老年脑梗死患者急性期瘦素动态测定的意义

目的探讨老年脑梗死患者急性期瘦素水平的动态变化及其与病情严重性之间的关系。方法 140例老年脑梗死患者,在发病后24 h内入院,分别在入院后第1、3、7天抽取空腹静脉血3 ml,采用放射免疫测定方法动态检测血清瘦素水平,采用欧洲卒中神经功能缺损评分量表（ESS）评价脑梗死的严重程度。同时检测70例健康体检者作为正常对照组。结果老年脑梗死组血清瘦素水平在发病后第1、3、7天均显著高于对照组（P均〈0.01）,ESS评分与血清瘦素水平无明显相关性（r=0.143,P〉0.05）。结论老年脑梗死患者存在高瘦素血症和瘦素抵抗,瘦素水平增高是老年脑梗死的危险标志。     

The role of erythrocytapheresis in secondary erythrocytosis therapy

In chronic respiratory insufficiency secondary erythrocytosis (SPC), causing pulmonary hypertension and dx ventricular insufficiency, is often noticed. An alternative therapy to phlebotomy for SPC is isovolemic large volume erythrocytapheresis performed with cell separator (CSE) in order to quickly remove a large volume of red blood cells (RBC) while saving plasma proteins and clotting factors. In order to evaluate the efficiency and safety of CSE in SPC we reported a retrospective analysis of our experience with 61 SPC patients: from April 1996 to May 1998 we performed 208 CSE using Haemonetics MCS3P (TAE protocol). Before every apheresis procedure we verified Hb (in median 18.8 g/dl), Ht (in median 58.4%), viscometry, coagulation test, EGA, PFR and ECG. 11 patients were treated with 1 CSE, 12 with 3, 29 with 4 and 9 with 5. The mean volume of RBC removed was 576 ml (range 426-800); Hb post CSE averaged 14.4 g/dl and Ht post CSE averaged 42.7%; hematic viscosity post CSE was significantly reduced while tissue oxygen tension increased: the improvement of symptomatology and hematochemical parameters was maintained on the average for 6.5 months. All the procedures were well tolerated and light side effects (paresthesias citrate-depending in 27 apheresis) were easily controlled. CSE, compared to phlebotomy, has the advantage of selectively removing RBC without loss of clotting factors, platelets and plasma proteins. Although CSE has relatively high costs we noticed a decrease of hospital recurrence (about 50-65%) in SPC patients treated with apheresis.     

A case of vertebral artery dissection associated with morning blood pressure surge.

We report a case of a middle-aged man who suffered a cerebral infarction resulting from dissection of a vertebral artery associated with morning blood pressure surge. A 56-year-old man was transferred to our hospital with dizziness and vomiting in the early morning on a cold day in winter. He reported that he had been standing in front of the sink after bathing when he suddenly felt dizzy and fell down. He did not lose consciousness, and by the time he reached the hospital by ambulance, his dizziness had subsided, but he complained of severe headache and vomited 3 times. On admission, he was alert, and there were no neurological or radiological abnormalities (CT, MR angiography) in the brain. However, infarction in the left cerebellar hemisphere was detected by brain MRI on the 5th day of hospitalization. String sign of the left vertebral artery was noted by angiography, confirming the diagnosis of dissection of the left vertebral artery. Ambulatory blood pressure monitoring was performed after discharge. Although the mean 24-h blood pressure was in the normal range, a marked morning blood pressure rise was observed. We speculated that the acute rise of blood pressure in the early morning might have contributed to the dissection of the vertebral artery.     

Acute myocardial infarction with variable clinical manifestations: probable catastrophic primary antiphospholipid antibody syndrome: a case report

A 62-year-old diabetic man was admitted to our hospital because of acute myocardial infarction. Emergent coronary angiography showed multiple thromboembolic occlusions in the distal circumflex and anterior descending arteries. For the first 2 weeks of hospitalization, he suffered multiple organ manifestations including the gastrointestinal, central nervous, renal and respiratory systems. The anticardiolipin beta2GP1 complex antibody titer on the 15th day was as high as 27.2 U/l (normal value < 3.5). These clinical manifestations and laboratory findings suggested catastrophic antiphospholipid antibody syndrome. He was discharged on the 83rd day with anticoagulant therapy and regular hemodialysis. Acute myocardial infarction is rare as the initial manifestation of catastrophic antiphospholipid antibody syndrome.     

