高负荷量阿托伐他汀对PCI围手术期患者的预后影响

目的观察经皮冠状动脉介入术(PCI)前12h服用80mg阿托伐他汀(立普妥),联合术前2h加服40mg阿托伐他汀,降低围手术期患者心肌梗死(MI)的发生率对预后的影响。方法 120例需择期PCI的患者随机分为阿托伐他汀强化组和对照组。阿托伐他汀强化组:给予冠状动脉粥样硬化性心脏病(冠心病,CHD)基础药物治疗的同时,术前12h给予阿托伐他汀80mg,术前2h阿托伐他汀40mg;对照组:仅给予CHD基础药物治疗,其中阿托伐他汀20mg。测定PCI术后18h测肌钙蛋白I(TnI)、肌酸激酶同工酶(CK-MB),并随访术后30d的主要心血管不良事件(MACE:心血管死亡、再发心肌梗死和靶血管重建)。结果阿托伐他汀强化组心肌梗死标志物水平显著低于对照组,CK-MB和TnI分别为(2.21±0.77)ng/ml比(12.30±7.89)ng/ml(P<0.01),和(0.196±0.112)ng/ml比(1.359±0.142)ng/ml,(P<0.01);且术后30d,阿托伐他汀强化组(3.08%)的主要不良心脏事件明显低于对照组(9.09%)比,P<0.01。结论对于稳定型心绞痛患者,PCI术前12h给予阿托伐他汀80mg,术前2h加服40mg,能显著降低PCI围术期MI的发生率,改善预后。     

急诊冠状动脉介入术强化阿托伐他汀治疗的临床疗效

目的:探讨急性ST段抬高心肌梗死(STEMI)急诊经皮冠状动脉介入治疗(PCI)术前单次口服大剂量阿托伐他汀和术后强化阿托伐他汀治疗的临床疗效。方法:选择STEMI并行急诊PCI治疗的118患者,随机分为2组:强化组(61例)术前阿托伐他汀80mg口服,术后40mg/d;常规组(57例)仅于术后给予阿托伐他汀20mg/d。两组均给予常规冠心病二级预防治疗。主要研究终点是术后30d主要心脏不良事件(MACE)发生率,次要研究终点包括心肌灌注TMPG分级、术后即刻和术后6hST段回降率(STR)和阿托伐他汀治疗前、后生化指标的变化。结果:PCI术后强化组CK-MB峰值明显低于常规组[(230.20±128.84)U/L∶(285.28±149.55)U/L,P<0.05]。PCI术后6h强化组STR≥50%的比例明显高于常规组(86.9%∶71.9%,P<0.05)。与常规组相比,强化组治疗30d后LDL-C、高敏C反应蛋白(hs-CRP)明显下降(P<0.05)。结论:STEMI急诊PCI术前大剂量阿托伐他汀80mg口服和术后40mg/d治疗安全有效,能够明显改善PCI术后6hSTR,降低CK-MB峰值和术后30d的LDL-C和hs-CRP。     

强化调脂治疗对经皮冠状动脉干预术后患者C反应蛋白的影响

目的　探讨阿托伐他汀 2 0mg/d对经皮冠状动脉干预 (percutaneouscoronaryintervention ,PCI)术后患者外周血C反应蛋白 (C reactiveprotein ,CRP)的降低能力是否强于 10mg/d。方法　连续选择因狭窄性病变行PCI的不稳定性心绞痛患者 4 8例 ,随机分为强化调脂组和常规调脂组 ,术后分别给予阿托伐他汀 2 0mg和 10mg,1次 /d。术前、术后 3d、3个月测定外周静脉血CRP、血脂等。结果　与术前比较 ,3个月后强化调脂组总胆固醇和低密度脂蛋白分别下降 2 1.6 %和 39.3% ,常规调脂组下降 11.6 %和 14 .8% ,阿托伐他汀 2 0mg/d降低总胆固醇和低密度脂蛋白的能力强于 10mg/d。强化调脂组术前 ,术后 3个月CRP中位数分别为 4 .1和 1.1mg/L ;常规调脂组为 7.1和 1.4mg/L。两组CRP的降低程度差异有显著性意义。阿托伐他汀的抗炎作用和术前的CRP水平相关 ,3个月后CRP的下降程度与血脂改变无相关性。结论　阿托伐他汀 2 0mg/d较 10mg/d能使PCI术后CRP进一步下降。     

