Disseminated non-tuberculous mycobacterium (dNTM) infection is rare in humans without human immunodeficiency virus (HIV) infection. Previous reports have shown autoantibodies to human interferon-gamma (IFN-γ), which play important roles in mycobacterium infection, in the sera of patients with non-HIV dNTM disease. Herein, we describe a 53-year-old male who was strongly suspected to have multicentric Castleman disease (MCD) based on bone marrow study and chest radiological findings. However, Mycobacterium kansasii was detected in respiratory samples including pleural effusion. We initiated anti-mycobacterial therapy under intensive care; he died on the 48th hospital day. We detected no hematological disorders, ruling out MCD postmortem. However, we detected M. kansasii in pulmonary, liver, spleen and bone marrow tissues. Moreover, anti-IFN-γ autoantibody was detected with strong neutralizing capacity for IFN-γ. We consider our present report to contribute to understanding of the relationship between anti-IFN-γ autoantibody and disease development.
Background:Because it remains unclear whether noninvasive ventilation (NIV) is an effective therapy for cardiogenic pulmonary edema secondary to acute myocardial infarction (AMI), we retrospectively evaluated our experience with NIV in the treatment of pulmonary edema secondary to AMI and other cardiac conditions.
Methods and Results:The study group included 206 patients with cardiogenic pulmonary edema, divided into an AMI group (53 patients) and a non-AMI group (153 patients). The weaning rate from NIV was similar in the AMI and non-AMI groups (90.6% vs. 90.8%, P=0.950). Heart rate, blood pressure, and respiratory rate decreased significantly 1 h after initiation of NIV in both groups, and were maintained until weaning from NIV. The frequency of endotracheal intubation after weaning from NIV was higher in the AMI group than in the non-AMI group (7.5% vs. 0.7%, P=0.016), although the overall frequency of intubation was similar in both groups. The in-hospital mortality rate was similar in the AMI and non-AMI groups (13.1% vs. 9.8%, P=0.489).Conclusions: NIV effectively improved vital signs and oxygenation and lowered the intubation rate in patients with cardiogenic pulmonary edema of all etiologies, including AMI. The outcome in patients with AMI treated with NIV depends primarily on the severity of the course of AMI and not on the severity of acute respiratory failure. (Circ J 2012; 76: 2586 - 2591
Limited information is available about histopathological reactions to the implanted endocardial electrodes of pacemakers (PM). Gross anatomic and histologic studies of tissue reactions to PM electrodes were made in thirteen autopsy cases (nine men and four women, ages 25 approximately 89 years, mean age 71.8) who died two months to twenty-one years after PM implantation. Nine of them had complete atrioventricular (AV) block, three had sick sinus syndrome, and one had bradycardia-tachycardia syndrome. The direct causes of death were not related to their PM. The tip with projecting tines was implanted in the right ventricle in all patients. At the contact area between the electrode and the endocardium, no tissue reaction was observed in one patient with a history of over sixteen years of PM implantation. However, cardiomyocytes under the tip had been replaced by fibrotic tissue in many other patients. In two patients in particular where the electrode had been implanted at the apex of each right ventricle, all cardiomyocytes had disappeared and only fibrotic tissue and adipose tissue were observed under the tip. These findings suggest that mechanical stress caused by attaching the tip tightly damages cardiomyocytes and brings about changes in the pacing thresholds. In three patients, a space was seen between the tip and the endocardium. A fibrous sheath covering the electrode extended to the tip and formed a thick fibrous cap. This non-excitable fibrous cap acted as a virtual electrode and possibly affected the elevation of the threshold in these patients. In four patients, extensive myocardial fibrosis due to disease, e. g. previous myocardial infarction, dilated cardiomyopathy, amyloidosis, or sarcoidosis, was found in the area surrounding the tip and also might affect the elevation of the threshold. We concluded that elevation of pacing thresholds after PM implantation is not due to reactive endocardial thickening. The space between the tip and the endocardium is occupied by a fibrous sheath, and an overly tight attachment damages cardiomyocytes causing replacement fibrosis. Thus, it is not desirable in some patients to insert the electrodes into the apex, where the myocardium is thin. To avoid the elevation of thresholds, development of further devices is necessary to allow electrode fixation to the endocardium with a more suitable pressure level.
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