BMC Pharmacology & Toxicology最新文献

{"title":"Coenzyme Q10 microemulsion ion-activated gel: a promising ophthalmic delivery system for enhanced corneal protection and sustained release.","authors":"Shao-Hua Dong, Yue Gao, Yue Li, Di Wu, Ying Chen, Shu-He Chen","doi":"10.1186/s40360-025-00922-2","DOIUrl":"https://doi.org/10.1186/s40360-025-00922-2","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to evaluate a novel microemulsion ion-activated gel system for the ophthalmic delivery of coenzyme Q10 (CoQ10).</p><p><strong>Methods: </strong>Various CoQ10 microemulsion ion-activated formulations were prepared and fully assessed for physical and chemical parameters, assay and related substances, in vitro release, rheological properties, in vitro cytotoxicity and ophthalmic retention. A preliminary pharmacokinetic study was also performed in rabbits.</p><p><strong>Results: </strong>The formulations met the specified criteria, showing a droplet size of 24.5 ± 2.0 nm for microemulsions, increasing slightly to 39.6 ± 3.5 nm for the microemulsion gels. They exhibited a 24-hour sustained in vitro release (80.0% ± 3.2%) and increased viscosity upon contact with artificial tears containing Ca²⁺ and K⁺ ions. The no-film dissolution method and in vitro models indicated first-order release kinetics (r = 0.987). The preparations demonstrated good tolerance and non-irritating properties, with a Draize score of 0-0.55 in rabbits, and provided a 2-hour extension in drug retention on the ocular surface compared with microemulsions alone. In ultraviolet B (UVB)-exposed rats, corneal epithelial damage was reduced and antioxidant marker levels (superoxide dismutase, malondialdehyde) were significantly improved.</p><p><strong>Conclusion: </strong>This novel system is a promising preparation for ophthalmic CoQ10 delivery, offering sustained release and protection against UVB-induced corneal damage.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"87"},"PeriodicalIF":2.8,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12008920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of key therapeutic targets in nicotine-induced intracranial aneurysm through integrated bioinformatics and machine learning approaches.","authors":"Qiang Ma, Longnian Zhou, Zhongde Li","doi":"10.1186/s40360-025-00921-3","DOIUrl":"https://doi.org/10.1186/s40360-025-00921-3","url":null,"abstract":"<p><strong>Background: </strong>Intracranial aneurysm (IA) is a critical cerebrovascular condition, and nicotine exposure is a known risk factor. This study delves into the toxicological mechanisms of nicotine in IA, aiming to identify key biomarkers and therapeutic targets.</p><p><strong>Methods: </strong>Gene Set Variation Analysis (GSVA), Weighted Gene Co-Expression Network Analysis (WGCNA), and enrichment analyses were conducted on differentially expressed genes (DEGs) from the GSE122897 dataset. Additionally, nicotine-related targets were identified using CTD, SwissTargetPrediction, and Super-PRED databases. Integrative machine learning approaches, such as Random Forest (RF) and Support Vector Machine (SVM), were employed to pinpoint key toxicity targets. Molecular docking and immune cell infiltration analyses were also performed.</p><p><strong>Results: </strong>DEGs in IA showed significant alterations in metabolic, secretory, signaling, and homeostatic pathways. Several immune and metabolic response pathways were notably disrupted. WGCNA identified 1127 DEGs with 37 overlapping toxic targets between IA and nicotine. ssGSEA revealed substantial upregulation in immune response and inflammation-related processes. Integrative analyses highlighted TGFB1, MCL1, and CDKN1A as core toxicity targets, confirmed via molecular docking studies. Immune cell infiltration analysis indicated significant correlations between these core targets and various immune cell populations.</p><p><strong>Conclusion: </strong>This study uncovers significant disruptions in metabolic and immune pathways in IA under nicotine influence, identifying TGFB1, MCL1, and CDKN1A as critical biomarkers. These findings offer a deeper understanding of IA's molecular mechanisms and potential therapeutic targets for nicotine-related toxicity.