D-dimer prognostic role in non thromboembolism conditions

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

D-dimer lab test can be elevated in conditions other than venous thromboembolism. Because D-dimer is a sensitive test that lacks specificity, it is considered only useful in ruling out DVT and/or PE. Since D-dimer elevation is a physiologic process related to fibrinolytic activity that counteracts the extrinsic coagulation pathway activation, it is understandably not exclusive to venous thromboembolism (VTE) and can be present in other physiologic and pathological processes.[1] D-dimer elevation is not diagnostic of PE and can sometimes be a misleading lab value that is cost-inefficient, predisposes patients to high doses of unnecessary computed tomography (CT) radiation exposure, and delays appropriate diagnostic and therapeutic work-up.[2][3]

D-Dimer and Non Thromboembolism Conditions

Age

D-dimer levels physiologically increase with age, making the usefulness of D-dimer among the elderly less significant. The exact mechanism of D-dimer increase with age is poorly understood. It is thought to be related to the expected increase in patient co-morbidities and thrombotic events that occur with age, and that also happen to elevate D-dimer levels. The use of D-dimer in elderly nonetheless remains helpful in diagnosing VTE in low and intermediate risk patients. Age-adjusted D-dimer levels are thought to be useful, especially for the elderly. However, specific age-adjusted values have not been released yet.[4]

Aortic Dissection

Elevated levels of D-dimer lab test has been used to rapidly rule out emergencies such as acute aortic dissection (AAD). More than 15 studies that enrolled more than 400 patients have evaluated the use of D-dimer in AAD. With the absence of specific biomarkers, the clinical diagnosis of AAD remains a challenge for clinicians based on clinical suspicion alone. A meta analysis for D-dimer testing in AAD revealed that D-dimer has 97% sensitivity and 59% specificity in diagnosis of AAD. The diagnostic cut-off D-dimer value for patients with AAD ranges between 0.1 and 0.9 µg/mL., with sensitivities ranging between 100% and 86% respectively. Using D-dimer cut-off value similar to that for PE at a level of 0.5 µg/mL is considered an appropriate level that has a negative predictive value that approximately reaches 100%.[1]

Atrial Fibrillation

D-dimer levels are also elevated in patients with atrial fibrillation (AF), especially in those who are known to have established several embolism risk factors.[5] In 2003, Somloi et al. measured D-dimer levels in 73 patients with AF prior to TEE-guided cardioversion; they concluded that although D-dimer is unspecific, D-dimer concentration < 0.06 µg/ml provides a negative predictive value of 98%.[6] Habara et al. concluded that D-dimer concentration of 0.115 µg/mL was an optimal cut-off value to detect left atrial appendange (LAA) thrombus; the NPV was 97% irrespective of co-morbidities, such as congestive heart failure, or stroke.[5] Even in AF patients receiving appropriate Warfarin anticoagulation therapy, D-dimer levels remained abnormally high.[7]

It was further found that AF patients with D-dimer levels > 0.15 µg/mL were at a significantly greater risk of thrombo-embolic events than other patient subgroups. As such, the level 0.15 µg/mL is currently considered an accepted threshold value for increased rate of thrombo-embolic events in patients with AF. Nonetheless, increased number of risk factors bypasses the importance of D-dimer in AF patients and thus, patients with multiple risk factors are at high risk of thrombo-embolic events regardless of D-dimer levels and anticoagulation therapy. As such, D-dimer alone in patients with AF must be coupled to clinical risk factors for adequate assessment of thrombo-embolic risk.[7]

According to Diego et al., elevated D-dimer level is significantly associated with increasing severity of atherosclerosis based on ultrasound detection of carotid plaques and overall cardiovascular decline.[8][9]

