Limulus amebocyte lysate (LAL)-reactive material other than endotoxin was detected in the plasma and urine of patients after intravenous immunoglobulin therapy. Thirty-seven vials of six different immunoglobulin products were analyzed for the LAL-reactive material by combined use of a conventional chromogenic Limulus test and a chromogenic endotoxin-specific test. The amount of LAL-reactive material in reconstituted immunoglobulin solutions ranged from a mean (standard deviation) of 10.2 (2.1) to 2,448.1 (988.9) pg/ml, and there were statistically significant differences among the six brands. The levels of LAL-reactive material in plasma increased in proportion to the amounts contained in the immunoglobulin products administered. The material accumulated in the blood with repeated administration. Urinary excretion of the material was less than 5% of the total amount administered. Such material seems to be derived from the cellulose-based membranes used during preparation of the blood products. Thus, interpretation of Limulus test results of patients receiving immunoglobulin therapy requires special consideration.

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The amebocytes of horseshoe crab (Limulus) hemolymph contain a coagulation system highly sensitive to bacterial endotoxins. Limulus amebocyte lysate (LAL) reactive material derived from cuproammonium rayon membranes, however, is not an endotoxin and acts upon the alternative pathway in the coagulation cascade found in Limulus amebocyte lysate. This study confirmed these facts by using the coagulation system of Limulus without factor G, which is a substrate of the alternative pathway. LAL reactive material lingered in the circulation for a relatively long time. In acute hemodialysis, its plasma concentration increased by an average of 100 pg/ml with each dialysis and eventually reached a plateau of approximately 300 pg/ml. In patients with chronic renal failure under regular hemodialysis, the mean level of LAL reactive material was 330.0 +/- 8.0 pg/ml before hemodialysis which increased by 70.6 +/- 20.7 pg/ml after four hours of hemodialysis.

SUMMARYThe relationship between delayed traumatic intracerebral haematoma and disseminated intravascular coagulation was investigated. Eighteen patients with delayed traumatic intracerebral haematoma were selected as the study subjects from 268 consecutive patients with head trauma and compared with another two groups of patients with closed head injury (20 cases) and with multiple injuries (24 cases). All cases had six laboratory studies for disseminated intravascular coagulation for 7 days. The results revealed no different clotting abnormalities among the three groups. From the laboratory point of view, it could be concluded there was no essential relationship between disseminated intravascular coagulation and the appearance of delayed traumatic intracerebral haematoma.With development of serial computed tomography (CT) for patients with acute severe head injuries, many reports have been published of delayed traumatic intracerebral haematoma. In several case reports and series, a relationship between delayed traumatic intracerebral haematoma and disseminated intravascular coagulation was noted. In this report, we found that there was no essential relationship between disseminated intravascular coagulation and delayed traumatic intracerebral haematoma. Materials and methodsEighteen cases of delayed traumatic intracerebral haematoma were selected from 268 consecutive patients with head trauma treated at our department during the period from March 1980 to October 1982. Delayed traumatic intracerebral haematoma patients (Group one) had a Glasgow Coma Score of 10 or less. As controls, 20 consecutive patients with closed head injuries having no other injuries (Group two) were included. In addition, 24

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