力蜚能治疗小儿缺铁性贫血的疗效观察

目的探讨多糖铁复合物力蜚能治疗小儿缺铁性贫血的疗效观察。方法60例患儿随机分为力蜚能治疗组和硫酸亚铁治疗组,前者给予力蜚能治疗;后者给予硫酸亚铁和维生素C治疗。结果治疗8周后力蜚能治疗组的血清铁（SI）水平明显高于硫酸亚铁治疗组（P〈0.01）;力蜚能治疗组的总有效率高于硫酸亚铁治疗组（P〈0.05）,且不良反应有显著性差异（P〈0.01）。结论力蜚能治疗小儿缺铁性贫血的疗效优于硫酸亚铁,且不良反应少,是治疗小儿缺铁性贫血的理想药物。     

多糖铁胶囊治疗妊娠合并缺铁性贫血的临床疗效

目的探讨多糖铁胶囊（商品名：红源达）治疗妊娠合并缺铁性贫血（IDA）的疗效及其安全性。方法采用多中心、临床试验,在广州市内4家医院按入选标准选择480例妊娠合并缺铁性贫血的患者,给予多糖铁胶囊治疗（口服,150mg/次,2次/d）,同时服维生素C片0.3g。治疗第2、4和8周后复查血常规和铁代谢,比较治疗前后红细胞（RBC）计数、血红蛋白（Hb）、血清铁蛋白（SF）、血清铁（SI）及可溶性血清铁蛋白受体（sTfR）变化及安全性。结果多糖铁胶囊治疗2周后SF、sTfR较治疗前改善（P〈0.05）;治疗4周后RBC计数、Hb、SF、sTfR较治疗前显著升高（P〈0.05）;治疗8周后RBC计数、Hb、SF及sTfR较治疗前升高非常明显（P〈0.01）,但SI在各检测时间的复查结果差异无统计学意义（P〉0.05）。治疗过程中患者均未发生明显的不良发应。结论多糖铁胶囊治疗妊娠合并IDA效果好,无明显不良反应。     

婴幼儿缺铁性贫血与维生素A营养状况关系及预防措施研究

目的通过对缺铁性贫血患儿血清维生素A的检测以及维生素A制剂辅助铁剂治疗缺铁性贫血的疗效分析,探讨缺铁性贫血与雏生素A缺乏之间的关系．为临床应用维生素A制剂辅助铁剂治疗缺铁性贫血提供循证医学的依据。方法对18个乡镇36个行政村的7个月-3岁的婴幼儿638名．采取末梢血进行血红蛋白、血清铁蛋白、锌原卟啉、维生素A测定。对缺铁性贫血合并亚临床维生素A缺乏的93婴幼儿,随机分为对照组37例。观察组56例。两组均给予健康教育和膳食指导,对照组单纯给予右旋糖酐铁口服液治疗;观察组给予右旋糖酐铁口服液＋维生素AD滴剂（胶囊型）治疗。治疗一个月后复查血红蛋白。结果638人中,缺铁性贫血136人,患病率为21．32％。其中7个月-1岁缺铁性贫血59人,患病率为28．23％;1—3岁77人,惠痛率为17．95％。轻度贫血89人,占65．44％;中度贫血36人,占26．47％;重度贫血11人,占8．09％。维生素A缺乏症。人。亚临床维生素A缺乏124人,患病率为19．44％。缺铁性贫血136人中,亚临床维生素A缺乏占缺铁性贫血患儿的68。38％,占非缺铁性贫血患儿的6．18％。对照组治愈16例,治愈率为43．24％;观察组治愈48例,治愈率为85．71％,经统计学处理,二者有极显著性差异（P〈0．01）。结论缺铁性贫血与维生素A缺乏是婴幼儿期最常见的两种营养缺乏性疾病,缺铁性贫血的发生与婴幼儿维生素A营养状况密切关系,维生素A制剂可以显著提高铁剂治疗缺铁性贫血的疗效,从而为临床应用维生素A制剂辅助铁剂治疗缺铁性贫血提供了循证医学的依据。     

