艾灸足三里、梁门穴对应激性溃疡大鼠胃黏膜细胞凋亡的干预作用

目的:探讨艾灸足三里、梁门穴对应激性溃疡胃黏膜细胞凋亡的影响,分析其与血浆多巴胺(DA)、胃黏膜内皮素(ET)的关系,揭示艾灸足三里、梁门穴对抗应激性损伤,进而保护胃黏膜的机制.方法:SD大鼠60只随机分为4组,即束缚对照组、模型组、艾灸足三里和梁门穴组、艾灸非穴点对照组,每组15只.束缚水浸应激法造模,免疫组化方法测定细胞凋亡指数(×10-6个/μm2).采用生物信号分析仪检测胃黏膜血流量(GMBF),高效液相色谱法测定血浆DA含量,放射免疫法测定胃黏膜ET含量.结果:预先艾灸足三里、梁门穴可显著降低随后的应激性胃黏膜损伤指数,降低胃黏膜ET和血浆DA含量,增加胃黏膜血流量,降低胃黏膜细胞凋亡指数.造模后,B组UI值(26.80±9.81vs12.00±5.94,P<0.01)、血浆DA(9.97±3.69μg/Lvs4.54±2.61μg/L,P<0.01)、胃黏膜ET(361.469±98.080ng/Lvs149.205±94.1425ng/L,P<0.01)以及凋亡指数(9.65±4.19vs4.36±2.60,P<0.01)显著高于A组,而GMBF低于A组(139.489±33.133mL/minvs377.090±85.840mL/min,P<0.01);C组UI值、凋亡指数显著低于B组和D组(UI:14.10±5.42vs26.80±9.81,26.20±7.23,P<0.01;凋亡指数:3.00±1.58vs9.65±4.19,8.20±5.17,P<0.01),而GMBF高于B组和D组(316.552±85.469mL/minvs139.489±33.133,141.512±58.450mL/min,P<0.01);C组血浆DA含量及胃黏膜ET显著低于B组(DA:4.41±2.48μg/Lvs9.97±3.69μg/L,P<0.01;148.271±69.113ng/Lvs361.469±98.080ng/L,P<0.01),但与D组比较无显著性差异(P>0.05).结论:艾灸足三里、梁门穴预处理可减轻束缚水浸应激所造成大鼠胃黏膜的损伤程度,这一作用可能是通过降低血浆DA和胃黏膜ET含量,增加胃黏膜血流量,抑制细胞凋亡实现的.     

艾灸预处理对应激性溃疡大鼠胃黏膜HSP70蛋白及mRNA表达的影响

目的:观察艾灸足三里和梁门穴预处理对应激性溃疡大鼠胃黏膜热休克蛋白70(HSP70)及其基因表达的影响,探讨艾灸足阳明经穴保护胃黏膜的作用机制.方法:将60只大鼠完全随机分为空白组(A)、模型组(B)、艾灸足三里等穴组(C)和对照组(D)4组,采用水浸-束缚应激法(WRS)制备应激性溃疡模型.按Guth法计算胃黏膜损伤指数(UI),用免疫组织化学法、逆转录聚合酶链式反应(RT-PCR)法和放射免疫法分别检测处理后大鼠胃黏膜HSP70,HSP70mRNA的表达和内皮素(ET)、前列腺素E2(PGE2)的含量.结果:SU大鼠胃黏膜损伤指数B组与A、C组(P=0.000,P=0.001),D组与A、C组(P=0.001)有显著性差异,艾灸足三里等穴可使SU大鼠胃黏膜损伤指数明显下降.胃黏膜PGE2含量A组与B、D组比较差异显著(P=0.011,P=0.028),C组与B、D组比较差异显著(P=0.020,P=0.048),经艾灸预处理的大鼠胃黏膜PGE2含量均有不同程度升高.ET含量B组与A组之间有显著差异(P=0.040),经艾灸预处理的大鼠ET含量下降显著,B组与C组相比差异显著(P=0.020).造模后胃黏膜的HSP70蛋白和mRNA表达均有不同程度的增强,B组与A组相比有显著性差异(P=0.039,P=0.008);经艾灸预处理后HSP70蛋白和mRNA显著增强,C组与B、D组比较有统计学意义(蛋白:P=0.003,P=0.035;mRNA:P=0.000,P=0.001).结论:艾灸足三里、梁门穴能通过增强HSP70的蛋白和基因表达,达到对胃黏膜的保护作用,并有一定的穴位特异性.     

