Latest Articles and News - Jul 1, 2025

Takotsubo Syndrome From Lisdexamfetamine Overdose and an FLNC Truncating Variant Requiring Venoarterial Extracorporeal Membrane Oxygenation.

https://pubmed.ncbi.nlm.nih.gov/40586014/

Nanoparticles Loaded with Pralidoxime Wrapped in Tumor Cell Membranes: A New Strategy to Counteract the Central Nervous System Effects of Organophosphate Poisoning.

In this study, cell membrane-coated nanoparticles (CMCNPs) were loaded with the organophosphorus antidote Pralidoxime Chloride (PAM) to improve the ability of the drug to penetrate the blood‒brain barrier (BBB) and evade immune clearance, providing a novel drug delivery strategy for the treatment of central organophosphorus poisoning. 1) The cell membranes of mouse melanoma cells (B16F10), breast cancer cells (4T1), glioblastoma cells (GL261), and monocytic macrophage leukemia cells (RAW264.7) were extracted, and their purities were verified. The cell membranes were combined with PAM in mesoporous silica (SiO₂) spheres by ultrasonic fusion to prepare the CMCNPs. 2) The immune evasion ability of CMCNPs was evaluated by laser confocal microscopy and flow cytometry after coculture with macrophages. 3) HPLC was used to screen the best CMCNPs through an in vitro BBB model. 4) After the CMCNPs were injected into malathion-poisoned mice, the phosphate chloride concentration in the peripheral blood and brain homogenates was tested, and the rate of acetylcholinesterase (AChE) reactivation was determined. All four types of CMCNPs were spherical particles with diameters of approximately 100 nm. Compared with unwrapped nanoparticles, CMCNPs exhibited a stronger immune evasion ability and enhanced BBB penetration ability in an in vitro BBB model. They also significantly prolonged the in vivo circulation time of PAM, increased its delivery dose to the central nervous system, and markedly increased cholinesterase activity in brain tissues. Furthermore, in an organophosphorus-poisoned mouse model, CMCNPs significantly improved the survival rate of intoxicated mice. In this study, CMCNPs with a significant BBB penetration ability and immune evasion ability were successfully prepared and improved the therapeutic effect of PAM on central organophosphate poisoning.

https://pubmed.ncbi.nlm.nih.gov/40584778/

Hyperkalemia combined with carbon monoxide poisoning, should hemodialysis or hyperbaric oxygen treatment be given first?: A CARE-compliant article.

Hyperkalemia and acute carbon monoxide (CO) poisoning are both life-threatening conditions. When these conditions coexist, there is a debate on whether hemodialysis or hyperbaric oxygen (HBO) therapy should be prioritized. Our discussion suggests that HBO therapy may help by lowering residual carbon dioxide levels and correcting electrolyte imbalances, consequently decreasing the risks linked to both CO poisoning and hyperkalemia. A 25-year-old man presented with hyperkalemia and CO poisoning. He was promptly taken to the emergency room where he received immediate interventions including intravenous infusion of 5% sodium bicarbonate solution, glucose plus insulin, diuretics, and calcium supplementation in a HBO environment. Subsequently, hemodialysis was performed. Following this treatment protocol, the patient showed significant improvements in hyperkalemia, CO levels, general weakness, cardiac arrhythmias, and other symptoms. This sequential therapy effectively eliminated the remaining CO in his system and addressed the electrolyte imbalances crucial to his recovery. After 4 weeks of comprehensive treatment, the patient's hyperkalemia and CO poisoning issues were successfully resolved. Based on the thorough history, electrocardiographs and the laboratory tests. The interventions included intravenous infusion of 5% sodium bicarbonate solution, glucose plus insulin, diuretics, calcium supplementation in a HBO environment, and followed by hemodialysis. The following clinical improvements were detected: consciousness was clear; the cardiac arrhythmia symptoms were improved (electrocardiograph became normal); normal electrolytes with no other abnormalities; displayed no nervous system symptoms. Sequential treatment of intravenous fluid rehydration, HBO, hemodialysis may be effective in treating patients with hyperkalemia combined with CO poisoning.

https://pubmed.ncbi.nlm.nih.gov/40587713/

Risk of self-harm and overdose after starting buprenorphine for opioid use disorder.

