硫酸镁治疗前置胎盘所致的妊娠晚期阴道出血

目的:观察硫酸镁治疗前置胎盘效果和安全性.方法:前置胎盘患者230例作为治疗组,30 min内快速静脉输入硫酸镁负荷量4 g(10%葡萄糖注射液250 mL加25%硫酸镁溶液16 mL),随后以1.5 g•h 1维持(10%葡萄糖注射液500 mL加25%硫酸镁溶液40 mL),宫缩消失及阴道流血停止12 h后停药.如复发,从负荷量开始重复治疗,但每天不应超过30 g.同期条件相同50例前置胎盘患者为对照组,肌肉注射苯巴比妥钠0.2～0.3 g,每4～6 h 1次.结果:治疗组有效227例(98.7%),对照组有效17例(34.0%),两组差异有极显著性(P＜0.01).治疗组新生儿窒息率低于对照组(P＜0.01).两组产后出血量及出血率差异均无显著性(P＞0.05).结论:硫酸镁治疗前置胎盘疗效显著,应用安全,可作为首选药物.     

Benefits of magnesium sulfate in the management of acute human poisoning by organophosphorus insecticides

Organophosphorus chemicals (OPs) are the pesticides most often involved in serious human poisoning. Treatment of intoxication with OPs conventionally involves atropine for reduction of muscarinic signs and oximes that increase the rate of hydrolysis of the phosphorylated enzyme acetylcholinesterase (AChE). Although atropine and oximes (pralidoxime or obidoxime) are traditionally used in the management of such poisoning, their efficacy remains a major issue of debate; thus, the goal of this prospective clinical trial was to elaborate the value of magnesium sulfate (MgSO4) in the management and outcome of OP insecticide poisoning. This unicenter, randomized, single-blind trial study was conducted on patients who were acutely poisoned with OPs and admitted to the Poisoning Center of Loghman-Hakim Hospital in Tehran, Iran. In a systematic sampling, every fourth eligible patient was chosen to undergo MgSO4 treatment. Magnesium sulfate was administered at dose of 4 g/day i.v. continued for only the first 24 hours after admission. The mean daily oxime requirement and the mean daily atropine requirement were not statistically significant between two treated groups. The mortality rate and hospitalization days of patients who received MgSO4 treatment were significantly lower than those who had not received MgSO4 (P < 0.01). It is concluded that administration of MgSO4, in a dose of 4 g/day concurrent to conventional therapy, in OP acute human poisoning is beneficial by reducing the hospitalization days and rate of mortality.     

Activities of rat cytochrome P450 3A and 2C isoforms are increased in vivo by magnesium sulfate as evidenced by enhanced oxidation of bupivacaine and testosterone in liver microsomes

We previously reported that magnesium sulfate (MgSO(4)) increases the threshold dose of bupivacaine in inducing seizure in rats. Cytochrome P450 (P450) isoforms involved in the biotransformation of bupivacaine to three oxidative metabolites and the effects of MgSO(4) in vivo on the P450 activities in rats were investigated. Of six cDNA-expressed rat P450 isoforms tested, CYP3A2 and CYP2C11 had high rates for N-debutlylation and 3'-hydroxylation of bupivacaine, respectively. The liver microsomes prepared from male rats pretreated with intravenous administration of MgSO(4) (a bolus dose of 25 mg/kg, followed by infusion of 2.0 mg/kg/min for 6 h) showed increased V(max) values for N-debutylation and 3'-hydroxylaiton of bupivacaine compared to the liver microsomes from control rats. Administration of MgSO(4) also increased the activities of testosterone 6beta- and 16alpha-hydroxylation. Although the level of expression of CYP3A and CYP2C isoforms in the liver microsomes were unchanged, NADPH-P450 reductase and cytochrome b(5) were found to be induced by intravenous administration of MgSO(4). These results suggest that CYP3A and CYP2C isoforms are activated by MgSO(4) in vivo as a consequence of enhanced microsomal electron transfer due to induction of NADPH-P450 reductase and cytochrome b(5), leading to the increased metabolism and clearance of bupivacaine.     

