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D. W. Bates, J. Parsonnet, P. A. Ketchum, E. B. Miller, T. J. Novitsky, K. Sands, P. L. Hibberd, P. S. Graman, P. N. Lanken, J. S. Schwartz, K. Kahn, D. R. Snydman, R. Moore, E. Black and R. Platt, “Limulus Amebocyte Lysate Assay for Detection of Endotoxin in Patients with Sepsis Syndrome,” Clinical Infectious Diseases, Vol. 27, No. 3, 1998, pp. 582-591. doi:10.1086/514713

has been cited by the following article:

• TITLE: Newly Developed Endotoxin Measurement Method (the Endotoxin Activity Assay) May Reflect the Severity of Sepsis

  AUTHORS: Kiyohide Ishihata, Yasuyuki Kakihana, Tomotsugu Yasuda, Tohru Imabayashi, Norifumi Nakamura

  KEYWORDS: Endotoxin Activity Assay; Endotoxin; Sepsis

  JOURNAL NAME: Open Journal of Pathology, Vol.3 No.1, January 28, 2013

  ABSTRACT: Objectives: Endotoxin (ET) is a structural molecule of the Gram-negative bacilli extracellular membrance, which activates targeted cells including macrophages and neutrophils, and causes septic shock. But it is known that the conventional ET measurement method has many problems; for example, a discrepancy between plasma ET concentration and clinical manifestation in the septic patients has been reported. The purpose of this study was to evaluate the usefulness of a newly developed method (Endotoxin Activity Assay (EAA)) to measure the ET activity (EA) in patients under sepsis compared with the prior method of the limulus amebocyte lysate (LAL) assay and explore the association between EA levels and patients’ severity. Method: We measured the EA levels in 40 patients (aged 63.5 +/－ 17.7 years) admitted to the ICU. EA level was measured using a chemiluminometer (Autolumat LB953; EG & Berthold). Patients were divided into 5 groups: 1) control group; 2) systemic inflammatory response syndrome (SIRS) group; 3) sepsis (SIRS and infection) group; 4) severe sepsis group and 5) septic shock group. We then compared the EA level between each group and control group. We made the statistical evaluation by unpaired t test and significant difference was p Results: The EA levels were significantly increased as sepsis severity rises. The measured EA levels were (0.18 +/－ 0.09), (0.33 +/－ 0.19), (0.39 +/－ 0.16), (0.65 +/－ 0.25) and (0.78 +/－ 0.34) in control, SIRS, sepsis, severe sepsis and septic shock groups, respectively. In the EA level measured by EAA, severe patients had a tendency to exceed the cutoff value. Conclusion: The EA levels were significantly correlated as patients’ severity rise. Measuring EA levels on admission to ICU may provide a mechanism to identify and target severe septic patients.