匹伐他汀与阿托伐他汀分别联合丹参多酚酸盐对脑梗塞患者血脂水平的影响研究

目的:探讨匹伐他汀与阿托伐他汀分别联合丹参多酚酸盐对脑梗塞患者血脂水平的影响.方法:回顾性分析,收集2018年10月至2019年10月我院采用常规治疗+丹参多酚酸盐+阿托伐他汀治疗的60例脑梗塞患者临床资料作为A组;收集同期采用常规治疗+丹参多酚酸盐+匹伐他汀治疗的60例脑梗塞患者临床资料作为B组.比较两组血脂水平及不良反应发生情况.结果:两组治疗1个月后三酰甘油(Triacylglyceride,TG)、总胆固醇(Total cholesterol,TC)、低密度脂蛋白胆固醇(Low density lipoprotein cholesterin,LDL-C)均降低,高密度脂蛋白胆固醇(High density lipoprotein cholesterin,HDL-C)升高,且B组更为显著(P<0.05).两组不良反应发生率无明显差异(P>0.05).结论:较阿托伐他汀方案,匹伐他汀联合丹参多酚酸盐改善脑梗塞患者血脂水平效果较好.     

阿托伐他汀钙联合硝苯地平、盐酸普萘洛尔治疗 冠心病的临床效果

目的 探讨阿托伐他汀钙片联合心血管药物治疗冠心病的临床效果。方法 选取我院2018年1月~2月收治的70例冠心病患者,随机分为研究组和对照组,各35例。两组患者均给予常规基础治疗,对照组在此基础上给予辛伐他汀钙片,研究组采用阿托伐他汀片治疗,比较两组患者三酰甘油（TG）、血总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）水平及治疗效果。结果 对照组TC、TG、LDL-C分别为（3.13±0.29）mmol/L、（5.74±0.32）mmol/L、（3.67±0.25）mmol/L,高于研究组的（2.05±0.32）mmol/L、（4.98±0.36）mmol/L、（3.01±0.22）mmol/L,差异有统计学意义（P＜0.05）;对照组HDL-C水平低于研究组[（1.08±0.05）mmol/L vs （1.63±0.07）mmol/L],差异有统计学意义（P＜0.05）;研究组治疗总有效率为94.29%,高于对照组的80.00%,差异有统计学意义（P＜0.05）。结论 阿托他汀钙片治疗冠心病临床效果较好,有助于调理患者脂代谢水平,延缓和控制疾病发展,改善患者血脂水平。     

国产阿托伐他汀治疗原发性高脂血症的疗效和安全性的随机临床对照研究

目的比较国产阿托伐他汀(阿乐)10mg与进口阿托伐他汀(立普妥)10mg每晚一次口服治疗原发性高脂血症的疗效和安全性。方法随机平行对照组研究94例原发性高脂血症患者被随机分为阿乐组和立普妥组,分别每晚口服阿乐10mg或立普妥10mg。结果服药8周阿乐与立普妥两组的血脂均明显下降,TC分别下降14.52%比14.38%,LDL-C下降19.38%比20.12%,TG下降6.29%比6.13%,HDL-C上升7.07%比7.18%,两组间无明显差异,均无明显不良反应或毒副作用,两组相似。结论国产阿托伐他汀(阿乐)10mg每晚一次治疗原发性高脂血症安全有效,其疗效与进口阿托伐他汀(立普妥)等同。     

4种给药方案治疗霉菌性阴道炎的成本-效果分析

目的：探讨不同用药方案治疗霉菌性阴道炎的药物经济学效果。方法回顾性分析我院门诊霉菌性阴道炎病例,选取4种治疗方案进行比较,每组随机抽取病例20例,A组：环吡酮胺阴道栓、B组：克霉唑阴道片、C组：保妇康栓、D组：硝呋太尔制霉素阴道软胶囊,治疗周期2疗程,运用药物经济学方法进行成本-效果分析。结果4组方案成本分别为188.6元、118.8元、52元、85.2元;有效率分别为95%、100%、90%、75%;成本-效果(C/E)比分别为1.99、1.19、0.58、1.14;A组增量成本-效果比为27.32,B组增量成本-效果比为6.68,D组增量成本-效果比为-2.21。结论克霉唑阴道片治疗霉菌性阴道炎疗效好、成本低,且不良反应少。     