Delayed manifestation and slow progression of cerebral infarction caused by polycythemia rubra vera

BACKGROUND: Polycythemia rubra vera is often found after the manifestation of cerebral infarction, though the pathogenesis is still controversial. We present a case of cerebral infarction secondary to polycythemia rubra vera, which presented a slow expansion on magnetic resonance imaging despite severe hemiplegia. This case suggests a possible mechanism for development of cerebral infarction in polycythemia rubra vera. METHODS: This case report was conducted in a university hospital. Magnetic resonance imaging and diffusion-weighted imaging were performed to assess the evolution of infarction, and the total blood volume and cerebral blood flow were determined with the use of isotopes, Cr and Tc, respectively. Phlebotomy was performed, but intervention was not applicable. The manual muscle test and sensory disturbance were assessed by the same physiotherapist throughout the clinical course. RESULTS: A 64-year-old male patient with polycythemia rubra vera had a cerebral infarction. A subtle change was observed on CT scan on the third day after the onset of infarction, and a small signal was demonstrated on magnetic resonance imaging on the fourth day. The cerebral infarction expanded slowly in size and reached a maximum on day 24. A diagnosis of cerebral infarction secondary to polycythemia rubra vera was made, and treatment by phlebotomy, hydration, and hydroxyurea was begun. Though the hemiplegia remained, he became ambulatory with a brace, as do patients with atherosclerotic infarction. CONCLUSIONS: It is suggested that the delayed manifestation and slow expansion of cerebral infarction caused by elevated hematocrit might be derived from a pathogenesis different from atherosclerotic infarction.     

Lethal pulmonary hemorrhage caused by Stenotrophomonas maltophilia pneumonia in a patient with acute myeloid leukemia

A 63-year-old man had been treated with intensive chemotherapy for acute myeloid leukemia. On the 49th hospital day, he had febrile neutropenia after the second course of induction chemotherapy. On the 53 rd hospital day, he presented with hemoptysis and developed acute respiratory failure requiring ventilator support within several hours. On the 54th hospital day, the patient died with hemorrhagic respiratory infection. Stenotrophomonas maltophilia was detected in bacterial cultures of his blood, bronchoalveolar lavage, and sputum. To our knowledge, nine cases of fatal hemorrhagic pneumonia caused by S. maltophilia have been reported in the literature. All the patients had hematological neoplasms and were severely neutropenic after one or two intensive chemotherapy regimens. They died shortly (within 3 days) after the onset of the hemorrhagic pneumonia. Management of the infection caused by S. maltophilia is hampered by high-level intrinsic resistance to multiple antibiotics and the increasing occurrence of acquired resistance to co-trimoxazole and fluoroquinolones. It would be important to keep in mind that hemorrhagic respiratory infection caused by S. maltophilia may lead to a fulminant and lethal course in severely neutropenic patients with hematological neoplasms and to recognize which antibiotic agents are more sensitive to S. maltophilia in each institution.     

Report of a case with fulminant hepatitis A associated with acute renal failure

A 34-year-old male presented with fulminant hepatitis A associated with acute renal failure. The patient was admitted four days after flu-like symptoms developed. Physical examination was unremarkable except for icteric sclerae. Laboratory studies showed SGOT 10719 U/l, SGPT 5780 U/l, prothrombin time 22%, BUN 25.5 mg/dl, and creatinine 2 mg/dl. Serum complements were within normal ranges, and circulating immune complexes were not detected. Anti-HAV IgM was positive. He developed hepatic coma on the fourth hospital day, and his renal function deteriorated progressively. He was treated with hemodialysis, but there was no improvement in consciousness. Although acute liver failure improved, he died on the 74th hospital day of subendocardial infarction. Autopsy examination showed acute renal tubular necrosis. The liver was enlarged and was in the residual stage of acute hepatitis without submassive necrosis. The development of fulminant hepatitis in hepatitis A has been rare, but in recent years acute renal failure in hepatitis A has been reported. Although the mechanisms responsible for renal failure in liver diseases are uncertain but could be multifactorial, immune complex-mediated nephritis and/or endotoxemia have been considered.     