艾灸预处理对大鼠应激性胃黏膜损伤增殖修复相关因子的影响

目的:观察艾灸预处理对应激性胃黏膜损伤大鼠血清和胃黏膜表皮生长因子(EGF)、转化生长因子-α(TGF-α)、胃黏膜三叶因子家族-1(TFF1)、增殖细胞核抗原(PCNA)的影响,探讨艾灸预处理促进胃黏膜损伤增殖修复的作用机制.方法:将48只健康SD大鼠随机分为4组,即空白组、模型组、艾灸穴位组、艾灸非穴组.束缚冷应激法制作大鼠应激性胃黏膜损伤模型.造模之前,艾灸组选取足三里、中脘、脾俞和胃俞等穴位行艾灸预处理8d,艾灸非穴组选取非穴对照点进行预处理.以Guth法计算胃黏膜损伤指数,光镜下观察大鼠胃黏膜组织学改变,放射免疫法测定血清EGF与TGF-α的含量,酶免法检测胃黏膜组织中EGF、TGF-α、TFF1和PCNA的含量.结果:与模型组和艾灸非穴组比较,艾灸足三里、中脘等穴位可使应激性胃黏膜损伤大鼠胃黏膜损伤指数明显下降(14.667±5.710vs27.250±7.448,24.750±7.300,P<0.01),血清EGF、TGF-α含量升高(2.167±0.756vs1.147±0.983,1.358±0.962,P<0.05;11.170±1.315vs4.585±0.720vs5.118±0.659,P<0.01),胃黏膜EGF、TGF-α和PCNA含量升高(343.560±27.644vs269.610±45.119,279.590±58.890,P<0.05;147.470±17.784vs115.530±24.319,116.620±14.908,P<0.01;191.910±37.262vs154.580±18.910,152.450±20.333,P<0.05);与模型组比较,艾灸穴位组胃黏膜TFF1含量明显升高(4.573±0.121vs3.654±0.507,P<0.05).结论:艾灸足三里、中脘等穴位预处理可减轻束缚水浸应激所造成大鼠胃黏膜损伤、促进胃黏膜损伤组织增殖修复,可能是通过上调胃黏膜损伤增殖修复相关因子(EGF、TGF-α、TFF1和PCNA)而达到其促胃黏膜损伤修复的作用.     

艾灸促进胃黏膜细胞HSP70表达上调对细胞凋亡线粒体信号转导途径的影响

目的:探讨艾灸预处理抑制细胞凋亡、保护胃黏膜损伤的机制.方法:32只健康Wister大鼠随机分为4组,即捆绑组(A组)、模型组(B组)、艾灸穴位组(C组)和艾灸非穴组(D组),每组8只.艾灸穴位组和艾灸非穴组大鼠艾灸预处理8 d,捆绑组和模型组大鼠只捆绑,不艾灸.除捆绑组外,其余各组采用无水乙醇灌胃法制备大鼠急性胃黏膜损伤模型.采用Western blot法检测大鼠胃黏膜细胞色素C(Cyt-C)的表达,免疫组织化学方法检测大鼠胃黏膜HSP70、胃黏膜细胞凋亡、凋亡活化因子1 (Apaf-1)、Caspase-9和Caspase-3的表达.结果:与A组相比,B组大鼠胃黏膜HSP70表达,胃黏膜细胞凋亡指数(AI),胞质Cyt-C、Apaf-1、Caspase-9和Caspase-3含量明显增加(2.93±0.29vs 2.51±0.22,3.52±0.77vs 2.25±0.53,1.63±0.36vs 0.75±0.23,4.32±0.67vs 3.44±0.86,4.05±1.01vs 3.76±0.82,3.55±0.86vs 2.35±0.71,P＜0.01或0.05).与B组相比,C组大鼠胃黏膜HSP70表达(3.93±0.36)明显增加(P＜0.01),而细胞凋亡指数(1.53±0.45),胞质Cyt-C(0.97±0.26)、Apaf-1(2.244±0.49)、Caspase-9(2.43±0.73)、Caspase-3(1.97±0.61)均显著降低(P＜0.01).与C组相比,D组大鼠胃黏膜HSP70表达(3.35±0.34)显著降低(P＜0.01),而凋亡指数(3.06±0.81),Cyt-C(1.45±0.29),Apaf-1(3.16±0.66),Caspase-9(3.33±0.76),Caspase-3(2.98±0.86),显著升高(P＜0.01或0.05).结论:艾灸通过上调大鼠胃黏膜细胞HSP70表达,继而作用于凋亡线粒体信号转导途径相关靶点,由此抑制胃黏膜细胞凋亡,达到保护胃黏膜损伤的作用,且这种保护作用具有一定的穴位特异性.     

