大鼠酒精性肝病细胞凋亡与细胞色素P4502E1和氧化应激的关系

目的:观察大鼠酒精性肝病组织病理形态学改变,探讨细胞凋亡与细胞色素P4502E1的表达以及和氧化应激的关系.方法:用酒精灌胃法制备酒精性肝病大鼠模型,模型组给予酒精8 g/kg,每天分2次灌胃连续8 wk,对照组给予等量的生理盐水灌胃.实验8 wk末,观察肝组织的病理形态学改变,用原位末端标记法(TUNEL)检测肝细胞凋亡,用免疫组化法检测肝组织中Caspase-3蛋白表达,用全自动生化仪检测ALT和AST的含量,用PCR法测定肝细胞色素P4502E1的基因表达,分别用硫代巴比妥酸法(TBA法)和黄嘌呤氧化酶法测定肝组织丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活力.结果:模型组凋亡的肝细胞明显增多,主要分布在中央静脉周围、点状和灶状坏死区;Caspase-3主要分布于中央静脉及肝细胞坏死灶周围细胞的胞质中.模型组肝细胞凋亡指数(AI)和Caspase-3蛋白表达强度明显高于对照组(AI:6.2%±1.7% vs 1.7%±0.8%;Caspase-3:66.7% vs 9.5%,P<0.05,P<0.01).CYP2E1表达:对照组c1基因频率为91.6%,c2基因频率为8.4%;模型组c1基因频率为53.4%,c2基因频率为46.6%,均有显著性差异(P<0.05).长期酒精摄入大鼠血清MDA含量增加(41.53±7.43μmol/L vs 15.72±2.06μmol/L,P<0.05),SOD活力下降(353.12±61.02 kU/L vs 636.82±138.60 kU/L,P<0.05),与酒精性肝病肝细胞凋亡程度有相关性(r=0.644,r=-0.511).结论:长期酒精摄入可引起大鼠酒精性肝病及及肝功能损伤,肝细胞凋亡明显增加.CYP2E1基因PstⅠ及RsaⅠRFLPs与酒精性肝病有关,其中c2基因可能与大鼠酒精性肝病的发生有关.MDA含量和SOD活力在酒精性肝病的肝细胞凋亡过程及脂质过氧化反应中发挥重要作用.     

茶多酚治疗慢性酒精性肝损伤的实验研究

目的 建立酒精性肝病大鼠模型,观察茶多酚对酒精性肝病大鼠血清氨基转移酶活性和肝脏病理变化的影响,探讨茶多酚对酒精性肝损伤的防治作用。 方法 SD大鼠分成3组:酒精组(酒精7g·kg-1·d-1灌胃)、茶多酚组(酒精7g·kg-1·d-1 茶多酚0.25g·kg-1·d-1灌胃)和对照组(等渗盐水灌胃)。各组分别于4周末、12周末和24周末处死大鼠留取肝脏标本,用于HE染色和Masson染色。 结果 酒精组大鼠血清氧基转移酶水平较对照组升高,茶多酚组大鼠与酒精组相比,其值有明显降低,差异有统计学意义(P<0.05)。HE染色显示酒精组大鼠肝细胞浆出现不同程度的脂肪变性,小叶各带可见不同程度的点、灶状或片状坏死,24周大鼠可见桥接坏死。Masson三色染色可见24周大鼠汇管区边缘有绿染胶原纤维包绕增生,肝窦中可见绿染胶原纤维分布。茶多酚组肝脂肪变和炎症程度轻于酒精组,未发现桥接坏死。 结论 茶多酚对酒精性肝损伤具有一定的保护作用。     

枳葛口服液防治大鼠酒精性肝病的相关机制

目的探讨枳葛口服液对酒精性肝病模型大鼠的防治作用及分子机制.方法以酒精灌胃加普通饲料造模酒精性肝损伤大鼠,干预组酒精灌胃同时给予不同剂量(高、中、低剂量)枳葛口服液,对照组酒精灌胃同时给予解酒灵口服液.12 wk后处死动物检测各组大鼠肝功、肝脏指数、脂质代谢、氧化应激及乙醇代谢酶活性等相关指标,同时观察各组肝组织病理学变化.结果相比正常组,除高剂量组外,各组大鼠肝脏指数、谷丙转氨酶、谷草转氨酶、总胆固醇、三酰甘油、乙醇脱氢酶(alcohol dehydrogenase,ADH)、乙醛脱氢酶(aldehyde dehydrogenase,ALDH)及CYP450 2E1含量均有明显变化(P0.01或0.05),且各组肝组织HE染色可见不同程度大面积的泡性脂肪空泡,其中模型组和枳葛口服液低剂量组差异最大(P0.01).相比模型组,各治疗组以上指标均呈现不同程度地逆转(P0.01或0.05),其中高剂量组逆转最显著(P0.01).枳葛口服液中剂量组疗效与解酒灵口服液对照组疗效近似(P0.05).结论枳葛口服液解酒护肝之功效可能与逆转ADH、ALDH等乙醇代谢酶活性进而抑制自由基、乙醛生成,抑制机体氧化应激,改善大鼠脂质代谢紊乱等密切相关.     