Triethylene glycol poisoning treated with intravenous ethanol infusion

INTRODUCTION: Poisoning with triethylene glycol has been rarely reported in humans. Triethylene glycol is thought to be metabolized by alcohol dehydrogenase to acidic products resulting in the production of a metabolic acidemia. Triethylene glycol metabolism has previously been shown to be inhibited by fomepizole (4-methyl pyrazole) administration. We report a case of triethylene glycol ingestion, presenting with a metabolic acidemia, treated with intravenous ethanol administration. CASE REPORT: A 23-year-old female presented to the emergency department approximately 1-1.5 hours following ingestion of a gulp of triethylene glycol (99%) brake fluid with coma (GCS-3) and metabolic acidemia (pH 7.03, PCO2 44 mm Hg, Bicarbonate 11 mmol/L, anion gap 30 mmol/L, serum creatinine 90 mumol/L). She was intubated and given 100 mmol of intravenous sodium bicarbonate. An ethanol loading dose was administered followed by an infusion to maintain serum ethanol at 100 mg/dL. Acidemia gradually resolved over the next 8 hours and she was extubated 12 hours later. The ethanol infusion was continued for a total of 22 hours. There was no recurrence of acidemia. Serum ethanol, ethylene glycol, and methanol levels were nondetectable on presentation, as was serum salicylate. Urine drug of abuse screen and thin-layer chromatography revealed no other coingested substances. The patient was discharged to a psychiatric ward 36 hours postingestion. CONCLUSION: Pure triethylene glycol poisoning results in coma and metabolic acidemia and may be treated with alcohol dehydrogenase inhibitors such as ethanol.     

Assessment of the effects of endothelin-1 and magnesium sulphate on regional blood flows in conscious rats, by the coloured microsphere reference technique

There is evidence to suggest that magnesium (Mg2+) is beneficial in the treatment of a number of conditions, including pre-eclampsia and acute myocardial infarction. The mode of action of Mg2+ in these conditions is not clear, although the vasodilator properties of Mg2+ are well documented both in vitro and in vivo. Previously, we demonstrated that i.v. infusion of magnesium sulphate (MgSO4) alone, or in the presence of vasoconstrictors, caused increases in flow and conductance in the common carotid, internal carotid and hindquarters vascular beds, in conscious rats. Therefore, the objective of the present study was to investigate the regional and subregional changes in haemodynamics in response to the vasoconstrictor peptide endothelin-1 (ET-1) and MgSO4 in more detail, using the coloured microsphere reference technique. Infusion of ET-1 and MgSO4 had similar effects on heart rate and mean arterial pressure as in our previous study. Infusion of ET-1 caused a rise in mean arterial pressure and a fall in heart rate, and infusion of MgSO4 returned mean arterial pressure to control levels with no effect on heart rate. The responses to MgSO4 in the presence of ET-1 showed considerable regional heterogeneity with blood flow increasing (e.g. skeletal muscle), decreasing (e.g. stomach) or not changing (e.g. kidney). Of particular interest was the finding that MgSO4 caused increases in flow in the cerebral and coronary vascular beds. This, and our previous studies, have shown that MgSO4 can reverse vasoconstriction in a number of vascular beds, and indicate that this compound may have therapeutic benefit in conditions associated with vasospasm.     

Assessment of serum magnesium levels and its outcome in neonates of eclamptic mothers treated with low-dose magnesium sulfate regimen

Objectives:

Magnesium historically has been used for treatment and/or prevention of eclampsia. Considering the low body mass index of Indian women, a low-dose magnesium sulfate regime has been introduced by some authors. Increased blood levels of magnesium in neonates is associated with increased still birth, early neonatal death, birth asphyxia, bradycardia, hypotonia, gastrointestinal hypomotility. The objective of this study was to assess safety of low-dose magnesium sulfate regimen in neonates of eclamptic mothers treated with this regimen.