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"86"},"PeriodicalIF":2.8,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12007307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trimetazidine effect on kidney function in patients undergoing coronary procedures.","authors":"Yasser Abdel-Hady, Mohammed Taha, Ahmed El Barbary, Osama Amin","doi":"10.1186/s40360-025-00913-3","DOIUrl":"https://doi.org/10.1186/s40360-025-00913-3","url":null,"abstract":"<p><strong>Background: </strong>CIN (Contrast-induced Nephropathy) was studied after Percutaneous Coronary Intervention (PCI) or Coronary Angiography (CA). Trimetazidine (TMZ) has been investigated as one of the potential molecules that may protect against CIN by its anti-ischemic, antioxidant, and mitochondrial protective effects. We aimed to observe the reno-protective value of TMZ when added to the Guidelines Directed Medical Therapy (GDMT) in patients receiving contrast.</p><p><strong>Methods: </strong>This cohort observational prospective study included 410 patients with Chronic Coronary Syndrome (CCS) undertaking elective CA or PCI. We observed the kidney function following the non-ionic contrast exposure in Group I (205 patients), who received all the GDMT and TMZ. We compared the results with another Group II (205 patients) who received all the GDMT without TMZ. The primary endpoint was the development of CIN, and the secondary endpoint was follow-up kidney function after one month.</p><p><strong>Results: </strong>The baseline characteristics of Group I and Group II were similar, with the weighted groups looking very well matched. All Standardized Mean Differences (SMDs) were either below or very close to 0.1.CIN rates at 72 h were lower in Group I (13.2%) than Group II (22.0%; unadjusted p = 0.019, Bonferroni-adjusted p = 0.352, FDR-adjusted p = 0.047), suggesting a modest protective effect of TMZ that weakens under stringent correction but remains borderline significant with FDR. By one month, CIN rates were 6.3% in Group I vs. 13.2% in Group II (unadjusted p = 0.020, Bonferroni-adjusted p = 0.060, FDR-adjusted p = 0.050), reinforcing TMZ's borderline significant potential long-term benefit.</p><p><strong>Conclusion: </strong>Our Cohort Observational Single-Center study showed that TMZ did not provide robust protection against CIN at 72 h. However, TMZ may offer a modest, clinically relevant, longer-term renal benefit at one month in patients undergoing elective coronary procedures. Further randomized trials are warranted to validate TMZ's efficacy and explore its mechanisms.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"85"},"PeriodicalIF":2.8,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sevoflurane reduces cardiomyocyte injury in a hypoxia/reoxygenation model of cardiomyocytes through the linc01278/miR-134-5pt regulatory axis.","authors":"Ling Wang, Changhua Zhu, Yangge Shao, Rui Chen, Hui Liang","doi":"10.1186/s40360-025-00909-z","DOIUrl":"https://doi.org/10.1186/s40360-025-00909-z","url":null,"abstract":"<p><strong>Background: </strong>Ischemia-reperfusion leads to varying degrees of myocardial cell injury. Notably, long noncoding RNA was associated with the protective effect of sevoflurane (Sev) preconditioning against myocardial ischemic injury. Therefore, we further investigated the protective mechanism of Sev-mediated linc01278 against damaged cardiomyocytes by constructing a hypoxia/reoxygenation (HR) model of cardiomyocytes.</p><p><strong>Methods: </strong>The expression of linc01278, miR-134-5p, and apoptotic biomarkers in cardiomyocytes was detected by RT-qPCR. The proliferation was detected by CCK8; apoptosis was observed by flow cytometry; and the degree of cardiomyocyte injury and the level of oxidative stress was observed by ELISA. Dual luciferase reporter assay and RIP verified linc01278 and miR-134-5p interactions.</p><p><strong>Results: </strong>linc01278 was down-regulated in the HR group and up-regulated after Sev pretreatment. Sev markedly mitigated the HR-impaired cell proliferation, reduced apoptosis, and oxidative stress, and downregulated the expression of myocardial injury markers including cTnI, CK-MB, and LDH. However, this protection was noticeably reversed by the downregulation of the linc01278 expression. Mechanistically, linc01278 binds to miR-134-5p. miR-134-5p was highly expressed in cardiomyocytes of the HR, and lowly expressed in the Sev groups. The cardioprotective effect of Sev weakened by si-linc01278 was typically restored by miR-134-5p inhibitor.</p><p><strong>Conclusions: </strong>Sev attenuates HR-stimulated myocardial injury through linc01278/miR-134-5p axis-mediated proliferation, apoptosis, and oxidative stress.