缺氧诱导因子1-α在酒精性肝病形成中的表达

目的 研究缺氧诱导因子1-α(HIF1-α)在洒精性肝病动物模型的表达情况,探讨其与酒精性肝病的关系。方法 采用酒精灌胃法建立酒精性肝病动物模型,应用逆转录聚合酶链反应(RT-PCR)法和免疫组织化学染色法检测大鼠肝组织HIF1-α mRNA和蛋白水平。结果 RT-PCR结果显示模型组大鼠HIF1-α mRNA表达阳性率为62.5％(5/8),对照组为16.7％(2/12),x~2=3.94,P<0.05。两组大鼠肝脏HIF1-α多克隆抗体免疫组织化学染色评分分别为3.13±0.83和0.83±1.27,差异有非常显著必,t=4.88,P<0.01。结论 HIF1-α在酒精性肝病动物模型的表达明显增高,缺氧是酒精性肝病的发病机制之一。     

软脉灵对大鼠非酒精性脂肪肝的预防作用

目的:观察软脉灵对非酒精性脂肪性肝病大鼠模型的预防作用.方法:采用高脂膳食喂养方式建立大鼠非酒精性脂肪性肝病模型.♂SD大鼠90只,随机分为模型组、药物组与空白对照组,每组30只.模型组应用高脂饲料喂养,药物组在高脂饲料喂养同时应用软脉灵灌胃,空白对照组应用基础饲料喂养.每组均于8,12及16 wk时各处死10只,观察肝脏指数,血清与肝组织生化指标及肝组织病理改变.结果:16 wk时与模型组相比较,药物组肝脏指数显著降低(F=51.626,P=0.000);血清胆固醇(CHOL)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-c),丙氨酸转氨酶(ALT)及谷草转氨酶(AST)水平明显降低(2.27±0.38 mmol/L VS 3.09±0.45 mmol/L;0.83±0.13 mmol/L vs 1.03±0.18 mmol/L;0.41±0.06 mmol/L vs 1.09±0.27 mmol/L;52.0±6.50 U/L vs 79.0±4.72 U/L;182.9±26.43 U/L vs 326.5±28.21 U/L;均P<0.01),但血清高密度脂蛋白胆固醇(HDL-c)水平提高(0.76±0.17 mmol/L vs 0.55±0.11 mmol/L,P<0.01);肝组织丙二醛(MDA)水平降低明显(167.2±14.00 mmol/g vs 263.6±26.84 mmol/g,P<0.01),超氧化物歧化酶(SOD)活力增加显著(9.95±0.33 U/g vs 4.36±0.46 U/g,P<0.01),肝组织脂肪变性程度(χ~2 =19.828-20.470,均P=0.000)和炎症活动度(F =10.170,P=0.000)明显减轻.结论:软脉灵具有预防大鼠非酒精性脂肪性肝病的作用.     

