<正>例1,女性,22岁,学生。患银屑病服用含铅、汞中药秘方5年,双眼视力逐渐下降,双眼失明1个月。尿铅0.308 mg/L(正常<0.08 mg/L)。驱铅治疗后,视力:右眼:指数/20cm,左眼:手动/20cm(图1)。

Objective. To study myocardial and lung injuries initiated by hydrogen sulfide, and evaluate the role and effectiveness of normobaric and hyperbaric oxygen (HBO) treatment in rats. Methods. One hundred healthy male Wistar rats were randomly divided into five groups: A: Normal control group (no H2S); B: H2S-exposed group; C: H2S+33% oxygen treatment group; D: H2S+50% oxygen treatment group; E: H2S+HBO group. The rats in groups C, D and E were exposed to H2S in an exposure chamber (1 m3) and were made to inhale 300 ppm hydrogen sulfide for 60 min, and then they were subjected to normobaric or HBO therapy. Normobaric oxygen was at concentrations of 33% or 50%, HBO was for 100 min including compression and decompression; the rats in group A inhaled air under the same conditions. Blood was sampled immediately after the experiment for analysis of arterial blood gases, myocardial enzymes and cardiac troponin I. Lung was rapidly removed to be made into tissue homogenates and then cytochrome c oxidase activity was measured; myocardial and lung ultrastructural changes were observed by electron microscopy. Results. Arterial blood gases: partial pressure of O2 (mmHg) (Group A, 97.6 ± 8.38; B, 76.5 ± 6.95*; C, 83.2 ± 2.66*; D, 86.20 ± 10.75*; E, 93.50 ± 4.97: *p < 0.01 compared to group A) was significantly lower than that in group in all but HBO rats. For myocardial enzymes and cardiac troponin I every parameter in groups B and C was significantly higher than that in group A (p<0.01),with no difference in D and E. Cytochrome c oxidase activity (u/mg) of lung tissue was reduced compared to group A after all treatments (A, 1.76 ± 0.02; B, 0.36 ± 0.04; C, 0.50 ± 0.12; D, 0.56 ± 0.07; E, 0.68 ± 0.05 (A vs. B p < 0.01; B vs. C,D,E p < 0.05 or p < 0.01 ), with a graded effect of oxygen dose in C, D and E. Pathological changes: (1) Myocardium – Mitochondrial swelling and autolysis with blurred or broken cristae was observed in the myocardium of H2S-exposed group; in group E, mitochondrial structure was basically normal, and clear cristae were found. (2) Lung tissue – In H2S-exposed group, alveolar epithelial cells disappeared, vacuolization of the organelle occurred, nuclear membrane was irregular and marginal condensation of heterochromatin was present; nucleus showed relatively normal morphology in group E, although some vacuoles still persisted within them. Conclusions. HBO therapy can effectively improve arterial oxygen partial pressure, and significantly reduce myocardial damage, as well as potentially relieve lung injury in this model. Further work in humans appears warranted.

Toxic nephropathy is the common disease in clinical practice,however its clinical features and prognosis are quite inconsistent owing to the different origins of disease and pathogenesis.There is only abnormal urine change in the mild patients,while in severe cases,acute renal failure and dead may occur if no timely medical treatment.In this paper,the etiology and clinical features of toxic nephropathy were reviewed according to the case reports published in journals.

目的 探讨36例急性氰化物中毒病例的发生及救治情况.方法 通过病例调查表的方法采集临床诊断观察的或尚未报道的中毒病例资料,应用相对数进行相关数据的统计分析.结果 36例急性中毒病例中,职业性中毒33例,以气道吸入为主要接触方式.出现意识障碍、抽搐、皮肤黏膜鲜红色改变等症状的患者病死率较高,为20.00%～53.85%.中毒后有关实验室检查很不完善,36例患者均未进行全血氰离子浓度的检测,7例死亡患者均未接受过解毒剂治疗.结论 急性氰化物中毒后临床潜伏期与接触方式及氰化物浓度有关,吸入高浓度者,发病快;表现为意识障碍、抽搐或皮肤黏膜颜色改变者临床病死率较高.临床实验室检测指标尚不完善,治疗仍以对症支持治疗为主,临床病死率仍高.

