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Coagulant and Fibrinolytic Status in Tuberculous Meningitis

Schoeman, Johan MD*; Mansvelt, Erna MD; Springer, Priscilla FCP (Paed)*; van Rensburg, Anita Janse*; Carlini, Sophia*; Fourie, Elba

The Pediatric Infectious Disease Journal: May 2007 - Volume 26 - Issue 5 - p 428-431
doi: 10.1097/
Original Studies

Background: The long-term neurologic sequelae of childhood tuberculous meningitis (TBM) mainly result from ischemia owing to cerebral vasculitis. Deep vein thrombosis occurs in adults with pulmonary tuberculosis owing to hypercoaguability. The present study aimed to investigate coagulation status during acute childhood TBM.

Methods: Coagulation status, including the natural anticoagulants, antithrombin, protein C and protein S; procoagulant FVIII; fibrinolytic factors, tissue plasminogen activator and plasminogen activator inhibitor-1 (PAI-1) as well as anticardiolipin antibodies (ACA), was determined in 16 children with TBM before and during treatment.

Results: A prothrombotic profile was found as expressed by a decrease of anticoagulant (protein S) and increase of the procoagulant (factor VIII) activity. Raised PAI-1 and normal tissue plasminogen activator values indicated deficient fibrinolysis. This hypercoagulable state was more pronounced in stage 3 patients than in stage 2 patients. The bleeding time on admission ranged from 1.2 to 10 minutes [mean 4.2 minutes]. The mean platelet count on admission was 577.9 ± 188.6 × 109/L and increased further during the course of the treatment.

Conclusions: The hypercoagulable state in childhood TBM is comparable to that described in adults with pulmonary tuberculosis and may further increase the risk for infarction. Therapeutic measures that reduce the risk for thrombosis could therefore be potentially beneficial in childhood TBM.

From the *Department of Paediatrics and Child Health; and †Department of Pathology: Haematological Pathology, Tygerberg Hospital, University of Stellenbosch and NHLS, Tygerberg, South Africa.

Accepted for publication February 2, 2007.

This study was supported by MRC (SA).

Address for correspondence: Johan F Schoeman, Department of Paediatrics and Child Health, Stellenbosch University, PO Box 19063, Tygerberg 7505, South Africa. E-mail:

© 2007 Lippincott Williams & Wilkins, Inc.