急性口服甲醇中毒血甲醇浓度与代谢性酸中毒的关系

目的探讨急性口服甲醇中毒血甲醇浓度与代谢性酸中毒的关系及其对血液透析(HD)适应症的影响.方法观察53例急性口服甲醇中毒患者血液甲醇浓度(M)、血二氧化碳结合力(CO2CP)和阴离子间隙(AG),按是否行HD治疗分为HD治疗组(GHD)、非HD治疗组(GNHD);用气相色谱顶空进样法(GC)测定M;并按不同M水平进行分析.结果①两组间logM、CO2CP和AG均有显著差异;②M在0.5～7.8mmol/L时,两组间出现例数无显著性差异;③CO2CP＜15mmol/L的HD患者中,大部分(22例,85%)M＜15.6mmol/L,其中有18例(69%)M＜7.8mmol/L.结论在应用M＞15.6mmol/L作为HD适应征时,应充分考虑其与代谢性酸中毒的关系.     

MARS治疗与血浆置换联合血液透析治疗肝性脑病的观察

目的观察并比较分子吸附再循环系统（MARS）与血浆置换（PE）联合血液透析（HD）对肝性脑病的治疗效果。方法60例有肝性脑病的急性或亚急性重型肝炎患者随机分为MARS治疗组、PE＋HD治疗组，每组30例。观察并比较两组治疗前后平均动脉压（MAP）、心率、血氨浓度、血浆渗透压（POP）以及肝性脑病的临床变化情况。结果MARS组治疗前与治疗9h后MAP、POP、血氨浓度分别为（63．5±5．2）mmHg、（81．1±19．3）mOsm／L、（314．1±4．6）mmol／L和（54．0±7．4）mmHg、（37．1±14．6）mOsm／L、（309．9±7．1）mmol／L；PE＋HD组对应值分别为（64．6±5．7）mmHg、（79．5±19．7）mOsm／L、（312．8±4．9）mmol／L和（63．7±7．3）mmHg、（84．7±22．1）mOsm／L、（300．9±7．8）mmol／1。治疗9h后两组间MAP、POP和血氨浓度的差异有统计学意义（P〈0．051。治疗过程中MARS组MAP、POP和血氨浓度的变化较PE＋HD组平稳。MARS组治疗9h后肝性脑病好转率为66．7％（20／30），PE＋HD组为10％（3／30），差异有统计学意义fP〈0．05）。结论与PE＋HD比较．MARS对血氨、血流动力学指标和POP的改善更为平稳，对肝性脑病的治疗效果更佳。     

甘精胰岛素联合格列美脲片治疗2型糖尿病的疗效观察

目的探讨甘精胰岛素联用格列美脲片治疗磺脲类药物继发性失效的2型糖尿病患者的疗效及安全性。方法60例口服磺脲类降糖药血糖控制不理想的2型糖尿病患者随机分为甘精胰岛素治疗组（GL组）和中性鱼精蛋白锌胰岛素（NPH）组,予睡前皮下注射胰岛素联合口服格列美脲治疗12周,观察12周前后空腹血糖、餐后2h血糖、糖化血红蛋白、空腹C肽、餐后C肽的变化。结果GL组治疗后FPG（6．3±1．41mmol／L,2hPG（8．7±1．4）mmol／L,HbAlc（6．7±0．6）％;NPH组治疗后FPG（6．4±1．0）mmol／L,2hPG（8．8±1．2）mmol／L,HbAlc（6．6±0．7）％,较治疗前差异有极显著性（P〈0．01）;但GL组的低血糖事件明显少于NPH组（P〈0．05）,且GL组治疗后C肽水平明显升高。结论甘精胰岛素联用格列美脲片治疗2型糖尿病的方案安全有效,简便易行,能减少低血糖事件的发生,且可能改善胰岛功能。     

