๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Hematologic dysfunction in Lassa fever

โœ Scribed by Dr. Susan P. Fisher-Hoch; J. B. McCormick; D. Sasso; Dr. R. B. Craven


Book ID
102906951
Publisher
John Wiley and Sons
Year
1988
Tongue
English
Weight
519 KB
Volume
26
Category
Article
ISSN
0146-6615

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โœฆ Synopsis


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 > 103.6 tissue culture infective dose (TCID) 501ml were found to have statistically significantly depressed lymphocyte counts when compared with patients with mild Lassa fever (AST < 150 IU/L or viremia, < 103.6TCID50/ml), (P<O.OOOl) and with febrile control patients, in whom Lassa infection had been excluded by laboratory criteria (P< O.OOO8).

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=O.0081 for collagen) when compared with patients with mild Lassa fever, and when compared with febrile controls, (P=0.0013 for ADP and P<O.OOOOl 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 X 109/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


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