.0% of whom we found aPTT to be prolonged without a significantly higher bleeding rate. The FXII deficiency was more common in patients with higher SAPS3 scores, septic shock, transfusion of red blood cells and platelet concentrates as well as in patients receiving renal replacement therapy. Patients with a FXII deficiency and prolonged aPTT less often received anticoagulatory therapy although they were more severely ill. The rate of thromboembolic events was higher in these patients although the difference was not statistically significant. Of all patients with spontaneous aPTT prolongation 50.6% had a FXII level of 42.5% or less. Those patients received insufficient thromboembolic prophylaxis.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31124034 · DOI · PMC6744379

Diabetes mellitus is associated with shortened activated partial thromboplastin time and increased fibrinogen values [3]

Research article Zhao Y, Zhang J, Zhang J, Wu J · · 2011 · cited 40 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
ObjectiveThis study was designed to examine the relationship between shortened activated partial thromboplastin time (APTT) and increased fibrinogen values with diabetes mellitus.
Closing excerpt
ConclusionsShorter APTT and increased fibrinogen levels might be useful hemostatic markers in patients with diabetes and in patients at high risk for diabetes.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (144 words)

ObjectiveThis study was designed to examine the relationship between shortened activated partial thromboplastin time (APTT) and increased fibrinogen values with diabetes mellitus.MethodsAPTT, prothrombin time (PT), fibrinogen, fasting plasma glucose (FPG) and glycosylated hemoglobin A1c (HbA1c) levels were measured in 1,300 patients. Patients were divided into three groups according to their HbA1c and FPG levels.ResultsWhen participants were grouped according to their HbA1c levels, we found significantly shorter APTT values (26.9±5.6 s) and increased fibrinogen levels (3.1, 1.9-6.3 g/L) in the diabetes group when compared with the other two groups. When participants were grouped according to their FPG levels, we found significantly shorter APTT values (26.9±6.2 s) and increased fibrinogen levels (3.1, 1.8-6.2 g/L) in the diabetes group when compared with the euglycemic group.ConclusionsShorter APTT and increased fibrinogen levels might be useful hemostatic markers in patients with diabetes and in patients at high risk for diabetes.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 21297995 · DOI · PMC3030587

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article How to interpret and pursue an abnormal prothrombin time, activated partial thromboplastin time, and bleeding time in adults [4]
    Kamal AH, Tefferi A, Pruthi RK · Mayo Clin Proc · 2007 · cited 234 times (Europe PMC)
  • Research article Monitoring unfractionated heparin with the aPTT: time for a fresh look [5]
    Eikelboom JW, Hirsh J · Thromb Haemost · 2006 · cited 112 times (Europe PMC)
  • Research article Genetic associations for activated partial thromboplastin time and prothrombin time, their gene expression profiles, and risk of coronary artery disease [6]
    Tang W, Schwienbacher C, Lopez LM, Ben-Shlomo Y, Oudot-Mellakh T, Johnson AD, et al. · Am J Hum Genet · 2012 · cited 91 times (Europe PMC)
  • Research article Towards standardization of clot waveform analysis and recommendations for its clinical applications [7]
    Shima M, Thachil J, Nair SC, Srivastava A, Scientific and Standardization Committee · J Thromb Haemost · 2013 · cited 66 times (Europe PMC)
  • Research article Tests of global haemostasis and their applications in bleeding disorders [8]
    Nair SC, Dargaud Y, Chitlur M, Srivastava A · Haemophilia · 2010 · cited 62 times (Europe PMC)
  • Research article Standardization and clinical utility of thrombin-generation assays [9]
    Berntorp E, Salvagno GL · Semin Thromb Hemost · 2008 · cited 60 times (Europe PMC)

References

  1. Ebner M, Birschmann I, Peter A, Spencer C, Härtig F, Kuhn J, et al.. Point-of-care testing for emergency assessment of coagulation in patients treated with direct oral anticoagulants. . 2017. PMID 28196509 · DOI · PMC5309971
  2. Bachler M, Niederwanger C, Hell T, Höfer J, Gerstmeyr D, Schenk B, et al.. Influence of factor XII deficiency on activated partial thromboplastin time (aPTT) in critically ill patients. . 2019. PMID 31124034 · DOI · PMC6744379
  3. Zhao Y, Zhang J, Zhang J, Wu J. Diabetes mellitus is associated with shortened activated partial thromboplastin time and increased fibrinogen values. . 2011. PMID 21297995 · DOI · PMC3030587
  4. Kamal AH, Tefferi A, Pruthi RK. How to interpret and pursue an abnormal prothrombin time, activated partial thromboplastin time, and bleeding time in adults. Mayo Clin Proc. 2007. PMID 17605969 · DOI
  5. Eikelboom JW, Hirsh J. Monitoring unfractionated heparin with the aPTT: time for a fresh look. Thromb Haemost. 2006. PMID 17080209 · DOI
  6. Tang W, Schwienbacher C, Lopez LM, Ben-Shlomo Y, Oudot-Mellakh T, Johnson AD, et al.. Genetic associations for activated partial thromboplastin time and prothrombin time, their gene expression profiles, and risk of coronary artery disease. Am J Hum Genet. 2012. PMID 22703881 · DOI · PMC3397273
  7. Shima M, Thachil J, Nair SC, Srivastava A, Scientific and Standardization Committee. Towards standardization of clot waveform analysis and recommendations for its clinical applications. J Thromb Haemost. 2013. PMID 23648068 · DOI
  8. Nair SC, Dargaud Y, Chitlur M, Srivastava A. Tests of global haemostasis and their applications in bleeding disorders. Haemophilia. 2010. PMID 20590862 · DOI
  9. Berntorp E, Salvagno GL. Standardization and clinical utility of thrombin-generation assays. Semin Thromb Hemost. 2008. PMID 19085768 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-31.

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At a glance

7,762
PubMed records on this heading
13%
published since 2020
438
review articles
447
randomized trials
9
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

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