阿托伐他汀对急性心肌梗死患者择期PCI术后胎盘生长因子水平及心肌灌注的影响

目的:探讨阿托伐他汀对急性心肌梗死患者择期经皮冠状动脉介入治疗(PCI)术后血清胎盘生长因子水平及心肌灌注的影响。方法:选择行择期PCI治疗的急性心肌梗死患者120例,随机分为阿托伐他汀组(60例)和对照组(60例)。阿托伐他汀组于PCI术前1周开始给予阿托伐他汀20mg,每晚1次。分别测定2组患者术前、术后1d、术后2周血清胎盘生长因子水平,观察2组PCI术后15min校正的TIMI帧数计数,同时行冠状动脉血流速度测定。术后2周行心肌核素显像分析,计算心肌灌注显像积分。结果:阿托伐他汀组术前、术后1d血清胎盘生长因子水平显著低于对照组[(9.13±2.56)ng/L∶(13.14±4.03)ng/L,(9.75±2.37)ng/L∶(14.53±3.41)ng/L,P<0.01],术后2周2组血清胎盘生长因子水平比较差异无统计学意义[(9.86±2.14)ng/L∶(10.02±2.01)ng/L,P>0.05)]。阿托伐他汀组校正的TIMI帧数计数明显低于对照组[(26.28±5.71)帧∶(35.12±6.18)帧,P<0.01],冠状动脉血流速度高于对照组[(151.23±36.7)mm/s∶(130.82±40.2)mm/s,P<0.05],阿托伐他汀组术后2周心肌灌注显像积分低于对照组[(2.0±0.5)∶(3.5±0.6),P<0.05]。结论:急性心肌梗死患者择期PCI术前给予阿托伐他汀治疗可能通过抗炎作用改善心肌灌注水平。     

阿托伐他汀对不稳定型心绞痛患者PCI术后心肌损伤及炎症反应的影响

目的探讨阿托伐他汀常规剂量治疗对不稳定型心绞痛（UAP）患者经皮冠状动脉介入术（PCI）后,心肌损伤的标记物血清肌酸磷酸激酶同功酶（CK-MB）、血浆肌钙蛋白Ⅰ（cTnI）及炎症反应标志物超敏C反应蛋白（hs-CRP）的变化。方法根据UAP患者PCI术前4周是否持续服用阿托伐他汀20mg/d分为试药组和对照组,于术前和术后8h、24h抽取肘静脉血检测血浆CK-MB、cTnI和hs-CRP。结果PCI术后两组心肌损伤及炎症反应的标记物均有不同程度升高,但试药组CK-MB、cTnI、hs-CRP水平显著低于对照组（均P<0.01）。结论UAP患者在PCI术前4周持续口服阿托伐他汀20mg/d能明显减少PCI术对UAP患者造成的心肌损伤及炎症反应。     

