The optimisation of nutritional support for the growing number of older individuals does not usually take into account medication. Paracetamol (acetaminophen; APAP) is the first intention treatment of chronic pain that is highly prevalent and persistent in the elderly. Detoxification of APAP occurs in the liver and utilises sulfate and glutathione (GSH), both of which are issued from cysteine (Cys), a conditionally indispensable amino acid. The detoxification-induced siphoning of Cys could reduce the availability of Cys for skeletal muscle. Consequently, APAP could worsen sarcopenia, an important component of the frailty syndrome leading to dependency. The present review provides the rationale for the potential pro-sarcopenic effect of APAP then recent results concerning the effect of chronic APAP treatment on muscle mass and metabolism are discussed. The principal findings are that chronic treatments with doses of APAP comparable with the maximum posology for humans can increase the requirement for sulfur amino acids (SAA), reduce Cys availability for muscle, reduce muscle protein synthesis and aggravate sarcopenia in animals. One clinical study is in favour of an enhanced SAA requirement in the older individual under chronic treatment with APAP. Few clinical studies investigated the effect of chronic treatment with APAP combined with exercise, in nutritional conditions that probably did not affect Cys and GSH homeostasis. Whether APAP can aggravate sarcopenia in older individuals with low protein intake remains to be tested. If true, nutritional strategies based on enhancing Cys supply could be of prime interest to cut down the pro-sarcopenic effect of chronic treatment with APAP.

The workup of the emergency patient with a raised anion gap metabolic acidosis includes assessment of the components of “MUDPILES” (methanol; uremia; diabetic ketoacidosis; paraldehyde; isoniazid, iron or inborn errors of metabolism; lactic acid; ethylene glycol; salicylates). This approach is usually sufficient for the majority of cases in the emergency department; however, there are many other etiologies not addressed in this mnemonic. Organic acids including 5-oxoproline (pyroglutamic acid) are rare but important causes of anion gap metabolic acidosis. We present the case of a patient with profound metabolic acidosis with raised anion gap, due to pyroglutamic acid in the setting of malnutrition and chronic ingestion of acetaminophen.

Increasing attention has been paid to Spirulina for its potential clinical uses. The present study investigated the protection by dietary Spirulina platensis against d-galactosamine (d-GalN)- and acetaminophen (APAP)-induced hepatitis in ICR mice. Mice in each group (n 6) were fed with a standard diet (American Institute of Nutrition (AIN)-93G), a positive control diet containing 0·5 % butylated hydroxytoluene (BHT), or a diet containing 3, 6 or 9 % S. platensis for 1 week. On the last day the mice were treated with d-GalN (300 mg/kg body weight, intraperitoneally) or APAP (150 mg/kg body weight, intraperitoneally) and 24 h later the mice were killed. The doses of both 6 and 9 % S. platensis were found to significantly alleviate the increase of serum glutamate oxaloacetoacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) activities in d-GalN- or APAP-intoxicated mice. The observation was very similar to that of the positive control groups. Two more experiments were carried out to investigate the involvement of thiobarbituric acid-reactive substances (TBARS) and IL-18 in the suppression of 6 % S. platensis on d-GalN- and APAP-induced hepatitis. The significant increase of GOT and GPT activities was found to be accompanied with the elevation of hepatic TBARS level, IL-18 mRNA expression and serum IL-18 concentration, and was significantly alleviated by supplementation with 6 % S. platensis in diets. These results showed that dietary S. platensis could provide a significant protection against d-GalN- and APAP-induced liver injuries, and IL-18 and lipid peroxidation might be involved in the protective influence of S. platensis.

Summary

Background: The purpose of this study was to assess whether the addition of intravenous magnesium sulphate (Mg) at the induction of anaesthesia to a balanced anaesthetic protocol including wound infiltration, paracetamol and tramadol resulted in improved analgesic efficiency after radical prostatectomy. Methods: We conducted a randomized, double-blind, controlled study. Thirty ASA I or II males scheduled to undergo radical retropubic prostatectomy with general anaesthesia were prospectively assigned to one of the two groups (n = 15 each). The Mg group (Gr Mg) received 50 mg kg−1 of MgSO4 in 100 mL of isotonic saline over 20 min immediately after induction of anaesthesia and before skin incision. The patients in the control group (Gr C) received the same volume of saline over the same period. At the time of abdominal closure, wound infiltration with 190 mg (40 mL) of ropivacaine was performed in both groups. Pain was assessed by a 10-point visual analogue scale in the recovery room starting from the time of tracheal extubation. Standardized postoperative analgesia included paracetamol and tramadol administered via a patient-controlled analgesia device. Results: In the postoperative period, both groups experienced an identical pain course evolution. Cumulative mean tramadol dose after 24 h was 226 mg in the magnesium group and 446 mg in the control group (P < 0.001). Postoperative nausea occurred in two patients in each group. Two vs. eight patients required analgesic rescue in magnesium and control groups, respectively (P = 0.053). Conclusions: This study shows that intravenous magnesium sulphate reduces tramadol consumption when used as a postoperative analgesic protocol in radical prostatectomy.

Fifty children (2–9 years) scheduled for tonsillectomy were enrolled in a double-blind randomized prospective study to compare postoperative analgesia provided with propacetamol/paracetamol (acetaminophen) or tramadol. A standard anaesthetic technique was used; each patient received sufentanil 0.25 μg kg−1 intravenously followed with either i.v. propacetamol 30 mg kg−1 or tramadol 3 mg kg−1 before surgical incision. For postoperative analgesia, each child received either tramadol drops (2.5 mg kg−1) or paracetamol (acetaminophen) suppositories (15 mg kg−1), 6 and 12 h after surgery the first day and three times a day during postoperative days 2 and 3. This dosage of paracetamol is lower than the current recommended dosage, which is 40 mg kg−1 loading dose followed by 20 mg kg−1 8 h−1. Rescue medication consisted of i.v. diclofenac (1 mg kg−1) during the first six postoperative hours and oral ibuprofen (6–9 mg kg−1) afterwards. Postoperative pain scores (Children's Hospital of Eastern Ontario Pain Scale) in recovery, numerical pain scale in the ward and at home, and rescue analgesic use were significantly lower in the tramadol group. No serious adverse effects were observed.