放射性皮肤损伤的机制与防治进展

皮肤是辐射中度敏感组织之一,受到一定剂量射线照射后,组织细胞内的物质代谢、酶的活性、染色体的形态和功能都会受到影响和损害,并产生一系列生物效应,使组织细胞呈渐进性和持久性的退行性改变及坏死,严重者形成创面难愈合的放射性溃疡,治疗上颇为困难。本文对放射性皮肤损伤的机制、防护与治疗方面的研究进行综述,为临床治疗提供理论依据。     

1例放射性皮肤损伤合并手癣诊疗体会

慢性放射性皮肤损伤是局部皮肤长期受到超过剂量限值的照射,致使累积剂量过大引起的.现将我院收治的1例放射性皮肤损伤合并手癣患者报告如下     

皮肤防护剂预防乳腺癌放射性皮肤损伤的观察

放射治疗是预防乳腺癌术后局部复发的最有效手段之一。     

Ⅲ度放射性皮肤损伤1例

笔者在放射工作人员身体健康调查中 ,发现 1例Ⅲ度放射性皮肤损伤患者。患者李×× ,骨科主治医师 ,从事骨科临床工作 2 5年。长期在X线照射下 ,为患者裸手四肢复位 ,无任何防护 ,短时间内接触射线频度过分集中 ,临床出现病理改变。估算手部皮肤累积剂量 10～ 15Gy。使用国产KE5 8型2 0 0mA、广州产 30mAX线机各 1台 ,平均每日工作量为 1～ 2名患者 ,每次裸手整骨 4 0min左右。1　临床症状1985年 3月 ,患者自感双手干燥、粗糙。 1990年发现双手皮肤角化过度 ,指甲呈灰黑色 ,纵嵴甲板增厚 ,呈典型舟状甲 ;近年左手手指出现功能障碍 ,中指…     

Ⅲ度慢性放射性皮肤损伤2例

慢性Ｘ射线皮肤损伤是由于Ｘ射线反复长期超剂量应用且防护设施不佳,致使累积剂量过大而引起的。本文报告２例Ｘ线致手部慢性Ⅲ度放射性皮炎的病例。１病例介绍 例１男性,４６岁,骨科医生,专业工龄２８年。使用Ｘ线机：三源产３０ｍＡ、天津产 １０ ｍＡ、上海产 １５ ｍＡ、山西产 ５０ｍＡ。徒手闭合手法复位：每天１０～２０人次,有时 ８ ｈ连续在机房内工作。 １９８６年前无任何防护,后有铅围裙、铅眼镜。工作２０年后双手指疼痛,多处溃疡长期不愈截指、拔甲。皮肤受照累积剂量：２．０５Ｓｖ。 查体：双手皮肤干燥、粗糙、脱屑…     

一例急性放射性皮肤损伤的医学追踪观察

1978年底,浙江省某部X射线金属探伤工王某因背部皮肤巨大溃疡伴白细胞减少,一年半未愈,到我室就诊。     

放射性皮肤损伤临床诊断与治疗

本文结合国内外文献、新制定的国家职业卫生标准及笔者的临床经验等解析了外照射急性及慢性放射性皮肤损伤的发病特点、临床表现、诊断标准和治疗原则，为放射性皮肤损伤的及时处理及规范化诊治提供依据。急性放射性皮肤损伤依据受照剂量的大小及临床表现分为Ⅰ、Ⅱ、Ⅲ、Ⅳ度，这四种程度急性放射性皮肤损伤临床经过既表现了损伤的量效关系，也体现了严重放射损伤的明显阶段性，早期通过皮肤损伤程度进行剂量估算有助于快速准确诊断、早期预测病变严重程度和决定治疗策略。慢性放射性皮肤损伤一方面是职业原因长期接触低剂量辐射所致，另一方面是急性放射性皮肤损伤迁延形成，分度为Ⅰ、Ⅱ、Ⅲ度，仅为皮肤损伤程度分类，与所受辐射没有严格的量效关系，急性和慢性放射性皮肤损伤的治疗根据损伤程度治疗有所不同，局部保守治疗以及应用修复手段的外科治疗，并且都考虑了全身治疗对创面愈合的促进作用。     

14例慢性放射性皮肤损伤及其临床特点

医用诊断Ｘ射线技术在我国城乡早已普及应用,以致使临床诊断技术得到进一步提高。然而,早年从事医用诊断Ｘ射线工作者,由于机器性能和防护条件普遍较差,导致手部职业性皮肤损伤已有不少报道。本文就我组８０年代以来诊断的１４例手部慢性放射性皮肤损伤及其临床特点报...     