阿托伐他汀治疗进展型脑梗死的临床研究

目的 评价阿托伐他汀治疗进展型脑梗死的疗效.方法 选择在本院就诊的进展型脑梗死患者94例,分成观察组和对照组,两组患者均采用阿司匹林肠溶片、神经营养剂、尼莫地平,大面积脑梗死降颅压等常规方法.对照组使用降纤酶;观察组阿托伐他汀,疗程结束评定疗效及安全性,两组均无退出受试者.结果 观察组临床总有效率为78.72%高于对照组的临床总有效率57.44%,差异有显著性(P<0.05);两组患者检测临床神经功能缺损程度评分(NDS)及患者日常生活能力BI(Barthel),差异具有统计学意义(P<0.05),两组患者在治疗期间均未见明显的不良反应.结论 采用阿托伐他汀治疗进展型脑梗死疗效佳,具有良好的安全性,建议临床进一步推广.     

76例急性缺血性脑卒中应用阿托伐他汀与阿司匹林治疗的疗效分析

目的：探讨急性缺血性脑卒中应用阿托伐他汀与阿司匹林治疗的疗效。方法将151例急性缺血性脑卒中患者分为两组,治疗组76例给予阿托伐他汀联合阿司匹林治疗,对照组75例给予单纯阿司匹林治疗。结果治疗组总有效率为96.05%,不良反应发生率为11.84%,对照组总有效率为74.67%,不良反应发生率为9.33%,两组总有效率差异有统计学意义(P<0.05),不良反应发生率差异无统计学意义(P>0.05)。结论阿托伐他汀联合阿司匹林治疗急性缺血性脑卒中,疗效较高,不良反应少。     

蛹油-亚麻酸乙酯胶丸联合阿托伐他汀治疗高脂血症合并脂肪肝的疗效观察

目的评价蛹油-亚麻酸乙酯胶丸联合阿托伐他汀治疗高脂血症合并脂肪肝的疗效。方法回顾性分析自2010年~2012年间的90例高脂血症合并脂肪肝患者的临床资料。对患者使用阿托伐他汀10 mg/d，同时联合蛹油-亚麻酸乙酯胶丸0.6 mg/d，持续治疗3个月。结果经3个月的治疗，患者血常规有明显的改善，血清中胆固醇水平由(7.69±1.42) mmol/L下降为(4.52±0.69) mmol/L，甘油三酯的水平由(3.53±0.79) mmol/L下降为(1.53±0.42) mmol/L；患者肝脏的 B 超结果表明其脂肪肝有显著的改善。结论蛹油-亚麻酸乙酯胶丸联合阿托伐他汀对患者的血脂和脂肪肝有良好的治疗效果。     

加替沙星与左氧氟沙星治疗泌尿系统感染的临床疗效及经济学分析

目的 比较加替沙星与左氧氟沙星治疗泌尿系统感染的临床疗效及成本-效果分析.方法 采用随机5组静脉治疗及药物经济学原理对两种治疗方案进行成本-效果分析.结果 加替沙星组与左氧沙星组治疗泌尿系统感染的有效率分别为92.86%、88.46%(P＞0.05);不良反应发生率分别为7.1%、9.0%(P＞0.05);成本-效果比(C/E)分别为7.99、6.53.与左氧氟沙星组相比,加替沙星组每增加一个单位效果需多花费37.43元.结论 左氧氟沙星治疗泌尿系统感染的成本-效果比优于加替沙星.     

阿托伐他汀联合依折麦布对缺血性脑卒中患者临床预后及颈动脉斑块的影响

目的 分析阿托伐他汀联合依折麦布对缺血性脑卒中患者临床预后及颈动脉斑块的影响.方法 回顾性分析381例缺血性脑卒中患者的临床资料,根据是否采取阿托伐他汀联合依折麦布治疗进行分组;对照组183例,单用阿托伐他汀治疗;观察组198例,采取阿托伐他汀联合依折麦布治疗;均连续治疗、观察24个月;对比两组患者治疗前后的血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平、改良RANKIN量表(mRS)、改良Barthel指数评定量表(MBI)评分、颈动脉斑块面积及分型,以缺血性脑卒中复发率、不良反应的观察指标水平.结果 治疗后,两组血清TC、TG、LDL-C、HDL-C水平均较治疗前显著改善(P＜0.05);但观察组血清TC、LDL-C水平改善幅度大于对照组,差异显著(P＜0.05);治疗后,两组mRS评分、MBI评分均较治疗前显著改善(P＜0.05);但观察组mRS评分、MBI评分改善幅度大于对照组,差异显著(P＜0.05);观察组颈动脉斑块面积较治疗前显著缩小(P＜0.05),分型显著改善(P＜0.05);对照组治疗前后的颈动脉斑块面积及分型差异不显著(P＞0.05);观察组缺血性脑卒中复发率显著小于对照组(P＜0.05),两组不良反应发生率差异不显著(P＞0.05).结论 阿托伐他汀联合依折麦布较单用阿托伐他汀治疗更能有效降低缺血性脑卒中患者血脂水平,改善预后,在缩小并稳定颈动脉斑块方面具有显著优势,且安全性较高,值得临床推广采用.     