胰岛素短期强化治疗恢复磺脲类降糖药敏感性30例的效果分析

目的探讨胰岛素短期强化治疗恢复糖尿患者对磺脲类降糖药敏感性。方法30例门诊和急诊糖尿病患者,其中男12例,女18例,均使用常规剂量磺脲类药物,但血糖控制不良。应用双相门冬胰岛素30后血糖达到控制良好3个月,之后停用胰岛素,继续以前的口服药物的治疗。结果停用口服降糖药之前3个月内平均血糖为（5．7±0．7）mmol／L,餐后2h血糖或随机血糖为（14．2±7．2）mmol／L;应用胰岛素达标时空腹血糖为（9．4±7．5）mmol／L,餐后2h血糖为（7．2±1．4）mmol／L;应用胰岛素期间空腹血糖为（6．0±0．8）mmol／L,餐后2h血糖为（7．8±1．2）mmol／L;停用胰岛素时,空腹血糖为（6．1±0．6）mmol／L,餐后2h血糖为（7．7±1．3）mmol／L。在改用原来口服降糖药后,1个月平均空腹血糖为（6．5±0．5）mmol／L。餐后2h血糖为（8．1±0．8）mmol／L,与应用胰岛素前相比,血糖降低的差异均有统计学意义（P〈0．05）。结论短期胰岛素强化治疗有可能恢复糖尿病患者对磺脲类药物敏感性。     

降脂护肝胶囊治疗脂肪肝临床观察

目的观察降脂护肝胶囊治疗脂肪肝的临床疗效。方法将190例脂肪肝患者完全随机分为降脂护肝胶囊组和血脂康胶囊组,各95例。降脂护肝胶囊组采用降脂护肝胶囊治疗,血脂康胶囊组采用血脂康胶囊治疗。治疗6个月后,对治疗前后的症状与体征、肝功能、血脂和B型超声等指标进行评价。结果降脂护肝胶囊组总有效率为96．8％（92／95）,明显高于血脂康胶囊组总有效率[76．8％（72／95）],差异有统计学意义（P〈0．05）。治疗后降脂护肝胶囊组和血脂康胶囊组患者AST、ALT、γ-谷氨酰转肽酶（γ-GT）、TC及TG、LDL—C水平均明显低于治疗前[降脂护肝胶囊组：（32±13）U／L比（67±30）U／L,（43±12）U／L比（89±31）U／L,（47±19）U／L比（96±42）U／L,（5．1±0．4）mmo]／L比（7．2±1．6）mmol／L,（1．5±0．7）mmol／L比（3．4±2．2）mmo]／L,（3．1±2．1）mmol／L比（3．8±1．6）mmol／L;血脂康胶囊组：（44±16）U／L比（69±30）U／L,（55±15）U／L比（87±31）U／L,（60±22）U／L比（99±46）U／L,（6．3±0．7）mmol／L比（7．5±1．4）mmol／L,（2．9±0．8）mmoL／L比（3．4±2．5）mmo]／L,（3．3±1．9）mmoL／L比（3．6±2．1）mmoL／L],HDL—C水平明显高于治疗前[降脂护肝胶囊组：（1．5±0．6）mmol／L比（1．0±0．7）mmol／L;血脂康胶囊组：（1．2±0．7）mmol／L比（0．9±0．9）mmol／L],差异均有统计学意义（P〈0．01或P〈0．05）;降脂护肝胶囊组治疗后AST、γ-GT、TC及TG水平均明显低于血脂康胶囊组,HDL—C水平明显高于血脂康胶囊组,差异均有统计学意义（P〈0．05）。结论降脂护肝胶囊具有良好的保肝降脂作用。     

对口服降糖药患者实施药学服务的临床效果评价

目的：探讨实施药学服务对2型糖尿病（ T2DM）患者口服降糖药物的影响。方法选择2012年1～6月145例实施药学服务的出院后口服降糖药治疗的T2 DM患者作为干预组,2011年1～12月150例未实施药学服务的出院后口服降糖药治疗T2 DM患者作为常规组,常规组出院时将药物发给患者,按常规的模式进行用药交待;干预组实施药学干预：进行T2 DM健康教育、加强降糖药物应用指导、开展药物咨询活动、注意与临床医生交流沟通。结果两组T2 DM患者出院时血糖控制情况及服药治疗依从性比较均无统计学意义差异（P＞0．05）;实施药学干预（9．56±2．18）个月;干预组空腹血糖（6．47±1．32）mmol／L、餐后血糖（8．66±1．86）mmol／L、糖化血红蛋白（7．01±1．34）％低于常规组的（7．42±1．50） mmol／L、（9．75±1．90）mmol／L、（8．17±1．42）％（P ＜0．05）;治疗依从性好87．14％,高于常规组的65．33％（P＜0．05）。结论通过多种药学方式全面服务于T2DM患者,提高T2DM患者用药依从性,使降糖药物更合理、更有效、更经济地发挥治疗和预防作用,提高药物疗效,值得临床应用。     

