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diazoxide toxicity in congenital hyperinsulinism:A case report

World Journal of Clinical Pediatrics 2024年第4期13卷 102-108页

作者： Roberta Pajno Camilla Visconti Carmen Bucolo Maria Pia Guarneri Paolo Del Barba Paolo Silvani Marco Gregnanin Graziano Barera Department of Pediatrics Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele InstituteMilan 20132LombardyItaly UniversitàVita-Salute San Raffaele Facoltàdi Medicina e ChirurgiaMilan 20132LombardyItaly Department of Anesthesia and Intensive Care Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele Scientific InstituteMilan 20132LombardyItaly Department of Neonatology Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele InstituteMilan 20132LombardyItaly

BACKGROUND diazoxide is the sole approved drug for congenital hyperinsulinism;however,diuretic administration and vigilant monitoring are crucial to prevent and promptly identify potentially life-threatening adverse *** report aims to highlight a seldom-considered rare side effect of *** believe that this brief report is of general interest to World Journal of Clinical Pediatric readership and increase the physicians’awareness of the guideline ***,it underlines the importance of stopping immediately the drug if suspected side *** SUMMARY The manuscript describes a patient diagnosed with congenital hyperinsulinism(CHI)treated with diazoxide not overlapping with *** resulted in sudden respiratory distress and therefore was transferred to the Neonatal Intensive Care *** cardiological evaluation showed pericardial effusion and left ventricular myocardial hypertrophy,absent *** suspicion of an iatrogenic effect of diazoxide it was progressively reduced until stop while introducing diuretic treatment,with resolution of *** clinically stabilized,an 18 fluoro-diydroxy-phenylalanine positron emission tomography/computed tomography(PET/CT)was performed to differentiate between a focal or diffuse form of *** PET/CT highlighted the presence of a single focal accumulation of the tracer located in the pancreatic tail,consistent with a focal form of *** the age of four months,the patient underwent a distal pancreatectomy with histological confirmation of a focal form of nesidioblastosis,resulting in a curative *** Diuretic administration and vigilant monitoring of diazoxide therapy are crucial to prevent and promptly identify potentially life-threatening adverse effects.

关键词： diazoxide Hypoglycemia Congenital hyperinsulinism Side effect Case report

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diazoxide preconditioning plus subsequent hypothermia increased resistance of rat cultured hippocampal neurons against hypoxia-reoxygenation injury

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Chinese Medical Journal 2006年第11期119卷 887-893页

作者： LIU Rong-guo WANG Wei-jian S0NG Na CHEN Yan-qing LI Li-huan Department of Anesthesiology Fujian Provincial Hospital Fuzhou 350001 China Department of Anesthesiology First Affiliated Hospital of Wenzhou Medical College Wenzhou 325000China Department of Anesthesiology Cardiovascular Institute Fuwai Hospital Peking Union Medical college and Chinese Academy of Medical Sciences Beijing 100037 China

Background Cerebral ischemia-reperfusion/hypoxia-reoxygenation insult triggers lots of pathophysiological and biochemical events that separately affect the evolution of cerebral damage. Accordingly, all known effective neuroprotective measures should be taken to get the optimal efficacy of therapy. This study was undertaken to investigate whether diazoxide （DZ） preconditioning combined with the following hypothermia could contribute to synergistic neuroprotection compared with either hypothermia or DZ preconditioning alone. Methods Cultured for 9-10 days in vitro, the hippocampal neurons of SD rats were preconditioned with DZ 0 pmol/L or DZ 250 pmol/L for 1 hour per day and this treatment lasted for 3 days. Subsequently, neurons were subjected to deprivation of oxygen for 4 hours at 37°0, 34°C, 30℃ and 22℃, respectively. This experiment consisted of 8 groups （4 temperature groups and 4 combination groups） and each group contained 12-well or 2-dish cells. Survival rate, expression of Bcl-2, fluorescence magnitude of intracellular calcium, and concentration of malondialdehyde （MDA） were determined at 24 hours after reoxygenation. Results The survival rate and expression of Bcl-2 were both increased in individually hypothermic conditions compared with those at 370G （P〈0.05）, whereas intracellular calcium and MDA did the opposite exhibition simultaneously （P〈0.05）. 22℃ contributed to a higher survival rate and greater expression of Bcl-2 in comparison with other hypothermia （P〈0.05）. Preceding administration of 250 pmol/L DZ took the similar effects on the neurons like hypothermia. Moreover, compared with individual hypothermia or DZ preconditioning, the neuronal survival rate and expression of Bcl-2 in the combination group were increased significantly （P〈0.05）, whereas the calcium fluorescence density and concentration of MDA were reduced further （P〈0.05）. 250 Iamol/L DZ preconditioning combined with 22℃ provided a maximal neuroprotection. Conclusions Compared with ei