Acquired hemophilia A in a patient with essential thrombocythemia

A 69-year-old woman with essential thrombocythemia (ET) developed giant ecchymosis, and she was admitted to hospital. Marked anemia (Hb 8.1 g/dl) accompanied by a prolonged activated partial thromboplastin time (89.6 s) was observed, and she received red blood cells (RBC) and fresh frozen plasma (FFP). On day 2 after admission, consciousness disturbance suddenly occurred, whereas computed tomography of the brain showed no evidence of bleeding. As the ecchymosis progressed, she developed shock. Although RBC and FFP transfusions were administered, she developed multi-organ failure and died 48 h after admission. Low factor VIII activity (<1%) accompanied by factor VIII inhibitor (17 Bethesda units) was found after her death. An autopsy revealed cerebral infarction without cerebral herniation. To date, acquired hemophilia A accompanying ET has been described in only one other patient. Although acquired factor VIII inhibitor is a rare disease, it should be tested for in ET patients with marked hemorrhagic tendency.     

急性脑缺血患者血浆NSE水平动态观察意义

目的：研究缺血性脑卒中患者血浆神经元特异性烯醇酶（Neuron-specific enolase,NSE)的变化及与预后的关系。方法：病例组50例,正常对照组30例。患者分别于入院24小时内,第2天至第7天连续采集血标本。血浆NSE测定采用酶联免疫分析方法,神经功能缺损评定按斯堪的纳维亚卒中量表（SSS）标准进行。结果：病例组3天内血浆NSE明显高于对照组（P＜0．01）。NSE 变化是一个动态变化过程,预后恶化组血浆NSE7天后仍明显高干预良好组（P＜0．01）。结论：脑缺血早期NSE血浆明显升高,NSE的动态变化反映了缺血后神经元的损伤是一个动态变化过程,7－10天血浆NSE居高不下者预后差。     

Acute promyelocytic leukemia accompanied by retinoic acid syndrome with complications of acute myocardial infarction and cerebral infarction during treatment with all-trans retinoic acid

A 71-year-old man visited our hospital complaining of fever and a bleeding tendency. The peripheral blood WBC count was 10,400/microliter with 90% promyelocytes. The bone marrow was hypercellular with 88% promyelocytes. Disseminated intravascular coagulation was recognized. The patient was diagnosed as having acute promyelocytic leukemia and was treated with daily oral administration of all-trans retionic acid (ATRA) (45 mg/m2/day) and cytarabine (160 mg/day, intravenous drip infusion for the initial five days). The ATRA treatment induced leukemic cells to undergo mature myeloid differentiation. On day 24 after the start of treatment, the WBC count rapidly increased and acute myocardial infarction appeared, with consciousness disturbance and bilateral Babinski reflex appearing three hours later. Magnetic resonance imaging showed a fresh lacunar infarction of the right lenticular nucleus, and serum levels of IL-6 and PAI-1 were found to be elevated at the onset of infarction. Since there was a possibility that the retinoic acid syndrome (RAS) might have helped bring about the infarctions, we stopped the ATRA treatment and started administration of methyl-prednisolone (500 mg/body/day for 3 days) and gabexate mesilate. The WBC count decreased immediately and the consciousness disturbance improved. In this case, ATRA treatment might have initiated the RAS and resulted in some endothelial damage, thus causing the infarctions.     

