23例HIV/AIDS病人HAART致乳酸酸中毒临床分析

目的探讨艾滋病病毒(HIV)感染者/艾滋病(AIDS)病人在高效抗反转录病毒治疗(HAART)过程中,出现乳酸酸中毒的情况,其临床表现、诊断、治疗和预后,以进一步采取预防措施,降低其发生率和致死率。方法采用回顾性分析的方法,分析HAART时间及不同方案发生乳酸酸中毒的情况。结果 2010年1月-2011年8月收治的住院病人中,已经进行HAART的共1 115例,出现高乳酸血症者74例,占6.64%;发生乳酸酸中毒的病人23例,发生率2.06%。所有发生乳酸酸中毒的病人都采用含司他夫定(D4T)的方案。经过综合治疗的18例治愈,死亡5例,总死亡率21.74%(5/23)。HAART 6个月以上及应用含D4T方案的病人发生率最高,为4.41%(23/521)。结论乳酸酸中毒的发生率虽低,致死率高,且临床表现多不典型,易被误诊、漏诊;危险因素包括肥胖、女性、合并HCV应用干扰素利巴韦林治疗的病人、以及同时合并其他机会性感染病人等。     

HIV／AIDS病人ART相关性高乳酸血症的预测因素分析

目的探讨艾滋病病毒（HIV）感染者/艾滋病（AIDS）病人进行抗反转录病毒治疗（ART）中,发生高乳酸血症（LAHL）的预测因素分析。方法回顾性分析2005年1月-2012年5月,门诊进行ART的随访AIDS病人出现LAHL的临床资料,对相关性数据进行统计学分析。结果在191例门诊进行ART随访的AIDS病人中,有71例发生LAHL,其中女性34例（χ2=6.147,P〈0.01）,服用D4T的42例（χ2=7.784,P〈0.01）,服用核苷类反转录酶抑制剂（NRTIs）药物超过1年以上59例（χ2=18.100,P〈0.01）。发生LAHL病人相比未发生LAHL病人更容易出现丙氨酸转氨酶（ALT）、天冬氨酸转氨酶、乳酸脱氢酶（LDH）、γ-谷酰转肽酶（GGT）升高,差异有统计学意义（P〈0.01）。在多因素非条件Logistic回归分析中,女性[比值比（OR）10.923,95%可信区间（CI）：1.067～111.836]、ALT升高（OR1.09,95%CI：1.017～1.168）、LDH升高（OR1.025,95%CI：1.007～1.043）,均为发生LHAL的预测因素。在ART中CD4T淋巴细胞计数升高病人中LAHL发生率低（OR0.991,95%CI：0.983～0.999）。结论 AIDS病人服用NRTIs药物,尤其是服用D4T、女性、服药时间超过1年以上,是发生LAHL的预测因素。在ART过程中出现ALT、GGT、LDH升高,要高度警惕是否存在LAHL风险,避免进一步发展成致死性的乳酸酸中毒。     

HAART伴乳酸酸中毒1例报告

某女,51岁,已发现艾滋病病毒(HIV)抗体阳性10个月,伴乏力、纳差、恶心、胸闷1月余,于2007年6月11日入院.患者于2006年8月因不明原因发热及腹泻而入住唐都医院传染科.     

HAART相关症状性高乳酸血症的临床特征及影响因素分析

目的初步研究中国艾滋病患者高效抗逆转录病毒治疗（HAART）过程中发生的症状性高乳酸血症的临床特征及相关影响因素。方法对北京地坛医院2005年1月至2007年12月,所有接受HAART的患者每1—2月进行临床随访,共发现8例症状性高乳酸血症患者,对其治疗前后的免疫状况、治疗方案、高乳酸血症的临床表现、实验室检测结果,以及临床处理和预后进行综合分析。结果所有8例症状性高乳酸血症患者,均在发病前服用过含有司他夫定的HAART方案9—24个月,临床症状以自觉疲乏、恶心、腹部胀痛、肌肉酸痛、运动后呼吸困难为多见,血乳酸水平3．4—10．0mmol／L。5例未出现乳酸酸中毒的症状性高乳酸血症患者,经换药或停药并对症处理后均好转;3例发展为乳酸酸中毒,病情严重,其中1例死亡。结论引起高乳酸血症的原因较多,司他夫定可能是主要因素。     