复方硫酸亚铁叶酸片联合促红细胞生成素治疗肾性贫血的疗效

目的 探讨复方硫酸亚铁叶酸片联合促红细胞生成素（EPO）治疗肾性贫血的临床效果。方法 选取2017年6月~2019年6月我院收治的50例肾性贫血患者,按照随机数字表法分为对照组和观察组,各25例。对照组给予复方硫酸亚铁叶酸片治疗,观察组在对照组基础上给予EPO治疗,比较两组临床疗效、贫血相关指标水平及不良反应发生率。结果 治疗后,观察组总有效率为84.00%,高于对照组的64.00%,差异有统计学意义（P＜0.05）;两组红细胞比容（Hct）、血红蛋白（Hb）、血清铁蛋白（SF）、血清铁（SI）、总铁结合力（TIBC）、血清转铁蛋白饱和度（TSAT）水平均较治疗前改善,且观察组高于对照组,差异有统计学意义（P＜0.05）;观察组不良反应发生率高于对照组,但差异无统计学意义（P＞0.05）。结论 复方硫酸亚铁叶酸片联合EPO治疗肾性贫血患者,有利于提高治疗效果,改善贫血指标,不良反应轻微,且均在机体耐受范围内。     

氟西汀合并奎硫平治疗躯体形式障碍的疗效

目的探讨氟西汀合并奎硫平治疗躯体形式障碍的疗效及安全性。方法70例躯体形式障碍患者随机分为两组．研究组以氟西汀合并奎硫平进行治疗，对照组单用氟西汀治疗，疗程均为8周。治疗前与治疗第2、8周采用症状自评量表（SCL-90）．汉密尔顿抑郁量表（HAMD）评定临床疗效，副反应量表（TESS）评定不良反应。结果治疗后两组SCL-90，HAMD评分较治疗前减少，差异有显著性（P〈0．01）。8周末研究组有效率88．2％，对照组有效率54．5％，两组差异有显著性（P〈0．05）。并且在治疗2周末研究组较对照组见效快，差异有显著性（P〈0．05）。两组不良反应均表现较轻，大多出现在治疗早期，经对症治疗逐渐缓解。结论氟西汀合并奎硫平治疗躯体形式障碍较单用氟西汀疗效好，起效快，且不增加副作用。     

海芋散在复治肺结核中的作用初探

目的探讨经炮制海芋散在复治肺结核中的作用。方法把102例多治病人随机分成两组。采用WHO推荐的复治方案3H3R3Z3E3／6H3R3E3为对照组（51例），将用复治方案3H3R3Z3E3／6H3R3E3，加口服经炮制海芋散作为治疗组（51例），对病例的症状体征、病灶吸收情况、空洞吸收和闭合情况、痰菌阴转情况及不良反应发生的情况进行观察研究。结果症状体征改变情况治疗组总有效率为96．0％，对照组为66．7％（P〈0．01）；病灶吸收情况治疗组为96．1％，对照组为64．7％，治疗组明显高于对照组（P〈0．01）：空洞吸收或闭合治疗组为98．0％，对照组为68．6％，治疗组明显高于对照组（P〈0．01）；痰菌阴转情况治疗组为94．1％。对照组为70．5％，治疗组明显高于对照组（P〈0．05）；不良反应发生情况治疗组为25．1％，对照组为52．2％．治疗组显著低于对照组（P〈0．01）。结论加服用经炮制海芋散联合抗痨化疗组合药物治疗复治肺结核的疗效优于单纯用抗痨化疗组合药的化疗方案，且可减轻抗痨化学药物的不良反应，作用肯定，值得在临床中进一步探讨研究。     