Fulminant autoimmune hemolytic anemia with multiple organ failure

We report a rare case of fulminant autoimmune hemolytic anemia (AIHA) with multiple organ failure (MOF). A 40-year-old man was emergently admitted to our hospital because of conscious disturbance and jaundice. The peripheral blood revealed RBC 68 x 10(4)/microliter, Hb 3.5 g/dl, Ht 8.9%, Ret 30% (20,400/microliter), WBC 20,300/microliter, Plts 16.9 x 10(4)/microliter, indirect bilirubin 9.4 mg/dl. Both direct and indirect Coombs test were positive and the IgG autoantibody was identified. Bone marrow aspiration revealed hypercellularity with increased megakaryocytes and erythroid hyperplasia. The patient was diagnosed as having idiopathic warm type of AIHA and the therapy was started with prednisolone 80 mg/day from the first day of admission but hemolysis with reticulocytopenia was so rapidly progressive that he was in acutely life-threatening state and MOF (acute renal failure, adult respiratory distress syndrome, congestive heart failure, liver dysfunction, rhabdomyolysis) appeared on the third hospital day. Plasma exchange therapy and hemodialysis were started and high dose methylprednisolone was given soon after rapid administration of sufficient blood transfusion. Dramatic improvement of hemolysis was noted and MOF was controlled after starting these therapies, but he died of exacerbation of MOF probably due to sepsis 40 days later.     

Neurally mediated syncope with significant cardiac arrest and asymptomatic multiple cerebral infarctions: a case report

A 32-year-old man had suffered episodes of loss of consciousness since childhood. He was admitted to another hospital because of three syncopal episodes in one day. He was referred to our hospital because of asymptomatic multiple lacunae indicating cerebral infarction on magnetic resonance imaging. He lost consciousness with convulsion followed by a 70-second interval of cardiac arrest during blood sampling. He reported the onset of his usual prodromal symptoms after 1 min in the 80 degrees head-up tilt position. He lost consciousness 2 min after returning to the supine position. Electrocardiography demonstrated a 10-second interval of cardiac arrest. Magnetic resonance angiography, carotid arterial echography, brain perfusion scintigraphy, and laboratory chemistry and hematology examinations identified no significant findings. Cerebral infarction had occurred in watershed areas, so hemodynamic change during cardiac arrest may be the main cause of the infarctions. He suffered no further syncopal or presyncopal episodes after implantation of a DDD pacing system.     

丹红注射液治疗急性脑梗死的疗效观察及对血液流变学和D-二聚体定量的影响

目的探讨丹红注射液治疗急性脑梗死的临床疗效及对血液流变学和D-二聚体定量的影响。方法将我院2010年6月—2011年10月收治的急性脑梗死患者80例,随机分为治疗组和对照组,各40例。治疗组在常规治疗的基础上给予丹红注射液30ml静脉滴注,1次/d;对照组给予丹参注射液20ml静脉滴注,1次/d,两组均治疗14d。观察两组临床疗效、治疗后血液流变学、D-二聚体定量。结果治疗后,治疗组的总有效率为92.5%,与对照组的75.0%比较,差异有统计学意义(P<0.05);治疗前后两组血浆黏度、纤维蛋白原浓度、D-二聚体定量均下降,与对照组比较,差异有统计学意义(P<0.05)。结论丹红注射液治疗急性脑梗死临床疗效确切,使用安全,值得临床推广。     

21例老年人基底动脉尖综合征临床及CT分析

目的 探讨老年人基底动脉尖综合征(TOBS)的临床特征、头颅CT表现，以加深对该病的认识，避免误诊。方法 对21例60岁以上老年TOBS患者的临床资料进行分析。结果 21例患者均以突发意识障碍为首发症状，能迅速恢复，但苏醒后睡眠过度7例(33．3％)；均有眼球运动障碍，且难于恢复；均无明显的肢体瘫痪。8例(38．1％)记忆力明显下降。少见的症状是视觉障碍(14．3％)、幻视(9．5％)、偏身感觉异常(9．5％)。21例患者中主要基础疾病有高血压15例(71．4％)、心脏病13例(61．9％)、糖尿病9例(42．9％)。8例(38．1％)被误诊，发病第3～5天行头颅CT薄层扫描均能明确诊断。结论 TOBS临床表现多样、复杂；老年人突发眩晕、意识障碍，伴有眼球运动障碍，无明显肢体瘫痪时应高度警惕TOBS。发病第3～5天复查头颅CT并薄层扫对基层医院诊断TOBS是行之有效的方法。TOBS可能以脑栓塞为主；高血压、心脏病、糖尿病是老年人TOBS最重要的危险因素。     