关键词： diazoxide hypothermia proto-oncogene protein c-bcl-2 calcium malondialdehyde

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diazoxide preconditioning antagonizes cytotoxicity induced by epileptic seizures

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Neural Regeneration Research 2013年第11期8卷 1000-1006页

作者： Qingxi Fu Zhiqing Sun Jinling Zhang Naiyong Gao Faying Qi Fengyuan Che Guozhao Ma Department of Neurology Linyi People's Hospital Department of Neurology Shandong Provincial Hospital Shandong University

diazoxide, an activator of mitochondrial ATP-sensitive potassium channels, can protect neurons and astrocytes against oxidative stress and apoptosis. In this study, we established a cellular mode of epilepsy by culturing hippocampal neurons in magnesium-free medium, and used this to investigate effects of diazoxide preconditioning on the expression of inwardly rectifying potassium channel （Kir） subunits of the ATP-sensitive potassium. We found that neuronal viability was significantly reduced in the epileptic cells, whereas it was enhanced by diazoxide preconditioning. Double immunofluorescence and western blot showed a significant increase in the expression of Kir6.1 and Kir6.2 in epileptic cells, especially at 72 hours after seizures. diazoxide pretreatment completely reversed this effect at 24 hours after seizures. In addition, Kir6.1 expression was significantly upregulated compared with Kir6.2 in hippocampal neurons after seizures. These findings indicate that diazoxide pretreatment may counteract epileptiform discharge-induced cytotoxicity by suppressing the expression of Kir subunits.

关键词： neural regeneration ATP-sensitive potassium channel activator of mitochondrial ATP-sensitivepotassium channel epilepsy diazoxide inwardly recti^ing potassium channel subunit hippocampal neuron cytotoxicity neuroprotection grants-supported paper neuroregeneration

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diazoxide attenuates ischemia/reperfusion injuryvia upregulation of heme oxygenase-1 after liver transplantation in rats

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World Journal of Gastroenterology 2012年第15期18卷 1765-1772页

作者： Zhong Zeng Han-Fei Huang Fei He Lin-Xi Wu Jie Lin Ming-Qing Chen Organ Transplantation Center the First Affili-ated Hospital of Kunming Medical CollegeKunming 650032Yunnan ProvinceChina

AIM:To evaluate the effects of diazoxide on ischemia/reperfusion(I/R)-injured hepatocytes and further elucidate its underlying ***:Male Sprague-Dawley rats were randomized(8 for donor and recipient per group)into five groups:I/R group(4 h of liver cold ischemia followed by 6 h of reperfusion);heme oxygenase-1(HO-1)small interfering RNA(siRNA)group(injection of siRNA via donor portal vein 48 h prior to harvest);diazoxide(DZ) group(injection of DZ via donor portal vein 10 min prior to harvest);HO-1 siRNA+DZ group;and siRNA control *** and liver samples were collected at 6 h after *** mRNA expressions and protein levels of HO-1 were determined by reverse transcription polymerase chain reaction and Western blotting,and tissue morphology was examined by light and transmission electron *** transaminases level and cytokines concentration were also ***:We observed that a significant reduction of HO-1 mRNA and protein levels in HO-1 siRNA and HO-1 siRNA+DZ group when compared with I/R group,while the increases were prominent in the DZ *** and transmission electron microscopy indicated severe disruption of tissue with lobular distortion and mitochondrial cristae damage in the HO-1 siRNA and HO-1 siRNA+DZ groups compared with DZ *** alanine aminotransferase,aspartate transaminase,tumor necrosis factor-αand interleukin-6 levels increased in the HO-1 siRNA and HO-1 siRNA+DZ groups,and decreased in the DZ ***:The protective effect of DZ may be induced by upregulation of *** inhibiting expression of HO-1,this protection pretreated with DZ was abolished.