广州市2005年中小学生贫血状况分析

目的分析广州市中小学生缺铁性贫血现况，以掌握缺铁性贫血的防治重点。方法分析2005年广州市学生体质健康调查研究资料，对象为7、9、12、14、17岁人群。采用WHO的方法和标准筛查贫血：同时收集调查对象的身高和体重等资料。结果广州市中小学生贫血患病率为9．47％，其中边缘性贫血占65．64％：女生贫血患病率为11．00％，高于男生的7．93％（Х^2=6．6，P〈0．05）；乡村学生贫血患病率为13．86％，远高于城区学生的5．08％（Х^2=53．8，P〈0．001）；不同年龄组、不同体格状况学生的患病率差别无统计学意义（P〉0．05）。结论应科学安排学生膳食，增加铁的摄入；重点防治乡村学生和青春发育期城区女生的贫血；应通过学校健康教育，增加学生营养知识。     

自知力对精神分裂症患者治疗依从性的影响

目的探讨自知力对精神分裂症治疗依从性的影响。方法符合入组条件的116例患者随机分为两组，对照组仅以药物维持治疗，研究组合并自知力教育。观察1年。以BPRS（简明精神病量表）评定病情轻重及自知力障碍程度，依从性分为完全依从，部分依从，不依从3个等级，并统计观察期间再入院率。结果研究组6个月后BPRS评分，自知力障碍评分均显著低于对照组（P〈0．05），至观察结束差异更趋明显（P〈0．01），治疗依从性，再入院率观察结束时．两组比较差异显著（P〈0．01或P〈0．05）。结论自知力教育可提高精神分裂症患者的治疗依从性。     

阿斯美治疗上呼吸道感染后咳嗽

目的研究阿斯美对上呼吸道感染后咳嗽的治疗作用。方法80例上呼吸道感染后咳嗽症状的患者随机分成两组。A组42例，给予阿斯美2片口服，tid；B组38例，给予复方甘草合剂口服，疗程均为10d。结果治疗前、后相比，A组咳嗽治疗总有效率为90．5％，远高于B组36．2％（P〈0．01），且A组治疗前后咯痰评分有明显差异，分别为（0．8±0．4）和（0．3±0．1）W〈0．05）；B组治疗前后咯痰无差异，两组咯痰评分治疗后比较差异有显著性（P〈0．05）。结论阿斯美对于慢性咳嗽的疗效确切，且还有相当的祛痰效果，对于痰量不多的患者可同时控制咳嗽和咯痰。     

帕罗西汀合用心理行为干预治疗老年期抑郁症的疗效

目的探讨帕罗西汀合用心理行为治疗对老年期抑郁症的疗效。方法将60例老年期抑郁症随机分成两组，进行为期6周的对照研究，出院后随访1年，分别用心理行为合并帕罗汀治疗（研究组）和帕罗西汀治疗（对照组）；采用汉密尔顿抑郁量表（HAMD）和临床疗效总评量表（CGI—SI）进行评定。结果研究组在治疗6周后HAMD评分（9．32±2．28）较对照组（13.17±3．39）有显著性差异（P〈0．01），研究组CGI—SI较对照组有显著性差异（P〈0．01），1年末随访时HAMD评分研究组（9.19±2．33）较对照组（13．98±4．96）有显著性差异（P〈0.01）。且研究组复发率低于对照组（P〈0.05）。结论帕罗西汀合用心理行为治疗对老年期抑郁症的疗效优于帕罗西汀，且复发率低。     

Korean Guideline for Iron Chelation Therapy in Transfusion-Induced Iron Overload

Many Korean patients with transfusion-induced iron overload experience serious clinical sequelae, including organ damage, and require lifelong chelation therapy. However, due to a lack of compliance and/or unavailability of an appropriate chelator, most patients have not been treated effectively. Deferasirox (DFX), a once-daily oral iron chelator for both adult and pediatric patients with transfusion-induced iron overload, is now available in Korea. The effectiveness of deferasirox in reducing or maintaining body iron has been demonstrated in many studies of patients with a variety of transfusion-induced anemias such as myelodysplastic syndromes, aplastic anemia, and other chronic anemias. The recommended initial daily dose of DFX is 20 mg/kg body weight, taken on an empty stomach at least 30 min before food and serum ferritin levels should be maintained below 1000 ng/mL. To optimize the management of transfusion-induced iron overload, the Korean Society of Hematology Aplastic Anemia Working Party (KSHAAWP) reviewed the general consensus on iron overload and the Korean data on the clinical benefits of iron chelation therapy, and developed a Korean guideline for the treatment of iron overload.     