针刺足三里穴对冷应激性胃溃疡大鼠下丘脑与肾上腺SP和POMC表达的影响

目的: 研究针刺足三里穴对冷应激性急性胃溃疡的保护作用, 以及应激大鼠下丘脑和肾上腺SP和POMC mRNA的表达情况.方法:大鼠22只随机分成3组: 正常对照组(6只)、单纯应激组(8只)、针刺预防应激组(8只). 针刺预防组先给于针刺足三里穴, 再冷应激.胃黏膜溃疡指数和RT-PCR法研究针刺足三里对大鼠的冷应激性溃疡的保护作用和下丘脑、肾上腺的SP、POMC的表达, 经图像分析系统照相并进行半定量.结果: 与单纯应激组比较, 针刺足三里穴可以明显减少冷应激造成的溃疡指数(9.75±1.91 vs 26.25±4.40, P<0.01), 抑制应激造成的皮质醇分泌增加(66.83 nmol/L±12.25 nmol/L vs 104.38 nmol/L±8.31 nmol/L, P<0.01),上调下丘脑的SP的表达(1.02±0.42 vs 0.45±0.12, P<0.05),下调肾上腺SP的表达(1.88±0.82 vs 2.93±1.08, P<0.05); 下丘脑POMC在应激过程中表达增高, 针刺能抑制POMC的表达, 刺预防应激组与单纯应激组相比差异显著(0.56±0.14 vs 0.82±0.19, P<0.01); 肾上腺中无POMC表达, 不参与应激过程.结论:针刺对冷应激溃疡具有保护作用, 该种保护作用是通过对生理性上调下丘脑SP的表达,下调POMC的病理性表达及抑制肾上腺SP而实现的.     

黄芪总苷对应激大鼠胃黏膜氧自由基及褪黑素受体的影响

目的:探讨黄芪总苷对应激大鼠胃黏膜褪黑素受体基因表达及氧自由基变化的影响.方法:SD大鼠48只分为4组,即正常对照组,模型组,黄芪总苷组和雷尼替丁组,每组12只.采用水浸-束缚应激模型,观察胃黏膜损伤指数,比色法检测胃黏膜SOD活性、MDA含量,RT-PCR法测定褪黑素受体1、2亚型mRNA表达变化.结果:与正常组比较,模型组大鼠胃黏膜损伤指数明显增高,MDA含量增高,SOD活性下降,褪黑素受体1、2基因表达降低,黄芪总苷预防给药后可明显降低应激大鼠胃黏膜损伤指数(6.75±4.10 vs 16.83±4.96,P＜0.01)和MDA含量(0.45±0.07 vs 0.79±0.36,P＜0.05),升高SOD活性(110.62±26.42 vs 71.74±22.20,P＜0.05)和褪黑素受体1、2基因表达(0.86±0.12 vs 0.54±0.05,0.79±0.14 vs 0.50±0.10,均P＜0.01).结论:黄芪总苷对水浸.束缚应激大鼠胃黏膜损伤有保护作用,其保护机制可能与调节胃黏膜褪黑素受体,并参与抗氧自由基损伤有关.     

损毁孤束核对电针足三里穴抗大鼠应激性胃溃疡作用的影响

目的:探讨孤束核(NTS)在电针(EA)足三里穴抗大鼠应激性胃溃疡中的作用.方法:健康♂SD大白鼠56只随机分为应激组、EA 应激组、NTS电损毁组、NTS假损毁组.通过脑立体定向仪电损毁大鼠孤束核,采用束缚-浸水制备大鼠应激性胃溃疡模型,分别测定各组胃黏膜损伤指数(UI)、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量.结果:与应激组比较,EA 应激组UI明显减少(t=9.5071,P<0.01),SOD活性升高(t=3.8729,P<0.01),MDA降低(t=2.3578,P<0.05).NTS电损毁组分别与假损毁组和EA 应激组比较UI提高(t=4.4223,7.2579,均P<0.01),SOD活性降低(t=3.5625,3.7242,均P<0.01),MDA含量升高(t=2.9045,2.4960,均P<0.05).结论:电损毁孤束核后,电针足三里穴对应激性胃黏膜损伤的保护作用减弱.     

