Coagulogram Above or Below Normal: Causes in Athletes and What to Do
Having received a coagulogram with “↑” or “↓” marks, a person often does not even understand the main thing — whether the blood has “thickened” or, on the contrary, clots worse. For different markers this logic is opposite, and some deviations are explained not by disease but by how the blood was drawn. The editorial team examines typical causes of deviations in athletes and offers a sequence of actions.
How to read the direction of a deviation
The main trap of a coagulogram is the markers measured in seconds. Prothrombin time, aPTT, and thrombin time show how much time plasma needs to clot in the tube. So if these values are higher than normal, the blood clots more slowly, meaning we are dealing with hypocoagulation. Lower values formally indicate accelerated clotting, although the clinical significance of a shortened time is less clear-cut.
INR behaves the same way as prothrombin time: an INR above normal means reduced clotting. Prothrombin by Quick, expressed as a percentage, changes in the opposite direction — its decrease corresponds to hypocoagulation. That is exactly why on one form you can see “INR ↑” and “Quick ↓,” and this is not a contradiction but the same result.
Fibrinogen and D-dimer are measured as concentrations. Elevated fibrinogen indicates inflammation or an increased potential for clot formation, a reduced level — its loss or insufficient synthesis. A D-dimer above the threshold means that fibrin has formed and is breaking down somewhere in the body, but it does not indicate where or why.
Reference intervals depend on the reagents and the analyzer, so you should be guided by the limits given specifically on your form. For D-dimer in people over 50, some laboratories apply an age-based adjustment of the threshold.
| Marker | Above normal | Below normal |
|---|---|---|
| PT / INR | Clotting reduced: vitamin K antagonists, vitamin K deficiency, liver diseases | Clinical significance small; often preanalytical causes |
| Prothrombin by Quick, % | Usually of no clinical significance | Clotting reduced (same as INR ↑) |
| aPTT | Heparin, deficiency of factors VIII, IX, XI, lupus anticoagulant | Activation of clotting, high factor VIII, collection errors |
| Fibrinogen | Inflammation, injury, infection, smoking, estrogens | Liver disease, DIC syndrome, hereditary defects |
| D-dimer | Thrombosis, pulmonary embolism, injury, surgery, inflammation, prolonged load | A normal level is a variant of the norm |
Changes toward increased clotting
The most frequent finding in athletes is moderately elevated fibrinogen. It is an acute-phase protein, and its level rises with any inflammation: an acute respiratory infection, an exacerbation of chronic tonsillitis, a fresh injury, after surgery. Smoking, excess body weight, and taking estrogens also raise fibrinogen. Such a result is not a diagnosis in itself, but it indicates that a source of inflammation should be sought.
An elevated D-dimer after a marathon, ultramarathon, or long cycling start has been described in a number of studies and, as a rule, normalizes within a day or two. That is exactly why a test given the morning after a competition can be misleading. However, if a high D-dimer is combined with leg swelling, calf pain, shortness of breath, or chest pain, it cannot be written off as being due to the load.
A shortened aPTT is often associated with a high level of factor VIII, which in turn rises with stress, inflammation, and intense physical exercise. But no less often it is the result of a poorly performed blood draw, in which clotting has already begun in the tube.
A separate group of causes is associated with hormonal pharmacology. Anabolic-androgenic steroids raise the hematocrit and change the balance of procoagulant and fibrinolytic proteins; the literature describes thrombotic complications in young people without other risk factors (Chang et al., 2018). Estrogen-containing contraceptives raise the levels of a number of coagulation factors. In such situations a coagulogram does not always look pathological, so the risk is assessed primarily by clinical factors.
- fibrinogen ↑ — look for inflammation, infection, injury;
- D-dimer ↑ after a race — retake it after a few days of rest, if there are no symptoms;
- D-dimer ↑ together with symptoms of thrombosis — emergency medical care;
- high hematocrit plus hormonal drugs — a mandatory doctor's consultation.
Changes toward decreased clotting
A prolongation of prothrombin time and an increase in INR in a person who is not taking anticoagulants is most often explained by vitamin K deficiency or impairment of the liver's synthetic function. Vitamin K deficiency is possible with a very restricted diet with a minimum of green vegetables, prolonged antibiotic use, or impaired fat absorption.
The liver synthesizes most coagulation factors, so with serious liver damage the INR rises. For athletes this is an important point: oral 17-alpha-alkylated steroids are known for their hepatotoxicity, and a prolongation of prothrombin time together with a rise in bilirubin is an alarming signal that requires evaluation by a hepatologist. At the same time, in chronic liver disease the natural anticoagulants are also reduced, so a “prolonged” INR does not mean protection from thrombosis (Tripodi, Mannucci, 2011).