益气补血法联合小剂量铁剂治疗对缺铁性贫血患儿的疗效分析

目的 分析益气补血法联合小剂量铁剂治疗对缺铁性贫血患儿的临床疗效。方法 选择本院2016年4月~2017年4月122例缺铁性贫血患儿的临床资料,随机分为对照组与研究组,每组61例,对照组实施小剂量的铁剂治疗,研究组实施益气补血法与小剂量铁剂联合治疗,分析两组铁代谢有关指标变化情况及治疗效果。结果 研究组SI（血清铁）及SF(铁蛋白)水平比对照组高,TIBC（总铁结合力）比对照组更低,研究组治疗效果高于对照组,存在统计学差异(P＜0.05)。结论 益气补血法联合小剂量铁剂治疗对缺铁性贫血患儿的临床疗效显著,值得推广。     

Iron accumulation during development and ageing of Drosophila

We examined Drosophila melanogaster fruit flies to determine whether iron accumulates with ageing as it does in mice. Iron concentrations were measured by atomic absorption for flies maintained at 11, 20, 25 and 30 degrees C where the average lifespans were 152, 81, 62 and 25 days, respectively. Iron was found to accumulate with ageing during both the adult and developmental stages with an overall increase of 186% at 25 degrees C. A similar increase was found at 20 degrees C and 30 degrees C. At 11 degrees C the increase was less than half that at 25 degrees C. The rate of iron accumulation also varied with environmental temperature with the logarithm of the rate proportional to temperature (log R = 0.0509T-0.384). The rate of iron accumulation with ageing was, thus, found to be proportional to the rate of ageing, suggesting that excess dietary iron may be an initiator of senescence.     

铁代谢及铁蛋白与心血管疾病关系的现状分析

铁是一种双面元素,铁稳态的紊乱对部分组织有害。研究表明心脏是受铁代谢紊乱影响的主要器官之一。铁代谢障碍无论是缺乏还是超载,都与心血管疾病的发生率和死亡率增加有关。铁蛋白是研究铁状态的唯一指标,被认为是诊断铁状态的最佳单一测定。就目前研究结果来看,多种心血管疾病与铁代谢紊乱有关,如冠心病、心力衰竭、心肌病、阿霉素导致的心肌损伤及心肌缺血再灌注。明确铁代谢紊乱引起细胞损伤的机制,并进一步研究铁蛋白与铁代谢紊乱所引起的心血管疾病的相关性,可以为临床上提供便捷、准确的检测方法,并可指导临床治疗。     

Iron medication-induced gastric mucosal injury

Severe gastrointestinal erosion, ulcer, necrosis and strictures after an acute iron overdose are well described. However, gastric mucosal injury in patients receiving therapeutic iron has received only scant recognition despite its wide use. We report a case of iron medication-induced gastric mucosal injury in a 76-year-old male who presented with iron deficiency anemia and had been taking ferrous sulfate tablet for 4 years. Esophagogastroduodenoscopy (EGD) revealed a pale, villous appearing flat lesion along the lesser curvature of gastric body. Histopathologic examination of EGD biopsies of the flat lesion showed brown crystalline materials deposited in the lamina propria of gastric mucosa, which was accompanied with fibrosis, chronic inflammation, and foreign body reaction. The crystalline materials were covered and admixed with gastric epithelium. Prussian blue iron stain confirmed that the brown crystalline materials were iron. The iron and hemosiderin accumulation was also seen in cytoplasm of epithelial cells and lumen of fundic gastric glands. The recognition and reporting by pathologists of iron-induced changes in EGD biopsies will alert clinicians to this underrecognized but easily correctable complication by alternative forms of iron therapy, such as liquid preparation.     