关键词： Ischemia/reperfusion injury diazoxide Heme oxygenase-1 Liver transplantation Rat

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Neuroprotective effects of a mitochondrial K^+-ATP channel opener (diazoxide) are mediated by Bcl-2 expression upregulation

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Neural Regeneration Research 2011年第12期6卷 956-960页

作者： Majid Katebi Mansooreh Soleimani Mehdi Mehdizadeh Department of Anatomy School of MedicineHormozgan University of Medical Sciences Cellular and Molecular Research Center Tehran University of Medical Sciences Department of Anatomy School of MedicineTehran University of Medical Sciences Research Institute for Islamic & Complementary Medicine Tehran University of Medical Sciences

Mitochondrial K＋-ATP （mito-KATP） channels play an important role in cellular function and survival following ischemic stress. The present results revealed that intervention with diazoxide, a mito-KATP channel opener, led to an increase in Bcl-2 expression in the cerebral cortex of rats subjected to cerebral ischemia reperfusion injury. In addition, the intervention also led to clear improvements in neuronal mitochondrial morphology and consciousness post-injury. Glibenclamide a mito-KATP channel blocker, exhibited the converse effects. Both diazoxide and glibenclamide exerted dose-dependent effects （in particular, at 18 mg/kg diazoxide and 25 mg/kg glibenclamide）. These findings suggest that diazoxide exerts a neuroprotective effect on cerebral ischemia reperfusion injury by opening mito-KATP channels and upregulating Bcl-2 expression.

关键词： K-ATP channel Bcl-2 cerebral ischemia reperfusion injury diazoxide

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Mechanism of diazoxide-mediated Cardioprotection

Mechanism of Diazoxide-mediated Cardioprotection

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第十五届国际药理学大会

作者： Mehta Neeraj arg Vivek Division of Pharmacology College of PharmacyOhio State University Columbus OHU.S.A. Division of Pharmacology College of PharmacyOhio State University Columbus OHU.S.A.

＜正＞ Ischemic preconditioning （IPC） can be mimicked by K+ channel openers such as diazoxide. diazoxide has multiple ATP-sensitive K+ channel （KATP）-indepen-dent actions, and the mechanism underlying diazoxidemediated cardioprotection remains inconclusive. Giving that the KATP pore-forming subunit Kir6.2-knock-out mice have shown no cardioprotection of IPC, we tested the hypothesis that diazoxide protects the heart by promoting import of Kir6.2-containing KATP into mitochondria from cytosol where they are synthesized. The effect of diazoxide on mitochondrial localization of Kir6.2 was examined in KATP deficient COS-7 cells transfected with HA tagged Kir6.2 and SUR2A by laser confocal microscopy. We found that the percentage of cells showing mitochondrial localization of Kir6.2 was significantly higher in diazoxide （100 micro M）-treated group than that in control group （68.0% vs. 11.0%）. The effect was almost completely prevented by the KATP channel inhibitors 5-hydroxydecanoate or glibenclamide, or a selective protein kinase C （PKC） inhibitor chelerythrine. We conclude that diazoxide increases Kir6.2-containing KATP channels in mitochondria by activation of PKC.

关键词： preconditioning diazoxide PKC

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Cardioprotective Effects of diazoxide on Myocardial Ischemia/Reperfusion Injury in Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2006年第6期26卷 690-692页

作者：张凯伦赵静杨运海胡志伟 Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology

In order to study the cardioprotective effects of diazoxide on the myocardial ischemia/reperfusion injury of rats and mechanisms, the healthy SD rats were randomly divided into 2 groups： the rats in the experimental group were injected with diazoxide for preconditioning with the dosage of 12.5 mg/kg through the right femoral vein and those in the control group was only administered with the equal volume of media. After 10 rain, a left thoracotomy was performed and the left anterior descending branch was occluded for 2 h. Two h later, the left anterior descending branch was reperfused for 2 h and then the heart was quickly excised to be used for measurement of MDA, SOD and the infarct size, in situ cell apoptosis detection and observation of the cell ultrastructure by electron microscopy. The results showed that as compared with the control group, MDA, the infarct size and cell apoptosis in the experimental group were greatly reduced （P〈0.05）. And the cell ultrastructure was obviously improved, But the activity of SOD had no change （P〉0.05）. It was concluded that diazoxide could protect the rats from myocardial ischemia/reperfusion injury, which might be contributed to the reduction of lipid peroxidation and cell apoptosis.