不同剂量瑞舒伐他汀对不稳定性心绞痛患者支架置入术后心肌损伤的保护和抗炎作用

目的探讨不同剂量的瑞舒伐他汀对不稳定型心绞痛(UA)患者支架置入术后心肌损伤的保护和抗炎作用。方法 150例UA并经皮冠状动脉介入(PCI)治疗的患者随机分为A组(阿托伐他汀20 mg/d)、B组(瑞舒伐他汀10 mg/d)、C组(瑞舒伐他汀20 mg/d),每组50例。三组患者连续3 d于睡前服用他汀类药物直至行PCI术,术后继续给予常规治疗并观察术前及PCI术后48 h外周血检测超敏C反应蛋白(hs-CRP)、肌酸激酶同工酶(CK-MB)和心肌肌钙蛋白(c Tn I)的水平,检测术后48 h的外周血CD4+T细胞的凋亡情况,同时比较PCI术后1个月与入院时血高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、甘油三酯(TG)和总胆固醇(TC)的水平。结果三组患者术前hs-CRP、CK-MB、c Tn I、TC、TG、HDL-C和LDL-C水平无明显差异(P0.05),而术后较术前相比有明显的改变(P0.05)。瑞舒伐他汀20 mg/d患者术后48 h hs-CRP、CK-MB、c Tn I、TC、TG、HDL-C和LDL-C水平与瑞舒伐他汀10 mg/d和阿托伐他汀20mg/d相比有显著的改善(P0.05);而瑞舒伐他汀10 mg/d和阿托伐他汀20 mg/d两组患者上述水平无明显差异(P0.05)。PCI术后48 h瑞舒伐他汀10 mg/d组患者CD4+T细胞凋亡比例明显高于阿托伐他汀20 mg/d组患者(P0.05),而瑞舒伐他汀20 mg/d组患者CD4+T细胞凋亡比例明显高于10 mg/d的患者。结论瑞舒伐他汀10 mg/d的常规剂量具有降脂,升高HDL-C水平、保护心肌和抗炎作用,而20 mg/d强化治疗能够显著增加PCI术后对心肌的保护和抗炎作用。     

单次高负荷量阿托伐他汀对PCI围术期心肌标志物的影响

目的观察经皮冠状动脉介入(PCI)治疗前服用80 mg阿托伐他汀能否降低围术期心肌标志物水平。方法将行择期PCI的87例冠心病患者随机分为两组,高剂量组予冠心病基础药物治疗,并在PCI前8 h内给予单次高负荷剂量(80 mg)阿托伐他汀;对照组仅予基础药物治疗。PCI后24 h检测两组肌钙蛋白T(TnT)、肌酸激酶同工酶(CK-MB)、C反应蛋白(CRP)水平。结果术后高剂量组TnT、CRP水平显著低于对照组(P<0.05);高剂量组术后TnT升高大于正常上限3倍者显著少于对照组(0 vs11.1%,P<0.05)。结论对于稳定型心绞痛及心肌标志物水平正常的不稳定型心绞痛患者,介入术前给予单次80 mg阿托伐他汀能显著降低围术期心肌标志物水平。     

急性冠脉综合征行PCI患者阿托伐他汀序贯治疗的疗效及安全性

目的:观察急性冠脉综合征(ACS)行PCI患者使用阿托伐他汀序贯治疗6个月的疗效以及安全性。方法:连续入选280例ACS患者,随机均分为序贯治疗组(术前2d给予阿托伐他汀80mg,术后给予40mg/d,1月后改为20mg/d)及常规治疗组(术前未服用阿托伐他汀,术后及维持量均予20mg/d),观察6个月,比较两组患者的疗效及安全性。结果:两组术后18h~24h肌酸激酶同工酶(CK-MB)、心肌肌钙蛋白I(cTnI)水平均明显高于治疗前,序贯治疗组的水平明显低于常规治疗组[CK-MB:(2.72±0.52)μg/L比(6.04±0.51)μg/L,cTnI:(0.28±0.13)μg/L比(0.42±0.16)μg/L,P均<0.01];术后2d,序贯治疗组高敏C反应蛋白(hsCRP)水平即显著低于常规治疗组,一直维持到术后6月[(1.49±0.78)mg/L比(2.34±0.51)mg/L,P=0.001],序贯治疗组血脂水平(除高密度脂蛋白水平显著升高外)较常规治疗组显著降低(P均<0.01);两组转氨酶大于3倍以上比例、主要不良心血管事件(MACE)发生率无明显差异(P均>0.05)。结论:急性冠脉综合征患者PCI术前80mg阿托伐他汀联合术后40mg阿托伐他汀治疗,可明显降低炎症反应,改善血脂;与常规剂量比较,未明显增加药物不良反应,安全有效。     

