Human immunodeficiency virus/acquired immunodeficiency syndrome training from a union perspective.

The authors developed a union sponsored 2-day human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) "train the trainer" program for healthcare workers in the San Francisco Bay Area. The program incorporated the "education for action" approach in an effort to respond to the inadequacies in many traditional, institutional trainings. Service Employees International Union (SEIU) and Labor Occupational Health Program (LOHP) conducted the HIV/AIDS "train the trainer" program for approximately 100 healthcare workers in county public hospitals and community health clinics. After completing the program, these workers went back to their healthcare facilities, or community organizations, and led additional classes on HIV/AIDS transmission and prevention for approximately 600 more people. The goal of the program was to empower healthcare workers to: 1) identify the occupational risks associated with exposure to blood and potentially infectious body fluids at the workplace; 2) develop strategies to reduce those risks; 3) discuss their feelings about caring for an HIV/AIDS patient; and, 4) conduct HIV/AIDS workshops at the workplace.     

A comparison of ceftazidime and aminoglycoside based regimens as empirical treatment in 1316 cases of suspected sepsis in the newborn

We report a prospective, non-blind, randomised, multicentre, parallel group, multinational investigation to compare ceftazidime to aminoglycoside based regimens as empirical treatment in 1316 cases of suspected sepsis in the newborn. In each of the 15 study centres either ceftazidime alone (CAZ) or ceftazidime + ampicillin (CAZ+AMP) was compared to an aminoglyocoside/ampicillin combination (AG+AMP). In all cases treatment was based on an intention to treat. Bacteria considered to be pathogenic were isolated from 176/1316 (13.4%) patients. The incidence of proven infection varied from 39% in a Yugoslav centre to 6% in a British centre; a further 489/1316 (37.1%) patients fulfilled the criteria for clinically suspected sepsis. A total of 210 bacterial isolates from 197 infection sites in 176 patients were considered to be clinically significant. The cure rate for evaluable patients with proven infection who were treated with CAZ+AMP (97%, 30/31) was significantly higher than that for the corresponding patients treated with AG+AMP (66%, 26/39), (P<0.002). The difference in cure rate between CAZ monotherapy (79%, 34/43) and AG+AMP (86%, 32/37) was not significant. Treatment failed in 28/150 (18.7%) evaluable patients. There were significantly fewer failures (P<0.001) with CAZ+AMP than with AG+AMP therapy. There were 55 staphylococcal infections. Treatment was successful in 16/19 evaluable patients treated with CAZ or CAZ+AMP and in 16/29 evaluable patients treated with AG+AMP. None of the study centres encountered problems with ceftazidime resistant bacteria. The cure rate for patients with only clinical and radiological evidence of sepsis was greater than 94% in all treatment groups. Of the study population 65 (4.9%) died, 15 deaths were attributed to infection, pathogenic bacteria were only isolated from 10. The mortality rate for infected babies was 5.7% compared to 4.8% for those without confirmed infection. All the deaths associated with infection were due to Gram-positive bacteria. This study suggests that the practice of continuing antibiotic therapy once pretreatment cultures are known to be negative should be seriously reconsidered. It is concluded that CAZ+AMP is superior to either AG+AMP or ceftazidime monotherapy for the treatment of infection in the newborn. Further studies are required to confirm these observations in neonates with proven infection.The ESPID Neonatal Sepsis Study Group: Recruitment >=50 patients included Prof. R. Dagan, Soroka Medical Centre, Beer-Sheva, Israel; Dr. I. Tessin, Hospital of Molndal, Molndal, Sweden; Dr. D. Harvey and Dr. J. de Louvois, Queen Charlotte's and Chelsea Hospital, London, UK; Dr. B. Trollfors and Dr. K. Thiringer, Ostra Sjukuset, Goteborg, Sweden; Dr. A. Valido, Maternidade, Dr. Alfredo Costa, Lisbon, Portugal; Dr. H. Baumer, Freedom Fields Hospital, Plymouth, UK: Prof. J. Brines and Dr. Diez, University of Valencia, Valencia, Spain; Dr. L. Benic, Dr. J. Kajfes Hospital, Zagreb, Yugoslavia; and Prof. J. Badoual, Hopital St. Vincent de Paul, Paris, France.Recruitment <50 patients included Prof. L. Corbeel, UZ Gasthuisberg, Leuven, Belgium; Prof. R. Roos, Univ.-Kinderklinik, Munich, FRG; Dr. D. Kafetzisa, University of Athens, Athens, Greece; Dr. S. Pedersen, Kolding Sykehus, Kolding, Denmark; and Prof. A. Columbo, Ospedali Riunuti di Bergamo, Bergamo, Italy.     