OBJECTIVE:To evaluate the effects of different oxygen therapy technique (different concentrations of normobaric oxygen and the hyperbaric oxygen) on the ultrastructure of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication.METHODS:One hundred healthy male Wistar rats were randomly divided into five groups: normal control group (A), poisoned group (B), oxygen therapy group (C), oxygen therapy group (D) and oxygen therapy group (E). After the exposure to 300 ppm H2S for 60 min in a static exposure tank (1 m3), the rats were treated with oxygen therapy, C, D and E groups were given 33% oxygen, 50% oxygen of atmospheric oxygen and hyperbaric oxygen therapy for 100 min, respectively. The rats in normal control group inhaled air under the same environment. After exposure and therapy, the tissues of lung, heart and liver were observed under light microscope and electron microscope.RESULTS:The results of light microscope examination showed that the broken and not well aligned cardiac myofilaments, cytoplasmic edema and pyknosis could be seen in group B. The well aligned and clear cardiac myofilaments appeared in group C, D and E. The alveolar hemorrhage, edema and inflammatory cells exudation could not be seen in group A. Alveolar epithelial cell edema, unsmooth alveolar edge and alveolar inflammatory cells exudation could be found in group B. The unsmooth alveolar septal borders and pulmonary edema could be seen occasionally in group C and D, the alveolar inflammatory cells exudation could not be seen in group E. The regular hepatic boards and the uniform hepatic cellular nuclei were found in group A. The disordered hepatic boards, widened cellular gaps and cytoplasmic edema could be seen occasionally in group B. The irregular hepatic boards and ballooning degeneration could be seen in group C and D. The regular hepatic boards and uniform cytoplasm could be found in group E. The results of electron microscope examination indicated that the mitochondrial swelling, autolyzing, fuzzy and breakage of myocardial cells were observed in group B; the clear mitochondrial structure appeared in group E. The apoptosis and organelle vacuole of alveolar epithelial cells could be observed in group B. The relatively normal nuclei of alveolar epithelial cells could be seen in group E. The lax cytoplast structure of hepatocytes, unclear nuclear membrane, lumped chromatin, slightly swelled mitochondria and phagosomes were observed in group B. However, no improved change was observed in group C, D and E.CONCLUSION:Hydrogen sulfide could induce the extensive and severe damage of myocardial mitochondria, alveolar epithelial cells and hepatocytes, the oxygen therapy in good time could reduce significantly the myocardial injury, and improve the lung injury to some extent. High-pressure oxygen therapy is better than the normobaric oxygen therapy.

The toxic mechanism of hydrogen sulfide(H2S) is not only inhibiting cytochrome oxidase but also inhibitingmonoamine oxidase and generating free radicals etc..Therefore,oxygen therapy should be very important and given as soon aspossible for H2S poisoning;hyperbaric oxygen therapy for acute hypoxic ischemic brain damage is reasonable and should also begiven early and appropriately.Additionally,evidences showed,that hydroxocobalamin(vitamin B12a) could work as an anti-dote against H2S poisoning as well.

A 46-year-old man received one Chinese herbal medicine pill prepared by a clinic ( each pill contained approximately 21 mg of calomel ) twice daily and he took 13 pills in total. On day 7,the patient developed dizziness,chest distress,and mouth ulcer accompanied by fever and generalized pain. His symptoms exacerbated and he was hospitalized. His temperature was 37.2℃. Physical examination showed congested erythema,which faded when pressed,in both face and trunk skin and oral-mucosal congestion,as well as gingival swelling. Laboratory tests revealed the following levels:blood mercury 0.029 mg/L,urine mercury 39.565 μmol/molCr,ALT 61 U/L,AST 28 U/L,BUN 7.42 mmol/L,SCr 67.0 μmol/L,blood β2-microglobulin 1 549.20 ng/mL,urine β2-microglobulin 167.0 ng/mL. Unithiol therapy was given. His condition improved,and urine mercury tended to normal. On reexamination,his liver functions,blood and urine β2-microglobulin levels returned to within normal range.