Materials and Methods:

This was a cross-sectional observational study of 100 eclampsia patients and their neonates. Loading dose and maintenance doses of magnesium sulfate were administered to patients by combination of intravenous and intramuscular routes. Maternal serum and cord blood magnesium levels were estimated. Neonatal outcome was assessed.

Results:

Bradycardia was observed in 18 (19.15%) of the neonates, 16 (17.02%) of the neonates were diagnosed with hypotonia. Pearson Correlation Coefficient showed Apgar scores decreased with increase in cord blood magnesium levels. Unpaired t-test showed lower Apgar scores with increasing dose of magnesium sulfate. The Chi-square/Fisher''s exact test showed significant increase in hypotonia, birth asphyxia, intubation in delivery room, Neonatal Intensive Care Unit (NICU) care requirement, with increasing dose of magnesium sulfate. (P ≤ 0.05).

Conclusion:

Several neonatal complications are significantly related to increasing serum magnesium levels. Overall, the low-dose magnesium sulfate regimen was safe in the management of eclamptic mothers, without toxicity to their neonates.KEY WORDS: Eclampsia, low-dose magnesium sulfate, serum magnesium level, neonatal outcome     

Prenatal MgSO4 treatment modifies the erythrocyte band 3 in preterm neonates.

Magnesium sulphate that is widely used to prevent preterm labour or treatment for imminent eclampsia is also suggested to decrease a cerebral palsy in preterm newborns. However, the molecular mechanism of MgSO4 protection in fetus remains unknown. Since Mg2+ very rapidly crosses the placenta, we assayed whether it may exert an effect on newborn erythrocytes, particularly on anion exchange band 3. The study groups consisted of preterm neonates born from mothers who received prenatally magnesium sulphate and a control group, without prenatal Mg2+ administration. We compared the selected erythrocyte parameters including ATP concentration, membrane lipids peroxidation, the band 3 amount and its phosphotyrosine level, assayed after delivery and 24h later. At birth, ATP concentration was higher in control newborns and decreased after 24h, reaching the level found in the MgSO4-treated group. Band 3 and P-Tyr amounts were unchanged in MgSO4-treated newborns during examined period. In the control group, the lower Mg concentration after delivery correlated with the lowered band 3 phosphorylation. We have also observed enlarged TBARS content in control membranes. Our results demonstrate that prenatal administration of magnesium sulphate significantly altered some erythrocyte parameters. These data suggest that MgSO4 may modify the erythrocytes metabolism in preterm newborns. Since band 3 exhibits the same structural and functional activities as in the brain, the elucidation of MgSO4 influence is of special importance.     

The efficacy of magnesium sulfate loading on microalbuminuria following SIRS: One step forward in dosing

Backgrounds

Magnesium has been known for its antioxidative and antiinflammatory properties in many studies. In this study two dosing regimens of magnesium were compared with a placebo control group in order to investigate safety and efficacy of high doses of intravenous magnesium sulfate infusion on critically ill trauma patients. Inflammatory and oxidative factors were measured in this trial.

Methods

45 trauma patients with systemic inflammatory response syndromes (SIRS) were randomly assigned into 2 treatment and one placebo groups. The high dose group received 15 g MgSO₄, low dose group received 7.5 g of MgSO₄ over 4 hour infusion, and placebo group received saline alone. The initial and post magnesium sulfate injections levels of tumor necrosis factor alpha (TNF-α), total antioxidant power and lipid peroxidation were measured after 6, 18 and 36 hours. The pre-infusion along with 6 and 36 hour level of microalbuminuria were also determined.

