Comment on “An update on toxicology of aluminum phosphide”

Omid Mehrpour

doi:10.1186/2008-2231-20-50

Abstract

Sir I read with interest the recent published article by Dr Moghadamnia titled “An update on toxicology of aluminum phosphide” [1]. Since aluminum phosphide (AlP) poisoning is an important medical concern in Iran, I have had the opportunities to work and publish many papers in this regard [2-11]. I would like to comment on paper as follows: The author stated that Leukopenia indicates severe AlP toxicity and also mentioned Increased serum glutamic oxaloacetic transaminase (SGOT) or serum glutamic pyruvic transaminase (SGPT) and induced metabolic acidosis indicate moderate to severe AlP overdose. Leukopenia and hepatotoxicity due to AlP poisoning is reported in the literature, but according to my knowledge there is no study supported they are good indicators of severity of AlP poisoning [2,3]. Even some studies indicated leukosytosis is known as a prognostic factor in AlP poisoning [3]. Shadnia et al. in a study found the prognostic factors in AlP poisoning are Simplified Acute Physiology Score II (SAPSII), low GCS, hypotension, hyperglycemia, acidosis, hemoconcentration, leukocytosis, hyperuremia and ECG abnormalities [3]. Moreover the author stated that The serum level of cortisol is usually decreased in severe AlP Very few studies have published about blood cortisol level changes in AlP poisoning. Generally in clinical situations such as stress, hypotension, shock or critically ill patients, there is evidence of increasing in plasma cortisol level. In addition, some surveys showed AlP poisoning has been postulated to stimulate cortisol, glucagon, and adrenaline secretion, or inhibit insulin synthesis [6,12]. Moreover Chugh, et al. (1989) reported findings in thirty cases showed a significant rise in plasma cortisol (greater than 1048 nmol/L) in 20 cases

Highlights

Obesity has reached epidemic proportions and is still escalating at an alarming rate worldwide
Obesity is associated with chronic activation of low-grade inflammation [3], which is implicated in the pathogenesis of obesity-associated diseases including insulin resistance, type-2 diabetes (T2D) [4, 5] and cardiovascular disease [6, 7]
A numerous of studies has been shown that shortchain fatty acids (SCFAs) inhibit inflammation with focus on butyrate and to a lesser extent on acetate and Propionic Acid (PA), [16]

Summary

Introduction

Obesity has reached epidemic proportions and is still escalating at an alarming rate worldwide. In Palestine the prevalence of obesity has been shown to be approximately 4. The etiology of obesity and low-grade inflammation is complex and involves intrinsic and extrinsic factors. The colonization of germ-free mice with microbiota derived from obese mice results in significantly greater adiposity than colonization with microbiota from lean mice [12]. Prebiotic diets such as fructans [13] are associated with general better health, including the decrease in body weight, fat mass and the severity of T2D [14,15,16]. The factors that influence the composition and metabolism of intestinal

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