Severity of adverse effects correlates with the extent of histamine release. Histamine release appears independent of tryptase suggesting a non-mast cell source. Acetaminophen is protective against adverse effects of NAC, and mechanisms by which acetaminophen might lessen histamine release require further attention.

This descriptive and retrospective study was conducted at the poisoning ward of Imam teaching hospital, Sari, Iran, with the aim of evaluating the pattern of poisoning. Hence, the medical profiles of 2057 patients, who were admitted, were carefully reviewed during the period from April 2006 to March 2008 for 2 years. During this period, 2057 cases, 53.9% female and 46.1% male, were admitted with the indication of acute poisoning. The greatest proportion of poisoning occurred between the ages of 18 and 29 years, with suicidal intentions. Most cases of poisoning were intentional (85%). The most common agents involved in acute poisoning were drugs (77.7%), especially sedatives/hypnotics such as benzodiazepines, followed by opioid analgesics. Organophosphate and carbamate insecticides were the third major agent that induced poisoning. Twenty-seven patients (1.3%) who were mostly females and young adults died. Death mostly occurred due to organophosphate and carbamate insecticides (19 cases) poisoning, followed by sedatives/hypnotics like benzodiazepines (3 cases). High prevalence of intentional overdose and mortality among young adults requires considerable attention and further studies to find out the underlying causes. In addition, strict rules must be followed regarding the sale of central nervous system drugs and pesticides, particularly organophosphate and carbamate insecticides. Establishing poison information centers in different parts of the country, preparing national treatment guidelines, training healthcare providers, and ensuring easy availability of the antidotes are also recommended.

What is already known about this subject • Paracetamol causes renal failure in overdose. Experimental studies have shown that paracetamol can inhibit COX II systemically in a manner similar to selective COX‐II inhibitors. • In overdose nonsteroidal anti‐inflammatory drugs such as ibuprofen, cause dose‐dependent increase in urinary potassium excretion (FeK) and sodium retention, probably due to vasoconstriction. What this study adds • Paracetamol overdose is associated with dose‐related hypokalaemia and kaliuresis of short duration (<24 h), suggesting a specific renal effect of paracetamol in overdose. • This effect seems likely to be via cyclo‐oxygenase inhibition and may be separate from the nephrotoxic effects of paracetamol. Aims To investigate the effects of acute paracetamol overdose on renal function, serum and urine electrolyte excretion in man. Methods Two studies were performed in patients admitted with paracetamol overdose: a retrospective study examining changes in serum electrolytes, and a prospective study evaluating changes in serum and urine electrolytes. A control group with SSRI overdose was included in the prospective study. Results There was a significant dose‐dependent relationship between admission (4 h) paracetamol concentration and fall in serum potassium in the retrospective study (P < 0.01) and a significant positive relationship between serum paracetamol at 4 h and fractional excretion of potassium at 12 h postingestion (P < 0.01) in the prospective study. No changes were seen in the control group. No cases developed renal failure. Conclusions Paracetamol overdose is associated with dose‐related hypokalaemia, and kaliuresis of short duration (<24 h), suggesting a specific renal effect of paracetamol in overdose perhaps via cyclo‐oxygenase inhibition. This effect seems distinct from any nephrotoxic effect of paracetamol.

ALP poisoning is a common toxicity in Iran causing high morality. This is a serious health problem in agricultural region where ALP is readily available. Withdrawal of ALP tablet from the market and introduction of safer products as rodenticides and insecticides is recommended.

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