职业性放射性皮肤损伤病人的甲襞微循环观察

职业性放射性皮肤损伤病人的甲襞微循环观察山东省医学科学院放射医学研究所（济南市经十路，２５００６２）金家美山东省劳动卫生职业病防治研究所沈祖期马希叔随着微循环研究的不断深入和发展，甲襞微循环检查已得到广泛应用，电离辐射致动物微循环障碍已有较深入的研究...     

2例Ⅲ度慢性放射性皮肤损伤的临床分析

目的 通过对Ⅲ度慢性放射性皮肤损伤的临床分析,了解和掌握电离辐射对皮肤的损伤状况。方法 按照GBZ106-2002《放射性皮肤疾病诊断标准》对病例进行临床分析。结果 根据例1、例2皮肤的受照剂量和临床分析,均诊断为Ⅲ度慢性放射性皮肤损伤。结论 电离辐射对皮肤的损伤具有一定的潜伏期和剂量效应关系。     

乳铁蛋白通过调节铁死亡改善小鼠放射性肠损伤

目的  探究乳铁蛋白(lactoferrin, Lf)对放射性肠损伤的防护作用及其机制。方法  小鼠随机分为对照组、10 Gy组及Lf+10 Gy组。于照射前7 d,Lf+10 Gy组给予250 mg/kg Lf灌胃,每天1次。10 Gy组和Lf+10 Gy组小鼠接受10 Gy的腹部照射。照射后3.5 d处死小鼠,收集样本测定相关指标。结果  照射引起放射性肠损伤,Lf干预缓解了体重下降、肝脏氧化应激,改善了小肠病理损伤,增加反映小肠细胞增殖再生能力的Lgr5和Ki67阳性细胞数。照射引起小肠组织的铁死亡。在铁代谢途径中,Lf干预显著下调小肠二价金属转运蛋白(divalentmetal-iontransporter-1, DMT1)的表达及Fe²⁺含量;在谷胱甘肽(glutathione, GSH)/谷胱甘肽过氧化物酶4(glutathione peroxidase 4, GPX4)-脂质过氧化途径中,Lf干预显著上调小肠溶质载体家族7成员(solute carrier family 7 member, SLC7A11)和GPX4蛋白表达,下调酰基辅酶A合成酶长链4(acyl-CoA synthase long chain 4, ACSL4)蛋白表达并降低丙二醛(malondialdehyde, MDA)水平。结论  Lf改善了放射性肠损伤,其作用机制可能与通过铁代谢与GSH/GPX4-脂质过氧化途径调节铁死亡有关。     

补体在放射性肺损伤中的作用与机制

目的 探明补体在⁶⁰Coγ射线单次20 Gy胸部照射所致小鼠放射性肺损伤中的作用。方法 ⁶⁰Coγ射线单次20 Gy胸部照射C57BL/6小鼠,观察早期(15 d内)肺组织炎性反应和后期(30 d、180 d)肺纤维化,ELISA测定照射后1 d、3 d、7 d、15 d、30 d、180 d肺组织C2、C3a、C4、C5b-9含量,RT-PCR检测Beas-2B细胞照射后补体mRNA的表达。结果 照射后小鼠放射性肺损伤表现为早期炎性反应和晚期纤维化。补体C2、C4和C5b-9复合物在照射后早期(3 d或7 d)增高(P <0.05),可能与照射引起的炎性反应有关。补体C3a在照射后3～180 d均明显高于对照组水平,提示其与放射性肺损伤关系密切。照射细胞中,补体C2、C3的mRNA表达增高,而C4、C5的m RNA水平无变化。结论 不同补体在放射性肺损伤中的反应存在差异,其中补体C3a与放射性肺损伤关系极为密切,提示通过调控补体C3a及其受体可能是防治放射性肺损伤的新途径。     