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"83"},"PeriodicalIF":2.8,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11998206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143979236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc sulphate attenuates metabolic dysfunctions induced by olanzapine via the reduction of insulin resistance, hepatic oxidative stress, and inflammation in albino rats.","authors":"Samir A E Bashandy, Rasha E Mostafa, Marawan A El-Baset, Fatma A A Ibrahim, Fatma A Morsy, Omar A Farid, Halima M Ibrahim, Bassim M S A Mohamed","doi":"10.1186/s40360-025-00889-0","DOIUrl":"https://doi.org/10.1186/s40360-025-00889-0","url":null,"abstract":"<p><p>Olanzapine, an atypical antipsychotic drug, is used to treat psychological diseases. However, it's use carries common side effects. Those include weight gain, dyslipidemia, elevated glucose levels, and disrupted oxidative balance. We aimed to test the effect of zinc coadministration to lessen metabolic disturbances, inflammation and oxidative stress in a rat model. Four treatment groups (n = 6) were involved in this investigation. Group 1 was the control group (received no intervention). Group 2 received olanzapine (10 mg/kg, p.o.; daily) for six weeks, whereas Groups 3 and 4 received 50 mg/kg and 100 mg/kg of zinc sulphate (ZnSO₄,p.o.; daily) respectively, in addition to olanzapine (10 mg/kg p.o.; daily). Following treatment completion, group 2 showed increased levels of stress markers (GSSG, MDA, and NO) and impaired levels of antioxidant markers (CAT, SOD, and GSH). Further, a strong positive correlation between insulin resistance index (HOMA-IR) and IL-6, TNF-α, and MDA of liver. Insulin resistance is a possible manifestation of the oxidative stress burden and the widespread inflammatory environment. In groups 3 and 4, however, ZnSO₄ recovered each of these markers in a dose-dependent manner. Improvements were also noted in other homeostatic markers, such as taurine, coenzyme Q10, ascorbic acid, and vitamin E. Remarkably, in both combination groups, there was a significant improvement in all metabolic indicators of dyslipidemia (triglycerides, total cholesterol) and insulin resistance index. The biochemical study and the histological assessment of the liver slices agreed with the results. Thus, the results clearly suggest that Zinc supplementation can significantly improve oxidative stress, inflammation, metabolic perturbation (dyslipidemia and insulin resistance), and liver injury caused by olanzapine in Albino rats.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"84"},"PeriodicalIF":2.8,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11998154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143979281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can vildagliptin protect against radiation-induced premature ovarian failure? Insights into the AMPK and AKT signaling pathways.","authors":"Nada A Mahgoub, Doaa A El-Sherbiny, Ebtehal El-Demerdash","doi":"10.1186/s40360-025-00903-5","DOIUrl":"https://doi.org/10.1186/s40360-025-00903-5","url":null,"abstract":"<p><strong>Background: </strong>Among the detrimental side effects caused by radiotherapy in young females is the ovarian damage, eventually causing premature ovarian failure (POF). While many signaling pathways contribute to the pathogenesis of POF, to date no sufficient data exist on the AMPK and AKT signaling pathways in irradiated ovaries. Both AMPK and AKT play crucial roles in the process of folliculogenesis. Vildagliptin (vilda) is a dipeptidyl peptidase-4 inhibitor with modulatory effect on both AMPK and AKT. Therefore, our study aimed to investigate the biochemical changes that occur in the AMPK/AKT signaling pathway, and the effect of co-administration of vildagliptin in radiation-induced POF.</p><p><strong>Methods: </strong>Female Sprague-dawley rats were randomly divided into four groups: control, radiation, radiation + vilda, or vilda alone groups. Vilda was administered orally once/day, and on the 10th day of the experiment, radiation and radiation + vilda group rats were subjected to 3.2 Gy of whole-body gamma irradiation. Behavioral activity was assessed on the 13th day of the experiment. On day 14 of the experiment, all rats were euthanized. Serum samples were collected, and ovaries were dissected for histological and biochemical analyses.