硫化氢（H2S）是具有致死性和危害性的环境和工业毒物。在我国，急性H2S中毒占职业性急性中毒的第二位，仅次于CO中毒。积极供氧对于急性H2S中毒者的治疗很重要。本研究评价常压下不同浓度吸氧及高压氧（HBO）对大鼠急性H2S中毒的治疗效果。

国内使用雄黄等含砷中药治疗银屑病等顽疾在民间十分常见,但由于缺乏用药规范,近年来含砷中药的内服与外用不当所导致的慢性砷中毒屡有发生,自2001年3月至2008年3月我科诊治慢性药源性砷中毒患者32例,以下就其临床特点进行分析.

目的分析急性三氯丙烷(TCP)中毒病例,了解其临床特点。方法对9例急性TCP中毒病例的发病过程、临床表现、实验室检查、诊断治疗、发病特点及事故原因进行分析。结果TCP可从皮肤、呼吸道吸收入体内,短时间、高浓度接触可造成急性肝脏损害。结论TCP中毒病人可采取予以保肝、利胆、降酶治疗,对于重度中毒者可予以血浆置换,临床效果显著。

The traditional Chinese medicine Xiaoerqizhen pills,which contain realgar and cinnabar,are used for treatment of acute infantile convulsion and constipation.This paper reports that two adults developed chronic arsenic poisoning after prolonged use of high-dose Xiaoerqizhen pills.Patient 1,a 36-year-old woman,received 40～80 Xiaoerqizhen pills once daily for three years for constipation.Two to three months after starting Xiaoerqizhen pills use,she developed fatigue,anorexia,and dark skin pigmentation on her abdomen.In recent one year,she developed dizziness,headache,insomnia,and numbness of her limb ends.After admission,an examination showed pigmentation on his face,trunk,and extremities,pachyderma on palms and soles.Her blood arsenic level was 7.3 μg/L,and her urine arsenic level was 0.117 mg/L.Chronic arsenic poisoning was diagnosed.After completing three courses of therapy with sodium dimercaptopropane sulfonate,her symptoms markedly improved.Patient 2,a 40-year-old man,received 20～80 Xiaoerqizhen pills one to two times daily for 7 years for constipation.During the treatment,he gradually presented with fatigue,anorexia,nausea,abdominal distension,pigmentation over his entire body,severe keratodermia,and numbness of extremities,hepatoemegaly,splenomegaly,and anemia.His urine arsenic level was 4.28 mg/L.He was diagnosed with chronic arsenic poisoning.After completing five courses of therapy with sodium dimercaptopropane sulfonate,his symptoms were markedly improved and he was discharged.

1例5月龄女婴因患湿疹外敷“一扫光”药膏[含红丹（Pb3O4）、铅粉及其他矿物类中药]。治疗10d后,出现精神萎靡、烦躁、轻度贫血等症状。实验室检查显示：ALT 61 U/L,AST 81 U/L,血铅342.3μg/L。疑为急性铅中毒。停用“一扫光”药膏,给予二巯丁二酸及对症治疗,症状好转。之后,给予甲硫氨酸治疗。半月后,血铅及其他实验室指标均恢复正常。

