Prothrombin time and what it reveals about liver function

Gain in-depth knowledge on liver function tests with this article on prothrombin time and partial thromboplastin time.
Last update26th Jan 2021

Let’s dive into prothrombin time (PT) and partial thromboplastin time (PTT) tests and discuss what PT can tell us about liver function.

The coagulation pathway is made up of the extrinsic, intrinsic, and common pathways. Prothrombin time is a coagulation test used to measure the integrity of the extrinsic and common coagulation pathways. Partial thromboplastin time measures the integrity of the intrinsic and common coagulation pathways.

Figure 1. The intrinsic, extrinsic, and common pathways of coagulation. Prothrombin time measures the integrity of the extrinsic and common pathways, while partial thromboplastin time measures the integrity of the intrinsic and common pathways.

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What are the normal ranges for PTT and PT?

Partial thromboplastin time has a normal range of 25–37 seconds. As well, prothrombin time is expressed in seconds or as a ratio called the international normalized ratio (INR). Prothrombin time has a normal range of 9.4–12.5 seconds or 0.9–1.1 INR.

Table 1. Normal ranges for partial thromboplastin time (PTT) and prothrombin time (PT).

What does an abnormal PT tell us?

Prothrombin time involves the interactions of factors I (fibrinogen), II (prothrombin), V, VII, and X. These factors are all synthesized by the liver. Remember, the common coagulation pathway is measured by both PT and PTT, but the extrinsic pathway is only measured by PT. So, if PT is abnormal and PTT is normal, we know the problem lies with the extrinsic pathway.

The clotting factors involved in the extrinsic pathway are factors III and VII. Factor VII has the shortest half-life of all the clotting factors, which is 4–6 hours. Thus, when the liver is injured and there is compromised liver function, factor VII levels quickly fall. Within a short time after significant liver dysfunction, PT is prolonged because the liver cannot make enough blood-clotting proteins. Consequently, it takes longer for the blood to clot.

So, if a patient has a normal PTT and an abnormal PT, we know that the abnormality must lie with one of the extrinsic pathway factors (e.g., III or VII). Since factor III is one of the reagents added when performing the PT test (and a factor III deficiency has never been described), we can conclude that the patient has low levels of factor VII.

Low factor VII levels may be due to reduced factor synthesis or the presence of a factor VII inhibitor (which is rare). Causes of reduced synthesis of factor VII include congenital or genetic disorders, liver disease, and warfarin. Liver disease is usually the culprit since congenital causes are rare and warfarin is easily ruled out.

Figure 2. Causes of reduced factor VII synthesis include congenital disorders, liver disease, and warfarin use.

As you can see, PT is an important test for assessing liver function. You can review the coagulation pathways and learn how to interpret PT and PPT in more detail in our Hematology and Coagulation Essentials course.

That’s it for now. If you want to improve your understanding of key concepts in medicine, and improve your clinical skills, make sure to register for a free trial account, which will give you access to free videos and downloads. We’ll help you make the right decisions for yourself and your patients.

Recommended reading

  • Chalasani, N, Younossi, Z, Lavine, JE, et al. 2012. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology142: 1592–1609. PMID: 22656328
  • Fuchs, S, Bogomolski-Yahalom, V, Paltiel, O, et al. 1998. Ischemic hepatitis: clinical and laboratory observations of 34 patients. J Clin Gastroenterol26: 183–186. PMID: 9600366
  • Lok, ASF and McMahon, BJ. 2007. Chronic hepatitis B. Hepatology45: 507–539. PMID: 17256718
  • Moussavian, SN, Becker, RC, Piepmeyer, JL, et al. 1985. Serum gamma-glutamyl transpeptidase and chronic alcoholism. Influence of alcohol ingestion and liver disease. Dig Dis Sci30: 211–214. PMID: 2857631
  • Myers, RP, Cerini, R, Sayegh, R, et al. 2003. Cardiac hepatopathy: clinical, hemodynamic, and histologic characteristics and correlations. Hepatology37: 393–400. PMID: 12540790
  • Rej, R. 1978. Aspartate aminotransferase activity and isoenzyme proportions in human liver tissues. Clin Chem24: 1971–1979. PMID: 213206
  • van de Steeg, E, Stránecký, V, Hartmannová, H, et al. 2012. Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver. J Clin Invest122: 519–528. PMID: 22232210

About the author

Amer Wahed, MD FRCPath
Professor and Vice Chair (Clinical Pathology) and Associate Residency Program Director in the Department of Pathology and Laboratory Medicine at the University of Texas, Health Science Center at Houston, USA.
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