Hypoglycemia is a rare but potentially serious adverse effect of second-generation antipsychotics (SGAs). Most studies have focused on SGA-induced hyperglycemia and metabolic syndrome, while hypoglycemia in non-diabetic adults remains underreported. We describe a case of severe hypoglycemia following risperidone initiation, demonstrating diagnostic challenges and safety concerns. A 41-year-old woman with treatment-resistant schizophrenia, Asperger's syndrome, and attention-deficit/hyperactivity disorder was admitted for worsening commanding auditory hallucinations and persecutory delusions. Risperidone was started at 2 mg nightly and increased to 3 mg after four days. The patient developed recurrent episodes of severe hypoglycemia (random blood glucose levels 35-50 mg/dL; hypoglycemia defined as <70 mg/dL), accompanied by hypotension, tachycardia, nausea, vomiting, dizziness, and altered mental status, shortly after increasing the dose of risperidone. Extensive laboratory and imaging evaluations were unremarkable except for persistent hypoglycemia. The episodes continued despite aggressive glucose replacement and supportive medical treatment. After risperidone was discontinued, blood glucose levels gradually normalized within 48-72 hours, and no further hypoglycemic episodes occurred. To contextualize this case, a systematic literature search was conducted following PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines using PubMed, PubMed Central, PsycINFO, Embase, and Google Scholar, with keywords including "risperidone", "second-generation antipsychotics", and "hypoglycemia", as well as MeSH terms. Studies involving adult non-diabetic psychiatric patients with antipsychotic-associated hypoglycemia were included. Nine relevant case reports and case series were identified and evaluated using the Joanna Briggs Institute (JBI) Critical Appraisal Checklist for Case Reports. Existing literature shows that hypoglycemia associated with SGAs is rare but has been reported with several agents, including risperidone, quetiapine, olanzapine, paliperidone, clozapine, and aripiprazole. Proposed mechanisms include hyperinsulinemia and impaired counter-regulatory responses related to antipsychotic receptor effects. Because symptoms such as confusion, dizziness, and weakness may mimic psychiatric symptoms or medication side effects, diagnosis may be delayed. This case highlights that risperidone can rarely cause severe hypoglycemia even in non-diabetic adults. Although limited by a single case and lack of insulin measurements, this study emphasizes the need for early recognition, glucose monitoring during SGA use, and multidisciplinary care to prevent serious complications. Further research is needed to better understand the underlying biological mechanisms and identify potential risk factors.

Curcumin is extensively existed in plants and is commonly used as food additives. However, excessive intake of curcumin may lead to side effects like nausea and vomiting. Traditional techniques such as high-performance liquid chromatography (HPLC) and liquid chromatography-tandem mass spectrometry (LC-MS) are constrained by cumbersome operations and low efficiency. Herein, a triple-emission surface molecularly imprinted fluorescence sensor (TPP&RhB-SMIPs) was fabricated via precipitation polymerization on halloysite nanotubes (HNTs), using aggregation-induced emission luminogen (AIEgen) TPP-M and allyl rhodamine B as fluorophores. This sensor exhibits distinct fluorescence color transitions (purple-fuchsia-carnation-yellow-chartreuse) with increasing curcumin concentrations, coupled with a linear range of 0.1-4.0 μmol L-1 and a low detection limit of 44 nmol L-1. It demonstrates excellent selectivity and achieves satisfactory recoveries in ginger and beverage samples. A smartphone-integrated portable device was further developed for on-site visual detection of curcumin. This work provides a reliable, rapid, and cost-effective strategy for curcumin analysis, holding great promise for food safety monitoring.

Posterior reversible encephalopathy syndrome (PRES) is a rare but potentially life-threatening neurological complication associated with vascular endothelial growth factor (VEGF)-targeted tyrosine kinase inhibitors. Although it is typically reported after prolonged exposure and at standard or high doses, early onset at reduced dosing may occur and requires prompt recognition. We report a 64-year-old woman with metastatic papillary renal cell carcinoma who developed PRES after two months of treatment with reduced-dose sunitinib (37.5 mg daily). She presented with severe headache, nausea, vomiting, impaired consciousness, and reduced mobility, accompanied by acute hypertension (170/100 mmHg). Brain magnetic resonance imaging demonstrated bilateral vasogenic edema without diffusion restriction, consistent with PRES, and electroencephalography revealed generalized background slowing indicative of encephalopathy. Sunitinib was immediately discontinued, and the patient was treated with corticosteroids, antiepileptic therapy, and antihypertensive agents, resulting in rapid clinical improvement. Follow-up imaging confirmed complete radiological resolution. Subsequent treatment with nivolumab and axitinib achieved limited disease control, and the overall survival was 11 months. This case highlights that PRES can develop early and at reduced doses of sunitinib, may present with severe neurological impairment, and can be supported by electroencephalographic findings. Early recognition and prompt discontinuation of the offending agent are essential to prevent irreversible neurological damage.