腰背部内外侧皮神经阻滞治疗腰肌劳损中糖皮质激素对血糖影响的观察

目的：研究腰背部内外侧皮神经阻滞治疗腰肌劳损中糖皮质激素对血糖的影响。方法对2013年6月至2014年4月96例腰肌劳损患者进行回顾性分析,分为4组,每组24例,患者进行不同浓度的镇痛液注射。分析对比4组治疗前后总的变化情况和治疗中血糖监测情况。结果通过治疗前与治疗后的血糖检测,第一组治疗前后血糖浓度差异无统计学意义（ P ＞0？．05）,第二组、第三组、第四组治疗前后比较血糖浓度均有显著提高（ P ＜0．05）;观察治疗过程中4 d的检查结果,第一组第1天（3．5±0．5） mmol／L,第2天（3．7±0．2） mmol／L,第3天（3．6±0．4） mmol／L,第4天（3．8±0．1）mmol／L;第二组（3．8±0．5）mmol／L,（4．3±0．3）mmol／L,（4．8±0．4）mmol／L,（5．3±0．2） mmol／L;第三组（4．0±0．2）mmol／L,（4．5±0．1） mmol／L,（5．1±0．4） mmol／L,（6．5±0．3） mmol／L;第四组（4．5± 0．6）mmol／L,（4．9±0．1）mmol／L,（7．3±0．4）mmol／L,（8．2±0．3）mmol／L。表明血糖随着糖皮质激素浓度的增大而增大,说明腰背部内外侧皮神经阻滞治疗腰肌劳损中糖皮质激素对血糖升高有明显作用。结论腰背部内外侧皮神经阻滞治疗腰肌劳损中使用糖皮质激素治疗疗效好具有安全性高、致死率低的特点。但会使血糖较为升高,只要用量得当,值得临床进一步推广。     

应用碘造影剂前后停用二甲双胍对糖尿病患者血糖水平的影响

目的探讨使用碘造影剂前后停用二甲双胍对糖尿病患者血糖水平的影响。方法研究对象选自2012年1月1日至12月31日在北京大学第一医院住院的糖尿病患者,入选标准为使用含二甲双胍方案治疗后血糖水平基本达标并维持平稳、应用碘造影剂前后48h内停用二甲双胍且有停药前后空腹、早餐后2h、午餐后2h、晚餐后2h和睡前血糖水平监测记录。停用二甲双胍期间调整降糖治疗方案者纳入调整组,未调整治疗方案者纳入未调整组。收集2组患者的病历资料进行回顾性分析。结果共收集到符合入选标准的患者80例,其中未调整组62例（87．5％）,调整组18例（22．5％）。二甲双胍停药时间为2—4d。未调整组停药后空腹、早餐后2h、午餐后2h、晚餐后2h和睡前血糖水平与停药前比较,均有不同程度的升高[（7．7±1．4）mmol／L比（7．0±1．2）mmol／L,（9．5±1．7）rnmol／L比（9．0±1．8）mmol／L,（10．9±2．3）mmol／L比（8．6±1．9）mmol,／L,（9．9±1．7）mmol／L比（8．6±1．7）mmol／L,（9．1±1．9）mmol／L比（8．5±1．6）mmo]／L],其中空腹、午餐后2h和晚餐后2h血糖水平与停药前比较差异有统计学意义（P=0．01,P=0．00,P=0．00）;调整组停用二甲双胍前后5个时间点血糖水平差异均无统计学意义[（7．9±1．2）mmol．／L比（8．1±1．8）mmol／L,（8．0±2．2）mmol／L比（8．5±2．4）mmo]／L,（9．2±2．9）mmol／L比（10．3±1．9）mmoL／L,（9．4±2．1）mmol／L比（9．1±2．4）mmol／L,（10．0±2．3）mmol／L比（9．3±2．2）mmol／L,均P〉0．05]。结论使用碘造影剂前后停用二甲双胍可导致停药期间未调整降糖治疗方案的糖尿病患者血糖水平出现有统计学意义的升高,调整降糖治疗方案有利于患者血糖水平控制更平稳。     