Results

Repeated measurements illustrated that there was no significant difference in TNF-α, total antioxidant power and lipid peroxidation levels among groups during the period of analysis. The microalbuminuria at 36 hour post infusion of high dose group was lower than that of control group (p = 0.024). Patient’s mortality (28 day) was similar among all treatment groups. Both magnesium infusion groups tolerated the drug without experiencing any complications.

Conclusion

No evidence for antioxidative and antiinflammatory effects of magnesium in traumatic SIRS positive patients was found. Magnesium in high doses may be recommended for traumatic patients with SIRS status to prevent microalbuminuria.     

Pre-eclampsia/eclampsia: a literature review

A review of literature on pre-eclampsia/eclampsia indicates that this is one of the commonest causes of high maternal and infant mortality and morbidity rates. Current information on the condition indicates that use of aspirin, phenytoin and magnesium sulphate are on the increase. However, in Malawi lytic cocktail and use of antihypertensives such as Hydralazine and, anticonvulsants such as Valium are currently in use. Even with this type of management, Malawi experiences high morbidity and mortality rates. This literature review was done to identify baseline data for a study to be carried out in some of the hospitals in Malawi to establish a protocol for effective management of pre-eclampsia and eclampsia in Malawi. It is hoped that after using low dose aspirin and magnesium sulphate, the morbidity and mortality caused by the disease will be reversed with time.     

静脉应用伏立康唑致急性肾损伤及肾小管性酸中毒

1例80岁男性患者因术后感染给予亚胺培南西司他汀钠、万古霉素、卡泊芬净、米卡芬净及美罗培南,效果不佳,后治疗改为联用美罗培南1.0 g,1次/8 h静脉滴注及伏立康唑200 mg(首日剂量400 mg,1次/12 h),1次/12 h静脉滴注。第5～9天,实验室检查示血清肌酐(SCr)154～208μmol/L,尿素氮(BUN)24.3～35.9 mmol/L,血清胱抑素C 4.54～5.44 mg/L;血pH值7.18～7.34,氯离子122～130 mmol/L,钾离子3.4～4.1 mmol/L,标准碳酸氢盐波动于12～15 mmol/L,实际碳酸氢盐13～14 mmol/L,阴离子间隙13～14 mmol/L。尿分析示红细胞3.8～4.8个/HP,蛋白±,pH值保持在5.5。诊断为肾小管性酸中毒、急性肾损伤。第9天,伏立康唑用法改为每晨静脉滴注200 mg,每晚鼻饲给药200 mg。调整用法后第3天患者出现高氯性酸中毒、低钾血症,第11天停用伏立康唑,美罗培南继续应用。停药2 d后,患者血清SCr及BUN水平升至最高,分别达282μmol/L及49.4 mmol/L,随后逐渐降低,分别于停药后第25天和停药后34天降至正常,血气分析各项指标于停药后第25天基本恢复正常。     

5-Fu静脉滴注不同持续时间对晚期大肠癌的疗效比较

目的　观察氟脲嘧啶 (5 Fu)持续静脉滴注不同时间联合醛氢叶酸 (LV)和奥沙利铂 (L OHP)治疗晚期大肠癌的疗效及毒性反应。方法　经病理组织学诊断的晚期大肠癌 39例。A组 :2 0例 ,L OHP 130mg/m2 静脉滴注 2h ,第 1d ;LV 2 0 0mg/m2 ,静脉滴注 2h ,随后 5 Fu 375mg/m2 静脉推注 10min ,再接 5 Fu3 0 /m2 用输液泵连续滴注 4 8h ,2 1d为 1个周期。B组 :19例 ,方案剂量同A组 ,其中 5 Fu 3 0 /m2 用输液泵连续滴注 12 0h ,2 1d为 1个周期。两组病例至少接受 2个周期治疗。结果　可评价的 35例中 ,A组 18例 ,B组 17例。A、B两组有效率分别为 38 9%、4 2 1% ,经统计学处理 ,差异无显著意义 (P >0 0 5 )。A组毒性大于B组。结论　L OHP 5 Fu LV方案延长 5 Fu持续滴注时间未能提高疗效 ,却减轻了毒性反应。     

