ABSTRACT
History and clinical findings | A 59-year-old man with metastasized rectum cancer presents at the interdisciplinary emergency care unit with a distinct cyanosis of his face. At that moment the patient himself is out of any complaints. Cyanosis is spreading from his face over his neck to both arms. During the last months he has been treated with folinic acid, 5-fluoruracil, irinotecan and aflibercept via a port-catheter. Except for smoking his further medical history is unremarkable. Examinations | CT-scan shows a port-catheter associated thrombosis with a consecutive superior vena cava syndrome (SCVS). No signs of an acute pulmonary embolism or thoracic aortic aneurysm are detected. Treatment and course | Anticoagulation is started immediately. Due to a short loss of consciousness glucocorticoids and vasopressors are given. As cyanosis continued during next days, a transfemoral percutaneous angioplasty with stent placement was performed. Cyanosis disappears completely and the patient can be discharged. Conclusions | SCVS due to port-catheter associated thrombosis in tumor patients is rare but its prevalence will grow because of increasing numbers of tumor patients, intravenous catheter-systems and pacemakers. Early CT-scan with contrast agent via femoral venous catheter is reasonable for diagnosis and therapy. For tumor percutaneous transluminal angioplasty is a safe and effective option.
Subject(s)
Cyanosis/etiology , Rectal Neoplasms/drug therapy , Superior Vena Cava Syndrome/diagnosis , Superior Vena Cava Syndrome/etiology , Vascular Access Devices/adverse effects , Antineoplastic Agents/administration & dosage , Diagnosis, Differential , Humans , Male , Middle Aged , Rectal Neoplasms/complications , Superior Vena Cava Syndrome/prevention & control , Treatment OutcomeSubject(s)
Lymphoma, Large B-Cell, Diffuse/diagnostic imaging , Neoplasm Recurrence, Local/diagnostic imaging , Osteolysis/chemically induced , Osteolysis/diagnostic imaging , Thalidomide/analogs & derivatives , Aged , Angiogenesis Inhibitors/adverse effects , Female , Humans , Lenalidomide , Lymphoma, Large B-Cell, Diffuse/drug therapy , Middle Aged , Neoplasm Recurrence, Local/drug therapy , Radiography , Thalidomide/adverse effects , Treatment OutcomeABSTRACT
The accumulation of beta-amyloid (A beta) plaques and neurofibrillary tangles consisting of hyperphosphorylated tau protein are pathological features of Alzheimer's disease (AD) commonly modeled in mice using known human familial mutations; however, the loss of neurons also found to occur in AD is rarely observed in such models. The mechanism of neuron degeneration remains unclear but is of great interest as it is very likely an important factor for the onset of adverse memory deficits occurring in individuals with AD. The role of A beta in the neuronal degeneration is a matter of controversial debates. In the present study we investigated the impact of extracellular plaque A beta versus intraneuronal A beta on neuronal cell death. The thalamus and the frontal cortex of the APP/PS1KI mouse model were chosen for stereological quantification representing regions with plaques only (thalamus) or plaques as well as intraneuronal A beta (frontal cortex). A loss of neurons was found in the frontal cortex at the age of 6 months coinciding with the decrease of intraneuronal immunoreactivity, suggesting that the neurons with early intraneuronal A beta accumulation were lost. Strikingly, no neuron loss was observed in the thalamus despite the development of abundant plaque pathology with levels comparable to the frontal cortex. This study suggests that plaques have no effect on neuron death whereas accumulation of intraneuronal A beta may be an early transient pathological event leading to neuron loss in AD.
