Etiological spectrum of arterial and venous thrombosis in a tertiary-care hospital
DOI:
https://doi.org/10.59736/IJP.24.03.1115Keywords:
Antiphospholipid Syndrome, Arterial Thrombosis, Myeloprolliferative Disorders, Thrombophilia, Venous ThrombosisAbstract
Background: There are heterogeneous pathogenesis of arterial and venous thrombosis, and little information exists locally on the etiological spectrum of these diseases. The objective of this study was to identify the etiological spectrum of arterial and venous thrombosis in patients who came to the tertiary care hematological service.
Methods: This cross-sectional research was done in the Department of Haematology, Shaikh Zayed Hospital, Lahore. A total of 70 patients with objectively recorded arterial or venous thrombosis aged 16-75 were used; it has excluded myocardial infarction and iatrogenic embolization/thrombosis. Clinical, available thrombophilia, demographic and imaging analyzes were checked. Etiological results were classified as APS / APS-compatible antiphospholipid-antibody results, myeloproliferative-neoplasm-associated mutation, Factor V Leiden, protein C deficiency, protein S deficiency or no known etiology. All participants were individually put under one major etiological category. The laboratory abnormalities were taken with caution because documentation of timing and repeat confirmation of certain thrombophilia tests was not always undertaken. Unadjusted comparisons were done using descriptive statistics and unpaired Fisher exact test.
Results: Of 70 patients, 45 (64.3%) had venous and 25 (35.7%) had arterial thrombosis. In 51 (72.9%), a specific category of etiology was determined. The 12 (17.1%), 10 (14.3%), 9 (12.9%), 8 (11.4%), 7 (10.0%), and 5 (7.1%) respectively consisted of APS/APS-compatible findings, myeloproliferative-neoplasm-related mutations, protein S deficiency, Factor V Leiden, protein C deficiency, and antithrombin deficiency respectively; 19 (27.1%) was of undetermined etiology.
Conclusion: This tertiary-care cohort had more venous than arterial thrombosis. The most common acquired etiological categories were APS/APS-compatible laboratory results and myeloproliferative-neoplasm-related mutations. Since not all thrombophilia abnormalities had repeat confirmation means that findings cannot be taken to be population prevalence or even definitive causal diagnoses but must be taken as implied etiological findings of the hospital setting. Selective and clinically whole-hearted testing of thrombophilia is endorsed.
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