RÉSUMÉ
Biliary cast describes the presence of casts within the biliary tree. It is resultant sequel of cholangitis and hepatocyte damage secondary to bile stasis and bile duct injury. Biliary cast syndrome was first reported in patient undergone liver transplantation. The pathogenesis of biliary cast is not clearly identified, but proposed etiologic factors include post-transplant bile duct damage, ischemia, biliary infection, or post-operative biliary drainage tube. Although biliary casts are uncommon, most of biliary cast syndrome are reported in the liver transplant or hepatic surgery patients. A few reports have been published about non-transplant or non-liver surgery biliary cast. We report two cases of biliary cast syndrome in non-liver surgery patients.
Sujet(s)
Femelle , Humains , Mâle , Adulte d'âge moyen , Maladie aigüe , Ascaridiose/diagnostic , Maladies des canaux biliaires/diagnostic , Conduits biliaires/imagerie diagnostique , Cholagogues et cholérétiques/usage thérapeutique , Cholangiopancréatographie rétrograde endoscopique/effets indésirables , Calculs biliaires/diagnostic , Cirrhose biliaire/diagnostic , Pancréatite/étiologie , Tomodensitométrie , Acide ursodésoxycholique/usage thérapeutiqueRÉSUMÉ
Thienopyridines are antiplatelet agents used in post-percutaneous coronary angioplasty patients and patients with acute coronary syndrome, stroke, and peripheral arterial disease. Ticlopidine has been shown to reduce the incidence of stent thrombosis, but it may also cause serious hematological side effects. Among the thienopyridines, clopidogrel is considered to be a safe alternative to ticlopidine because of its decreased incidence of hematological adverse effects. However, some hematological side effects can occur and may be fatal. In this case, a 47-year-old man complained of dyspnea and generalized edema. He had been taking clopidogrel after coronary angioplasty. His laboratory findings showed acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia, which were consistent with hemolytic uremic syndrome (HUS). After discontinuing clopidogrel and undergoing plasma exchange, he recovered fully. To our knowledge, this is the first reported case of clopidogrel-induced HUS in Korea.
Sujet(s)
Humains , Adulte d'âge moyen , Syndrome coronarien aigu , Atteinte rénale aigüe , Anémie hémolytique , Angioplastie , Dyspnée , Oedème , Syndrome hémolytique et urémique , Incidence , Corée , Maladie artérielle périphérique , Échange plasmatique , Antiagrégants plaquettaires , Endoprothèses , Accident vasculaire cérébral , Thiénopyridines , Thrombopénie , Thrombose , TiclopidineRÉSUMÉ
A 37-year-old woman presented to our hospital with a 1-month history of fever. She also complained of lower leg pain. Transthoracic echocardiography showed large vegetations on the mitral valve leaflets. Staphylococcus lugdunensis was isolated from blood cultures. She was diagnosed with infectious endocarditis due to S. lugdunensis and was treated with antibiotics and surgery. Infective endocarditis caused by S. lugdunensis can be invasive and often resembles endocarditis due to Staphylococcus aureus. Thus, whenever this organism is found in patients with endocarditis, early surgical treatment of the infected valve should be considered.
Sujet(s)
Adulte , Femelle , Humains , Antibactériens , Échocardiographie , Endocardite , Fièvre , Jambe , Valve atrioventriculaire gauche , Staphylococcus , Staphylococcus aureus , Staphylococcus lugdunensisRÉSUMÉ
Acquired factor VIII deficiency is very rare, often fatal. It is associated with pregnancy, autoimmune diseases, malignancy, and drugs, although no underlying cause is found in 50%. A 49-year-old male was referred with right shoulder bruising. The coagulation test showed a prolonged activated partial thromboplastin time. The factor VIII level was less than 1%, and the factor VIII inhibitor antibody titer was 246 Bethesda units/mL. The findings were compatible with acquired factor VIII deficiency. He had consumed the dried gallbladder of a cobra, Naja naja, for two weeks, it contained venom. After the initial treatment with factor VIII, he did not take supplemental coagulation factor VIII. The patient was readmitted with left forearm swelling. He lost consciousness suddenly and brain computed tomography (CT) revealed a subdural hematoma. Despite administering recombinant factor VII, his bleeding was not controlled and he died.