关键词： diazoxide cardioprotection ischemia/reperfusion injury apoptosis rat

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Effects of diazoxide Treatments on Electrophysiologyic Properties in Guinea Pig Papillary Muscles Undergoing Ischemia/Reperfusion

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2005年第3期25卷 257-259页

作者：杨运海韩召敏胡志伟张凯伦 Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Department of Pharmacy Union Hospital Tongji Medical College Huazhong University of Science and Technology

The effects of diazoxide treatments on electrophysiologyic properties in guinea pig papillary muscles undergoing ischemia/reperfusion was studied using intracellular microelectrode technique. Twenty-four guinea pigs were randomly divided into three groups (n=8 in each group). In control group, *** solution was given. In experimental group, *** solution with diazoxide (100 mol/L) was given. In pretreatment group, the muscle was treated with diazoxide 20 min before arrested with *** cardioplegia. The results showed that the APD_50 and APD_90 in experimental and pretreatment groups were significantly shorter after 5 and 10 min reperfusion (Pdiazoxide is better than that of pretreatment with diazoxide or *** solution alone.

关键词： diazoxide cardioplegia electrophysiology cardioprotection

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Differentially expressed phosphoproteins in diazoxide-pretreated ventricular myocytes by two-dimensional electrophoresis and mass spectrometry in vitro

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Journal of Medical Colleges of PLA(China) 2006年第3期21卷 143-147页

作者：李洪肖颖彬高玉琪杨天德 Departments of Anesthesiology Xinqiao HospitalThird Military Medical UniversityChongqing 400037China Department of Pathophysiology College of High Altitude Military MedicineThird Military Medical UniversityChongqing 400038China

Objectives To analyze and identify differentially expressed phosphoproteins associated with mitochondrial KATP channel opening. Methods： Adult rat ventricular myocytes were isolated, cultured, and identified, and pretreated without or with 100 μmol/L diazoxide for 10 min. Phosphoproteins prepared and enriched from the control and diazoxide-pretreated cells were separated by two-dimensional gel electrophoresis （2-DE） followed by sliver staining. The obtained interesting phosphoproteins were further identified by mass spectrometry. Results. Associated with diazoxide preconditioning, the proteins of chaperonin containing TCP-1 and hypothetical protein XP-346548 were phosphorylated significantly （P〈0. 01）, while the 94-kDa glucose-regulated protein, calpactin I heavy chain and ferritin were dephosphorylated markedly （P〈0. 01）. Conclusion： These findings suggest that cardiomyocytes undergo significant posttranslational modification via phosphorylation in a multitude of proteins in order to respond diazoxide preconditioning, and these phosphorylated protein may mediate the downstream signaling of cardioprotection by mitochondrial KATp channel opening induced by ischemic preconditioning.

关键词： preconditioning mitochondrial KATP channel two-dimensional gel electrophoresis ventricular myocytes diazoxide

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氯苯甲噻二嗪(diazoxide)的评价

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国外医学参考资料.药学分册 1974年第5期 305-307页

作者：张楠森

恶性（即急进型）高血压的特征为舒张压突然升高并持续在130毫米汞柱以上,3～4级眼底病变,视神经乳头水肿,肾功能损害及脑病常见发生。氯苯甲噻二嗪为治疗恶性高血压及脑病的药物,快速静脉注射后可迅速减低舒张压。其化学结构式为: 氯... 详细信息

恶性（即急进型）高血压的特征为舒张压突然升高并持续在130毫米汞柱以上,3～4级眼底病变,视神经乳头水肿,肾功能损害及脑病常见发生。氯苯甲噻二嗪为治疗恶性高血压及脑病的药物,快速静脉注射后可迅速减低舒张压。其化学结构式为: 氯苯甲噻二嗪的化学结构虽与噻嗪类和尿药相似,但无利尿作用。本品的分子式为C8H7ClN2O2S,分子量230.67,熔点325℃。其性状为白色结晶、无嗅,略溶于水及碱性氢氧化物溶液,其水溶液可用氢氧化钠调节pH至11.6,澄明无色,在室温避光条件下可稳定二年,如变色失效,不可应用。作用原理

关键词：恶性高血压氯苯氯代烃降压效应血浆半衰期 diazoxide 快速静脉注射降压幅度舒张压高血糖

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