Intractable hyponatremia secondary to syndrome of inappropriate antidiuresis complicated with empty sella: A case report.

RATIONALE: Hyponatremia is a common electrolyte disorder in elderly critically ill patients, and it may be associated with poor outcomes, higher morbidity, and mortality. Syndrome of inappropriate antidiuresis (SIAD) is one of the main causes of hyponatremia, with an insidious onset that is highly misdiagnosed. Primary empty sella lesions are specific, mostly asymptomatic, and easily overlooked. SIAD combined with empty sella is much rarer in clinic, this article focuses on the diagnosis and management of an elderly patient with intractable hyponatremia secondary to syndrome of inappropriate antidiuresis complicated with empty sella. PATIENT CONCERNS: An 85-year-old male patient with severe pneumonia presented with progressive and intractable hyponatremia. DIAGNOSES: The patient had clinical signs of persistent hyponatremia, low plasma osmolality, elevated urinary sodium excretion, and hyponatremia that worsened with increased intravenous rehydration and was effective with appropriate fluid restriction. The diagnosis of SIAD combined with empty sella was made in combination with the findings of the pituitary and its target gland function. INTERVENTIONS: Numerous screenings were performed to clarify the cause of hyponatremia. His overall condition was poor due to recurrent episodes of hospital-acquired pneumonia. We treated with ventilation support, circulatory support, nutritional support, anti-infection, and continuous correction of electrolyte imbalance. OUTCOMES: His hyponatremia gradually improved through aggressive infection control, appropriate fluid restriction (intake controlled at 1500-2000mL/d), continuous electrolyte correction, supplementation with hypertonic salt solution, and potassium replacement therapy. LESSONS: Electrolyte disorders, especially hyponatremia, are very common in critically ill patients, but the etiology of hyponatremia is challenging to diagnose and treat, and timely attention and proper diagnosis of SIAD and individualized treatment are the significance of this article.

Exploring the Mechanism of Curcumin on Retinoblastoma Based on Network Pharmacology and Molecular Docking.

Background: Curcumin shows great effects of inhibiting tumor cell proliferation, inducing apoptosis, inhibiting tumor metastasis, and inhibiting angiogenesis on a variety of tumors. However, the biological activity and possible mechanisms of curcumin in the treatment of retinoblastoma have not been fully elucidated. This study explored the potential therapeutic targets and pharmacological mechanisms of curcumin against retinoblastoma based on network pharmacology and molecular docking. Methods: The genes corresponding to curcumin targets were screened from the HERB, PharmMapper, and SwissTargetPrediction databases. Protein-protein interaction (PPI) networks were constructed for the intersecting targets in the STRING database. Cytoscape 3.7.0 was used for network topology analysis and screening of important targets. R 4.1.0 software was used for Gene Ontology (GO) function enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of intersection targets. The molecular structures of curcumin and core target proteins were obtained from PubChem and PDB databases, and the two were preprocessed and molecularly docked using AutoDockTools and PyMOL software. Results: Through network data mining, we obtained 504 curcumin targets and 966 retinoblastoma disease targets, and 44 potential targets for curcumin treatment of retinoblastoma were obtained by mapping. Three core targets were obtained from network topology analysis. 462 biological processes, 21 cellular compositions, and 34 molecular functions were obtained by GO enrichment analysis. KEGG pathway analysis revealed 94 signaling pathways, mainly involving chemical carcinogenesis-receptor activation, chemical carcinogenesis-reactive oxygen species, viral carcinogenesis, Th17 cell differentiation, etc. The molecular docking results indicated that the binding energy of curcumin to the core targets was less than 0 kJ mol-1, among which the binding energy of RB1 and CDKN2A to curcumin was less than -5 kJ mol-1 with significant binding activity. Conclusion: Based on molecular docking technology and network pharmacology, we initially revealed that curcumin exerts its therapeutic effects on retinoblastoma with multitarget, multipathway, and multibiological functions, providing a theoretical basis for subsequent studies.