冷诱导RNA结合蛋白在放射性肺损伤模型中的表达变化

目的探讨冷诱导RNA结合蛋白(CIRBP)在放射性肺损伤模型中的表达变化。方法将30只雄性C57BL/6小鼠按体重随机分为2组,每组15只,对照组小鼠不做任何处理,模型组小鼠经20 Gy X射线单次胸部照射,构建放射性肺损伤模型,于照射后5周解剖。采用苏木素-伊红(H&E)染色和Masson染色观察肺组织病理改变及胶原的沉积;采用免疫组织化学法检测肺组织炎症因子白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的表达;采用qRT-PCR技术检测肺组织中CIRBP mRNA的表达;采用免疫荧光技术和Western blotting技术检测肺组织中CIRBP蛋白的表达。结果与对照组相比,模型组肺组织血管扩张充血、炎细胞浸润、部分肺泡间隔增厚,IL-6的表达[(187.22±34.77) vs (129.41±5.58),t=3.179,P <0.05]和TNF-α的表达[(187.02±19.16)vs (137.52±23.53),t=5.069,P <0.05]均升高,差异具有统计学意义,而且模型组肺组织中CIRBP mRNA的表达明显升高[(1.97±0....     

The effect of tuberculin skin test and BCG vaccination on the expansion of PPD-specific IFN-gamma producing cells ex vivo

Understanding the immunogenicity of BCG in a population where it has failed will facilitate the design of new TB vaccines. We assessed the immunogenicity of M. bovis BCG over 12 months by ELISPOT assay. Forty-one adolescents and young Gambian male adults received a tuberculin skin test (TST) which was followed one week later by BCG vaccination, but the 23 control subjects received neither of these. TST alone significantly induced PPD-specific IFN-γ producing cells. Twenty-three percent of subjects did not respond to BCG, which was associated with higher pre-existing ex vivo response to PPD. Paradoxically, amongst BCG responders there was a correlation between pre-existing response and subsequent response to BCG. We conclude that BCG is immunogenic, but this effector response is short-lived and can be limited in higher pre-existing anti-mycobacterial immunity, suggesting a possible threshold beyond which BCG immunogenicity is inhibited.     

Nicaraven mitigates radiation-induced lung injury by downregulating the NF-κB and TGF-β/Smad pathways to suppress the inflammatory response

Radiation-induced lung injury (RILI) is commonly observed in patients receiving radiotherapy, and clinical prevention and treatment remain difficult. We investigated the effect and mechanism of nicaraven for mitigating RILI. C57BL/6 N mice (12-week-old) were treated daily with 6 Gy X-ray thoracic radiation for 5 days in sequences (cumulative dose of 30 Gy), and nicaraven (50 mg/kg) or placebo was injected intraperitoneally in 10 min after each radiation exposure. Mice were sacrificed and lung tissues were collected for experimental assessments at the next day (acute phase) or 100 days (chronic phase) after the last radiation exposure. Of the acute phase, immunohistochemical analysis of lung tissues showed that radiation significantly induced DNA damage of the lung cells, increased the number of Sca-1⁺ stem cells, and induced the recruitment of CD11c⁺, F4/80⁺ and CD206⁺ inflammatory cells. However, all these changes in the irradiated lungs were effectively mitigated by nicaraven administration. Western blot analysis showed that nicaraven administration effectively attenuated the radiation-induced upregulation of NF-κB, TGF-β, and pSmad2 in lungs. Of the chronic phase, nicaraven administration effectively attenuated the radiation-induced enhancement of α-SMA expression and collagen deposition in lungs. In conclusion we find that nicaraven can effectively mitigate RILI by downregulating NF-κB and TGF-β/pSmad2 pathways to suppress the inflammatory response in the irradiated lungs.     

Development of a porcine skin injury model and characterization of the dose-dependent response to high-dose radiation

A porcine skin model was developed to characterize the dose-dependent response to high-dose radiation. The dorsal skin of a mini pig was divided into four paraspinal sections, with 11 small irradiation fields (2 cm × 2 cm) in each section, and a single fraction of 15, 30, 50 or 75 Gy was delivered to each section using a 6 MeV electron beam. A spectrophotometer measured gross skin changes, and a biopsy for each radiation dose was performed in the 1st, 2nd, 4th, 6th and 9th weeks for histology, immunostaining with anti-CD31, and western blotting with IL-6 and TGF-β1 to determine the degree of skin damage. After a 4-week latency period, erythema and dry desquamation, moist desquamation, and ulceration appeared at 4, 6 and 9 weeks, respectively. Gross skin toxicity was more pronounced, occurred early and continued to progress with irradiation >50 Gy, whereas complete healing was observed 12 weeks after 15 Gy. Spectrophotometry showed erythema indices rapidly increased during the first 4 weeks after irradiation. The number of eosinophils began rising sharply at 4 weeks and normalized after reaching peaks at 7–8 weeks. Microvessel density showed a biphasic pattern with a transient peak at 1 week, a nadir at 4–6 weeks, and maximum recovery at 9 weeks. Increase in the levels of IL-6 and TGF-β1 was detected soon after irradiation. Most of these parameters indicated complete healing of the skin 12 weeks after 15 Gy. Our porcine skin model provides an effective platform for studying high-dose radiation-induced skin injury, in particular histologic and molecular changes, during the early latency period.     