Iron homeostasis and organismal aging

Iron is indispensable for normal body functions across species because of its critical roles in red blood cell function and many essential proteins and enzymes required for numerous physiological processes. Regulation of iron homeostasis is an intricate process involving multiple modulators at the systemic, cellular, and molecular levels. Interestingly, emerging evidence has demonstrated that many modulators of iron homeostasis contribute to organismal aging and longevity. On the other hand, the age-related dysregulation of iron homeostasis is often associated with multiple age-related pathologies including bone resorption and neurodegenerative diseases such as Alzheimer’s disease. Thus, a thorough understanding on the interconnections between systemic and cellular iron balance and organismal aging may help decipher the etiologies of multiple age-related diseases, which could ultimately lead to developing therapeutic strategies to delay aging and treat various age-related diseases. Here we present the current understanding on the mechanisms of iron homeostasis. We also discuss the impacts of aging on iron homeostatic processes and how dysregulated iron metabolism may affect aging and organismal longevity.     

Iron acquisition by Mycobacterium tuberculosis residing within myeloid dendritic cells

The pathophysiology of Mycobacterium tuberculosis (M.tb) infection is linked to the ability of the organism to grow within macrophages. Lung myeloid dendritic cells are a newly recognized reservoir of M.tb during infection. Iron (Fe) acquisition is critical for M.tb growth. In vivo, extracellular Fe is chelated to transferrin (TF) and lactoferrin (LF). We previously reported that M.tb replicating in human monocyte-dervied macrophages (MDM) can acquire Fe bound to TF, LF, and citrate, as well as from the MDM cytoplasm. Access of M.tb to Fe may influence its growth in macrophages and dendritic cells. In the present work we confirmed the ability of different strains of M.tb to grow in human myeloid dendritic cells in vitro. Fe acquired by M.tb replicating within dendritic cells from externally added Fe chelates varied with the Fe chelate present in the external media: Fe-citrate > Fe-LF > Fe-TF. Fe acquisition rates from each chelate did not vary over 7 days. M.tb within dendritic cells also acquired Fe from the dendritic cell cytoplasm, with the efficiency of Fe acquisition greater from cytoplasmic Fe sources, regardless of the initial Fe chelate from which that cytoplasmic Fe was derived. Growth and Fe acquisition results with human MDM were similar to those with dendritic cells. M.tb grow and replicate within myeloid dendritic cells in vitro. Fe metabolism of M.tb growing in either MDM or dendritic cells in vitro is influenced by the nature of Fe available and the organism appears to preferentially access cytoplasmic rather than extracellular Fe sources. Whether these in vitro data extend to in vivo conditions should be examined in future studies.     

Iron appetite and latent learning in rats

Two experiments are reported which show that rats are capable of forming an association between the presence of iron in a solution when it is not specifically needed and a subsequent state of iron deficiency. Specifically, rats were trained to lever press for water while thirsty. One group received ferrous ions in addition to the water. When these rats were subsequently rendered iron deficient, they lever pressed more under extinction conditions as a graded function of lower hemoglobin levels. Controls that either did not receive ferrous ions during training or received solutions other than ferrous solutions during training did not respond this way under extinction conditions. This is therefore a type of latent learning previously demonstrated only for sodium appetite.     

Small Bowel Pseudomelanosis Associated with Oral Iron Therapy

An accumulation of pigment deposits on mucosa, called melanosis or pseudomelanosis, of the small bowel is observed infrequently during endoscopic examination. We describe 6 cases of small bowel pseudomelanosis; the possible etiology of which was chronic iron intake. We observed numerous brown spots in duodenum, jejunum, and terminal ileum during upper and lower endoscopy. Interestingly, all patients have been taking oral iron for several years. Histology showed pigment depositions within macrophages of the lamina propria and a positive Prussian blue stain indicating hemosiderin deposition. Herein, we demonstrate that long term iron therapy may result in pseudomelanosis of small bowel, such as duodenum, jejunum, and ileum.