姜黄素对酒精诱导的大鼠脂质过氧化反应的影响

目的:观察姜黄素对酒精性肝病大鼠肝脏氧化应激指标SOD,MDA和NO及血清ALT,AST和ALP水平的影响,探讨姜黄素对酒精诱导的大鼠脂质过氧化反应的影响.方法:将40只SD大鼠随机分为对照组、模型组、姜黄素治疗Ⅰ组(40 mg/kg)、姜黄素治疗Ⅱ组(80 mg/kg)和姜黄素治疗Ⅲ组(160mg/kg),每组8只.除对照组用等量生理盐水灌胃外,其他组均采用56度白酒6.72 g/(kg·d)灌胃的方法制作酒精性肝病大鼠模型,6 wk后姜黄素治疗Ⅰ、Ⅱ、Ⅲ组分别加用姜黄素ig,至12 wk末,处死大鼠,抽取血标本测定血清ALT、AST及ALP水平;留取肝组织标本测定SOD活性、MDA及NO含量,常规HE染色观察肝脏病理变化.结果:与对照组相比,模型组大鼠血清ALT、AST及ALP水平显著升高(86.4±7.5 vs 33.5±10.3;201.0±16.8 vs 116.5±12.0;205.1±20.0 vs 104.6±9.4:均P<0.01);肝组织SOD活性明显下降(80.21±4.55 vs 180.24±27.53,P<0.01),MDA及NO含量显著升高(3.29±0.34vs 1.35±0.12;4.37±0.21 vs 2.72±0.13:均P<0.01).与模型组相比,各姜黄素治疗组血清ALT、AST及ALP水平(Ⅰ组:66.5±9.6,171.4±10.8,176.4±13.7:Ⅱ组:52.4±12.0,145.8±11.9,146.9±13.8:Ⅲ组:40.9±7.9,135.0±11.8,127.1±12.6)明显降低(P<0.05或P<0.01),肝组织MDA及NO含量(Ⅰ组:2.84±0.27,4.01±0.17;Ⅱ组:1.95±0.23,3.60±0.16;Ⅲ组:1.65±0.08,3.22±0.13)均显著降低(P<0.05或P<0.01),而SOD活性(92.36±6.47,117.69±21.96,146.70±27.361明显提高(P<0.05或P<0.01),其中以Ⅱ、Ⅲ治疗组较为显著.模型组大鼠肝细胞出现不同程度的脂肪变性,伴有点、灶状坏死,炎性细胞浸润,各姜黄素治疗组肝脏病理变化不同程度的轻于模型组.结论:姜黄素能抑制脂质过氧化,减轻或防治酒精诱导的肝损伤.     

葛根素对大鼠酒精性肝炎的影响及其机制

目的:探讨葛根素对酒精性肝炎的作用机制.方法:21只Wistar大鼠,随机分为3组,正常对照组(n=7)用玉米油+500 g/L葡萄糖20 mL/(kg·d)灌胃,模型组(n=7)用400 mL/L乙醇按8 g/(kg·d)+玉米油灌胃,葛根素组(n=6):葛根素+酒精,按葛根素5 mg/(kg·d)腹腔注射给药.采用比色法测定血清AST,ALT及GST,放免法测定血浆PGE2,TNF及IL-6,Westem blot方法检测肝组织COX-2表达,并通过光镜观察肝组织病理变化.结果:血浆ALT,AST及GST模型组与正常对照组比较有明显升高(107.5±6.81 vs 33.20±10.55,138.29±9.72 vs 47.86±14.3,3.57±0.53 vs 1.43±0.43,均P＜0.01);与模型组比较,葛根素组血浆ALT及AST水平(52.33±13.19,63.33±7.03)有明显下降(P＜0.01).GST有下降趋势,但无明显著意义;模型组与正常对照组比较血浆PGE2.TNF及IL-6明显上升(274.13±26.15 vs 193.84±23.97,1.85±0.11vs 0.90±0.18,68.07±12.64 vs 40.50±5.09,均P＜0.01);与模型组比较,葛根素组血浆PGE2,TNF及IL-6明显下降(227.05±21.55,1.35±0.19,53.16±5.62,均P＜0.01),COX-2正常对照组呈弱表达,模型组显著高表达,与正常对照组比较差别显著(P＜0.01),葛根素组COX-2表达下调,与模型组相比有明显下调(F=27.94,P＜0.01).结论:葛根素通过抑制肝脏COX-2的表达,从而减少炎症介质PGE2、TNF及IL-6的生成.最终减轻酒精对肝脏的损伤作用.     

柴胡皂苷对大鼠酒精性肝损害的保护作用

目的 研究柴胡皂苷对大鼠酒精性肝损害保护作用的机制.方法 将60只雄性Wistar大鼠随机分为正常对照组、酒精性肝病模型对照组、柴胡皂甙低、中、高剂量组.通过长期酒精灌胃方法建立酒精性肝病大鼠模型,观察柴胡皂甙对大鼠血清AST、ALT活性和甘油三脂(TG)水平,以及肝组织超氧化物歧化酶(SOD)、谷胱甘肽(GSH)及谷胱甘肽过氧化物酶(GSH-PX)含量变化的影响.结果 与正常对照组相比,模型组大鼠血清AST、ALT活性及TG含量明显升高(P＜0.05),肝组织SOD、GSH及GSH-PX活性明显降低(P＜0.05),与模型组及柴胡皂甙低剂量组比较,柴胡皂甙中、高剂量组血清AST、ALT活性及TG含量明显降低(P＜0.05),肝组织SOD、GSH及GSH-PX活性明显增高(P＜0.05).结论 中、高剂量的柴胡皂苷能有效的改善大鼠酒精性肝损害造成的影响.     