Coronary Artery Disease

Since D-dimers alterations reflect thrombus turnover, levels are expected to be increased in ischemic heart disease and coronary angina. D-dimer levels are significantly associated with a 1.5 fold increase in coronary artery disease (CAD) and in subclinical atherosclerosis.[10] In patients with CAD, the median D-dimer value was 0.112 µg/mL vs. only 0.0028 µg/mL in patients without CAD. The positive correlation between D-dimer, fibrinogen, plasma viscosity, and interleukin-6 seem to be of importance in understanding the association of D-dimer with inflammatory products.[11] The most important value that D-dimer carries is its prediction of future cardiac events in various patient age groups, in both genders, and in patients with known peripheral arterial disease and myocardial infarction.[12][13][14][15][16][17] Despite obvious associations, some still question the use of D-dimer in providing informative or additional clinical data in the diagnosis or management of myocardial ischemia.[18]

According to a prospective study and metaanalysis, D-dimers level were found to correlate with CAD with an odds ratio of 1.67 (95% CI, 1.31 to 2.13; P<0.0001).[19] This finding can be explained by the fact that CAD might be associated with activation of the coagulation cascade and increased fibrin turnover.[20]

In a study by Tataru et al. in 2000 that recruited 1112 male and 299 female patients, the significant association between and previous MI was further emphasized.[21]

Liver Disease

Cirrhosis is considered a hypercoagulable state due to altered physiology of hemostasis secondary to the disease due to the physiological role the liver plays in the synthesis of thrombopoietin and coagulation factors,[22] decrease in fibrinolytic inhibitors, and reduced clearance of tissue plasminogen activator.[23] Platelet dysfunction and thrombocytopenia are frequent in liver cirrhosis, along with prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT).[22] Elevated D-dimer level is seen in more than 75% of patients with advanced liver disease. Significant elevation correlates with worse liver outcomes, as demonstrated by Child-Pugh classification. It demonstrates features of fibrinolysis in these patients when levels are just above 0.2 µg/mL.[24][25] In a study that included 188 patients, D-dimer was considered of high specificity in patients with Child-Pugh class A or B, of cut-off values > 0.56 µg/mL and > 1.18 µg/mL respectively; whereas it was highly sensitive in patients with class C with cut-off value > 0.77 µg/mL with lower specificity in this particular class probably due to patients’ advanced state of liver dysfunction. [26]

D-dimer is suggested to have a prognostic role in liver disease because it was found to be a significant predictor of death.[27]

D-dimer elevation is notably seen in patients with portal vein thrombosis (PVT) regardless of Child-Pugh class, a complication of portal hypertension that affects approximately 0.6-26% of patients with liver cirrhosis in general and approximately 35% of patients with cirrhosis from hepatocellular carcinoma (HCC).[23] In patients with worse outcomes of chronic liver disease Child-Pugh class C, D-dimer level of ≥ 0.55 µg/mL was 100% sensitive to diagnose PVT when measured.[28]

Malignancy

D-dimer is significantly associated with increased incidence of malignancy. The younger patient population, especially under 60 years, seem to be of particular concern for overt or occult cancer forms when D-dimer values are > 4 µg/mL .[29] Data regarding the correlation of malignancy with D-dimer shows that increasing D-dimer values are significantly more associated with malignancy than lower, yet abnormal, values. In patients with D-dimer > 8 µg/mL, the rate of malignancy following an episode of DVT was approximately 50%.[30] Similarly, patients with thrombosis who have low D-dimer values < 1 µg/mL are less likely to have an underlying malignancy.[31]

According to the Vienna Cancer and Thrombosis Study (CATS) that evaluated 1178 cancer patients, D-dimer was highest at a median of approximately 1.2 µg/mL in pancreatic cancer, followed by 1.08 µg/mL in gastric cancer, then 0.84 µg/mL in lung cancer, 0.81 µg/mL in colorectal cancers.[32] Significant association was also seen with lower D-dimer values and other malignancies, such as brain cancer (0.66 µg/mL), lymphomas (0.61 µg/mL), prostate cancer (0.46 µg/mL) and finally breast cancers (0.46 µg/mL).[32]