阿托伐他汀对62例早期糖尿病肾病的疗效观察

目的:探讨阿托伐他汀早期干预糖尿病肾病的临床效果。方法:将62例符合2型糖尿病并发早期肾病患者随机分为治疗组和对照组,每组31例。在常规治疗的基础上,治疗组给予阿托伐他汀40 mg及拜阿司匹林0.1 g;对照组给予阿托伐他汀20 mg及拜阿司匹林0.1 g,均为Qd,口服,疗程4周,并进行疗效评价。结果:治疗前后两组患者的U-m Alb、UAER、Scr、TG等指标均明显下降(P<0.05),且治疗组(口服阿托伐他汀40 mg)各项指标改善优于对照组(口服阿托伐他汀20 mg)(P<0.05)。结论:中等剂量的阿托伐他汀辅助治疗早期糖尿病肾病,可有效改善肾功能,不良反应较少,有着积极的临床价值。     

Schizophrenia in a North Swedish geographical isolate, 1900–1977. Epidemiology, genetics and biochemistry

Over 200 schizophrenic patients belonging to three major and interrelated pedigree complexes have been investigated over the past 30 years in a North Swedish geographically isolated population, presently numbering about 6,000. An intensive investigation of a number of biochemical correlates and genetic markers in a few selected families belonging to one of the major pedigrees has indicated new strategies for the current research program.
Schizophrenia, as defined operationally, is significantly associated with decreased activities of two enzymes (1) blood platelet monoamine oxidase, (2) plasma dopamine-β-hydroxylase, and (3) with the genetic marker Gc² (group specific antigen). Both enzymes are subject to genetic variation. A positive score for linkage between schizophrenia and low plasma DBH activity has been calculated, but, so far, available data are insufficient for discrimination between linkage and partial contribution of genetically controlled low plasma DBH to the pathogenesis of the disease. Alternatively, both mechanisms could be involved.
As a model for continued research, schizophrenia is explained as based on a double dominant-recessive genotype (Aabb), representing a vulnerability which in about 50 % of cases develops into clinical schizophrenia. It is suggested that the dominant mutation (A) operates on or affects MAO activity, and that the recessive genotype (bb) is instrumental in low variates of DBH activity and very likely such variates within the normal range of physiological variation. Moreover, it is suggested that the combined effects of MAO- and DBH-reduced efficiency on the metabolism of e.g. dopamine could be an essential pathogenic mechanism for the schizophrenic illness which is segregating in this population.     

The universal muscular chain reaction,muscle spasm,Torsions, ruptures and extravasations. Chameleons of pathology and some manifestations of simple muscular disorders

Most bodily functions require the coordinated actions of complementary and supplementary paired muscle groups. Where this essential muscular cooperation is lacking, hollow organs may burst and others become literally screwed up, giving rise to many similar spastic diseases such as Torticollis, Twisted ovarian cyst, Torsion of the Testis, Volvulus of the intestines, Varicose Veins, Megacolon, Aortamegaly, Scoliosis, Erb's Palsy, Peyronie's Disease, Main-en-Griffe, Undescended Foot (Pes Cavus), Talipes, Strabismus. Spasm is “panenepidemic” and unclassified examples of Torsion Dystonia and Dyskinesia really are as common as debt and taxes.     