OBJECTIVE:To probe into the clinical features and the rescue of pneumoconiosis with pulmonary thromboembolism (PTE). METHODS:26 patients with pneumoconiosis and PTE, male 16, female 10, were collected from June 2002 to June 2006 and 42 patients only with pneumoconiosis served as control. Tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), thrombomodulin (TM), plasma protein S, C (Ps, Pc), homocysteine (Hcy) were measured by the methods of ILISA, and antithrombin (AT-III) by chromo substrate method before and after the treatment of heparin. RESULTS:The average age of patients with pneumoconiosis and PTE was 66.0 +/- 11.9 years old. The number of patients with pneumoconiosis of degree 1, 2, 3 was 3, 16 and 7 respectively. After anticoagulant therapy of heparin, 23 were well improved, and 3 died of acute respiratory failure. Dyspnea, chest pain, hemoptysis, syncope were the conspicuous symptoms. The levels of D-Dimer (0.63 +/- 0.14 mg/L), TM (5.02 +/- 1.24 microg/L) were significantly higher than those of the control (P < 0.05), and significantly lower again after the treatment (P < 0.05). The level of AT-III (96.68 +/- 7.23%) was significantly lower than that of the control, and higher again after the treatment (P < 0.05). CONCLUSION:PTE is often developed in the elder patients with high degree of pneumoconiosis (> or = 2 degree). Clinical features are complicated and non-specific, with the high negative ratio of D-Dimer (7/26), high mortality and high complications of anticoagulant therapy.

Human saliva offers a unique noninvasive approach for populational study. Purposes of this study were to investigate the feasibility of using saliva manganese (Mn) concentration as a biomarker of Mn exposure among career welders and to study the variations of Mn, copper (Cu), zinc (Zn), cadmium (Cd), and lead (Pb) in saliva as affected by the welding profession. Forty-nine male welders, of whom 28 were in the low exposed group and 21 in the high exposed group, were recruited. Control subjects were 33 military soldiers without metal exposure. Ambient Mn levels in breathing zones were 0.01, 0.24 and 2.21mg/m(3) for control, low, and high exposed groups, respectively. Saliva samples were collected to quantify metals by inductive coupled plasma mass spectrometer (ICP-MS). Saliva concentrations of Mn and Cu were significantly higher in welders than in controls (p<0.01); the variation in saliva levels appeared likely to be associated with airborne Mn levels among study populations. Saliva levels of Zn were significantly lower in welders than in controls (p<0.05), while Cd and Pb levels in saliva were unchanged. Significant associations were observed between saliva and serum for Mn (r=0.575, p<0.05) and Cu (r=0.50, p<0.05). Moreover, saliva Mn concentrations were higher among welders with 5-10years of employment than those with less than 5years of employment. Linear regression analysis revealed a significant correlation between saliva Mn and Cu and between saliva Mn and Zn. Taken together, these data suggest that Mn concentrations in saliva appear reflective of welders' exposure to airborne Mn and their years of welding experience, respectively. Elevated Mn levels among welders may alter the homeostasis of Cu and Zn.

患者女,25岁.因阵发性腹痛、呕吐伴贫血1个月入院.入院前曾多次发作腹痛,伴腹胀、干呕、排气、排便减少收住某医院消化内科.实验室检查:RBC 3.32×1012/L、WBC 9.44×102/L、Hb 78～82 g/L、AST 65 U/L、ALT150 U/L、血清铁四项、叶酸均为正常、溶血全套、CD55、CD59、尿Rous试验均阴性.

目的 探讨唾液锰是否可作为锰接触的生物检测指标.方法 选择电焊锰作业工人49名,其中高浓度接触组21人、低浓度接触组28人,采用电感耦合等离子体质谱法(ICP-MS)测定唾液锰和血清锰,用石墨炉原子吸收分光光度法测定尿锰.结果 高浓度接触组的车间空气锰浓度达2.21 mg/m3,低浓度接触组为0.24 mg/m3.接触组的唾液锰和血清锰分别为(4.45±2.17)、(4.64±1.30)μg/L,均明显高于对照组[分别为(3.04±1.40)、(2.70±1.50)μg/L],差异有统计学意义(P＜0.01),尿锰略高于对照组,但差异无统计学意义(P＞0.05).高浓度接触组的唾液锰和血清锰升高者分别为85.71%和100.00%,升高均值为3.04和3.00μg/L;低浓度接触组的唾液锰和血清锰升高者为71.43%和89.29%,升高均值为1.04和1.40 μg/L.唾液锰和血清锰未见伴随工龄的升高趋势.结论 唾液锰与血清锰测定均可反映工人的近期锰接触状况,尿锰的变化不敏感.唾液锰测定方便、准确,可作为新的生物检测指标。