In a different study investigating endothelial, platelet and coagulation factors activation, patients with multiple myeloma undergoing treatment were found to have elevated D-dimers. In fact, 3 out of 4 patients who had elevated D-dimer levels beyond 500 mg/L developed DVT. Hence, D-dimer might play a role in stratifying patients with multiple myeloma who are at high risk of DVT.[33]

Not only is D-dimer associated with the presence of malignancy, but also it correlates with tumor bulk, metastasis, and overall patient prognosis and mortality.[34]

Normal Pregnancy

It is well known that physiological changes in the hypercoagulable state of normal pregnancy include alterations in coagulation and fibrinolysis systems. Pregnant women are at increased risk of VTE, and consumptive coagulopathies, such as DIC. D-dimer levels gradually increase in pregnancy and are believed to reach their peak values on day one post-partum, after which steady decline is observed to reach normal pre-pregnancy values approximately 42 days after delivery.[35] D-dimer surpasses normal range of 0.5 µg/mL in pregnant women starting the first trimester; where 79- 84% of pregnant women have normal D-dimer levels in the first trimester. This percentage declines to reach 22-33% in the second trimester, and only 0-1% in the third trimester. When studying D-dimer levels in 89 healthy pregnant women, Kovac and colleagues proposed in 2010 a new threshold of D-dimer levels for pregnancy to rule out VTE. They suggested D-dimer cut-off values of 0.286 µg/mL, 0.457 µg/mL, and 0.644 µg/mL in pregnant women in their first, second and third trimesters, respectively.[36][37]

Primary Pulmonary Hypertension

Elevated D-dimer levels are shown to be associated with idiopathic primary pulmonary hypertension (PPH) and correlates with severity of disease, New York Heart Association (NYHA) functional class, and survival when evaluated in a small study that included 14 patients.[38][39]

The sensitivity of D-dimer in diagnosing chronic thromboembolic pulmonary hypertension (CTEPH) is low in comparison to its sensitivity in other utilities. In a study that included 34 patients with CTEPH, the sensitivity of D-dimer in diagnosing CTEPH was only 37%, whereas the specificity was 46%. Hence, it cannot be used to rule in or rule out CTEPH.[38][39]

Renal Disease

D-dimer levels is correlated with nephrotic syndrome and other renal diseases. While some postulate that D-dimer elevation is associated with renal clearance,[40] data is conflicting as to whether D-dimer elevation may be less likely correlated with renal clearance as much as it is associated with proteinuria.[41] Nevertheless, the increase of hemostatic markers, such as D-dimer in renal disease, are considered risk factors for VTE in patients with renal disease.[42]

Nephrotic syndrome is considered a hypercoagulable state that is notoriously associated with DVT and PE. Among 100 patients with proteinuria, 53% had elevated D-dimer levels. When proteinuria was more than 1g/24 hours, elevation of D-dimer levels was seen in 69% of patients with proteinuria. D-dimer is believed to be related to the heavy proteinuria in nephrotic syndrome and subsequent hepatic synthesis of fibrinogen, where strong association between D-dimer elevation and hypoalbuminemia is found. It is also suggested that elevated serum fibrinopeptide A, thrombin-antithrombin III complex, along with products of thrombin and prothrombin, and the state of activated hemostasis in nephrotic syndrome causes the elevation of D-dimer with no evidence of clinical thrombosis.[43][44][41]

Sepsis and Septic Shock

D-dimer levels are almost always increased in patients with sepsis, septic shock, and disseminated intravascular coagulation (DIC). According to the Recombinant Human Activated Protein C Woldwide Evaluation in Severe Sepsis (PROWESS) trial that included 1,690 septic patients, D-dimer was elevated in approximately 100% of patients.[45][46][47] Increase level of D-dimer is correlated with worsening severity and death. For instance, according to one study higher D-dimer levels were correlated with high risk of 28 day mortality such as the odds ratio are 2.07 (CI=95%) and 3.03 (CI=95%) in patients having a D-dimer level >1180 and >2409 respectively.[48] On the other hand, its decrease was associated with resolution of sepsis.[45][46][47] Higher D-dimer levels were correlated with high risk of 28 day mortality such as the odds ratio are 2.07 (CI=95%) and 3.03 (CI=95%) in patients having a D-dimer level >1180 and >2409 respectively.[48]