Hypo- und Hypermagnesämie aus kardiologischer Sicht

Zusammenfassung Eine Reihe pathologischer Zustände bedingen Magnesiummangel. Zustände mit Hypermagnesämie sind ebenfalls bekannt, doch wesentlich seltener. Für den Kardiologen beachtenswert ist, daß unter Therapie mit bestimmten Diuretica bei Herzinsuffizienz, bei Herzinfarkt, Kardiomyopathie, Digitalisintoxikation und bestimmten Herzrhythmusstörungen Hypomagnesämie beobachtet wurde. Leider kann in der klinischen Routine nur ein extracelluläres Magnesiumdefizit durch Serumbestimmungen gemessen werden; über Magnesiummangel einzelner Organe kann nichts ausgesagt werden. Hinweise für Magnesiummangel geben aber neben der Messung des Serumspiegels Anamnese, klinischer Befund, bestimmte EKG-Veränderungen wie auch evtl. Hypokalämie, ein Zustand, bei dem sich oft — besonders bei Aldosteronismus — parallele Veränderungen zeigten.Tierexperimente deuten darauf hin, daß infarktähnliche Läsionen unter Magnesiummangel entstehen, doch ob Herzinfarkt beim Menschen durch Magnesiummangel ausgelöst werden kann, ist noch ungeklärt. In Leichenherzen zeigte sich im Infarktgebiet neben Calciumakkumulation signifikanter Magnesiumverlust, wobei unklar blieb, ob sich Ursache oder Folge des Infarktes widerspiegelten. Falls ein ursächlicher Zusammenhang besteht, ist er im Myokardstoffwechsel selbst zu suchen, wie bei der Alkoholkardiomyopathie, wo myokardialer Magnesiummangel zumindest als pathogenetischer Teilfaktor anerkannt wird. Andererseits versucht man aber auch Beziehungen zwischen Atherosklerose, Blutgerinnung und Hypomagnesämie herzustellen, in der Meinung, daß Magnesiummangel auch über den coronaren Pathomechanismus des Herzinfarktes wirken könnte. Sicher scheint, daß gewisse EKG-Veränderungen und Herzrhythmusstörungen durch einen irritierten Magnesiumhaushalt bedingt sein können, da sie bei Gabe bzw. Entzug von Magnesium verschwinden. Daß Magnesiummangel die Glykosidtoleranz verringert, wird tierexperimentell bestätigt. Unter Hypomagnesämie bewirkt Acetylstrophanthidin eher und länger Rhythmusstörungen als ohne, außerdem lassen diese sich durch Magnesiumgaben eliminieren. Da in gewissen Fällen spontane und digitalisinduzierte Herzrythmusstörungen durch Magnesiuminjektionen beseitigt wurden, scheint Magnesium als Therapeuticum angebracht. Einsatz verschiedener Magnesiumsalze bei Angina pectoris, degenerativen Herzerkrankungen und Herzinsuffizienz ohne geprüften und offensichtlich gestörten Magnesiumhaushalt ist fragwürdig, weil keine eindeutigen klinischen Erfolgsbeweise vorliegen. Immerhin mag es aber larvierte, durch Serumbestimmungen nicht erfaßbare Mangelzustände geben. Allgemein erscheint es aus kardiologischer Sicht ratsam, den Magnesiumhaushalt zu überwachen und in entsprechenden Fällen auszugleichen, um möglichen Myokardläsionen oder fatalen Herzrhythmusstörungen entgegenzuwirken.     

Environmental risk factors and their role in the management of atopic dermatitis

Introduction: The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.

Areas covered: We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.

Expert commentary: The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.     

HLA genes in Amerindians from Mexico San Vicente Tancuayalab Teenek/Huastecos

Huastecos or Teenek Amerindians are presently living at North East Mexico (San Luis Potosi State). They have probably one of the most ancient culture of Mexico and Central America together with Mayas and Olmec groups with which also show close relationships. Proximity to Atlantic Ocean/Mexican Gulf originated that Spaniards had very early contact with them at about 1519 CE or before. In the present paper we have aimed to study HLA gene profile which may be useful for HLA and disease epidemiology and transplant programs in Teeneks. HLA-DRB1*04:07, -DRB1*14:06 and -DRB1*04:11 have been found in high frequency like in other Amerindian groups. High frequency typical Amerindians HLA extended haplotypes have been found, such as A*02-B*35-DRB1*04:07-DQB1*03:02; A*68-B*39-DRB1*04:07-DQB1*03:02 and A*02-B*39-DRB1*04:07-DQB1*03:02; also new haplotypes have been described, like A*02-B*52-DRB1*04:11-DQB1*03:02, A*68-B*35-DRB1*14:02-DQB1*03:01 and A*68-B*40-DRB1*16:02-DQB1*03:01. Genetic proximity is observed not only to linguistically close Mayans, but also to Mazatecans, Mixtecans and Zapotecans, who speak an altogether different languages; it shows once more that genes and languages do not correlate. This population was greatly diminished after European contact between 1500 and 1600 years CE; in fact, North and South America First Inhabitants population was brought from 80 down to 8 million people because of diseases (i.e.: measles, smallpox or influenza), slavery and war.     