Magnesium levels after magnesium-containing cathartics

To determine the effect on serum Mg++ levels of oral Magnesium-containing cathartics (MgCC) used in the treatment of suspected drug overdose, a prospective, non-randomized study of 24 cases of suspected drug overdose was conducted. Ten cases admitted to the observation unit were assigned to the single dose MgCC group. Fourteen cases admitted to either the ICU or the observation unit were assigned to the multiple dose MgCC group. Single dose cases received 30 gm of magnesium sulfate (MgSO4) at 0 hours. Multiple dose cases received 3 30 gm doses of MgSO4 at 0, 4, and 8 hours. Mg++ levels were measured prior to each MgSO4 dose and 1 and 4 hours after the final dose in both groups. In the single dose group, there was no difference between baseline Mg++ levels and post MgSO4 levels, and only 2/10 developed slightly elevated levels (2.2, 2.3 mEq/L). In the multiple dose group, levels increased and remained significantly higher than baseline after the second MgSO4 dose, and 9/14 developed elevated levels (2.2 to 5.0 mEq/L). All patients who developed elevated Mg++ levels had normal BUN and creatinine values. When the single and multiple dose groups were compared, baseline Mg++ levels were no different (1.68 +/- 0.21 vs 1.69 +/- 0.24, p = 0.952), but peak Mg++ levels were significantly higher in the multiple dose group (1.80 +/- 0.31 vs 2.61 +/- 0.86, p = 0.004). Cases that developed hypermagnesemia had slightly higher baseline Mg++ levels (1.78 +/- 0.22 vs 1.60 +/- 0.19 mEq/L, p = 0.041). In the multiple dose group, higher peak Mg++ levels were noted in cases involving ingestions of anticholinergic or opioid drugs (2.83 vs 1.98, p = 0.025). Hypermagnesemia developed in some cases with normal renal function, blood pressure, and urine output. We conclude that significant hypermagnesemia can occur rapidly after use of multiple dose Mg++ cathartics in standard doses in patients with normal renal function.     

Absorption of magnesium from orally administered magnesium sulfate in man

The use of magnesium sulfate (Epsom salt) as a cathartic in patients with impaired renal function can lead to severe toxicity due to hypermagnesemia. Although toxicity is uncommon in healthy subjects, little is known concerning the extent of absorption of magnesium after a cathartic dose of magnesium sulfate. The bioavailability of magnesium following a large oral dose of magnesium sulfate in normal volunteers was examined in the present investigation. Baseline 24-hour urinary excretion rates of magnesium and creatinine were determined over 3 consecutive days in 6 healthy men. The oral administration of 13.9 g (56.5 mmoles) magnesium sulfate U.S.P., in 4 equal hourly increments, resulted in the urinary excretion (corrected for baseline excretion rate) of 4.0 +/- 2.9% (mean +/- SD) of the dose of magnesium during the first 24 hours and 6.9 +/- 7.0% of the dose during a 72-hour interval. Magnesium sulfate administration had no effect on the 24-hour urinary excretion rate of creatinine. The baseline excretion rate of magnesium was significantly correlated with that of creatinine (r = 0.875) and inorganic sulfate (r = 0.921). All of the subjects experienced mild or moderate diarrhea. Therefore, magnesium is absorbed to a limited and variable extent in healthy adults following a cathartic dose of magnesium sulfate.     