己酮可可碱对小鼠酒精性肝病酒精代谢酶和核受体PPAR-α的影响

目的：研究己酮可可碱（PTX）对酒精性肝病小鼠酒精代谢酶和过氧化物酶增殖物激活受体（PPAR-α）的影响。方法将64只 C57BL/6小鼠随机分为模型组、治疗组和对照组,用50%酒精灌胃建立急性肝损伤模型,以20%酒精连续灌胃6周建立慢性酒精性肝病模型;采用比色法检测各组小鼠血清乙醇脱氢酶（ADH）和细胞色素 P4502E1（CYP2E1）活性;采用 RT-PCR 法检测肝组织 ADH、CYP2E1和 PPAR-α mRNA 水平;采用免疫组化法检测肝组织 CYP2E1和 PPAR-α蛋白表达。结果急性和慢性酒精性肝损伤模型小鼠血清 ADH 活性分别为（11.2±1.6）U/ml 和（5.8±1.4）U/ml,与相应对照组比无显著性差异[分别为（12.5±1.2）U/ml 和（4.3±0.6）U/ml];急性和慢性酒精性肝损伤小鼠 CYP2E1活性分别为（12.2±1.8）U/ml 和（11.8±1.7）U/ml,均显著高于对照组[（7.9±1.4）U/ml 和（6.5±1.2）U/ml,P〈0.01）]和治疗组[（8.1±1.5）U/ml 和（7.8±1.5）U/ml,P〈0.01];急性和慢性酒精性肝损伤小鼠肝组织 CYP2E1阳性细胞相对表达强度为（765±21）和（682±25）,均显著高于对照组[分别为（308±12）和（305±18）,P〈0.01）]和大剂量 PTX 治疗组[分别为（521±18）和（418±12）,P〈0.01];急性和慢性酒精性肝损伤小鼠肝组织 ADH mRNA 水平与对照组比无显著性差异,但肝组织 CYP2E1 mRNA 相对水平分别为（1.47±0.32）和（1.13±0.52）,显著高于对照组[（0.89±0.23）和（0.45±0.28）,P〈0.01）]及大剂量 PTX 治疗组[分别为（0.92±0.27）和（0.48±0.32）,P〈0.01）];急性酒精性肝病动物肝组织 PPAR-α mRNA 水平与对照组或 PTX 治疗组比无统计学差异,但慢性酒精性肝损伤小鼠肝组织 PPAR-α mRNA 相对水平[（0.45±0.31）]显著低于对照组[（0.85±0.21）,（P〈0.05）];急性和慢性酒精性肝损伤小鼠肝组织 PPAR-α阳性相对表达强度为（322±15）和（262±23）,均显著低于对照组[分别为（721±18）和（689±14）,（P〈0.01）]和大剂量 PTX 治疗组[分别为（548±20）和（725±19）,P〈0.01）]。结论 PTX 能够减轻急慢性酒精性肝损伤,可能与其上调酒精代谢酶 CYP2E1和下调 PPAR-α表达有关,而与ADH 无关。     

老年男性非酒精性脂肪肝患者腹部脂肪面积及血清脂联素和瘦素水平的变化

目的 研究老年男性非酒精性脂肪肝(NAFLD)患者腹部脂肪面积及血清脂联素和瘦素水平的变化.方法 选择238名年龄≥60岁的老年男性,应用B超诊断脂肪肝,依据病史排除酒精性及病毒性脂肪肝.分为3组:脂肪肝组76例,年龄、体重指数与脂肪肝组匹配的非脂肪肝组77名(肥胖组),非肥胖非脂肪肝组85名(对照组).采用放射免疫法测定血清脂联素、瘦素水平;采用CT扫描测定腹部内脏脂肪面积.组间比较采用方差分析.结果 (1)脂肪肝组与肥胖组的体重指数、腹部皮下、内脏、总脂肪面积分别为(26.87±2.62)kg/m2与(26.63±1.97)kg/m2、(166.59±54.27)cm2与(147.89±50.14)cm2、(148.94±53.72)cm2与(150.06±45.47)cm2、(315.25±89.42)cm2与(297.93±75.12)cm2,均高于对照组(P＜0.01).脂肪肝组的腹部皮下脂肪面积高于肥胖组(P＜0.05),而两者的腹部内脏及总脂肪面积差异无统计学意义.(2)脂肪肝组与肥胖组间的瘦素水平差异无统计学意义,但均高于对照组.NAFLD组的脂联素水平明显低于肥胖组[(6.31±3.31)μg/ml对比(9.87±7.07)μg/ml,P＜0.01],也明显低于对照组[(6.31±3.31)μg/ml对比(11.05±7.19)μg/ml,P＜0.01];肥胖组与对照组间脂联素水平差异无统计学意义.(3)非酒精性脂肪肝的高危因素包括天冬氨酸转氨酶、甘油三酯、腹部内脏及皮下脂肪面积.血脂联素水平是非酒精性脂肪肝的保护性因素.结论 老年男性非酒精性脂肪肝患者的特征是腹型肥胖,瘦素水平高,脂联素水平低.其中脂联素水平的下降在其中起关键作用.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Presence of immunoreactive growth hormone and prolactin in the ovine pineal gland