经颅多普勒超声联合巴曲酶治疗脑梗死急性期的疗效观察

目的:评估在巴曲酶治疗同时应用经颅多普勒超声连续监护照射病变血管是否能够提高巴曲酶对脑梗死急性期的疗效.方法:发病12h内的急性脑梗死患者90例,随机分为对照组(47例)和治疗组(43例),对照组接受巴曲酶10U治疗1次,治疗组患者在巴曲酶治疗的同时应用经颅多普勒超声连续监护照射病变血管1h.监测治疗前及用药后3d的血浆纤维蛋白原,比较2组患者就诊时、巴曲酶治疗后24h、第3日、第5日及1周时的NIHSS评分、进展性卒中及梗死后出血的发生率.结果:2组患者就诊时血浆纤维蛋白原差异无显著性,治疗后第3日治疗组血浆纤维蛋白原低于对照组(P=0.033);2组患者就诊时、治疗后24h、第3日NIHSS评分差异无显著性,治疗组治疗后第5日及1周时NIHSS评分低于对照组(P=0.030,P =0.002),治疗组进展性卒中的发生率低于对照组(P=0.049),梗死后出血的发生率无显著差异(P=1.000).结论:巴曲酶治疗同时应用经颅多普勒超声对病变血管连续监护照射1h能够增强巴曲酶的降纤作用,提高巴曲酶对脑梗死急性期的疗效.     

高敏C反应蛋白水平对急性心肌梗塞并发心衰死亡率的预测价值

目的：探讨高敏C反应蛋白（CRP）预测急性心肌梗塞（AMI）并发心力衰竭（HF）死亡率的价值。方法：采用免疫比浊法测定51例AMI组,40例冠心病对照组患者入院第1d（1d）、第3d（3d）、第7d（7d）的高敏CRP（hs—CRP）水平。结果：AMI组的hs—CRP水平（3d,60mg／L）显著高于冠心病对照组（3d,13mg／L）,P〈0．001。AMI并发HF患者（31例）的hs—CRP水平[1d,（30±4）mg／L]显著高于未并发HF患者（20例）的[1d,（15士3）mg／L],P〈0．01。AMI者在1年内的总死亡率：第3dhs—CRP峰值≥85mg／L者为47％,hs-CRP峰值〈85mg／L者为8．8％,P〈0．001;HF的死亡率：第3dhs-CRP峰值≥85mg／L者为23．5％,hs-CRP峰值〈85mg／L者为2．9％,P〈0．001。说明第3d的hs-CRP水平峰值与1年内的死亡率有关。结论：hs—CRP水平可做为预测AMI1年内总死亡率和HF死亡率的一项重要指标。     

Prognostic value of troponin T in hospitalized patients with angina or non-ST-segment elevation myocardial infarction

INTRODUCTION AND OBJECTIVES: Cardiac troponins are highly specific and sensitive for detecting minimal myocardial damage. The aim of our study was to determine the prognostic value of troponin T levels in patients hospitalized for suspected angina or myocardial infarction without ST-segment elevation. PATIENTS AND METHOD: We recorded the frequency of death, acute myocardial infarction, heart failure, or need for coronary revascularization in the three months after the onset of symptoms in 346 consecutive patients admitted for suspected acute coronary syndrome, excluding those who developed myocardial infarction with persistent ST-segment elevation. RESULT:. Serum troponin T levels were > or = 0.1 ng/ml in 133 patients (troponin T positive group) and lower in 213 patients (troponin T negative group). The relative risk (RR) and 95 percent confidence intervals (95% CI) of individual and grouped events for the troponin T positive group were 3.2 (95% CI, 1.4-7.3; p = 0.006) for death; 2.8 (95% CI, 1.43-5.51; p = 0.003) for death or myocardial infarction; and 2.8 (95% CI, 1.6-5.0; p < 0.001) for death, myocardial infarction or heart failure. Diabetes mellitus and troponin T levels > or = 0.1 ng/ml had independent prognostic value after adjusting for age, sex, and electrocardiographic changes; with RR 2.5 (95% CI, 1.01-5.9) for death, myocardial infarction or heart failure. CONCLUSIONS: The prognosis of patients hospitalized for chest pain who do not immediately develop transmural necrosis depends on serum troponin T levels at hospital admission. Troponin T levels > or = 0.1 ng/ml almost triple the risk of major events in the three months after the acute episode. The prognostic value of troponin T is independent of age, sex, presence of diabetes mellitus, and electrocardiographic changes.     

