Comparison between various scoring systems in predicting the need for intensive care unit admission of acute pesticide-poisoned patients.

The decision of intensive care unit (ICU) admission in acute pesticide poisoning is often challenging, especially in developing countries with limited resources. This study was conducted to compare the efficacy of the Acute Physiology and Chronic Health Evaluation II (APACHE II), Modified Early Warning Score (MEWS), and Poisoning Severity Score (PSS) in predicting ICU admission and mortality of acute pesticide-poisoned patients. This prospective cohort study included all patients admitted to Tanta University Poison Control Center with acute pesticide poisoning from the start of March 2018 to the end of March 2019. Patient data, including demographic and toxicological data, clinical examination, laboratory investigation, and score values, were collected on admission. Out of 337 acute pesticide-poisoned patients, 30.5% were admitted to the ICU, including those poisoned with aluminum phosphide (ALP) (81.5%) and organophosphates (OP) (18.5%). Most non-survivors (86.6%) were ALP poisoning. The PSS had the best discriminatory power in predicting ICU admission and mortality, followed by APACHE II and MEWS. However, no significant difference in predicting ICU admission of OP-poisoned patients was detected between the scores. Additionally, no significant difference in mortality prediction of ALP-poisoned patients was found between the PSS and APACHE II. The PSS, APACHE II, and MEWS are good discriminators for outcome prediction of acute pesticide poisoning on admission. Although the PSS showed the best performance, MEWS was simpler, more feasible, and practicable in predicting ICU admission of OP-poisoned patients. Moreover, the APACHE II has better sensitivity for mortality prediction of ALP-poisoned patients.

Hepatic alcohol dehydrogenase deficiency induces pancreatic injury in chronic ethanol feeding model of deer mice.

The single most common cause of chronic pancreatitis (CP, a serious inflammatory disease) is chronic alcohol abuse, which impairs hepatic alcohol dehydrogenase (ADH, a major ethanol oxidizing enzyme). Previously, we found ~5 fold greater fatty acid ethyl esters (FAEEs), and injury in the pancreas of hepatic ADH deficient (ADH-) vs. hepatic normal ADH (ADH+) deer mice fed 3.5g% ethanol via liquid diet daily for two months. Therefore, progression of ethanol-induced pancreatic injury was determined in ADH- deer mice fed ethanol for four months to delineate the mechanism and metabolic basis of alcoholic chronic pancreatitis (ACP). In addition to a substantially increased blood alcohol concentration and plasma FAEEs, significant degenerative changes, including atrophy and loss of acinar cells in some areas, ultrastructural changes evident by such features as swelling and disintegration of endoplasmic reticulum (ER) cisternae and ER stress were observed in the pancreas of ethanol-fed ADH- deer mice vs. ADH+ deer mice. These changes are consistent with noted increases in pancreatic injury markers (plasma lipase, pancreatic trypsinogen activation peptide, FAEE synthase and cathepsin B) in ethanol-fed ADH- deer mice. Most importantly, an increased levels of pancreatic glucose regulated protein (GRP) 78 (a prominent ER stress marker) were found to be closely associated with increased phosphorylated eukaryotic initiation factor (eIF) 2α signaling molecule in PKR-like ER kinase branch of unfolded protein response (UPR) as compared to X box binding protein 1S and activating transcription factor (ATF)6 - 50kDa protein of inositol requiring enzyme 1α and ATF6 branches of UPR, respectively, in ethanol-fed ADH- vs. ADH+ deer mice. These results along with findings on plasma FAEEs, and pancreatic histology and injury markers suggest a metabolic basis of ethanol-induced pancreatic injury, and provide new avenues to understand metabolic basis and molecular mechanism of ACP.