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Hematologic dysfunction in Lassa fever
Author(s) -
FisherHoch Susan P.,
McCormick J. B.,
Sasso D.,
Craven R. B.
Publication year - 1988
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.1890260204
Subject(s) - lassa fever , medicine , viremia , gastroenterology , lassa virus , sierra leone , immunology , virus , disease , development economics , economics
Lassa fever is widespread in West Africa, where the case fatality is about 16% in hospitalized adult patients. The clinical course is highly variable, with a few patients developing severe disease with bleeding, adult respiratory distress syndrome, encephalopathy and hypovolemic shock. We studied 70 patients admitted with suspected Lassa fever to a hospital in Sierra Leone, West Africa. Fourteen patients classified as having severe Lassa fever on the basis of serum aspartate amino transferase (AST) > 150 IU/L or viremia of > 10 3.6 tissue culture infective dose (TCID) 50 /ml were found to have statistically significantly depressed lymphocyte counts when compared with patients with mild Lassa fever (AST <150 IU/L or viremia, <10 3.6 TCID 50 /ml), ( P <0.0001) and with febrile control patients, in whom Lassa infection had been excluded by laboratory criteria ( P <0.0008). Maximum depression occurred a mean of 10.9 days post onset. Patients with severe Lassa fever also had moderate thrombocytopenia, which was statistically significant when compared with febrile control patients ( P <0.0003) and this occurred a mean of 10.8 days postonset. The most significant changes were in platelet function, which was markedly depressed in patients with severe Lassa fever ( P <0.0035 in response to ADP and P =0.0081 for collagen) when compared with patients with mild Lassa fever, and when compared with febrile controls, ( P =0.0013 for ADP and P <0.00001 for collagen). This abnormality was usually maximal on admission to hospital, and probably is an early event, preceding hospitalization in these patients. Characteristically it is present even when circulating platelet numbers remain above 100 × 10 9 /L. Though this defect was significantly associated with Lassa fever in the patients studied, platelet dysfunction was also observed in a small number of patients with laboratory confirmed malaria within the febrile control group of patients. In contrast, prothrombin times and partial thromboplastin times in Lassa fever patients were rarely abnormal, and there were no statistically significant differences between Lassa fever patients and febrile controls in coagulation tests or in fibrinogen degradation product levels.