Effects of administration of oral magnesium on plasma glucose and pathological changes in the aorta and pancreas of diabetic rats

1. Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of the complications of diabetes. The purpose of the present study was to determine the relationship between oral Mg supplementation and changes in plasma glucose, calcium, haemoglobin, Ca/Mg ratio, blood pressure and the histology of the pancreas and vascular system in streptozotocin-induced diabetic rats. 2. Ten days after the induction of diabetes in male Wistar rats, half the diabetic animals were divided into six groups, receiving 0, 1, 3, 10, 30 or 50 g/L MgSO4 added into the drinking water for 8 weeks. Plasma glucose and Mg were measured at days 1, 2, 3, 5, 7, 14 and 21 to find the optimum dose of Mg and the time-course of its effect. In addition, histological observations were undertaken. Eight weeks later, all animals were decapitated, the pancreas and thoracic aorta were removed carefully and immersed immediately in 10% formaldehyde for histological study. 3. To evaluate the effects of Mg on plasma glucose, calcium, haemoglobin, Mg and blood pressure, another group of animals was divided into four experimental groups, as follows: (i) non-diabetic controls received tap water for 8 weeks; (ii) acute diabetics received tap water for 10 days; (iii) chronic diabetic controls received tap water for 8 weeks; and (iv) Mg-treated chronic diabetic rats received 10 g/L MgSO4 added into the drinking water 10 days after the induction of diabetes for 8 weeks. 4. Magnesium dose dependently affects plasma glucose levels. The peak effect was reached during the first 24 h following oral administration. Administration of 10 g/L MgSO4 results in the return of normal structure in the diabetic pancreas and aorta. Moreover, this concentration of MgSO4 causes glucose, haemoglobin, calcium, the Ca/Mg ratio and blood pressure to reach normal levels. Although the Mg level increases slightly following the administration of 10 g/L MgSO4 to diabetic rats, it never reaches control levels. 5. On the basis of the results of the present study, it may be concluded that chronic Mg administration may have beneficial effects on diabetes.     

大剂量甲氨蝶呤化疗致急性肾衰竭2例

2例患者大剂量甲氨蝶呤（MTX）化疗导致急性肾衰竭。第l例为53岁女性，因非霍奇金淋巴瘤给予大剂量MTX化疗：先用MTX500mg0．5h时内静脉滴注、3500mg24h内泵入，然后用亚叶酸钙进行解救，首次剂量为30mg／m^2，以后15mg／m^2，每隔6h肌内注射1次，解救8次。患者无慢性肾脏病史，化疗前肾功能正常（SCr97．1μmot／L，BUN4．78mmol／L）。化疗后第4天，出现颜面及双手轻度水肿，尿量减少，SCr升至151Ixmol／L。给予甲泼尼龙、呋塞米和碳酸钙一维生素D3对症治疗，并碱化尿液，监测肾功能（SCr最高达275μmot／L），化疗后第13天肾功能恢复至正常（SCr96μmol／L）。第2例为29岁男性，因急性淋巴细胞白血病给予大剂量MTX化疗：MTX500mg0．5h内静脉滴注、4500mg24h内泵入，解救方案同例1。患者无慢性肾脏病史，化疗前肾功能正常（SCr86．9μmol／L，BUN5．35mmol／L）。化疗后第3天出现全身水肿、尿量减少，SCr升至235μmol／L（最高达360μmol／L）。给予对症治疗，同例1。化疗后第30天肾功能恢复至正常（SCr89ttmol／L）.     

帕珠沙星静脉滴注引发低血糖

1例89岁男性2型糖尿病和高血压患者，因肺部感染住院。患者于停用降血糖和降血压药物后，静脉滴注帕殊沙星0.3g，2次／d。在第3次静脉滴注1h后突然出冷汗，血糖自10mmol／L降至2．7mmol／L。立即停用帕殊沙星，静脉注射50％葡萄糖注射液60ml，静脉滴注10％葡萄糖注射液，并增加进食量。24h后血糖逐渐上升至5．6mmol／L。     

血栓通注射液致低血钾

患者女,46岁,入院诊断为脑梗死,首次静脉滴注血栓通注射液0.6g 5%葡萄糖注射液250ml时,约50min后突现严重烦燥、软弱无力、大汗淋漓;实验室检查:血钾2.7mmol/L,ECG示T波低平,U波增高。治疗后血钾恢复至4.5mmol/L,3h后患者安静入睡,第2天症状完全缓解。     