不同剂量阿托伐他汀治疗心肌梗死合并心衰患者的效果对比

目的观察对比不同剂量阿托伐他汀治疗心肌梗死合并心衰患者的临床效果。方法选取我院2009年5月至2011年5月42例心肌梗死合并心衰的患者,均行经皮冠状动脉介入术（PCI）,随机分为观察组和对照组,各21例。观察组患者术前口服40mg／d阿托伐他汀;对照组患者术前口服20mg／d阿托伐他汀,观察比较两组患者入院前24h、术前1d、术后1d、术后3d、术后4周血清高敏C-反应蛋白（hs—CRP）的变化。结果两组术后3d血清hs—CRP与入院前24h、术前1d相比差异有统计学意义（P〈0．05）;两组术后3dhs—CRP比较差异有统计学意义（P〈0．05）。结论心肌梗死合并心衰患者在行PCI术前给予口服40mg／d阿托伐他汀治疗,能有效降低血清中的炎症因子,增高血清中的炎症保护因子,从而保护心功能。     

PCI术前单次服用不同剂量阿托伐他汀对ACS病人的心肌保护作用及其安全性分析

目的研究经皮冠状动脉介入(PCI)术前单次服用不同剂量阿托伐他汀对急性冠脉综合征(ACS)病人的心肌保护作用及其安全性。方法选取2014年6月—2015年6月我院接诊的60例急性冠脉综合征择期PCI术病人作为研究对象。按照随机数表法分为观察组(30例)和对照组(30例)。观察组强化阿托伐他汀治疗,对照组予以小剂量阿托伐他汀治疗。观察两组治疗前后心肌损伤标记物肌钙蛋白(cTnl)、肌酸激酶同工酶(CK-MB)水平、C反应蛋白(CRP)、谷丙转氨酶(ALT)、肌酸激酶(CK)水平。结果治疗后,观察组cTnl、CK-MB水平分别为(0.30±0.09)μg/L、(2.85±0.65)μg/L,均低于对照组的(0.42±0.13)μg/L、(6.09±0.61)μg/L,差异有统计学意义(P0.05);观察组CRP水平(5.22±1.69)mg/L,低于对照组(6.72±1.71)mg/L,差异具有统计学意义(P0.05);观察组ALT、CK水平(29.10±8.03)U/L、(93.10±11.10)U/L,与治疗后(32.92±9.17)U/L、(92.35±10.02)U/L比较差异无统计学意义(P0.05)。结论 PCI术前单次强化服用阿托伐他汀对急性冠脉综合征病人心肌保护作用疗效显著,安全性良好。     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Study of constancy of hydrogen-consuming flora of human colon

The constancy of the hydrogen consuming flora of the human colon was studied in 15 healthy subjects via two measurements obtained 18 to 36 months apart. Hydrogen disappearance rate and the major products of H₂-consuming bacteria, methane and sulfide, were measured during incubation of fecal homogenates with excess hydrogen and sulfate. In 11/15, the hydrogen consumption rate and the predominant hydrogen-consuming pathway (methanogenesis, sulfate reduction, or neither) remained constant. However, major shifts in these pathways were observed in four subjects, with two losing and two gaining the ability to produce methane. Methanogenesis was associated with the highest hydrogen consumption rate. This study demonstrates that clinically unrecognizable, major alterations of the colonic flora occur in healthy subjects. Understanding of the factors responsible for these alterations might allow for therapeutic manipulation of the colonic flora.Supported in part by the Department of Veterans Affairs and NIDDKD RO1 DK 13309-25.