Four patients(3 men and 1woman aged 19～51 years)developed acute thallium poisoning.The clinical presentations were the triad of gastroenteritis,polyneuropathy,and alopecia.Their urine thallium concentration was 885～7 143 μg/L.The four patients were treated with Prussian blue 250 mg/kg daily,and hemoperfusion was added to their regimen in three of them.Later,the patient's symptoms were relieved and their urine thallium concentration decreased to 0.01～216 μg/L.

Introduction. Exposure to arsine gas can cause fatal hemolysis and multiorgan damage. Whole blood exchange transfusion and hemodialysis have been recommended to treat severe acute arsine poisoning, but are associated with significant complications and sub-optimal outcomes. Plasma exchange is another method of blood purification technique but there are no data on its use in acute arsine poisoning. This retrospective study evaluated the clinical and effects and arsenic clearance from the use of plasma exchange treatment of patients with acute arsine poisoning. Methods. Data from patients with severe acute arsine poisoning, treated with plasma exchange from December 2000 to December 2005 were collected and analyzed. Measured laboratory factors, performed before and after plasma exchange treatment included routine biochemistry and hematology tests as well as arsenic concentrations in blood, urine, and discarded plasma. Results. During the study period, 12 patients with severe acute arsine poisoning were treated with plasma exchange. Plasma exchange was performed one or two times on each patient, during which the replacement fluid was fresh frozen plasma (total volume ranged from 1400 to 4000 mL). The range of concentrations of arsenic in discarded plasma was 27.7 to 88.7 mg/L and the range of total arsenic removed by plasma exchange was 55.4 to 177.4 mg. Plasma exchange appears to rapidly terminate arsine-induced hemolysis and favorably modify damage to the kidneys and other organs. Laboratory factors that showed significant association with treatment response were creatine kinase, lactate dehydrogenase, blood urea nitrogen, total bilirubin, and heart-related enzymes. All patients recovered from the poisoning and were in good condition at a 2 to 3 months follow-up. Conclusions. Plasma exchange appears to be an effective treatment intervention for patients with severe acute arsine poisoning. It is suggested that it be used as early as possible.

Thallium is a very toxic heavy metal,the lethal dose for adults is approximately 12 mg/kg.The exact mechanism of thallium poisoning is unclear;however,it may competitively inhibit potassium action,bind to sulfydryl group of proteins and enzymes,and form insoluble complexes with riboflavin.The triad of gastroenteritis,polyneuralgia,and alopecia is regard as the classic syndrome of thallium poisoning.Gastrointestinal symptoms,such as nausea,vomiting,and abdominal pain,occur early.Neurologic symptoms are pain and paresthesias of the lower extremities,convulsions,and coma.Hair loss may appear within 1 to 3 weeks after thallium poisoning.Other signs and symptoms are skin eruptions,renal injury,tachycardia and visual disturbances,etc.Death may result from respiratory failure.A 24-hours urine thallium concentration is the most accurate way to assess thallium poisoning.If urine thallium concentration is more than 0.3 mg/L,it is of diagnostic significance.Differentiation of thallium toxicity from Guilliam-Barre syndrome,lead poisoning,and arsenic toxicity should be made.Oral thallium poisoning may be treated with activated charcoal,magnesium sulfate,Prussian blue,etc.The usual dose of Prussian blue is 250 mg/kg daily,given in 4 divided doses by mouth.Hemoperfusion has been reported to be effective in eliminating absorbed thallium.

例1患者男,70岁,1952年参加工作,某制药厂化学合成车间操作工。1955年曾因短时间吸入高浓度氯气确诊为急性氯气中毒并发肺水肿。1988年后,出现气喘、憋气、胸闷,且症状逐渐加重,日常生活中稍闻到异味如花露水、油烟