促甲状腺激素释放激素在应激性溃疡致病过程中的作用

目的:探讨促甲状腺激素释放激素(TRH)在冷束缚应激性溃疡发病中的作用及其机制．方法:选用SD大鼠制备应激性溃疡模型,观察侧脑室注射TRH或TRH抗血清后对胃黏膜、胃液的分泌量和胃运动的影响．结果:侧脑室注射TRH 3h后,可使室温条件下禁食24h的清醒大鼠胃黏膜严重损伤,胃液量(5．5±0．7 mL/2 h vs 2．7±0．6 mL/2h, P<0．01)和总酸排出量(539．4±50．5μmol HCl/2h vs 317．7±45.3 μmol HCl/2 h,P<0．05) 均比对照组明显增加,胃壁结合黏液的分泌减少(1．35±0．08 vs 2．21±0．11,P<0．01),胃收缩频率(1．2±0.2 vs 0．4±0．1,P<0．01)、收缩波宽度(17．2±2．0 vs 8．1±1．1,P<0．01)和每分胃运动指数(90．3±14．2 vs 13．2±3．1,P<0．01)均明显高于对照组,冷束缚应激引起的大鼠胃黏膜损伤作用能被侧脑室注射TRH抗血清明显抑制(溃疡指数:10．2±3．9 vs 30．3±5．5,P<0．01)．结论:侧脑室注射TRH可使胃黏膜产生与应激相类似的溃疡,脑内TRH合成分泌增多是冷束缚应激时胃黏膜损伤的重要原因．     

聚普瑞锌诱导HSP70保护大鼠胃黏膜损伤

目的探讨聚普瑞锌诱导热休克蛋白70(heat shock protein 70,HSP70)减轻大鼠胃黏膜损伤的作用机制。方法无水乙醇灌胃致大鼠胃黏膜损伤后分别应用聚普瑞锌100 mg/kg、200 mg/kg灌胃及赋形剂灌胃,同时以空白组作对照,检测胃黏膜HSP70蛋白表达。同时检测各实验组大鼠胃黏膜IGF-1含量和SOD活性。结果聚普瑞锌100 mg/kg治疗组治疗3 d时HSP70表达的相对灰度值为278.3%±10.8%;聚普瑞锌200 mg/kg治疗组治疗3 d时HSP70表达的相对灰度值为471.1%±24.7%,与空白组和赋形剂组相比,差异均有统计学意义(P0.01)。各实验组大鼠胃黏膜IGF-1含量和SOD活性差异无统计学意义(P0.05)。结论聚普瑞锌能够诱导损伤后大鼠胃黏膜产生大量HSP70,发挥保护胃黏膜的作用。     

有烟艾灸、无烟艾灸对急性胃黏膜损伤大鼠血清中SOD、MDA的影响

目的:观测有烟艾灸、无烟灸对急性胃黏膜损伤修复作用的差异.方法:40只SPF级SD大鼠随机分为4组,即正常对照组、模型组、有烟艾灸组、无烟灸组,每组10例,采用无水乙醇灌胃制备急性胃黏膜损伤模型.采用比色法检测体内超氧化物歧化酶(super oxide dismutase,SOD)的活性、丙二醛(malondialdehyde,MDA)的含量,HE染色光镜下观察胃黏膜组织形态学变化.结果:(1)胃黏膜组织炎症病理学评分比较:与正常对照组比较(0.75±0.46),模型组病理组织学评分明显升高(7.75±1.67vs0.75±0.46,P<0.01);有烟艾灸组、无烟灸组明显低于模型组(4.63±0.52vs7.75±1.67、4.75±0.46vs7.75±1.67,P<0.01);有烟艾灸组与无烟灸组比较无显著差异(4.63±0.52vs4.75±0.46);(2)血清中SOD、MDA值比较:与正常对照组比较(301.48±16.675、6.77±0.529),模型组SOD值明显降低(260.07±15.481vs301.48±16.675,P<0.01)、MDA值明显升高(9.73±0.704vs6.77±0.529,P<0.01);与模型组比较,有烟艾灸组、无烟灸组SOD值明显升高,且有显著性差异(281.03±17.713vs260.07±15.481、278.61±17.550vs260.07±15.481,P<0.05)、MDA值降低,有显著性差异(7.52±0.361vs9.73±0.704、7.78±0.387vs9.73±0.704,P<0.01);有烟艾灸组较无烟灸组SOD值稍高(281.03±17.713vs278.61±17.550)、MDA值稍低(7.52±0.361vs7.78±0.387),但两组无显著性差异.结论:(1)有烟艾灸、无烟灸对急性胃黏膜损伤具有修复作用,且两者之间抗氧化比较没有明显差异;(2)有烟艾灸、无烟灸通过上调SOD活性、降低MDA含量,调节氧化/还原的动态平衡,使胃黏膜达到抗氧化损伤的作用.     

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.     

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.     

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.     

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.