Sujet(s)
Humains , Mâle , Adulte d'âge moyen , Grossesse , Maladies auto-immunes , Encéphale , Conscience , Elapidae , Facteur VII , Facteur VIII , Avant-bras , Vésicule biliaire , Hématome subdural , Hémophilie A , Hémorragie , Temps partiel de thromboplastine , Épaule , VeninsRÉSUMÉ
Placenta growth factor (PIGF) was originally described as a placenta produced homodimeric protein that shares substantial structural similarity with vascular endothelial growth factor (VEGF). It is becoming increasingly evident that PIGF may directly or indirectly modulate several key vascular events in various tissues. These include angiogenesis or vasculogenesis, vascular maturation and stabilization, vascular permeability, and endothelial cell survival. Inflammatory reaction in the nasal mucosa increases mucosal vascular permeability, resulting in edematous nasal mucosa with polypoid change. In this respect, PIGF may play a role in the formation of nasal polyp. In the present study we evaluated the expression of PIGF mRNA and protein in human inferior turbinate mucosa and nasal polyp. The expression and localization of PlGF mRNA and protein were investigated in the inferior turbinate mucosa and nasal polyps using reverse transcription-polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry. These results showed that the mRNA transcripts and protein for PlGF are expressed in human turbinate mucosa and nasal polyps. Semiquantitative RT-PCR revealed that PIGF mRNA in nasal polyps increased in its expression level than that in nasal turbinate mucosa. Likewise, immunoblot analysis demonstrated a higher expression of PIGF protein in nasal polyp tissues, compared with that of the nasal turbinate mucosa. However, immunohistochemical findings revealed that PlGF is localized in the endothelial lining of blood vessels in the inferior turbinate mucosa, whereas it is expressed in the epithelial cells of nasal polyps. These results indicate that PlGF mRNA and protein are expressed in normal turbinate mucosa and nasal polyp. Further, based on the fact showing that the expression site of PIGF is different in both tissues, the action mechanism of PIGF may be different in human nasal mucosa and nasal polyp. That is, the PIGF may play a role in the physiological function of normal nasal mucosa, possibly the maintenance of blood vessel and in the pathogenesis of nasal polyp formation.
Sujet(s)
Humains , Vaisseaux sanguins , Technique de Western , Perméabilité capillaire , Cellules endothéliales , Cellules épithéliales , Immunohistochimie , Muqueuse , Muqueuse nasale , Polypes du nez , Placenta , ARN messager , Cornets , Facteur de croissance endothéliale vasculaire de type ARÉSUMÉ
BACKGROUND AND OBJECTIVES: Electrolyte transport by nasal epithelia has been suggested to be important for controlling the quantity and composition of the nasal fluid and may play an important role in the development of nasal polyps. Transepithelial transport of ion and water in various fluid-transporting epithelia is strictly dependent on the localization of specific membrane proteins in the polarized epithelial cells. Na+ : HCO3-cotransporter (NBC) transports Na+ and HCO3- into the intracellular from extracellular space and induces the evacuation of H+, regulating pH. K+ : Cl- cotransporter (KCC) controls the cell volume and resorption of NaCl which is associated with the extracellular transport of K+ and Cl-. The present study evaluated the presense of mRNA for NBC and KCC in human inferior turbinate and nasal polyp. MATERIALS AND METHOD: The expression of NBC and KCC mRNA isoforms in inferior turbinate mucosa and nasal polyp was evaluated, using RT-PCR and in situ hybridization. RESULTS: RT-PCR revealed that the inferior turbinate and nasal polyp mucosa expressed kNBC, KCC1 and 4 mRNA. In in situ hybridization, their distribution was noted in the epithelial layer and submucosal glands of both mucosa. CONCLUSION: These results indicate that these types of ion transporters are expressed in human nasal mucosa and nasal polyp, controlling the fluid and ion transport in nasal epithelium and submucosal glands.