An isolated prolongation of aPTT with a normal INR may indicate a deficiency of intrinsic-pathway factors (mild forms of hemophilia or von Willebrand disease, which are sometimes first detected in adulthood before surgery) or the presence of a lupus anticoagulant. Paradoxically, a lupus anticoagulant in the body is associated not with bleeding but with an increased risk of thrombosis.
A reduced fibrinogen in an athlete is rare and is usually associated with liver disease, massive bleeding, or hereditary disorders. Aspirin, nonsteroidal anti-inflammatory drugs, and omega-3 in usual doses mainly affect platelets and hardly change a standard coagulogram — so mild bleeding tendency with a normal test does not rule out a platelet problem.
False results and laboratory errors
A coagulogram is among the tests most sensitive to preanalytical errors, that is, to everything that happens before the sample reaches the analyzer. An insufficiently filled tube with citrate changes the ratio of blood to anticoagulant and prolongs the clotting time. Too long an application of the tourniquet, a difficult draw over several attempts, and hemolysis activate clotting and can shorten the aPTT.
A delay in delivering the sample to the laboratory or an incorrect storage temperature affects labile factors, especially factor VIII. Blood taken from a catheter through which heparin was administered gives a sharply prolonged aPTT.
In athletes with a very high hematocrit (over 55%) there is less plasma in the tube, and thus an excess of citrate, which artificially prolongs PT and aPTT. For such cases laboratory standards recommend adjusting the volume of preservative — a high hematocrit should be reported in advance.
Finally, results obtained in different laboratories may differ because of different reagents. If you are tracking a trend, retake the test at the same place.
What to do with a deviating result
The first step is to assess whether there are symptoms. Unilateral swelling and pain in the lower leg, sudden shortness of breath, chest pain, hemoptysis, as well as heavy bleeding that does not stop, require emergency care regardless of the numbers on the form.
If there are no symptoms, it is worth analyzing the circumstances of the collection: whether the test was given on an empty stomach, whether there was a competition or hard training the day before, whether you were ill at the time, which medications and supplements you were taking. Often it is exactly this that explains the deviation, and a control test after 1–2 weeks under correct conditions turns out to be normal.
Persistent deviations require a consultation with a general practitioner or hematologist. The doctor may order additional tests: a complete blood count with hematocrit, liver tests, individual coagulation factors, tests for lupus anticoagulant, genetic markers of thrombophilia. If thrombosis is suspected, an ultrasound examination of the veins is ordered.
Taking anticoagulants, aspirin “to thin the blood,” or vitamin K preparations on your own based on coagulogram results is unacceptable. These agents have a narrow therapeutic window and can cause both dangerous bleeding and the masking of a real problem. If the deviation is related to taking hormonal drugs, it is important for the doctor to know about this honestly — the risk assessment depends on it.
Editorial conclusions
To read a coagulogram it is important to remember the direction: prolonged PT, INR, and aPTT mean slowed clotting, while elevated fibrinogen and D-dimer indicate inflammation or activation of clot formation. Prothrombin by Quick changes in the opposite direction to INR.
In athletes most minor deviations are associated with inflammation, recent heavy load, injury, or blood-collection errors. More serious attention is required for persistent changes, a combination with symptoms, taking estrogens or hormonal drugs, a high hematocrit, and signs of liver damage.
The right strategy is to assess symptoms, retake the test under standard conditions, and discuss the result with a doctor without resorting to self-treatment.
We also recommend reading our materials on what a coagulogram shows, on the hematocrit in athletes, and on liver tests when using pharmacology.
References
- Tripodi A, Mannucci PM. The coagulopathy of chronic liver disease. N Engl J Med. 2011;365(2):147–156.
- Wells PS, Anderson DR, Rodger M, et al. Evaluation of D-dimer in the diagnosis of suspected deep-vein thrombosis. N Engl J Med. 2003;349(13):1227–1235.
- Chang S, Münster AB, Gram J, Sidelmann JJ. Anabolic androgenic steroid abuse: the effects on thrombosis risk, coagulation, and fibrinolysis. Semin Thromb Hemost. 2018;44(8):734–746.
- Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
- Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest. 2016;149(2):315–352.
- Hoffman M, Monroe DM 3rd. A cell-based model of hemostasis. Thromb Haemost. 2001;85(6):958–965.
Andriy Melnyk
A strength-sports coach and author of programs for beginner and intermediate levels. Writes about training planning.
