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PubMed · 11322838

An update on hypercoagulable disorders.

D G Federman·R S Kirsner
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Abstract

Venous thrombosis is a cause of considerable morbidity and is often responsible for chronic venous disorders that frequently lead to visits to dermatologists and others involved in wound healing. Over the past several years, many new causes of thrombophilia have been identified and have dramatically altered the approach to patients presenting with thrombosis. Newly described abnormalities associated with thrombophilia include the syndrome of activated protein C resistance, the prothrombin 20210A mutation, hyperhomocysteinemia, and elevated levels of coagulation factors VIII and XI. Clinicians can now frequently determine causes of thromboses that have previously been deemed idiopathic.

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Activated Protein C ResistanceAnticoagulantsBlood Coagulation DisordersContraceptives, OralFactor VFemaleHumansHyperhomocysteinemiaMutationPregnancyPregnancy Complications, CardiovascularProthrombinRecurrenceRisk FactorsWarfarinJournal ArticleReview

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D G Federman, R S Kirsner. 2001-04-23. An update on hypercoagulable disorders.. https://doi.org/10.1001/archinte.161.8.1051

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PubMed2002

Laboratory evaluation of hypercoagulable states in patients with central retinal vein occlusion who are less than 56 years of age.

PURPOSE: To investigate whether hypercoagulability plays a role in thrombus formation in patients with central retinal vein occlusion (CRVO) who are less than 56 years of age. DESIGN: Prospective, observational case series with retrospective comparative controls. PARTICIPANTS AND CONTROLS: Participants included 55 consecutive patients with CRVO less than 56 years of age. The laboratory's age-matched control groups were used to compare results for the same tests. METHODS: Fifty-five patients with CRVO less than 56 years old (mean age, 44 years) underwent laboratory evaluation for homocysteine, activated protein C resistance, protein C activity, protein S activity, antithrombin III activity, antiphospholipid antibodies, and anticardiolipin antibodies. The results were compared with previously drawn age-matched control groups obtained by the same laboratory for statistical significance. MAIN OUTCOME MEASURES: Patients were considered to have a positive test if their results were outside the laboratory's established range. RESULTS: Fifteen of 55 patients (27%) had one positive test result suggesting hypercoagulability. Compared with the control groups, these patients less than 56 years old with CRVO had a higher incidence of coagulation abnormalities by laboratory testing. Among the parameters tested, hyperhomocysteinemia and circulating antiphospholipid antibodies were significantly more common in the CRVO patients (P < 0.05) compared with age-matched controls. CONCLUSIONS: Hypercoagulability may play a role in the pathogenesis of CRVO in patients less than 56 years old. The cause of CRVO remains multifactorial, and laboratory tests suggesting hypercoagulable states alone cannot account for the cause in most of these patients less than 56 years of age. The authors recommend examining blood pressure, intraocular pressure, complete blood count, glucose levels, and a lipid panel on all patients with CRVO. When tests for these common risk factors for CRVO are negative, consider ordering selected tests in young patients with CRVO to rule out thrombophilias, especially in patients with bilateral CRVO, a history of previous thrombosis, or family history of thrombosis.

Activated Protein C Resistance↗
PubMed2002

Hereditary thrombophilia in elite athletes.

PURPOSE: Although under normal circumstances exercise prevents thrombosis, there are cases in the literature that indicate a connection between exercise and the onset of thrombosis. In the average population, hereditary thrombophilia is a major cause of thrombosis. However, nothing is known about the prevalence of hereditary thrombophilia in elite athletes. Because high-performance sports are known to carry an increased risk of thrombogenesis, measures to avoid thrombosis must be initiated in cases of known hereditary thrombophilia. METHODS: Hereditary thrombophilia was checked for in 173 elite athletes, members of the German national team. Antithrombin III, protein C, protein S, and the APC ratio, followed by a molecular genetic analysis, were measured, and molecular analysis of factor II G20210A mutation was used to detect the presence of an antithrombin III-, protein C- and protein S-deficiency, as well as factor V Leiden (factor V 506Arg to Gln) and factor II G20210A mutation. RESULTS: No definite antithrombin III-, protein C- or protein S-deficiency was found. In 12 cases, an APC resistance caused by a factor V Leiden mutation (11 heterozygous; 1 homozygous) was detected. In 10 cases, a heterozygous factor II G20210A was observed; a combination of both mutations was not found. For factor V Leiden, this corresponds to a prevalence of 6.9% (CI 95% 3.6-11.8%) in our group, similar to prevalence rates in the general population. Additionally, the observed prevalence of 5.8% (CI 95% 2.8-10.4%) of factor II G20210A is nearly within the range as reported by several authors. CONCLUSION: Based on the observed prevalence of APC resistance and factor II G20210A mutation in our group of athletes, along with consideration of additional circumstantial risks, screening tests for elite athletes should be considered to allow the undertaking of preventive measures.

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