Abstract: The use of antisera raised against bovine growth hormone (GH) and ovine prolactin (PRL) enabled the detection of related immunoreactive (ir) sequences of proteins in ovine pineal tissue. The isolation of PRL-like ir-material was accomplished using a 0.25 M ammonium sulphate (pH 5.5) extraction followed by ethanol precipitation, whereas the resulting 2.0 M ammonium sulphate (pH 7.0) precipitate contained a GH-like immunoreactivity. Gel chromatography of the GH-like immunoreactivity (Sephadex G-100) indicated the presence of several GH-like fragments ranging in the M_r range of 7,000 to 55,000. Analyses of the PRL-like ir-material found in pineal tissue on HPLC using a TSK 545-DEAE column led to the resolution into a single peak of immunoreactivity. A single peak of activity was also observed following chromatofocusing and hydrophobic interaction chromatography of the ir-peak from the TSK 545-DEAE column. The PRL-like ir-material inhibited the binding of [¹²⁵I]ovine PRL-S14 to anti-ovine PRL antibodies without showing an affinity for binding to anti-rat PRL or anti-bovine GH antibodies. Scatchard analysis of the binding of pineal PRL-like ir-material and pituitary ovine PRL-S14 to liver membranes from day-20 pregnant rats revealed similar affinity constants (K_a of 4.7 ± 0.2 × 10⁹ M^-1). In addition, the replication of Nb 2 Node rat lymphoma cells was stimulated by pineal PRL-like ir-material, an effect known to be specific for lactogenic hormones. The pineal PRL-like immunoreactivity appeared on sodium dodecyl sulfate polyacrylamide gels as a single major band of M_r 24,000. The functional status of PRL-and GH-like ir-material in the ovine pineal remains to be determined, but evidence is presented that the overall protein synthesis rate of the rat pineal responded to circulating concentrations of PRL.     

Microbiology of human immunodeficiency virus anorectal disease

PURPOSE: Individuals who are seropositive for the human immunodeficiency virus are at high risk for opportunistic infection and anorectal disorders. Little prospective information is available regarding anorectal pathogens in these patients. METHODS: One hundred sixty-three HIV-seropositive patients presented to the colorectal clinic between 1989 and 1992. Forty-seven (29 percent) patients were thought to have an infectious process and were prospectively studied using a standardized multiculture protocol. RESULTS: Mean age was 33 (range, 19–59) years. All were male; high-risk behavior accounted for 87 percent of HIV transmissions. Presenting complaints included anorectal pain (79 percent), pus per anum (28 percent), and blood per anum (26 percent). Examination revealed perianal tenderness (60 percent), condyloma (38 percent), perianal ulcers (38 percent), and anal fissures (34 percent). Sixty-six sets of cultures were performed; 28 patients had one set, 15 had two sets, and 4 had three sets. Thirty-two of these 47 patients (68 percent) had positive cultures including herpes (50 percent), cytomegalovirus (25 percent),Neisseria gonorrhoeae (16 percent), chlamydia (16 percent), acidfast bacilli (2 percent), and others (9 percent). Six of 32 patients with positive cultures had more than one organism cultured. Sixteen (50 percent) patients with positive cultures were treated medically, 8 (25 percent) were treated surgically and 8 (25 percent) were treated with both modalities. Sixty-one procedures were performed on 17 patients for condylomata. Eighteen patients had 20 procedures for abscesses, 50 percent of whom had positive cultures for other than common bowel flora; all improved. Fourteen patients underwent 33 procedures for perianal fistulas.Mycobacterium fortuitum was cultured from one patient who required 13 procedures for abscesses and fistulas. Forty-five (96 percent) patients were followed for an average of 12.5 months ±2.9 SEM (range, 1–94 months). Symptoms were improved or resolved in 22 of 32 (69 percent) patients with positive cultures and in 11 of 13 (84 percent) with negative cultures. CONCLUSIONS: Specific pathogens may often be identified in human immunodeficiency virus-seropositive patients with anorectal disorders if aggressively sought. Although patients without specific pathogens identified may be expected to improve with planned empiric treatment, positive identification allows more directed therapy.