The Last Articles summary in 2025-05-31

Amlodipine and quetiapine are widely utilized medications that are generally well-tolerated at therapeutic doses. However, overdoses can lead to severe, life-threatening cardiovascular effects, leading to refractory vasoplegia. The management of poly-ingestion overdoses is challenging and often requires aggressive, multimodal treatment strategies especially when the causative agent is unknown. In this case report, a 38-year-old male intentionally ingested a large amount of amlodipine and quetiapine resulting in refractory shock despite high doses of vasopressors, calcium, and insulin therapy. After conventional therapies failed, the administration of exogenous angiotensin II (Ang II), a vasoconstrictor traditionally used for septic shock, led to a marked improvement in the patient's blood pressure and stabilization of hemodynamics. Sixty minutes after initiation of Ang II, the patient's mean arterial pressure (MAP) improved, allowing for the weaning of other vasopressors and a gradual reduction in insulin therapy. This case highlights the potential role of Ang II as a salvage therapy in polysubstance ingestions when other therapies fail.
Link: https://pubmed.ncbi.nlm.nih.gov/40445505/

Minamata disease, officially identified in 1956, refers to methylmercury food poisoning that occurred in Minamata City, Japan. Although many children in the affected areas were born with severe neurological signs after birth (known as congenital Minamata disease [CMD]), little investigation has been conducted to elucidate the health effects on those who were born at the same time in the affected areas. We used historical data from a clinical study conducted in 1970 in the city of Minamata (a methylmercury-polluted area) and the island region of Amakusa (a less polluted area) to evaluate the association between prenatal methylmercury exposure and neurocognitive impairment in a total of 416 junior high school students. We divided the participants into three categories: those who lived in a highly exposed area, those who lived in a moderately exposed area (both in Minamata City), and those who lived in a less exposed area (in the Amakusa island region). We then calculated the prevalence of neurocognitive impairment in each category and estimated prevalence ratios with 95 % confidence intervals (CIs) for neurocognitive impairment compared with the less exposed area, adjusting for potential confounders. We then found that the prevalence for both neurocognitive impairment and severe neurocognitive impairment among students in the highly exposed area were 2.08 (95 % CI: 1.26 to 3.44) and 2.84 (95 % CI: 1.18 to 6.81) times higher, respectively, than those in the less exposed area. Prenatal methylmercury exposure affected neurocognitive function in CMD patients and in Minamata residents born at the same time as CMD patients in the affected areas.

Link: https://pubmed.ncbi.nlm.nih.gov/40440848/

This study demonstrates that Al-rich, high-Cu-loaded Cu-SSZ-13 exhibits superior resistance to SO<sub>2</sub> poisoning under actual SCR conditions. The high Cu content mitigates the risk of SO<sub>2</sub>-induced structural degradation. A key finding is that lower regeneration temperatures can lead to more severe secondary poisoning, while high temperatures induce hydrothermal aging. Thus, controlling the regeneration temperature is critical for maintaining long-term catalyst stability. Additionally, experimental results and DFT calculations show that SO<sub>2</sub> preferentially reacts with dimer-Cu species, especially hydrogenated dimer-Cu ([Cu<sup>II</sup><sub>2</sub>(NH<sub>3</sub>)<sub>4</sub>(OH)O]<sup>+</sup>), resulting in significant sulfate accumulation. This interaction inhibits the redox cycle of Cu<sup>+</sup>/Cu<sup>2+</sup>, thereby suppressing low-temperature activity. Overall, this work elucidates the mechanisms of SO<sub>2</sub>-induced deactivation in Cu-zeolite SCR catalysts and provides valuable insights into designing Cu-SSZ-13 catalysts with enhanced sulfur resistance through Cu-Al co-optimization.

Link: https://pubmed.ncbi.nlm.nih.gov/40440499/

A drug-related fatality involving 3,4-methylenedioxy-α-pyrrolidinohexanophenone (MDPHP) is here reported. Belonging to the class of synthetic cathinones (SCs), MDPHP is a 3,4-methylenedioxy-derived designer (MDDs) drug with a pyrrolidine moiety and an alkyl portion with six carbon atoms. Other MDD pyrrolidine derivatives belong to the alkyl homologous series (C3-C5) and are known as 3,4-methylenedioxy-α-pyrrolidinopropiophenone (MDPPP), 3,4-methylenedioxy-α-pyrrolidinobutyrophenone (MDPBP) and 3,4-methylenedioxypyrovalerone (MDPV). MDDs are psychostimulant drugs of abuse that primarily act on monoamine transporters; little is known about their off-target liability. Recently, MDPHP has gained attention due to increasing seizures and involvement in human intoxications, but currently there is a lack of data about its pharmaco-toxicological effects. In the case reported here, a 58-year-old man with a history of MDPV addiction was found dead in a waterway. While no evidence of natural disease or trauma was found to account for the death, toxicological analysis revealed the presence of MDPHP in addition to MDPPP, MDPV, MDPBP, clonazepam and citalopram. Since no standards of MDPPP and MDPBP were available at the time of the analysis, LC-QTOF analysis of the drugs and their metabolites were performed. The following concentrations of MDPHP were reported: 354.5 ng/mL in femoral blood (FB), 110.9 ng/mL in cardiac blood (CB), 1900 ng/mL in urine, 3000 ng/mL in bile, 490 ng/g in kidney, 80 ng/g in liver, 480 ng/g in lung, 98 ng/g in brain, 700 ng/mL in gastric content and 8.3 ng/mg in pubic hair. Other MDDs concentrations in biological fluids and tissue were significantly lower than MDPHP suggesting their presence as synthetic impurities. Finally, to better understand the binding properties of the abovementioned MDDs to several documented transporters and receptors, an in-silico evaluation was performed. The medical examiner reported that the cause of death was an acute multidrug intoxication by MDPHP and clonazepam in presence of MDPPP, MDPV, MDPBP and citalopram.

Link: https://pubmed.ncbi.nlm.nih.gov/40440133/