Sickle Cell Disease

The pathogenesis and clinical manifestations of sickle cell disease are mostly related to its hypercoagulable sickle-shaped red blood cells that contain phosphatydil serine moieties that contribute to their thrombogenic nature. In addition, endothelial dysfunction, sluggish blood flow, and increased transit time, all of which are associated with generation of subclinical or clinically relevant thrombin, are all factors generally augmented in patients with sickle cell disease. Elevated D-dimer levels is commonly found in up to 68% of homozygous sickle cell disease patients experiencing sickling crises and frequently associated with abnormal chest X-ray (CXR) findings.[49][50]

Stroke

Elevated D-dimer values can also be used to predict acute cerebrovascular events and subtypes. Levels increase remarkably during first 6 hours of stroke onset in patients with large occlusion and those being treated with intravenous thrombolytics regardless of time of artery recanalization.[51] D-dimer seems to have shown association with infarction volume[52] and with cardioembolic strokes but not atherothrombotic or lacunar strokes. According to Ageno et al. in 2002, the optimal D-dimer cut-off point for predicting cardioembolic stroke is 2 µg/mL with 93.2% specificity and 59.3% sensitivity. In contrast, the cut-off point for predicting lacunar stroke in the same study was 0.54 µg/mL with 96.2% specificity and 61.3% sensitivity.[53] Although it is suggested as a screening test for patients presenting with acute-onset headaches,[54] triage for high-risk patients who require antithrombotic therapy, and evaluating progressing strokes, defined by clinical worsening of symptoms following admission, the prognostic role of D-dimer in cases of strokes is unclear and yet to be determined.[55]

Surgery

D-dimer levels may be elevated after surgery and trauma independent of VTE and PE. The diagnosis of post-operative VTE, a common complication following surgery, becomes even a more challenging diagnosis for this specific subset of patients given the unpredictable and heterogeneous variation of post-operative D-dimer levels. The dynamics behind D-dimer elevation following surgery and trauma are poorly understood.[56]

In a study of 154 patients categorized according to different types of abdominal surgeries, surgeries that did not include entering the abdominal cavity did not reveal elevation in D-dimer. In contrast, approximately 44% of open and laparoscopic intra-abdominal and retroperitoneal (and liver) surgeries were associated with elevated D-dimer levels that normalized after 25 and 38 days post-operatively respectively. D-dimer was found to generally peak around day 7 post-operation. The right time post-operatively to use D-dimer without the effect of the surgery itself is yet to be determined, but believed to be more than 5 weeks following intra-abdominal and retroperitoneal. It is thought that following peak, D-dimer levels decline at a rate of 6% every day.( PMID: 19474701 - Dindo et al. 200). The length of the surgery was associated with the elevation of D-dimer. However, no cut-off surgery length is determined.[57]

Orthopedic surgeries are also associated with an increase in D-dimer levels. In a study that recruited 78 patients with cemented or hybrid total hip replacement and uncemented total knee replacement. During the first 7 days post-op, D-dimers were significantly elevated particularly on day 1 and 7 post-operatively, showing a double-peak distribution.[58][59]