放射性肺损伤发病机制及分子靶向治疗研究进展

放射性肺损伤是胸部肿瘤放疗的常见并发症,通常包括早期的放射性肺炎和晚期的放射性肺纤维化,严重影响患者的治疗和预后.目前常用的治疗放射性肺纤维化的方法包括糖皮质激素治疗、抗炎治疗、抗氧化治疗等.随着人们对放射性肺损伤的深入研究,分子靶向治疗受到广泛关注.分子靶向抑制剂是一类新兴的治疗放射性肺损伤的药物,主要针对各类细胞因...     

早期肠内营养对重症颅脑外伤病人炎性因子及免疫功能的影响

目的:探讨早期肠内营养(EEN)对重症颅脑外伤病人康复过程中炎性因子及免疫功能的影响.方法:将84例重症颅脑外伤病人随机分为观察组(n=44)和对照组(n=40).检测和比较两组病人入院时、治疗后1周和2周的炎性因子(IL-2、6、8),肿瘤坏死因子-α(TNF-α)和免疫功能指标(IgG、IgA、IgM、TLC)的变化,以及并发症的发生率和康复时间等. 结果:治疗2周后,观察组病人炎性因子水平明显下降,免疫功能指标明显恢复,并发症的发生率明显降低,与对照组比,差异均有显著性统计学意义(P＜0.05). 结论:对重症颅脑外伤病人EEN可有效地改善病人康复过程中的免疫功能,降低炎性因子水平和并发症的发生率.     

Alcohol and inflammation and infection: clinical and experimental systems—summary of the 2010 Alcohol and Immunology Research Interest Group Meeting

The 15th annual meeting of the Alcohol and Immunology Research Interest Group was held on November 19, 2010, at Loyola University Medical Center in Maywood, IL. This year, the focus of the meeting was on alcohol’s effect on the immune system in both clinical and experimental systems. The event consisted of three sessions, which featured plenary talks from invited speakers along with oral presentations from selected abstracts, in addition to a poster session. Participants presented a variety of information on ethanol-induced effects on infection susceptibility and resolution, oxidative stress, and organ inflammation. Specifically, speakers presented new insights on the mechanism of alcohol-mediated deleterious effects in the lung, liver, skin, and neuroendocrine system, as well as on immune cells in both in vivo and in vitro systems. Additional oral presentations suggested possible mechanisms of how alcohol-induced reactive oxygen species promote immune dysregulation both locally and systemically.     

吡菲尼酮的抗氧化能力及其对大鼠油酸性急性肺损伤的防护作用

目的探讨新型抗炎药物吡菲尼酮(PFD)对大鼠油酸(OA)性急性呼吸窘迫综合征(ARDS)的氧化-抗氧化的影响。方法129只SD大鼠,分为正常对照组、油酸组和3个不同剂量的PFD干预组(20、40、80mg/kg灌胃);根据取材观察时间每组又分为0.5、1、2、6、24h5个亚组。动态观察PFD对氧自由基生成酶[如NADPH氧化酶、黄嘌呤氧化酶(XO)和髓过氧化物酶(MPO)等]及清除氧自由基物质如谷胱甘肽过氧化物酶(GSH-Px)活力和总抗氧化能力(TAC)的作用。结果PFD可降低OA性ARDS大鼠肺组织的自由基含量和氧自由基生成酶(如NADPH氧化酶、XO和MPO等)活力;同时可增强肺组织中GSH-Px活力和TAC。结论PFD对OA性ARDS具有早期干预作用,主要是抑制产生自由基的酶类尤其是NADPH氧化酶活力,从而达到避免自由基直接损伤肺组织的目的。