Compare risk of intentional self-harm and overdose after visits for opioid use disorder (OUD) followed by starting vs. not starting buprenorphine. Records from four health systems identified visits during 1/1/2012-12/31/2019 by health system members aged 13 or older with OUD diagnosis and no recent OUD medication. Following a target-trial emulation approach, visits followed by buprenorphine dispensing within 7 days were matched to unexposed visits. Analyses compared risk of diagnosed self-harm injury or poisoning (primary outcome) as well as opioid-involved poisoning and any injury or poisoning (secondary outcomes) within 90 days. Among 183,809 visits by 30,955 patients, 15,508 (8.4 %) had buprenorphine dispensing within 7 days, and 2260 (1.2 %) had self-harm diagnosis within 90 days. Average duration of buprenorphine treatment before interruption was 44.3 days (SD 32.1). In primary intention-to-treat analyses using logistic regression and adjusting for baseline risk of self-harm, starting buprenorphine was not associated with significant difference in self-harm (odds ratio [OR] 1.01, 95 % CI 0.81-1.24) or opioid-involved poisoning (OR 1.09, 95 % CI 0.86-1.38). In secondary as-treated analyses censoring outcomes after treatment change, buprenorphine initiation was associated with no significant difference in hazard of self-harm (Hazard Ratio [HR] 0.74, 95 % CI 0.53-1.02) and with significantly lower hazard of opioid-involved poisoning (HR 0.63, 95 % CI 0.43-0.94). Among people with OUD, starting buprenorphine was not followed by lower risk of self-harm, likely reflecting frequent discontinuation and high risk of self-harm or overdose shortly after discontinuation. These findings reinforce the need to improve treatment continuity among those starting buprenorphine.

https://pubmed.ncbi.nlm.nih.gov/40580781/

Combined carbon monoxide poisoning and smoke inhalational injury in a case of severe underlying lung disease.

https://pubmed.ncbi.nlm.nih.gov/40580197/

Hyperbaric oxygen for paroxysmal sympathetic hyperactivity syndrome after acute carbon monoxide poisoning.

JOURNAL/mgres/04.03/01612956-202603000-00002/figure1/v/2025-06-28T140100Z/r/image-tiff Paroxysmal sympathetic hyperactivity syndrome (PSH) is common in patients with severe craniocerebral injuries. Carbon monoxide poisoning (ACOP) may lead to secondary PSH, and hyperbaric oxygen (HBO) is an important treatment method for ACOP that can promote the dissociation of carboxyhemoglobin and reduce the long-term sequelae of ACOP. To explore the risk factors and clinical characteristics of PSH secondary to acute ACOP and to investigate the efficacy of HBO treatment, a retrospective analysis was performed on patients with moderate to severe ACOP admitted to the Hyperbaric Oxygen Department of Beijing Chaoyang Hospital, Capital Medical University, from January 1, 2018 to December 31, 2024. Three patients developed PSH during hospitalization and were classified into the PSH group, while the remaining 50 patients were in the non-PSH group. Univariate Fisher's exact test indicated that a coma duration of more than 72 hours was related to the occurrence of PSH after ACOP, and irregular HBO treatment after onset might be associated with the occurrence of PSH after ACOP. All three PSH patients developed paroxysmal postural or dystonic disorders after onset, accompanied by sympathetic excitation manifestations such as increased heart rate, respiratory rate, elevated blood pressure, and fever. Antiepileptic drugs had poor effects, and the attacks were effectively controlled after HBO treatment combined with adjusted drug therapy. The results indicate that for patients with severe carbon monoxide poisoning, especially those with a long coma duration or irregular HBO treatment after onset, if epileptic seizures occur during the disease course and are accompanied by sympathetic excitation manifestations, the possibility of PSH should be considered. Regular HBO treatment is of great significance for controlling the onset of symptoms.

https://pubmed.ncbi.nlm.nih.gov/40580183/