肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肾综合征出血热合并严重心脏并发症一例

患者男,43岁.入院前5 d无明显诱因地开始发热伴持续性头痛、腰痛、呕吐伴轻微腹痛、腹泻,在当地诊所疑为"急性胃肠炎"应用"丁胺卡那霉素"治疗2 d无效.     

肿瘤病人弓形虫感染分析

在肿瘤的发生和发展进程中 ,多伴有免疫功能低下或缺陷 ,从而极易遭受各种感染。弓形虫是机会感染因子 ,当患者免疫功能受损时 ,易于感染 ,还会使隐性感染激活 ,引起低热不退、淋巴结肿和脑神经系统的反应 ,此现象尚未引起临床医师的重视。近年来 ,我们对 4 0 9例肿瘤病人进行了弓形虫感染及弓形虫病的分析观察 ,报告如下 :1　材料与方法1 1　材料　 30 4例病人血清取自江西省肿瘤医院住院或门诊病人 ,随机抽样后低温保存待检 ,10 5例取自其他医院送检样品 ,有急性症状者随到随检 ,以便及时做病原学检测。1 2　弓形虫病诊断方法1 2 1　免疫…     

A patient with rectal ulcer with severe stenosis presenting with perforated peritonitis

We report a patient with rectal ulcer with severe stenosis, who underwent urgent surgical treatment for perforated peritonitis. The 54-year-old man suddenly developed cramping abdominal pain and fever while hospitalized, with signs of peritoneal irritation. An emergency laparotomy was performed, and severe stenosis of the rectum and a perforated lesion on the oral side approximately 10 cm distant from the stenosis were found, with massive abdominal purulent fluid. He was treated by rectosigmoid colon resection with transverse colon loop colostomy. Histopathologically, the stenosis was caused by ulceration extending to all muscular layers of the rectum, with inflammatory changes. Benign rectal stenosis is so rare that differential diagnosis from malignancy may be difficult when there are inflammatory changes in the surrounding tissues. However, it is necessary to keep in mind the likelihood of this disease in differentiation from rectal cancer. Received: December 21, 1998 / Accepted: May 28, 1999     

Infection with Rhodococcus equi in a patient with sarcoidosis treated with corticosteroids

A 51-year-old female farmer was diagnosed as having sarcoidosis. During 4 years of observation, slow radiological progression was observed. Cough then developed, necessitating treatment with corticosteroids. After 28 months of continuous treatment with prednisolone in low doses (5-7.5 mg daily), she suffered fever episodes, recurrent haemoptyses, general malaise and loss of weight. A chest roentgenogram showed a left upper lobe infiltrate, which progressed and finally cavitated, and rib destruction. Despite efforts, including a thoracotomy, 22 months passed before a diagnosis could be made. Blood and sputum cultures and cultures from the destroyed rib showed growth of Rhodococcus equi, a common soil organism which can cause infections in foals and other animals. Treatment with rifampicin and erythromycin was successful. R. equi has been reported to cause infection in patients with neoplastic disease and/or immunosuppression, but the disease might be more common than is suggested by the sparse case reports in the literature, owing to lack of familiarity with the organism, which will tend to be overlooked as a contaminant.     

Evaluation of atrial vulnerability with transoesophageal stimulation in patients with atrioventricular junctional: Comparison with patients with ventricular pre-excitation and with normal subjects

The aim of our work was to evaluate the inducibility of atrialfibrillation in a group of patients with atrioventricular junctionalreentrant tachycardia and to compare it with that of patientswith a Kent-type ventricular pre-excitation (Wolff-Parkinson-Whitesyndrome) and a control group. One hundred and twenty-five subjects were separated into groups.Group 1 comprised 49 Wolff-Parkinson-White patients, with amean age of 26.4, range 10.66 years; group 2, 51 patients withatrioventricular junctional reentrant tachycardia inducibleby transoesophageal atrial stimulation andlor clinically documented,with a mean age of 43.4, range 16–78 years; group 3, 25control subjects with a mean age of2.64, range 13–76 years. Each subject underwent atrial transoesophageal stimulation withthe following protocol: programmed atrial stimulation with 1and 2 stimuli during atrial pacing of 100. min^–1 and 150.min^–1; atrial stimulation for 10 s at a rate of 200–300–400–500–600.min^–1 with intervals of 10 s between stimulations, fivesuccessive ‘ramp-up’ atrial stimulations for 9 swith the rate increasing from 100 to 800. min^–1 with intervalsof 10 s between stimulations. The end point was the completionof the protocol or induction of sustained atrial fibrillation(>1 min). The chi-square test was used for statistical analysis. Our resultsshowed that in group 1 atrial fibrillation was induced in 27149patients (55.1%); this was sustained in 13149 (26.5%) and non-sustainedin 14149 (28.5%); in group 2, atrial fibrillation was inducedin 22151 patients (43.0%); it was sustained in 7151 (13.7%)and non-sustained in 15151 (29.4%); in group 3, sustained atrialfibrillation was not induced in any subject and in only onesubject was a non-sustained atrial fibrillation (4 s) induced. The chi-square test showed that group 2 vs group 1 were non-significant,while group 2 vs group 3 and group 1 vs group 3 were significant(P<0.003 and P<0.0007, respectively). Therefore group 2 patients showed a greater atrial vulnerabilityin comparison to the control subjects and a similar vulnerabilityto group 1 patients. It is possible that the greater atrialvulnerability in the patients of group 2 was due to the doublenodal pathway.     

Treating patients with lupus with B-cell depletion

A new era in the treatment of systemic lupus erythematosus has dawned with the increasing introduction of monoclonal antibodies and other approaches, that target the key molecules involved in the pathogenesis of the disease. At present the ability to block the CD20 molecule on those B cells that carry this marker has proved the most effective way to treat patients resistant to conventional immunosuppressive drugs. However, these studies have all been open label and the results of double blind controlled studies are eagerly awaited.