HAART疗法致HIV/AIDS病人血液毒性反应及中药治疗的相关研究进展

高效抗反转录病毒疗法(HAART)是目前对艾滋病病毒(HIV)感染者、艾滋病病人唯一有效的治疗方法,能够有效抑制病毒复制,重建病人机体免疫,显著改善病人预后。但也出现了毒副作用大、依从性差等问题。针对HAART的主要毒副作用如血液毒性反应,近年来国内外进行了一些相关的临床和实验研究。发现了一批以增强免疫力为主的中药更具有发展潜力,文章对相关研究进展进行综述。     

艾滋病抗病毒治疗乳酸酸中毒及高乳酸血症32例临床分析

乳酸酸中毒和高乳酸血症被认为是核苷类反转录酶抑制剂（NRTI）引起的严重甚或致命的远期副作用。广西壮族自治区疾病预防控制中心（CDC）门诊收治32例艾滋病（AIDS）抗病毒治疗乳酸酸中毒及高乳酸血症病人,现将其临床表现、诊疗经过及预后总结报告如下。     

湖南省6558例HIV/AIDS病人HAART疗效及不良反应分析

目的了解湖南省开展艾滋病病毒（HIV）感染者/艾滋病（AIDS）病人（简称HIV/AIDS病人）高效抗反转录病毒治疗（HAART）的疗效、不良反应及耐药等情况。方法采用回顾性研究,对湖南省2003年9月至2012年12月间接受HAART的病例进行分析。结果共有6558例HIV/AIDS病人接受了HAART：1）CD＋4T淋巴细胞（简称CD4细胞）计数随治疗时间的延长明显升高,按照基线CD4细胞水平划分为≤99个/μL、100~199个/μL、200~350个/μL三组,然后做两两比较,差异有统计学意义（P〈0.01）。2）在治疗后7-12个月,64%的病人体内病毒复制得到了完全抑制,病毒载量检测值〈50拷贝/mL;在治疗后7-12个月,病毒载量〈50拷贝/mL的比例及病毒载量常用对数值lgVL变化幅度最大,12个月以后下降趋势减缓,约3年后进入平台期。3）服药后较常见的不良反应是胃口改变、恶心呕吐、皮疹及疲倦等,因不良反应更换治疗方案的病例占总换药病例的70.1%（1719/2451）,因不良反应停药占总停药病例的33.6%（178/529）。4）最近一次病毒载量检测〈50拷贝/mL的2739例病人中,连续2次CD4细胞计数较基线水平增幅〈20%,或治疗一年以上未达200个/μL的共375例,免疫无应答比例13.7%。5）2011及2012连续两年耐药监测显示,总耐药率为2.6%,处于较低水平。结论湖南省艾滋病HAART在免疫学和病毒学方面均取得了较好的疗效,需进一步加强不良反应、免疫无应答及耐药情况的监测和处理。     

