Use of immobilized histidine in assay for endotoxin in patients with liver disease

Shiomi, Susumu; Kuroki, Tetsuo; Ueda, Tadashi; Takeda, Tadashi; Nishiguchi, Shuhei; Nakajima, Shinya; Kobayashi, Kenzo; Yamagami, Sakae; Watanabe, Taizo; Minobe, Satoshi

doi:10.1007/bf02349282

Cited by 6 publications

(2 citation statements)

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“…11,12 Last, but not least, the interpretation of endotoxin levels in patients with liver disease is particularly challenging, as they may be related to a reduced clearing efficiency of the hepatic reticuloendothelial system and/or an increased presence of liver-derived X-l,3-D-glucans, which can account for false-positive results. 13,14 In view of these concerns, there is an urgent need for an alternative method to assess endotoxin exposure of the liver in human NASH using peripheral blood. For this purpose, we here assessed the level of Immunoglobulin G (IgG) antibodies in the systemic circulation directed against the inner core of endotoxin, using the Endotoxin Core Antibodies assay (EndoCab).…”

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confidence: 99%

Novel Evidence for Chronic Exposure to Endotoxin in Human Nonalcoholic Steatohepatitis

Verdam¹,

Rensen²,

Driessen

et al. 2011

Journal of Clinical Gastroenterology

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confidence: 99%

Novel Evidence for Chronic Exposure to Endotoxin in Human Nonalcoholic Steatohepatitis

Verdam¹,

Rensen²,

Driessen

et al. 2011

Journal of Clinical Gastroenterology

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“…The liver plays an important role in innate immunity; its functions include reserving fixed‐tissue macrophages, including Kupffer cells, and regulating the synthesis of proteins responsible for pathogen recognition and opsonization [25]. Previous studies have reported that innate immunity impairment due to liver dysfunction after liver surgery was associated with both changes in innate immune response and postoperative infection [26–28]. Meanwhile, we demonstrated that RLHA division was an independent risk factor for postoperative transaminase elevation, suggesting the possible presence of innate immune impairment in patients with RLHA division.…”

Section: Discussionmentioning

confidence: 74%

Preserving a Replaced Left Hepatic Artery Arising from the Left Gastric Artery During Laparoscopic Distal Gastrectomy for Gastric Cancer

Waki

Kamiya

et al. 2020

World j. surg.

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Background A replaced left hepatic artery (RLHA) arising from the left gastric artery (LGA) is occasionally encountered during laparoscopic gastrectomy. Although the RLHA is usually divided at the root level as RLHA preservation might result in inadequate lymph node dissection, blood flow disruption by RLHA division may lead to hepatic ischemia. To date, there is no consensus on RLHA preservation. Thus, we aimed to evaluate the efficacy of RLHA preservation by investigating the short-term outcomes of patients with RLHA who underwent laparoscopic distal gastrectomy (LDG). Methods A total of 106 patients with an aberrant LHA from the LGA were identified as having gastric cancer and underwent LDG from 2012 to 2018. Finally, 55 patients were retrospectively diagnosed with RLHA by preoperative computed tomography and included in this study. Patients were classified into the divided (n = 18) or preserved (n = 37) group. Clinicopathological factors and surgical outcomes were compared between the two groups. ResultsThe RLHA preservation rate in patients who had been preoperatively diagnosed with RLHA was 88%. No significant difference was found in the number of harvested lymph nodes between the groups. The incidence of hepatic infarction was significantly higher in the divided group (16.7% vs. 0%, p = 0.031). Moreover, RLHA division caused postoperative transaminase elevation and was an independent risk factor for postoperative transaminase elevation (odds ratio: 55.8, p \ 0.001). Conclusions Surgical procedures of RLHA preservation reduced postoperative transaminase elevation and hepatic infarction in patients who underwent LDG. Surgeons should confirm the RLHA preoperatively and preserve it to prevent hepatic damage.

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Endotoxemia in Alcoholic Liver Disease†

Rao

2009

Hepatology

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As described in an interesting review by Rao, 1 much evidence derived from numerous experimental studies of alcoholic liver disease (ALD) support the association of endotoxemia with the initiation and progression of ALD. The review focuses on the role of endotoxemia and the mechanisms of gut barrier dysfunction in ALD. The author mentions that endotoxemia is conventionally believed to exist when the plasma endotoxin level rises higher than 2.5 endotoxin units (EU)/mL, and the endotoxin levels in ALD patients, ranging from 8.5 to 206 pg/mL, are 5-to 20-fold higher than those in normal subjects. First, I would like to comment on the determination and interpretation of endotoxemia in the clinical setting. Historically, the rabbit pyrogenic test was introduced to detect the contamination of endotoxins and other toxins in biological preparations in 1940. In the early 1960s, dose-dependent endotoxin-induced coagulation of lysates from the horseshoe crab amoebocyte was found, leading to the development of a new method of quantifying the endotoxin in 1970s, which is now called the limulus amoebocyte lysate (LAL) assay. This assay was quickly approved by the US Food and Drug Administration (FDA) because the LAL test is more sensitive, less time-consuming, more costeffective, and better standardized than the rabbit test. For interpreting the results of the LAL assay, it should be noted that LAL is not prepared for the detection of endotoxemia but is intended only for in vitro diagnostic purposes. Endotoxin antagonists, antibiotics, plasma proteins, and unknown substances in the blood can interfere with or activate the LAL test. The term EU indicates the national standard biological activity in the LAL assay, which was determined by the FDA and other organizations on the basis of the relationship between the LAL assay and the rabbit pyrogenic test. Although the FDA initially defined 1 EU as the endotoxin activity of 200 pg of a reference standard endotoxin, the conversion ratio is variable because it is dependent on the source of the endotoxin used for each assay, ranging from 1 EU to 20 pg to 1 EU to 500 pg. Commercially available LAL kits use a control standard endotoxin because a reference standard endotoxin is very expensive. There are substantial variations in endotoxin potency among the control standard endotoxins. Additionally, substantial variation in the reactivity of lysates from different horseshoe crabs has been observed. Therefore, I would like to ask the author whether it was quite difficult to define endotoxemia and assess the differences in endotoxin levels among the studies.The author concludes that the evidence is clear that alcohol consumption leads to increased intestinal permeability and endotoxemia, which are involved in the pathogenesis of ALD. However, there is no definite clinical evidence showing that improvements in intestinal permeability or anti-endotoxin therapy can ameliorate liver injury in ALD. Also, in an experimental study, ethanol-induced liver damage was not markedly enhanced by the lon...

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Use of immobilized histidine in assay for endotoxin in patients with liver disease

Cited by 6 publications

References 8 publications

Novel Evidence for Chronic Exposure to Endotoxin in Human Nonalcoholic Steatohepatitis

Novel Evidence for Chronic Exposure to Endotoxin in Human Nonalcoholic Steatohepatitis

Preserving a Replaced Left Hepatic Artery Arising from the Left Gastric Artery During Laparoscopic Distal Gastrectomy for Gastric Cancer

Endotoxemia in Alcoholic Liver Disease†

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