银杏达莫注射液治疗早期糖尿病肾病的临床观察

目的观察银杏达莫注射液对早期糖尿病肾病的治疗效果。方法将80例早期糖尿病肾病患者通过随机数字表法分为治疗组和对照组各40例。对照组给予常规治疗,治疗组在常规治疗基础上加用银杏达莫注射液20ml,静脉滴注,1次／d,共3周。治疗前后分别检测尿白蛋白排泄率,血、尿β2-微球蛋白。结果治疗组治疗后尿蛋白排泄率为（45±21）μg／min,对照组为（96±28）μg／min;治疗组血β2-微球蛋白为（2．6±1．3）mg／L,对照组为（3．7±1．2）mg／L;尿β2-微球蛋白治疗组为（40．5±13．2）mg/L,对照组为（40．1±10．8）mg／L,与本组治疗前相比,差异有统计学意义（均P〈0．05）。治疗后2组尿自蛋白排泄率、血β2-微球蛋白均下降,而以治疗组更明显,2组之间差异有统计学意义。对照组治疗前血糖值（12．01±2．14）mmol／L,治疗后（7．91±2．36）mmol／L;治疗组治疗前血糖值（11．91±2．36）mmol／L,治疗后（7．81±2．89）mmol／L。2组与本组治疗前相比,差异有统计学意义（P〈0．05）;2组间治疗后相比,差异无统计学意义。治疗组治疗过程中未见相关药物不良反应。结论银杏达莫注射液对早期糖尿病肾病治疗效果较好,且较安全。     

法舒地尔联合山莨菪碱治疗糖尿病足疗效观察

目的：观察法舒地尔联合山莨菪碱治疗Ⅱ级以上糖尿病足的临床疗效。方法将29例糖尿病足患者随机分为治疗组17例和对照组12例。对照组给予常规治疗,治疗组在对照组基础上采用山莨菪碱联和法舒地尔全身静脉滴注治疗,比较2组临床疗效,空腹血糖和餐后2h血糖。结果治疗组总有效率为94．1％高于对照组的41．7％,差异有统计学意义（P＜0．01）。治疗组在治疗后空腹血糖（6．9±3．2）mmol／L,餐后2h血糖（10．1±2．8） mmol／L;对照组治疗后空腹血糖（7．1±2．6）mmol／L,餐后2h血糖（9．8±2．7）mmol／L,2组空腹血糖、餐后2h血糖差异无统计学意义（P＞0．05）。结论法舒地尔联合山莨菪碱用药治疗糖尿病足明显优于常规治疗效果,值得临床推广应用。     

Methanol poisoning

AIMS: This study examines clinical experience with methanol poisoning during a one-year period. METHODS: All admissions with the diagnosis of suspected methanol toxicity were analysed and the current guidelines for the management of this problem were reviewed. RESULTS: Twenty-four subjects were identified. Most had a history of chronic use of methylated spirits. Four died before admission to hospital and the other 20 patients had 26 admissions to hospital and form the basis for this report. Four patients died in the Intensive Care Unit. In total 11 patients were admitted to the Intensive Care Unit. Seven patients received haemodialysis. There was no correlation between the methanol level and the outcome. The strongest predictor of death or a poor outcome was a blood pH < 7.0. Some patients, in spite of potentially lethal methanol levels of up to 160 mmol/L, did not develop signs of toxicity. CONCLUSIONS: The overall mortality was high and ethanol was given to most of the patients for up to several days. Some patients did not show any toxicity and some of those were not given ethanol. It is recommended that chronic meths drinkers, who are not acidaemic and are generally well, do not require ethanol treatment. Only the complete removal of methanol from methylated spirits will reduce the morbidity of this condition.     