214例HIV/AIDS病人的HAART不良反应及换药原因分析

目的探讨艾滋病病毒（HIV）感染者/艾滋病（AIDS）病人（简称HIV/AIDS病人）高效抗反转录病毒治疗（HAART）的不良反应及换药原因。为保证HAART合理用药及用药安全提供依据。方法全部病人均使用国家免费艾滋病HAART药物,按照国家免费艾滋病抗病毒药物治疗手册要求,全部病例均在HAART后1、2、3、6、9、12个月随访1次,统计病人不良反应及换药原因,数据分析用SPSS 19.0软件处理,以P〈0.05为差异有统计学意义。结果 95例病人中90例出现抗病毒药物不良反应、3例一线治疗失败、2例因药物配伍禁忌更换抗病毒药物。其中90例病人因AZT、NVP、D4T不良反应更换抗病毒药物。另有3例初始HAART方案包含EFV的病人,出现神经系统症状,均自行缓解,未更换药物。将初始HAART方案包含AZT、NVP、D4T的病例分为未换药组和换药组,将两组病人的基线CD＋4T淋巴细胞（简称CD4细胞）计数值进行统计学比较,差异无统计学意义。结论HAART的主要换药原因为抗病毒药物不良反应。在包含AZT、D4T、NVP的HAART方案中,治疗前3个月着重监测AZT、NVP的不良反应,治疗6个月后着重监测D4T的不良反应,且不良反应的出现与基线CD4细胞计数无关。同时须及早发现耐药,并须掌握药物配伍禁忌。     

HIV/AIDS病人HAART致肝功能损害66例分析

目的探讨高效抗反转录病毒治疗（HAART）对艾滋病病毒（HIV）感染者/艾滋病（AIDS）病人（简称HIV/AIDS病人）肝功能的影响。方法回顾性分析HIV/AIDS病人抗病毒治疗24个月内肝功能的变化情况。结果共计调查755例HIV/AIDS病人,肝功能损害发生率为8.7%（66/755）,以单项转氨酶或胆红素升高为主,轻、中度肝损害占84.8%（56/66）,发生异常的时间为30-485天,中位数75天。其中含奈韦拉平（NVP）方案治疗者肝功能损害的发生率为7.1%（33/467）、含依非韦伦（EFV）方案发生率为11.5%（33/288）。肝损害级别：1级34例,2级22例,3级10例。结论 HIV/AIDS病人在抗病毒治疗过程中轻中度肝损害常见,应严密观察,及时处理,以保证HAART的顺利进行。     

An Experimental model of phenformin-induced lactic acidosis in rats

Summary An experimental model of phenformininduced lactic acidosis was established in rats. Following a subtotal nephrectomy, renal failure developed (serum creatinine 4.5±0.1mg/100ml and 2.8±0.1 mg/100 ml on the 1st and 8th postoperative days respectively). Immediately after nephrectomy intra-peritoneal phenformin treatment, 16 mg/day, was commenced. Lactic acidosis developed progressively within 8 days, or earlier in the rats with the most severe renal insufficiency. The metabolic pattern was very similar to that observed in diabetic patients with a biguanide-induced lactic acidosis: on the 8th day, 2 h after the last phenformin injection, blood lactate was 10.8±1.0 mmol/1 (controls: 1.50±0.03); pyruvate was 0.56±0.06 mmol/1 (controls: 0.10±0.01) and blood pH: 7.00 ± 0.02 (vs 7.34±0.02); 3-hydroxybutyrate was 1.41±0.37 mmol/1 (vs 0.32 ±0.03); acetoacetate: 0.51±0.15 mmol/1 (vs 0.17 ±0.01), and free glycerol: 0.63 ±0.07 mmol/1 (vs 0.14 ±0.02). Increased concentrations of alanine (1.66±0.26 mmol/1, vs 0.48 ± 0.04 in controls) and low blood glucose levels (23± 8 mg/ 100 ml vs 70 ± 2, after a 12 hours fast) accompanied the lactic acidosis in spite of high glucagon levels (2030±170 pg/ml vs 108±10 in controls) and low insulin/glucagon molar ratio (0.19 vs 6.9 in controls). Normal rats, treated with phenformin at same doses, and nephrectomized rats injected with saline served as controls and remained free of lactic acidosis. Hydroxyphenformin (16 mg/day) injected in nephrectomized rats, was biologically inactive. Glucose production from¹⁴C-lactate was 425 ±85 mol/100 g body wt/h, vs 1050 ± 90 in control animals. Blood lactate specific activity declined more slowly in the lactic acidotic rats than in controls, suggesting that a decrease in lactate utilization contributed to hyperlactataemia more than an increased lactate production.     

