ABSTRACT
In contrast to widely recognized venous thrombotic complications, peripheral arterial thrombosis as a complication of nephrotic syndrome, especially without preceding iatrogenic venous puncture, corticosteroid treatment, or coagulation factor abnormalities, has rarely been reported in adult female patients. We report the case of a 39-year-old woman who presented with pain in the right lower leg accompanied by minimal change nephrotic syndrome. Lower-extremity angiography showed total occlusion of the right superficial femoral artery. Thrombectomy was performed with a balloon catheter, and the thrombi were successfully aspirated. Our experience indicates that even if few traditional risk factors for atherosclerosis are identified, a high index of suspicion and aggressive treatment of arterial thrombosis in adult nephrotic syndrome are crucial to minimize serious ischemic injuries.
Subject(s)
Adult , Female , Humans , Angiography , Atherosclerosis , Blood Coagulation Factors , Catheters , Femoral Artery , Leg , Nephrosis, Lipoid , Nephrotic Syndrome , Peripheral Arterial Disease , Punctures , Risk Factors , Thrombectomy , ThrombosisABSTRACT
In contrast to widely recognized venous thrombotic complications, peripheral arterial thrombosis as a complication of nephrotic syndrome, especially without preceding iatrogenic venous puncture, corticosteroid treatment, or coagulation factor abnormalities, has rarely been reported in adult female patients. We report the case of a 39-year-old woman who presented with pain in the right lower leg accompanied by minimal change nephrotic syndrome. Lower-extremity angiography showed total occlusion of the right superficial femoral artery. Thrombectomy was performed with a balloon catheter, and the thrombi were successfully aspirated. Our experience indicates that even if few traditional risk factors for atherosclerosis are identified, a high index of suspicion and aggressive treatment of arterial thrombosis in adult nephrotic syndrome are crucial to minimize serious ischemic injuries.
Subject(s)
Adult , Female , Humans , Angiography , Atherosclerosis , Blood Coagulation Factors , Catheters , Femoral Artery , Leg , Nephrosis, Lipoid , Nephrotic Syndrome , Peripheral Arterial Disease , Punctures , Risk Factors , Thrombectomy , ThrombosisABSTRACT
Duloxetine is a balanced serotonin and norepinephrine reuptake inhibitor available for treating peripheral neuropathic pain. The occurrence of hyponatremia as an adverse event of duloxetine treatment, but it has not yet been reported in Korea. Here, we report two cases of hyponatremia induced by duloxetine for treatment of peripheral neuropathic pain. Our findings highlight the need for special attention when using duloxetine in elderly patients taking thiazide diuretics.
Subject(s)
Aged , Humans , Hyponatremia , Korea , Neuralgia , Norepinephrine , Serotonin , Selective Serotonin Reuptake Inhibitors , Sodium Chloride Symporter Inhibitors , Thiophenes , Duloxetine HydrochlorideABSTRACT
BACKGROUND: Statins can regulate the production of pro-inflammatory cytokines and inhibit MMP production or activation in a variety of types of cells. This study evaluated whether statins would inhibit MMP release from human lung fibroblasts, which play a major role in remodeling processes. METHODS: This study, using an in-vitro model (three-dimensional collagen gel contraction system), evaluated the effect of cytokines (tumor necrosis factor-alpha, TNF-a and interleukin-1beta, IL-1b) on the MMP release and MMP activation from human lung fibroblasts. Collagen degradation induced by cytokines and neutrophil elastase (NE) was evaluated by quantifying hydroxyproline. RESULTS: In three-dimensional collagen gel cultures (3D cultures) where cytokines (TNF-a and IL-1b) can induce the production of MMPs by fibroblasts, it was found that simvastatin inhibited MMP release. In 3D cultures, cytokines together with NE induced collagen degradation and can lead to activation of the MMP, which was inhibited by simvastatin. CONCLUSION: Simvastatin may play a role in regulating human lung fibroblast functions in repair and remodeling processes by inhibiting MMP release and the conversion from the latent to the active form of MMP.