References

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  39. ↑ 39.0 39.1 Arunthari V, Burger CD (2009). "Utility of d-dimer in the diagnosis of patients with chronic thromboembolic pulmonary hypertension". Open Respir Med J. 3: 85–9. doi:10.2174/1874306400903010085. PMC 2703202. PMID 19572023.
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  46. ↑ 46.0 46.1 Kinasewitz GT, Yan SB, Basson B, Comp P, Russell JA, Cariou A; et al. (2004). "Universal changes in biomarkers of coagulation and inflammation occur in patients with severe sepsis, regardless of causative micro-organism [ISRCTN74215569]". Crit Care. 8 (2): R82–90. doi:10.1186/cc2459. PMC 420030. PMID 15025782.
  47. ↑ 47.0 47.1 Nguyen HB, Rivers EP, Abrahamian FM, Moran GJ, Abraham E, Trzeciak S; et al. (2006). "Severe sepsis and septic shock: review of the literature and emergency department management guidelines". Ann Emerg Med. 48 (1): 28–54. doi:10.1016/j.annemergmed.2006.02.015. PMID 16781920.
  48. ↑ 48.0 48.1 Rodelo JR, De la Rosa G, Valencia ML, Ospina S, Arango CM, Gómez CI; et al. (2012). "D-dimer is a significant prognostic factor in patients with suspected infection and sepsis". Am J Emerg Med. 30 (9): 1991–9. doi:10.1016/j.ajem.2012.04.033. PMID 22795996.
  49. ↑ Dar J, Mughal I, Hassan H, Al Mekki TE, Chapunduka Z, Hassan IS (2010). "Raised D-dimer levels in acute sickle cell crisis and their correlation with chest X-ray abnormalities". Ger Med Sci. 8: Doc25. doi:10.3205/000114. PMC 2975260. PMID 21063468.
  50. ↑ Setty BN, Rao AK, Stuart MJ (2001). "Thrombophilia in sickle cell disease: the red cell connection". Blood. 98 (12): 3228–33. PMID 11719358.
  51. ↑ Skoloudík D, Bar M, Sanák D, Bardon P, Roubec M, Langová K; et al. (2010). "D-dimers increase in acute ischemic stroke patients with the large artery occlusion, but do not depend on the time of artery recanalization". J Thromb Thrombolysis. 29 (4): 477–82. doi:10.1007/s11239-009-0372-9. PMID 19568692.
  52. ↑ Park YW, Koh EJ, Choi HY (2011). "Correlation between Serum D-Dimer Level and Volume in Acute Ischemic Stroke". J Korean Neurosurg Soc. 50 (2): 89–94. doi:10.3340/jkns.2011.50.2.89. PMC 3206284. PMID 22053225.
  53. ↑ Ageno W, Finazzi S, Steidl L, Biotti MG, Mera V, Melzi D'Eril G; et al. (2002). "Plasma measurement of D-dimer levels for the early diagnosis of ischemic stroke subtypes". Arch Intern Med. 162 (22): 2589–93. PMID 12456231.
  54. ↑ Squizzato A, Ageno W (2005). "D-dimer testing in ischemic stroke and cerebral sinus and venous thrombosis". Semin Vasc Med. 5 (4): 379–86. doi:10.1055/s-2005-922484. PMID 16302160.
  55. ↑ Barber M, Langhorne P, Rumley A, Lowe GD, Stott DJ (2006). "D-dimer predicts early clinical progression in ischemic stroke: confirmation using routine clinical assays". Stroke. 37 (4): 1113–5. doi:10.1161/01.STR.0000209240.63821.1a. PMID 16527998.
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  58. ↑ Shiota N, Sato T, Nishida K, Matsuo M, Takahara Y, Mitani S; et al. (2002). "Changes in LPIA D-dimer levels after total hip or knee arthroplasty relevant to deep-vein thrombosis diagnosed by bilateral ascending venography". J Orthop Sci. 7 (4): 444–50. doi:10.1007/s007760200077. PMID 12181657.
  59. ↑ Rafee A, Herlikar D, Gilbert R, Stockwell RC, McLauchlan GJ (2008). "D-Dimer in the diagnosis of deep vein thrombosis following total hip and knee replacement: a prospective study". Ann R Coll Surg Engl. 90 (2): 123–6. doi:10.1308/003588408X261627. PMC 2443306. PMID 18325211.

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