An uncommon cause of lactic acidosis: MELAS

Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) is a rare clinical entity in adults transmitted by mitochondrial inheritance. Absence of family history and spatial distribution of clinical features can pose a diagnostic dilemma. We report a 36-year-old male who presented with recurrent strokes, seizures and lactic acidosis. A muscle biopsy revealed red ragged fibers pointing to the diagnosis of MELAS.     

二甲双胍导致糖尿病乳酸性酸中毒合并急性肾功能衰竭1例报告

报道1例因服用二甲双胍导致乳酸性酸中毒合并急性肾功能衰竭患者,提示早期诊断、治疗及尽早的血液净化治疗可改善预后。     

Buformin concentrations in a case of fatal lactic acidosis

Summary A fatal case of lactic acidosis in a 84 year old diabetic woman taking buformin is reported. Buformin concentrations in serum, other body fluids and tissues were measured by gas chromatography. Serum buformin concentration at admission was 5.5 mg/l. Postmortem concentrations were: in serum 3.2 mg/l; in lung 2.8 mg/kg wet weight; in heart 3.0 mg/kg; in pericardial fluid 3.5 mg/l; in liver 5.2 mg/kg; in bile 6.3 mg/l; and in kidney 98 mg/kg.     

A case risk study of lactic acidosis risk by metformin use in type 2 diabetes mellitus tuberculosis coinfection patients

Metformin (MET) has possibilities to be utilized as an adjunct of tuberculosis (TB) therapy for controlling the growth of Mycobacterium tuberculosis (M. tuberculosis). MET enhances the production of mitochondrial reactive oxygen species and facilitates phagosome–lysosome fusion; those mechanism are important in M. tuberculosis elimination. Moreover, MET-associated lactic acidosis (MALA) needs to be considered and the incidence of MALA in patients with type 2 DM–TB coinfection remains unknown. This result contributes much to our understanding about the clinical effect of MET use in type 2 DM–TB coinfection.For the purpose of understanding the MET effect as an adjuvant therapy in TB therapy and insulin simultaneous therapy, an observational clinical study was done in type 2 DM newly TB coinfection outpatients at Surabaya Paru Hospital. Patients were divided into two groups. First group was MET group, in which the patients were given MET accompanying insulin and TB treatment regimens, the golden standard therapy of DM–TB coinfection. MET therapy was given for at least 2 months. Second group was non-MET group, in which the patients were given insulin and TB treatment regimens. The lactate levels in both groups were measured after 2 months.Among 42 participants, there was no case of lactic acidosis during this study period. Data were normally distributed; thus, we continued analysis of the difference using paired T-test with 95% confidence. There was no difference in lactate levels (p = 0.396) after MET therapy compared to non-MET group.In this study involving patients with TB pulmonary diseases, there is neither evidence that MET therapy induced lactic acidosis event nor that it increased lactate blood level. Thus, we concluded that MET use in type 2 DM–TB coinfection did not induce lactic acidosis.     

Acute renal failure and metformin-associated lactic acidosis following colonoscopy

Two patients with type 2 DM developed acute kidney injury and lactic acidosis following colonoscopy despite withholding metformin. We recommend that DM patients on metformin also withhold ACEI, ARB until their dehydration is reversed after colonoscopy. This should reduce the risk of acute renal failure (ARF) and of lactic acidosis.     

The relation between phenformin therapy and lactic acidosis

Summary Two cases of lactic acidosis are described in which the time sequence of events made it certain that phenformin was the precipitating cause. In one patient the condition arose because of self administration of an overdose; in the other, phenformin had been administered to a patient on maintenance dialysis. After recovery, and in the absence of phenformin therapy the second patient was able to clear an intravenous lactate load at a rate similar to that observed in other patients on chronic dialysis. — A review of the literature re-emphasizes the possible danger of phenformin in the presence of diminished renal or hepatic function, which should be shown to be normal before starting the drug and assessed periodically during therapy.