Valeria Margherita Petrolini

Although bupropion is known to be associated with pharmacobezoar formation, it remains understudied in this context. Upper gastrointestinal endoscopy has emerged as a potential adjunctive decontamination technique for managing acute overdoses associated with pharmacobezoar formation. We aim to evaluate its role in acute bupropion overdoses. We retrospectively analysed intentional bupropion overdoses referred to the Pavia Poison Control Centre (2015-2024) in which upper endoscopy was performed. Data on patient characteristics, overdose details, co-ingestants, decontamination procedures, endoscopy indications, and findings were collected. Endoscopy outcomes were classified as positive (pharmacobezoars, intact tablets, or paste-like residues) or negative. In parallel, an in vitro model was used to assess the propensity of bupropion to form pharmacobezoars. Forty-seven patients were included (median age 44 years, IQR 27-55; 75% female). The median ingested bupropion dose was 4,500 mg (IQR 4,500-6,750 mg). The median ingested tablets count was 59 (IQR 29-100 mg), and co-ingestants were present in 79% of cases. Upper gastrointestinal decontamination endoscopy was positive in 28 cases (60%). Pharmacobezoars or tablet residues were identified even in patients who had undergone prior decontamination, including orogastric lavage (60%). The only variable significantly associated with positive endoscopic findings was the total number of ingested tablets (P in vitro experiment showed early pharmacobezoar formation within four hours of incubation, persisting for up to 72 hours. Acute bupropion overdoses, alone or with co-ingestants, can cause gastric pharmacobezoars and retained tablets/residues despite standard decontamination. Upper gastrointestinal decontamination endoscopy is effective early post-ingestion and may complement or replace conventional methods. Gastric pharmacobezoars and tablet residues are frequently observed in bupropion overdoses, particularly with ingestions of ≥30 tablets, making these patients potential candidates for early endoscopic removal.

Dear editor,We read with interest the the case report by Friedman et al., whose patient did well without acetylcysteine after ∼100 mg/kg IV paracetamol (APAP) [1].Their case leaves unresolved quest...

Introduction: Most of the molybdenum (Mo) is used in metallurgical applications, the tetrathiomolybdate form is an experimental chelating agent for Wilson's disease. Human data of acute Mo exposure are lacking and, no report of no-observed-adverse-effect level (NOAEL) has been described until now. Case-study: We report a case of acute occupational exposure to molybdenum, with the related plasma and urine molybdenum concentrations, caused by an accidental ingestion of a sip of an anti-corrosion liquid for metal containing sodium molybdate. Our purpose was to evaluate potential systemic toxicity of molybdenum and to evaluate the dose-response/dose-effect relationship. We estimated the amount of ingested molybdenum to make a mg/kg relationship and performed repeated urine and plasma molybdenum determinations. The patient was hospitalized for three days to monitor possible development of acute symptoms/biochemical alterations. Discussion: We estimated the amount of the sip around 50 ml, with an estimation of a total of 5 gr of sodium molybdate that, for the patient bodyweight of 80 kg, would mean 62,5 mg/kg of ingested Mo. Blood and urine samples collected 2 hours after ingestion showed 50 mcg/L (reference range: 0.43 – 1.8 mcg/L) and 630 mcg/L (refence range: up to 116 mcg/L) of Mo respectively, confirming acute exposure. The patients remained asymptomatic confirming that an estimated oral dose of Mo of 62.5 mg/kg was not associated with adverse effects. Conclusions: Our value, being extrapolated by a single case, will require further confirmations from other studies to allow a full evaluation of a NOAEL. Nevertheless, it does not preclude its use in evaluating the probable absence of adverse effect in the context of acute Mo exposure.

Aims To study the predictive factors for the development of clinical manifestations in poisoning due to the erroneous taking of low-dose methotrexate (MTX). Methods A retrospective observational study was performed. Only cases of erroneous administration in non-oncologic outpatients were included (July 2008-March 2020). Results Forty-one cases were included. All patients were taking MTX for the first time. In 36 cases, patients took MTX daily instead of weekly. In the other five patients, MTX was sold instead of methylergometrine. Clinical manifestations were absent in 12/41 patients (29.3%). All 29 (70.7%) symptomatic patients recognized the medication error when they developed clinical manifestations: dermatological, haematological and gastrointestinal symptoms. Statistical results showed that symptomatic patients were older, received a higher amount of total dose and were treated for longer. Moreover, the probability of being symptomatic increases as a function of age and of total dose. Asymptomatic patients were treated with folinic acid (30 mg/m(2)/day) for 5 days. Symptomatic patients were treated with folinic acid together with treatments for the specific clinical manifestations. No patients were treated with glucarpidase. All patients fully recovered. Conclusions When MTX is prescribed for the first time, it is important to clearly communicate with patients to avoid therapeutic errors. In our experience, age, total dose taken and number of days of assumption are predictive for the presence/absence of clinical manifestations. These parameters must be evaluated together to identify patients needing maximum starting treatment with folinic acid and closer monitoring.

Systemic toxicity associated with cobalt (Co) and chromium (Cr) containing metal hip alloy may result in neuropathy, cardiomyopathy, and hypothyroidism. However clinical management concerning chelating therapy is still debated in literature. Here are described two metal-on-metal hip-implanted patients in which N-acetyl-cysteine decreased elevated blood metal levels. A 67-year-old male who underwent Co/Cr hip implant in September 2009 referred to our Poison Control Centre for persisting elevated Co/Cr blood levels (from March 2012 to November 2014). After receiving oral high-dose N-acetyl-cysteine, Co/Cr blood concentrations dropped by 86% and 87% of the prechelation levels, respectively, and persisted at these latter concentrations during the following 6 months of follow-up. An 81-year-old female who underwent Co/Cr hip implant in January 2007 referred to our Centre for detection of high Co and Cr blood levels in June 2012. No hip revision was indicated. After a therapy with oral high-dose N-acetyl-cysteine Co/Cr blood concentrations decreased of 45% and 24% of the prechelation levels. Chelating agents reported in hip-implanted patients (EDTA, DMPS, and BAL) are described in few cases. N-acetyl-cysteine may provide chelating sites for metals and in our cases reduced Co and Cr blood levels and resulted well tolerable.