</p><p><strong>Results: </strong>Irradiation of female rats resulted in increased locomotor hyperactivity, impaired memory, and ovarian damage as evidenced by the marked histopathological deterioration. Additionally, irradiation led to a significant decrease in body weight gain, gonadosomatic index, and serum estradiol level. Further, it caused a significant increase in serum AMH, phosphorylated AMPK, phosphorylated AKT, cytoplasmic Nrf2 expression and phosphorylated CREB levels. Co-administration of vilda exhibited neuroprotective effects, preserved the ovarian histological architecture but failed to preserve the primordial follicle pool in irradiated rats.</p><p><strong>Conclusion: </strong>In conclusion, AMPK/AKT signaling pathway is upregulated in radiation-induced POF. It possibly contributes to POF pathogenesis by accelerating the activation of primordial follicles, hence leading to their premature depletion. Coadministration of vilda can protect the ovaries and temporarily preserve its endocrine function; however, it does not sustain the ovarian reproductive capacity due to the early depletion of the pool of primordial follicles. Women undergoing radiotherapy should be cautious with the use of AKT-activating drugs.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"81"},"PeriodicalIF":2.8,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143979272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safety profile of faricimab: a multi-source pharmacovigilance analysis using FAERS and JADER.","authors":"Chuanya Liu, Shangze Li, Ziyi Wang, Zhifu Li, Zhou Fang, Yuan Zhang, Yu Gao","doi":"10.1186/s40360-025-00902-6","DOIUrl":"https://doi.org/10.1186/s40360-025-00902-6","url":null,"abstract":"<p><strong>Background: </strong>Faricimab is a bispecific antibody targeting vascular endothelial growth factor (VEGF) and angiopoietin-2 (Ang-2), offering a novel therapeutic approach for ocular diseases. However, its long-term safety profile remains under evaluation. This study analyzes its adverse events (AEs) using the U.S. FDA Adverse Event Reporting System (FAERS) and the Japanese Adverse Drug Event Report (JADER).</p><p><strong>Methods: </strong>AEs from FAERS (2004-2024) and JADER (2004-2024) were analyzed using disproportionality algorithms. Subgroup analyses assessed differences by age and sex. AE onset time was also assessed.</p><p><strong>Results: </strong>Several newly identified adverse events (AEs) were observed, including macular ischemia, keratic precipitates, and optic nerve injury, with strong safety signals detected in both FAERS and JADER. For instance, macular ischemia showed a high association with faricimab use (ROR = 260.46), suggesting a potential risk of retinal circulation impairment. Similarly, keratic precipitates (ROR = 739.65) indicate a notable inflammatory response. All these findings highlight the need for closer monitoring of ocular complications, particularly in high-risk patient groups. The FAERS database mainly reported retinal occlusive vasculitis, ocular vasculitis, and keratic precipitates, while JADER predominantly featured retinal occlusive vasculitis and retinal vascular occlusion. Sex-based differences indicated a higher risk of inflammatory AEs in females (e.g., uveitis and eye inflammation) and a greater incidence of retinal vascular events in males (e.g., retinal vasculitis). Age-related differences showed that older patients (≥65 years) had lower inflammatory AE risks but were more prone to optic nerve damage and retinal atrophy, while younger patients (<65 years) exhibited a higher risk of vitreous hemorrhage and cataracts.</p><p><strong>Conclusions: </strong>This study identified previously unreported safety signals, suggesting the need for potential updates to faricimab's safety labeling. Faricimab's dual-target mechanism presents unique safety concerns. Clinicians should monitor ocular inflammation and vascular complications, particularly in younger males and Asian patients. Further studies using real-world data are needed to validate these findings.