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D-dimer Interference

With reference to our September 8, 2016 discussion entitled Still More on Xarelto and D-dimer, attached is information on another individual with whom I have been corresponding for several months whose D-dimer remains moderately to markedly elevated but whose lab results have demonstrated there is no human anti-mouse antibody or rheumatoid factor present. This person, who remains exceptionally active, has osteoarthritis and has had knee and hip replacement surgery. Please review the attached file below and offer your opinion on what may be the source of her chronically elevated D-dimer. Thank you, Geo.


Comments (3)
Nov 18, 2016 7:27pm

I discussed this case with a
I discussed this with a colleague who thought it may describe a classic case of “laboratory incidentaloma”. The problem is that we don’t know the historical picture for this case. The d-dimer may have been high for years. My colleague described a case of a lab tech he has who has had elevated d-dimers between 2000 and 3000 ng/L for 20 years now, but describes this person as healthier than him. This was originally discovered when she was included as a control for evaluation of a ‘new’ d-dimer kit many years ago. She’s still perfectly healthy and she had 2 children in the meanwhile. The reason for continued elevated d-dimer remains unknown. I guess the case could be retested with a range of different kits, but it is likely this person has had raised ‘d-dimers’ for many many years. As stated by others, likely associated with the osteoarthritis in this case.

Nov 15, 2016 2:31pm

I agree with David McGlasson
I agree with David McGlasson that age and osteoarthritis likely contribute to chronically elevated levels of D-Dimer.
(From Geo, don’t the values seem a little high for these explanations?)

Nov 13, 2016 8:58pm

See the below abstract that
See the below abstract that addresses the elevated d-dimer in osteoarthritis. The patients age may also explain some of the d-dimer levels. No disrespect intended.
Cheras PA, Whitaker AN, Blackwell EA, et al .Hypercoagulability and hypofibrinolysis in primary osteoarthritis. Clin Orthop Relat Res 1997; 334:57ā€“67

Histologic evidence of venous thrombosis and lipid abnormalities have previously been reported in osteoarthritis. Hypofibrinolysis has been recorded in patients with ischemic necrosis of bone, and it has been proposed as a major cause of osteonecrosis. This study determines whether systemic evidence of coagulation and lipid abnormalities could be detected in osteoarthritis. Global and specific tests were used to assess coagulability and fibrinolysis in 44 patients with degenerative osteoarthritis of the hip and 52 matched control subjects. In patients with osteoarthritis, an increase in factor VIIl, increased platelet sensitivity over a range of adenosine diphosphate concentrations (0.05 umol/Lā€“4 umol/L) and elevated D dimer levels were found. Euglobulin clot lysis time was prolonged in this group and plasminogen activator inhibitor Type 1 activity was increased. Relative hyperlipidemia was observed in the osteoarthritis group, with increased cholesterol, low density lipoprotein cholesterol, and triglyceride levels. It is concluded that there is a hypercoagulable and prothrombotic condition in osteoarthritis, with hypofibrinolysis and indirect evidence of increased fibrin generation. The possible contribution of lipid abnormalities to hemostatic imbalance in osteoarthritis is discussed.

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