Increased whole blood chemiluminescence in patients with Shwachman syndrome: therapy trial with thiamine and α-tocopherol

Neutrophils purified from peripheral blood of patients with the Shwachman syndrome show enhanced chemiluminescence (CL) and depressed chemotaxis. Here we present data showing that the increased CL response can be demonstrated by using a whole blood CL assay. This assay is well-suited for studies in infants, because the blood sample volumes needed are small. Increase in CL was most distinct in the initial (1 min) activation induced by N-formyl-methionyl-leucyl-phenylalanine. The 1-min response is considered to derive from extracellular production of oxygen radicals. Such an extracellular oxygen radical production may render the patients susceptible to undue oxidant stress. We therefore treated the patients with two antioxidants, thiamine and -tocopherol, for 3 months. This supplementation, however, failed to exert any significant effect on either whole blood CL or migration of the patients' neutrophils under agarose.     

Severe hypoaldosteronism due to corticosterone methyl oxidase type II deficiency in two boys: metabolic and gas chromatography-mass spectrometry studies

Infection-triggered, life-threatening salt-loss and hyperkalaemia developed in two male infants with wasting, inappropriately low plasma aldosterone concentrations and elevated plasma renin activity. The presumptive diagnosis of a defective terminal step in aldosterone biosynthesis was made by the presence of large amounts of 11-dehydrotetrahydrocorticosterone and its 18-hydroxylated metabolite (18-OH-THA), free 18-hydroxycorticosterone (18-OH-B) and 18-hydroxytetra-hydrocorticosterone in the urine of both patients. The diagnosis of corticosterone methyl oxidase type II (CMO II) deficiency was confirmed by an elevated urinary 18-OH-THA to tetrahydroaldosterone ratio in one boy and by an elevated plasma 18-OH-B to aldosterone ratio in the other boy. Unknown steroids responsible for the salt-loss were not identified. Sodium supplementation but not short-term high dose oral 9-fluorcortisol (FF) normalized the hyponatraemia in one patient, in whom sodium (Na⁺)/potassium (K⁺) co-transport was decreased. Both patients eventually received long-term FF treatment to prevent impairment of longitudinal growth caused by chronic salt-loss. The diagnosis of CMO II deficiency should always be confirmed by elevated precursor-product ratios in urine or plasma, using radioimmunoassays with prior chromatographic separation. Metabolic studies as the short-term response of serum Na⁺ to high dose FF may not be helpful in differentiating aldosterone biosynthetic defects from endorgan resistance to mineralocorticoids.Dedicated to Professor Dr. Walter Teller, on the occasion of his 60th birthdayPresented in part at the 27th Annual Meeting of the European Society for Paediatric Endocrinology, Copenhagen, Denmark, June 1988     

Spastic paraplegia associated with addison's disease: Adult variant of adreno-leukodystrophy

Summary Clinical and pathological features of an adult variant of adreno-leukodystrophy (ALD) are presented. A male with clinical and laboratory signs of Addison's disease (AD) developed at age 22 a slowly progressing paraplegia with slight sensory deficits in both legs and bladder and sphincter dysfunctions; he died at age 24 in an AD crisis. Autopsy revealed hyperplasia of lymphatic tissues, lymphocytic infiltrates in various organs including the CNS and adrenocortical atrophy with prominence of large ballooned, sometimes bizarre and occasionally striated cortical cells. CNS lesions consisted in incomplete demyelination of long tracts of brain stem and spinal cord with accentuation in the pyramical tracts; in these areas, perivascular cuffs of epitheloid histiocytic cells contained a strongly PAS-positive non-sudanophilic material. Electron microscopy demonstrated massive storage of leaflet structures in perivascular histiocytes identical to the lamellar profiles previously described as specific for ALD. Some leaflets were found in close contact with compact lamellar arrays and with an electron-dense fingerprint material within astrocytes.In our case, the spastic paraplegia-AD syndrome which has been described previously in several clinical observations could be neuropathologically classified as an adult variant of ALD. Several differences to classical ALD occurring in young boys are stressed: the predominance of the endocrine disorder probably accounting for some of the perivascular lymphocytic infiltrates within the CNS; the absence of both clinical and pathological signs of diffuse cerebral involvement and the peculiar topistic pattern of CNS lesions and the very slow evolution of neurological signs paralleled by the absence of active sudanophilic demyelinating lesions. The possible mechanism of demyelination and the nature of the suggested metabolic defect in ALD are discussed. The ultrastructurally prominent leaflet structures may originate from myelin remnants, thus relating ALD to pathological storage of a myelin degradation product.

