ABSTRACT
Encapsulating peritoneal sclerosis (EPS) is a potentially fatal complication after long-term peritoneal dialysis, and tamoxifen can be used for its prevention and treatment. However, tamoxifen is known to increase the risk of venous thromboembolism. A 49-year-old woman was admitted with sudden abdominal pain. The patient had received peritoneal dialysis for 20 years and switched to hemodialysis after the diagnosis of EPS. Tamoxifen (10 mg) and prednisolone (20 mg) had been administered for 8 months. On computed tomography, the left hepatic lobe was hardly illuminated, leading to a diagnosis of liver infarction. A month later, she was re-admitted due to abdominal pain and extensive deep vein thrombosis of the leg. The administration of tamoxifen was stopped and prednisolone was reduced to 10 mg. As her malnutrition progressed, she succumbed to death of gram negative sepsis. The patient was concluded to have liver infarction and extensive venous thrombosis as a side effect of tamoxifen.
ABSTRACT
Encapsulating peritoneal sclerosis (EPS) is a potentially fatal complication after long-term peritoneal dialysis, and tamoxifen can be used for its prevention and treatment. However, tamoxifen is known to increase the risk of venous thromboembolism. A 49-year-old woman was admitted with sudden abdominal pain. The patient had received peritoneal dialysis for 20 years and switched to hemodialysis after the diagnosis of EPS. Tamoxifen (10 mg) and prednisolone (20 mg) had been administered for 8 months. On computed tomography, the left hepatic lobe was hardly illuminated, leading to a diagnosis of liver infarction. A month later, she was re-admitted due to abdominal pain and extensive deep vein thrombosis of the leg. The administration of tamoxifen was stopped and prednisolone was reduced to 10 mg. As her malnutrition progressed, she succumbed to death of gram negative sepsis. The patient was concluded to have liver infarction and extensive venous thrombosis as a side effect of tamoxifen.
ABSTRACT
Invasive aspergillosis has emerged as a major cause of life-threatening infections in immunocompromised patients. Recently, patients with chronic obstructive pulmonary disease, who have been receiving corticosteroids for a long period, and immunocompetent patients in the intensive care unit have been identified as nontraditional hosts at risk for invasive aspergillosis. Here, we report a case of invasive pulmonary aspergillosis after influenza in an immunocompetent patient. The patient's symptoms were nonspecific, and the patient was unresponsive to treatments for pulmonary bacterial infection. Bronchoscopy revealed mucosa hyperemia, and wide, raised and cream-colored plaques throughout the trachea and both the main bronchi. Histologic examination revealed aspergillosis. The patient recovered quickly when treated systemically with voriconazole, although the reported mortality rates for aspergillosis are extremely high. This study showed that invasive aspergillosis should be considered in immunocompetent patients who are unresponsive to antibiotic treatments; further, early extensive use of all available diagnostic tools, especially bronchoscopy, is mandatory.
Subject(s)
Humans , Adrenal Cortex Hormones , Aspergillosis , Bacterial Infections , Bronchi , Bronchoscopy , Hyperemia , Immunocompetence , Immunocompromised Host , Influenza A virus , Influenza, Human , Intensive Care Units , Invasive Pulmonary Aspergillosis , Mortality , Mucous Membrane , Pulmonary Disease, Chronic Obstructive , TracheaABSTRACT
PURPOSE: To study the short term effects of hypercholesterolemia on corpus cavernosal tissue, we performed isometric tension studies and RT-PCR was used to identify mRNA expression of VEGF on isolated strips of corpus cavernosum, on rabbits which underwent partial ligation of the abdominal aorta and received a diet containing 2% cholesterol. MATERIALS AND METHODS: New Zealand White rabbits were divided into a control group(n=6) fed with a regular diet and a hypercholesterolemic group(n=10) which underwent partial ligation of the abdominal aorta and received a diet containing 2% cholesterol. After 3 weeks, the relationship between hypercholesterolemia and cavernosal smooth muscle pathophysiology was studied. To characterize the cavernosal smooth muscle reactivity in hypercholesterolemia, we performed isometric tension studies with phenylephrine(PE), acetylcholine(Ach), sodium nitroprusside(SNP) and electrical field stimulation(ES). RT-PCR was used to identify the mRNA expression of VEGF. RESULTS: PE-induced cavernous smooth muscle contraction in the hypercholesterolemic group was increased compared with the control group(p<0.05), while relaxation by Ach and ES in PE pretreated cavernosal smooth muscle in the hypercholesterolemic group was decreased(p<0.05). Relaxation by SNP in PE pretreated cavernosal smooth muscle was not different between any experimental groups. Expression of VEGF mRNA in cavernosal smooth muscle was significantly increased in the hypercholesterolemic group compared with the control group. CONCLUSIONS: Hypercholesterolemia caused a significant increase in PE-induced contraction of cavernosal tissue. Hypercholesterolemic cavernosal tissue retained the ability of relaxation induced by endothelium-independent, but relaxation induced by endothelium-dependant was impaired. Furthermore, expression of VEGF mRNA in cavernosal tissues was up regulated in the hypercholesterolemic group. This study showed that a short period of hypercholesterolemia could induce pathophysiologic change of cavernosal tissue.