Acute Methanol Toxicity in Minipigs

The pig has been proposed as a potential animal model for methanol-inducedneuro-ocular toxicosis in humans because of its low liver tetrahydrofolatelevels and slower rate of formate metabolism compared to thoseof humans. To examine the validity of this animal model, 124-month-old female minipigs (minipig YU) were given a singleoral dose of water or methanol at 1.0, 2.5, or 5.0 g/kg bodywt by gavage (n = 3 pigs/dose). Dose-dependent signs of acutemethanol intoxication, which included mild CNS depression, tremors,ataxia, and recumbency, developed within 0.5 to 2.0 hr, andresolved by 52 hr. Average maximum methanol concentrations inplasma, of 3100 ± 700 (SD), 6200 ± 2300, and 15,200± 900 µg/ml were reached within 0.5 to 4 hr followingmethanol administration in animals given 1.0, 2.5, or 5.0 gmethanol/kg, respectively. The mean initial elimination half-livesof methanol were 9.0 ± 1.6, 22.4 ± 6.1, and 18.9± 4.3 hr, for 1, 2.5, and 5.0 g/kg doses, respectively.In 3 minipigs, a transient increase in plasma formate concentration(1.74–3.40 mEq/liter vs control = 0.5 + 0.3 mEq/liter)occurred 4 to 30 hr following methanol administration. Methanol-and formate-dosed pigs did not develop optic nerve lesions,toxicologically significant formate accumulation, or metabolicacidosis. Based on results following a single dose, female minipigsdo not appear to be overtly sensitive to methanol and thus maynot be a suitable animal model for acute methanol-induced neurooculartoxicosis.     

Perinatal Methanol Exposure in the Rat: I. Blood Methanol Concentration and Neural Cell Adhesion Molecules

Although the acute toxicity of methanol is well documented,few studies have addressed the consequences of perinatal exposuresto the low concentrations that are expected to arise from itsproposed use as a component of automobile fuel. This reportdescribes the general research design of a series of studies,the effects of methanol exposures on blood concentrations indams and neonates, and indices of brain development. Four cohortsof Long-Evans pregnant rats, each cohort consisting of an exposure(n=12) and a control (n=12) group, were exposed whole-body to4500 ppm methanol vapor or air for 6 hr daily beginning on GestationDay 6. Both dams and pups were then exposed through PostnatalDay 21 (PND 21). Blood methanol concentrations determined bygas chromatography from samples obtained immediately followinga 6-hr exposure reached approximately 500–800 µg/mlin the dams during gestation and lactation. Average concentrationsfor pups attained levels about twice those of the dams. Selectedoffspring from Cohort 4 were exposed for one additional 6-hrsession at ages that extended out to PND 52. Regression analysesshowed that the blood methanol concentrations of the pups declineduntil about PND 48, at which time their levels approximatedthose of their dams. Such pharmacokinetic differences mightincrease the risks posed to developing organisms. Light-microscopicanalysis showed no significant abnormalities in the brains ofthe methanol-treated animals. However, assays of neural celladhesion molecules (NCAMs) in brains of pups sacrificed on PND4 showed staining for both the 140 and the 180 kDa isoformsto be less intense in the cerebellum of exposed animals. NCAMdifferences were not apparent in animals sacrificed 15 monthsafter their final exposure.     

Photolyse des Prenazons in Methanol und Wasser

Photolysis of Prenazone in Methanol and Water Photolysis of 4-prenyl-1,2-diphenylpyrazolidine-3,5-dione (prenazone) in methanol leads to (3,3-dimethylallyl)methoxymalonic dianilide, 1-hydroxy-1-isopropylcyclopropane-2,2-dicarboxylic dianilide, 1-isopropylidenecyclopropane-2,2-dicarboxylic dianilide and (3,3-dimethylallyl)malonic dianilide.     

Methanol levels in methylated spirit drinking alcoholics

On three different occasions, blood samples sent to this laboratory from the accident and emergency department were found to contain potentially toxic amounts of methanol (30, 34 and 41 mmol/l) during analysis for ethanol by a gas chromatographic method. It is suggested that the simultaneous determination of both alcohols may be clinically important in methylated spirit drinking alcoholics.