Q and A
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October 2007 In the June 2007 issue was a question and answer related to livedo reticularis patients possibly having platelet antiphospholipid antibodies that are treated with anticoagulants. The question was whether the antiphospholipid antibody test can be negative (within normal limits) in an LR patient who is taking Coumadin for chronic atrial fibrillation. Here, Elizabeth M. Van Cott, MD, member of the CAP Coagulation Resource Committee, and Rajni Mandal, MD, both of Massachusetts General Hospital, Boston, provide additional information. A. Livedo reticularis, or LR, is characterized by a violaceous reticular or mottled pattern of the skin on the trunk, arms, or legs due to increased visibility of the cutaneous venous plexus by either venodilation or deoxygenation of the blood.1,2 LR can also be seen as a physiologic response to cold exposure (cutis marmorata), or as a primary disorder due to spontaneous arteriolar vasospasm. Secondary causes of LR commonly lead to increased resistance to venous outflow, such as due to vasculitis, embolic phenomena, or a hypercoagulable state. Medications such as amantadine have been associated with LR. Livedo vasculitis, which is the formation of cutaneous nodules and ulcerations secondary to ischemia and tissue infarction, can occur with occlusion of vascular lumina. Antiphospholipid antibody syndrome, or APS, is defined as thrombotic or pregnancy complications that occur in temporal concordance with a persistently positive test, or tests, for a lupus anticoagulant, anticardiolipin antibodies, or anti-beta-2-glycoprotein-I antibodies. LR can be seen in APS and has been associated with a poor outcome in patients with both APS and systemic lupus erythematosus.2 In Sneddon syndrome, which is characterized by ischemic cerebrovascular events with LR, patients with livedo racemosa—in which the thickness of the reticular pattern was greater than 10 mm—had a higher likelihood of having anticardiolipin antibodies.3 Histological examination of skin biopsies is not clinically indicated, since classic findings of LR—vascular dilation without inflammation—can be nonspecific. However, a biopsy can help exclude vasculitis, if suspected. In a patient with LR and negative antiphospholipid antibodies, a clinical evaluation, including the response to ambient temperature, can help distinguish between primary or secondary LR. In addition, investigating autoimmune connective tissue disease, infection such as hepatitis C, hypercoagulability, or other causes for emboli is also recommended. Since the causes for secondary LR are extensive and can be due to systemic disease, a full clinical evaluation is warranted. Warfarin does not affect the presence or absence of antiphospholipid antibodies. In addition, warfarin is not expected to interfere with anticardiolipin antibody or beta-2-glycoprotein-I antibody testing because these are enzyme-linked immunosorbent assays. On the other hand, a number of coagulation experts have anecdotally reported that warfarin can cause false-positive lupus anticoagulant tests when using a dilute Russell viper venom time assay. In our experience, the presence of warfarin can make interpreting dilute partial thromboplastin time-based screening tests more difficult, possibly leading to false-negative mixing study results. In theory, warfarin should not interfere with the hexagonal phase lupus anticoagulant assay, but as this has not been validated with certainty, it is recommended that such results be interpreted cautiously. According to a consensus group, specimens containing anticoagulants should not be tested for lupus anticoagulants, but if such patients must be tested, the results must be interpreted with caution.4 References
Q. Is there a time frame after blood collection within which a prothrombin time or activated partial thromboplastin time must be run to ensure accurate results? A. There is no consensus on the stability of prothrombin time or activated partial thromboplastin time after collection in an appropriately filled 3.2 percent citrate tube. It is good practice to centrifuge the specimen as soon as it arrives in the laboratory, leaving the plasma on top of the cells. The Clinical Laboratory Standards Institute (CLSI) document H21-A4 (2003)1 recommends that a PT test be completed within 24 hours from the time of collection if stored at room temperature (between 18° and 24°C). Other investigators have reported that the PT was stable for 24 hours if the plasma was stored at room temperature2,3 or on ice (4°C).2 However, room-temperature storage has also been recommended for a maximum of six hours4 and eight hours.5 Always follow the manufacturer's recommendations for your specific coagulation analyzer/reagent combination, especially if these instructions are more restrictive for the maximum storage time. For example, the Dade Behring Innovin PT reagent package insert6 indicates plasma should be tested within four hours after collection. CLSI recommends that an APTT test be completed within four hours from the time of collection if stored between 18° and 24°C.1 This time interval is suggested for patients on heparin therapy.2 Other investigators have recommended eight hours5 and 12 hours3 after the collection time. However, the Dade Behring Actin FSL APTT reagent package insert recommends testing be completed within two hours after blood collection.7 When PT and APTT testing cannot be completed within the recommended time frame, the plasma should be removed from the cells and frozen at -20°C for up to two weeks2 or three months8, or at -70°C for up to six months1 or 18 months.8 References
Peggy Fuller, MT (ASCP) Frederick L. Kiechle, MD, PhD |