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"82"},"PeriodicalIF":2.8,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Commentary on \"real world results of ibrutinib in patients with relapsed or refractory chronic lymphocytic leukemia: a meta-analysis of clinical studies\".","authors":"Ali Beheshti Namdar, Masoud Keikha","doi":"10.1186/s40360-025-00923-1","DOIUrl":"https://doi.org/10.1186/s40360-025-00923-1","url":null,"abstract":"","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"80"},"PeriodicalIF":2.8,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11992757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Saikosaponin D inhibits the inflammatory response of secretory otitis media through FTO-mediated N⁶-methyladenosine modification of TLR4 mRNA.","authors":"Minjing Yin, Xiuli Han","doi":"10.1186/s40360-025-00910-6","DOIUrl":"https://doi.org/10.1186/s40360-025-00910-6","url":null,"abstract":"<p><p>Secretory Otitis Media (SOM) is a non-suppurative inflammatory disease of the middle ear. Saikosaponin D (SSD), a compound with significant anti-inflammatory and immunomodulatory properties, was investigated for its preventive effects and underlying mechanisms against SOM. A rat model of SOM was established through intraperitoneal ovalbumin injection. Middle ear lavage fluid (MELF) and tissue samples were collected for comprehensive analysis, including bacterial load quantification, neutrophil enumeration, and inflammatory factor assessment. HEK293T cells were utilized for mechanistic validation. Our findings demonstrated that SSD preventive treatment significantly reduced colony-forming units (CFUs) in SOM-induced rats, attenuated middle ear mucosal thickening, and suppressed pro-inflammatory cytokine levels (TNF-α, IL-6, and INF-γ). Mechanistically, SSD treatment counteracted SOM-induced m⁶A level elevation and reversed the downregulation of FTO expression. Functional studies revealed that FTO inhibition exacerbated inflammatory responses, while SSD treatment mitigated these effects. Further investigation demonstrated that SSD decreased TLR4 mRNA stability through FTO-mediated m⁶A modification. In conclusion, SSD alleviates SOM progression by reducing bacterial load and neutrophil infiltration. The therapeutic effects are mediated through FTO upregulation and subsequent m⁶A-dependent TLR4 mRNA degradation. This study elucidates a novel molecular mechanism underlying SSD's preventive action against SOM development.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"79"},"PeriodicalIF":2.8,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11987459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of the efficacy of sucroferric oxyhydroxide and lanthanum carbonate in the hyperphosphatemia of maintainable Hemodialysis.","authors":"Min Li, YiJing Kang, Chao Zhang, XiQuan Ni","doi":"10.1186/s40360-025-00914-2","DOIUrl":"https://doi.org/10.1186/s40360-025-00914-2","url":null,"abstract":"<p><strong>Objective: </strong>To study the efficacy of sucroferric oxyhydroxide (SFOH) and lanthanum carbonate (LC) in the treatment of hemodialysis hyperphosphatemia.</p><p><strong>Methods: </strong>A total of 60 hemodialysis patients with secondary hyperparathyroidism combined with hyperphosphatemia from January 2024 to April 2024 in China Rongtong Medical & Healthcare Group Tai'an 88 Hospital were selected. All patients were randomly divided into 2 groups. One group was treated with SFOH, and the other with LC. Patients in the 2 groups were treated for 3 months continuously, and clinical outcomes, serum phosphorus, serum calcium, and intact parathyroid hormone (iPTH) levels were compared before treatment, and at 1, 2, and 3 months after treatment.</p><p><strong>Results: </strong>When compared with before treatment, the serum phosphorus levels of both groups of patients decreased significantly after 1 month, 2 months, and 3 months of treatment, with statistical significance (P < 0.01). The degree of serum phosphorus decrease in SFOH group was higher than that in LC group (P < 0.01, P < 0.05). There was no statistically significant difference in the effect of serum calcium between the two groups (P > 0.05). Both groups of patients showed a significant decrease in iPTH after treatment, with a statistically significant difference (P < 0.01). The degree of iPTH decrease in SFOH group was more pronounced than in LC group (P < 0.05). After treatment, the serum hosphorus compliance rates of SFOH group and LC Group were 80% and 53.3%, respectively, and the difference in effective rates between the two groups was statistically significant (P < 0.05).</p><p><strong>Conclusion: </strong>SFOH was superior to LC in lowering patients' blood phosphorus and iPTH levels in patients with maintenance hemodialysis hyperphosphatemia combined with secondary hyperparathyroidism.</p>","PeriodicalId":9023,"journal":{"name":"BMC Pharmacology & Toxicology","volume":"26 1","pages":"78"},"PeriodicalIF":2.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}