Phase I trial of continuous infusion recombinant human interleukin-4 in patients with cancer

BACKGROUND: A phase I study using recombinant human interleukin-4 (rhuIL-4) administered as a continuous intravenous infusion was conducted in patients with advanced cancer to study the toxicity profile and to determine the maximum tolerated dose (MTD) of this cytokine. METHODS: Twenty-six patients with non-hematologic malignancies were treated with escalating doses of rhuIL-4 administered as 24-hour continuous intravenous infusion on days 1-5 and 15-19 every 28 days. The dose levels of rhuIL-4 were: dose level I-0.25 microg/kg/day (3 patients), dose level II-0.5 microg/kg/day (5 patients), dose level III-1.0 microg/kg/day (3 patients), dose level IV-2.0 microg/kg/day (10 patients) and dose level V-4.0 microg/kg/day (5 patients). RESULTS: Dose limiting toxicity of continuous infusion rhuIL-4 occurred at 4.0 microg/kg/day D1-5 and 15-19, in three of five patients and consisted of hematologic (thrombocytopenia and prolongation of PT) and neurologic (headache and neurocortical toxicity) toxicity. A mild flu-like syndrome characterized by fever, chills, fatigue, headache, anorexia, arthralgias and myalgias was seen almost universally, occurred more commonly and with increasing severity with higher dose levels and resolved completely on discontinuing therapy with rhuIL-4. None of the enrolled patients had an objective response to treatment with continuous infusion rhuIL-4. CONCLUSIONS: A five-day continuous infusion of rhuIL-4 given biweekly is well tolerated with a MTD of 2.0 microg/kg/day.     

Increase in magnesium plasma level after orally administered trimagnesium dicitrate

Magnesium plasma concentrations were measured in healthy probands before and after administration of trimagnesium dicitrate by the oral and intravenous routes. There was a notable circadian fluctuation of the plasma concentration with a peak in the evening hours. After oral administration of 12 and 24 mmol magnesium, a long-lasting, statistically significant increase in plasma magnesium concentration measured as the increase in area under the curve (AUC) between 0 and 12 h, of 3.1% and 4.6%, respectively, was found. After intravenous administration of 4 and 8 mmol magnesium, AUCs increased by 9.5% and 16.1%, respectively. The decline in the plasma magnesium concentration after i.v. administration was compatible with a three-compartment model with a terminal half-time of about 8 h. Although no absolute value of the oral bioavailability of trimagnesium dicitrate could be determined from the data, our results may be important in helping to elucidate the influence of magnesium preparations on the plasma magnesium concentration. By comparing the effects of different preparations, it should be possible to estimate the relative oral bioavailability and the bioequivalence of these preparations.     

加替沙星致高血糖2例

2例患者静脉滴注加替沙星引发高血糖。第1例为81岁男性,因慢性阻塞性肺疾病急性加重,给予加替沙星0.4g 5%葡萄糖注射液250ml静脉滴注,1次/d。3d后患者出现烦躁、多尿、口渴、疲劳,血糖由用药前6.01mmol/L升至28.84mmol/L。立即停用加替沙星,给予12U胰岛素静脉滴注,2d后血糖恢复到5.2mmol/L。第2例为61岁男性梗阻性胆管炎、胆汁淤积性肝硬化患者,给予加替沙星0.4g 5%葡萄糖注射液250ml静脉滴注,1次/d,谷胱甘肽1.2g 葡萄糖氯化钠注射液250ml静脉滴注,1次/d,消炎利胆片6片,3次/d。治疗后第4天,血糖由用药前的5.60mmol/L升为13.81mmol/L。遂停用加替沙星,改为克林霉素静脉滴注。3d后血糖降至5.84mmol/L。