Takotsubo cardiomyopathy associated with torsades de pointes and long QT interval: a case report

A 77-year-old man was admitted to our hospital for pneumonia. On admission, electrocardiography showed ST segmental elevation and echocardiography showed abnormal movement of the left ventricular walls. Emergent coronary angiography was not performed because of his high C-reactive protein values and negative troponin T value. On the 3rd day, electrocardiography showed torsades de pointes and long QT interval, then intravenous lidocaine (1,000 mg/day) was started. Left ventriculography demonstrated takotsubo cardiomyopathy on the 9th day. Torsades de pointes disappeared with intravenous lidocaine therapy, and he was discharged on the 27th day. Takotsubo cardiomyopathy has a relatively good prognosis, and rarely causes sudden death and congestive heart failure. Ventricular tachycardia and fibrillation complicate this disease in 9% of patients. To prevent fatal arrhythmia, appropriate therapy against torsades de pointes should be considered.     

Circulating hepatocyte growth factor as a diagnostic marker of thrombus formation in patients with cerebral infarction.

Circulating levels of hepatocyte growth factor (HGF) are increased in the early stage of an acute myocardial infarction because of arterial thrombosis. The purpose of this study was to use a new sensitive enzyme-linked immunosorbent assay to investigate whether circulating HGF is increased in patients with cerebral infarction. Circulating HGF was measured in 32 patients with cerebral infarction on admission to hospital and on days 2, 3, 7 and 14 after the onset of symptoms. Serum HGF levels exceeded the mean value +2SD (329pg/ml) measured in controls in 10 of 20 patients (50%) within 6 h after onset and in 15 of 32 patients (47%) within 24 h. Plasma D-dimer was increased in more than half of the patients with elevated HGF values. HGF levels in 16 patients who were measured serially were persistently increased throughout the study period. The results suggests that circulating HGF is a reliable early marker of cerebral infarction, and that this new sensitive HGF assay may be useful for diagnosing cerebral thrombosis.     

Iron status and its relationship with lipid peroxidation in patients with acute myocardial infarction.

AIM: The aim of this study was to investigate iron status and its relationships with lipid peroxidation in patients with acute myocardial infarction (MI). METHODS: The study included 30 male patients aged between 32 and 73 years (mean 55 +/- 6) with acute MI.We measured the levels of plasma iron, transferrin (TF), ferritin (FER), ceruloplasmin (CER), cardiac enzymes, and erythrocyte malondialdehyde (e-MDA) in patients with acute MI on the admission and 1st, 3rd, 5th, 7th, 15th, 45th post MI day and investigated the variations of these parameters in acute MI. RESULTS: The e-MDA level started to increase on the admission day and showed a peak value on the post MI 1st day (88 +/- 23 and 98 +/- 26 nmol/g Hb, respectively). Afterwards, the e-MDA level minimally changed until post Ml 45th day, which showed a minimum level (57 +/- 13 nmol/g Hb) (p < 0.05). In addition, the iron concentration of serum reached its maximum level on the 1st post Ml day (99 +/- 30 mg/dl, p < 0.05) and relatively decreased after the 3rd day. Courses of MDA and iron levels were similar. The FER level started to increase from the admission day of the patients (230 +/- 375 mg/dl), showed a mean peak value on the 3rd day (296 +/- 568 mg/dl) and decreased to a minimum level on the 45th day (121 +/- 85 mg/dl) (p < 0.05). Contrarily, the TF level started to decrease on the 1st day (221 +/- 44 mg/dl), decreased minimum level on the 3rd day (211 +/- 37 mg/dl) and continued approximately the same level until the 45th day (244 +/- 45 mg/dl) (p < 0.05). The CER level started to increase from the first day of admission of the patients (43 +/- 12 mg/dl), reached a maximum level on the 7th day (59 +/- 12 mg/dl) and similar levels were observed until the 15th day. On the 45th day, the CER level was higher than on the first day (52 +/- 13 mg/dl) (p < 0.05). CONCLUSION: There was an association of higher iron status with increased lipid peroxidation in patients with myocardial infarction.