État de l’art : nouveaux anticoagulants et transfusion

Direct oral anticoagulants (DOAC) are indicated for stroke prevention in atrial fibrillation and for the prevention and treatment of venous thromboembolism. As any anticoagulant, they are associated with a bleeding risk. Management of DOAC-induced bleeding is challenging. Idarucizumab, antidote for dabigatran, is currently available and is part of the therapeutic strategy, whereas antidotes for anti-Xa agents are under development. Activated or non-activated prothrombin concentrates are proposed, although their efficacy to reverse DOAC is uncertain. We propose an update on DOAC-associated bleeding management, integrating the availability of idarucizumab and the critical place of DOAC concentration measurements.     

HLA in North Colombia Chimila Amerindians

HLA-A,-B,-C,-DRB1 and -DQB1 alleles have been studied in Chimila Amerindians from Sabana de San Angel (North Colombian Coast) by using high resolution molecular typing. A frequent extended haplotype was found:HLA-A*24:02-B*51:10-C*15:02-BRB1*04:07-DQB1*03:02 (28.7%) which has also been described in Amerinndian Mayos Mexican population (Mexico, California Gulf, Pacific Ocean). Other haplotypes had already been found in Amerindians from Mexico (Pacific and Atlantic Coast), Peru (highlands and Amazon Basin), Bolivia and North USA. A geographic pattern according to HLA allele or haplotype frequencies is lacking in Amerindians, as already known. Also, five new extended haplotypes were found in Chimila Amerindians. Their HLA-A*24:02 high frequencies characteristic is shared with aboriginal populations of Taiwan; also, HLA-C*01:02 high frequencies are found in New Zealand Maoris, New Caledonians and Kimberly Aborigines from Australia. Finally, this study may show a model of evolutionary factors acting and rising one HLA allele frequency (-A*24:02), but not in others that belong to the same or different HLA loci.     

The universal muscular chamber. A basic unit of the genitourinary, cardiovascular, gastro-intestinal, skeletal, cutaneous, respiratory and other systems, endocameral hypertension; and spasm, the key to their idiopathic diseases and arthropathies

Starting with the integument, we see many organs are contractile sacs or multiples thereof, which tubes or bags constitute the major part of the entire body. Recognition of this basic unit and its characteristics sheds new light, individually and collectively, on many disorders previously considered unrelated. Muscular tears and perforations develop in the walls of these chambers, being no way peculiar to those organs, wherein, hydrochloric acid occurs. So, it is not necessary to explain the absence of excessive acid from patients who exhibit holes in the gastric, uterine, aortic, duodenal, rectal, pulmonary, retina, and other walls. Muscle, not acid is the great common factor relating idiopathic disorders in the gastrointestinal tract to each other and to similar diseases in other systems. When the units are linked together, the lesions tend to appear as arthropathies, i.e. at the joints. Rephrasing common-place observations, frees us from conventional, conceptual cul-de-sacs. An observation is only as good as its interpretation, so all possibilities must be considered, otherwise, we will remain blinded by our misconceptions.     

Renal dysplasia and asplenia in two sibs

A family is reported in which two sibs, one male and the other female, both died within 24 hours of birth with enlarged polycystic kidneys. Postmortem histology in the second child showed gross renal dysplasia. In both children the pancreas was enlarged, nodular and cystic but the liver appeared macroscopically normal. In the second child, histological examination confirmed pancreatic fibrosis with cystic dilation of ducts, but showed portal fibrosis with bile duct proliferation in the liver.
This combination of findings is very reminiscent of those in a girl and her brother reported by Ivemark et al. (1959). The children reported here also showed absence or hypoplasia of the spleen, cardiac anomalies and other features of the Ivemark syndrome (Ivemark 1955), a quite different, usually sporadic, congenital disorder. It is suggested that the children described here have a distinct lethal congenital disorder, probably inherited in an autosomal recessive manner.