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Zusammenfassung Klinische und pathologische Befunde einer adulten Form der Adrenoleukodystrophie (ALD) werden dargestellt. Ein Patient mit klinischem Bild und Laboratoriumsbefunden der Addison-Krankheit (AD) entwickelte im Alter von 22 Jahren eine sehr langsam zunehmende Paraspastik mit geringer Hypaesthesie in beiden Beinen und Blasenund Mastdarmstörungen; er verstarb im Alter von 24 Jahren in einer AD-Krise. Bei der Autopsie fanden sich eine Hyperplasie des lymphatischen Apparats und lymphocytäre Infiltrate in verschiedenen Organen einschließlich des ZNS; beide Nebennieren waren atroph mit Hervortreten großer ballonierter, etwas bizarrer Rindenzellen mit gelegentlicher cytoplasmatischer Streifung. Im ZNS fanden sich pseudosystematische inkomplette Entmarkungen der langen Bahnen in Hirnstamm und Rückenmark mit Betonung der Pyramidenbahn, charakterisiert durch perivasale Manschetten epitheloider histiocytärer Zellen, die ein stark PAS-positives sudannegatives Material enthielten. Elektronenoptisch wurde eine massive Speicherung eines lamellären Materials in perivasalen Histiocyten nachgewiesen, welches mit den als spezifisch für die ALD angesehenen Einschlüssen übereinstimmte. Einige derartige Strukturen zeigten einen engen Zusammenhang mit kompakten Lamellenaggregaten und mit einem elektronendichten fingerprint-Material innerhalb von Astrocyten.In diesem Fall konnte das Paraplegie-AD-Syndrom, welches mehrfach bereits klinisch beschrieben worden war, aufgrund neuropathologischer Befunde als adulte Variante der ALD klassifiziert werden. Die Unterschiede dieser Form zur klassischen ALD, welche üblicherweise Knaben betrifft, werden hervorgehoben: das Überwiegen der endokrinen Symptomatik, was das Auftreten perivasaler Lymphocytensäume im ZNS zum Teil bedingen dürfte; das Fehlen klinischer und pathologischer Hinweise auf diffuse Beteiligung des Großhirns und die spezielle Topik der ZNS-Läsionen und die geringe Progredienz der neurologischen Symptomatik, welche im Einklang mit dem Fehlen florider sudanophiler Entmarkungsvorgänge steht. Der Mechanismus der Entmarkung und die Art der vermuteten metabolischen Störung bei der ALD werden diskutiert. Die elektronenoptisch charakteristischen lamellären Strukturen könnten aus dem Myelinabbau stammen, und damit könnte bei der ALD eine pathologische Speicherung eines Myelinabbauprodukts vorliegen.

     

胰腺癌的临床表现

胰腺的临床表现因病变而异。腹痛、黄疸及体重减轻是胰腺癌的主要临床表现。部分病人同时可表现为发热、焦虑、抑郁、胆囊肿大及血栓性静脉炎等。     

头颈部坏死性筋膜炎7例临床分析

目的：探讨头颈部坏死性筋膜炎的病因、临床表现、诊断和治疗，加强对这一罕见疾病的认识。方法：回顾分析1992-2002年10年收治的7例头颈部坏死性筋膜炎的病例资料并复习文献。结果：7例全部行积极的内科保守治疗和外科处理（包括局部切开引流、清创术和气管切开术），其中2例死亡。结论：临床上对该病应有足够的认识，以期早期诊断。及时有效的外科处理是治疗成功的关键。     

国际海员疾病发生与治疗的社会因素浅析

从３０００例国际海员疾病发生率原因着手,结合国际海员群体工作游动性和成员多国性的特点,从社会医学和心理医学角度,分析国际海员健康工作中存在的问题,并对如何实现国第员“人人享有卫生保健”提出初步见解。国际海员群体的特殊性及他们的健康问题值得中国及国际航海医学界和社会医学界的关注。     

N-甲基-D-天门冬氨酸受体及其调控的钙内流在大鼠感染性脑损伤中的变化

为探讨Ｎ－甲基－Ｄ－天门冬氨酸（ＮＭＤＡ）受体及其调控的钙内流在感染性脑损伤发病机制中的作用，采用Ｆｕｒａ－２／Ａｍ荧光法检测大鼠大脑皮质突触体内游离钙浓度（［Ｃａ＋＋］ｉ）。结果表明，注射百日咳杆菌组的［Ｃａ＋＋］ｉ较对照组显著增加（Ｐ均＜０．０１），并与注菌时间呈正相关关系（４小时ｖｓ０．５小时和２４小时ｖｓ４小时，Ｐ＜０．０５和＜０．０１）。ＮＭＤＡ受体的非竞争性拮抗剂ＭＫ－８０１预处理组（ＭＢＰ）的［Ｃａ＋＋］ｉ、脑含水量和伊文思蓝含量均较注菌组显著减少（Ｆ值分别为７２．２５、１６．８９、１４．３６，Ｐ＜０．０１和＜０．０５），并以２４小时［Ｃａ＋＋］ｉ减少最为明显（Ｐ＜０．０１）。提示ＮＭＤＡ受体调控的神经元内钙超载在感染性脑损伤、尤其在迟发性脑损伤的发病机制中起着重要作用。     

耳蜗急性纯音损伤后下丘及耳蜗核快速功能重组

实验比较高强度纯音损伤耳蜗局部区域前后，耳蜗背核及下丘接近损伤区边缘的神经元反应特性的改变。致损纯音的频率高于神经元的特征频率，且位于其兴奋区以外，所以不影响其兴奋性输入。结果发现此种纯音损伤在逾半数的神经元产生不同程度的去抑制效应，提示皮层的功能重组可能部分地起源于低位中枢的功能改变，下丘和耳蜗背核的抑制性神经网络具有相当程度的侧抑制组分。