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d-dimer is a reliable and sensitive index of fibrin deposition and stabilization. As such, its presence in plasma should be indicative of thrombus formation. There are many conditions unrelated to thrombosis in which d-dimer concentrations are high, however, making its positive predictive value rather poor.

Notwithstanding these limitations, d-dimer can be regarded as a most valuable laboratory tool to diagnose and manage a vast array of thrombosis-related clinical conditions, including (a) diagnosis of venous thromboembolism (VTE), (b) identification of individuals at increased risk of first thrombotic event (both arterial and venous), (c) identification of individuals at increased risk of recurrent VTE, (d) establishment of the optimal duration of secondary prophylaxis after a first episode of VTE, (e) pregnancy monitoring, and (f) diagnosis/monitoring of disseminated intravascular coagulation (DIC). This article is aimed at reviewing the merits and pitfalls of these applications.

From my analysis of the literature, I draw the following conclusions. (a) d-dimer, as measured by a sensitive test, can be safely used to exclude VTE in symptomatic outpatients, provided that it is used in combination with the pretest clinical probability. (b) High concentrations of d-dimer are associated with an increased risk of recurrent VTE. (c) Patients who present with d-dimer above cutoff after stopping the regular course of oral anticoagulation benefit from extended prophylaxis. (d) Finally, d-dimer can be used as a fibrin-related degradation marker for the diagnosis/management of patients with DIC.

Background: A reduced comeback to aspirin and clopidogrel predicts ischemic events, but reputable tests are needed to relate low responders. We compared 3 platelet-function tests during long-term dual treatment with aspirin and clopidogrel.

Methods: Patients who underwent a percutaneous coronary intervention and were receiving a colloid of 325 mg/day aspirin and 75 mg/day clopidogrel were followed for 1 year. Blood was sampled 5 times during this term for 3 tests: light-headed forwarding aggregometry (LTA) assay, with 5.0 µmol/L ADP or 1.0 mmol/L arachidonic acid (AA) adapted to as an agonist; VerifyNow^TM assay, with the P2Y₁₂ or aspirin cartridge (Accumetrics); and thrombelastography (TEG), stimulated by 2.0 µmol/L ADP or 1.0 mmol/L AA.

Results: Twenty-six of 33 patients completed all scheduled visits. A low retort to clopidogrel was bring about in a few patients at mutable frequencies and at new visits, depending on the method and criteria tolerant of. We found a non-reactionary correlation intercessor the LTA (ADP) and VerifyNow (P2Y₁₂ cartridge) results, but the TEG (ADP) results correlated improperly with the LTA and VerifyNow results. A low return to aspirin was organize with the VerifyNow (aspirin cartridge) and TEG (AA) methods on 6 and 2 occasions, respectively, but not with the LTA (AA) method, except for 1 prompting caused by probable noncompliance.

Conclusions: Detecting a low rejoinder to clopidogrel depends on the whole on the method acclimatized. Which method best predicts ischemic events remains uncertain. A low answer to aspirin is rare with AA-dependent methods used at the chosen cutoffs. In some patients, the response to clopidogrel or aspirin may be classified differently at unheard-of times, equable with the just the same method.

Background: The antiphospholipid syndrome (APS) is an egotistical motive of acquired thromboembolic complications and pregnancy morbidity. Its diagnosis is based on clinical and laboratory criteria, defined by pitiless guidelines. The fresh clinical and laboratory criteria for the denomination of APS patients were published in 1999, in the so-called Sapporo criteria. In 2006 these criteria were revised, and recently more precise guidelines for breakdown of the lupus anticoagulant procure been provided. However, dissimilar questions correlated to the diagnosis of APS balance unanswered.

Content: In over to providing a historical perspective, this criticize covers several challenges in the diagnosis of APS with respect to clinical and laboratory features, while highlighting pathogenic pathways of the syndrome. We debate ongoing dilemmas in the diagnosis of this complex disorder. Although antiphospholipid antibodies are institute in association with diversified clinical manifestations, the older established clinical criteria were not substantively altered in the 2006 update. Several laboratory tests recommended in the latest criteria, including phospholipid-dependent coagulation tests for the detection of the lupus anticoagulant and ELISAs for measuring anticardiolipin and β2-glycoprotein I antibodies, still show methodological and diagnostic shortcomings. In addition, antiphospholipid antibodies be experiencing been described against other antigens, but their clinical impersonation remains uncertain.

Conclusions: Regardless of updated APS criteria, diagnosis of this syndrome remains challenging. Over investigation on clinically related antibodies and standardization of their detection are needed to improve clinical hazard assessment in APS.