Chronic eosinophilic pneumonia is a very rare disorder of unknown etiology characterized by striking systemic and pulmonary manifestations such as fever, weight loss, dyspnea, blood eosinophilia, and fluffy peripheral opacities on chest radiograph. A number of these patients developed asthma before or with the onset of illness. The roentgenographic lesion rapidly resoluted with corticosteroid and recurrence was occasionally occured in the same location. Histopathologic features of chronic eosinophilic pneumonia include dense aggregates of eosinophils, histiocytes, and multinucleated giant cells within alveolar spaces, interstitium, and bronchioles associated with scattered lymphocytes and plasma cells. We report a case of chronic eosinophilic pneumonia diagnosed by clinical, radiographic, and histologic findings with review of the literature.
Asthma ; Bronchioles ; Dyspnea ; Eosinophilia ; Eosinophils* ; Fever ; Giant Cells ; Histiocytes ; Humans ; Lymphocytes ; Plasma Cells ; Pneumonia ; Pulmonary Eosinophilia* ; Radiography, Thoracic ; Recurrence ; Strikes, Employee ; Weight Loss

Ticlopidine is an antiplatelet agent used as a drug to prevent the recurrence of cerebral infarction or ischemic heart disease. Close attention has recently been paid to the superiority of this drug to aspirin in the prevention of stroke. Its mechanism of action differs from aspirin, dipyridamole, and sulfinpyrazone. Inhibition of the adenosine diphosphate induced pathway of platelet aggregation, along with the activation of adenylate cyclase and suppression of platelet-activating factor and thromboxane A2, are the postulated mechanisms of action of ticlopidine. Because ticlopidine causes neutropenia and agranulocytosis in roughly 1% of treated patients, usually within the first 3 months of treatment, this drug has been reserved for patients intolerant to aspirin therapy. We reported two cases of ticlopidine-induced neutropenia and one patient hospitalized with severe neutropenia and pneumonia.
Adenosine Diphosphate ; Adenylyl Cyclases ; Agranulocytosis ; Aspirin ; Cardiovascular Diseases* ; Cerebral Infarction ; Dipyridamole ; Humans ; Myocardial Ischemia ; Neutropenia* ; Platelet Aggregation ; Pneumonia ; Recurrence ; Stroke ; Sulfinpyrazone ; Thromboxane A2 ; Ticlopidine

Ticlopidine is an antiplatelet agent used as a drug to prevent the recurrence of cerebral infarction or ischemic heart disease. Close attention has recently been paid to the superiority of this drug to aspirin in the prevention of stroke. Its mechanism of action differs from aspirin, dipyridamole, and sulfinpyrazone. Inhibition of the adenosine diphosphate induced pathway of platelet aggregation, along with the activation of adenylate cyclase and suppression of platelet-activating factor and thromboxane A2, are the postulated mechanisms of action of ticlopidine. Because ticlopidine causes neutropenia and agranulocytosis in roughly 1% of treated patients, usually within the first 3 months of treatment, this drug has been reserved for patients intolerant to aspirin therapy. We reported two cases of ticlopidine-induced neutropenia and one patient hospitalized with severe neutropenia and pneumonia.
Adenosine Diphosphate ; Adenylyl Cyclases ; Agranulocytosis ; Aspirin ; Cardiovascular Diseases* ; Cerebral Infarction ; Dipyridamole ; Humans ; Myocardial Ischemia ; Neutropenia* ; Platelet Aggregation ; Pneumonia ; Recurrence ; Stroke ; Sulfinpyrazone ; Thromboxane A2 ; Ticlopidine

Transcatheter arterial chemoembolization (TACE) is a therapeutic option for unresectable hepatocellular carcinoma. Supraumbilical skin rash is a rare complication of TACE caused by patent hepatic falciform artery. We report herein two cases of supraumbilical skin rash developed after TACE for hepatocellular carcinoma, with discussion on the pathogenesis, prophylaxis, and treatment.
Arteries ; Carcinoma, Hepatocellular* ; Exanthema* ; Humans ; Skin*

BACKGROUND/AIMS: The prevalence of hepatitis delta virus (HDV) infection has been estimated as being approximately 5% among global HBsAg carriers. The anti-delta positive rate in Koreans had been reported as being 0.85% in 1985. While the prevalence of HBV has been decreased from nearly 10% to 5% during the past twenty years, there have been no more studies on the anti-delta prevalence in Koreans. The aim of this study was to estimate the anti-delta prevalence in Koreans and to study the clinical characteristics of anti-delta positive patients in a single center. METHODS: Serum anti-delta was measured in one hundred ninety four HBsAg-positive patients who were admitted to our hospital from February 2003 to August 2003. We checked the genotypes of the HBV in the anti-delta positive patients. The clinical features of the anti-delta positive patients were compared to those clinical features of the anti-delta negative patients from the aspect of age, gender, mode of transmission, the positivity of HBeAg and serum HBV DNA. RESULTS: Serum anti-delta was positive in seven patients among the 194 subjects, giving a 3.6% positive rate. Among these seven patients, six had hepatocellular carcinoma (HCC) and the other one had cholangiocarcinoma. All of the anti-delta positive patients had the C genotype of HBV. The anti-delta positive patients showed significantly suppressed HBV DNA replication compared to the anti-delta negative patients. CONCLUSIONS: In Koreans, anti-delta was positive mainly in HCC patients with an approximate prevalence of 4%, and this rate has not changed much for the past twenty years. HBV DNA replication was suppressed by HDV infection.
Adult ; Carcinoma, Hepatocellular/virology ; English Abstract ; Female ; Hepatitis Antibodies/analysis ; Hepatitis D/complications/*epidemiology/immunology ; Hepatitis Delta Virus/immunology ; Hepatitis delta Antigens/analysis ; Humans ; Korea/epidemiology ; Liver Neoplasms/virology ; Male ; Middle Aged ; Prevalence

BACKGROUND AND OBJECTIVES: Ischemic preconditioning reduces the size of myocardial infarct in animal models, however its role in humans remains unclear. Clinical data suggests that episodes of angina immediately before acute myocardial infarction may be associated with a protective effect on the human myocardium. We performed an analysis on the effect of prodromal angina on infarct size, in-hospital outcome and newly developed Q-wave in patients with acute myocardial infarction. SUBJECTS AND METHODS: 65 patients who had received thrombolytic therapy were enrolled in the study. Eleven patients (17%) had experienced previous angina within 24 hours prior to acute myocardial infarction (group I), and the remaining 54 patients (83%) did not have a history of previous angina (group II). Killip class, cardiac enzyme, ECG findings, echocardiographic data and in-hospital outcomes were compared between the two groups. RESULTS: Group I tended to have lower peak creatine kinase (CK) and CK-MB levels, although the difference between the two groups in regards to the level of cardiac enzyme was statistically insignificant. Despite similar patient characteristics, Group I showed a lower incidence of heart failure during hospitalization than group II. 6/11 patients (55%) in group I and 47/54 (87%) in group II had a Q-wave at discharge ECG. Group I showed better left ventricular systolic function during admission. None of the DM patients (14 patients) had prodromal angina and 13 of 14 patients (93%) demonstrated Q-wave infarction. CONCLUSION: Prodromal angina prior to acute myocardial infarction as a marker of ischemic preconditioning may also confer beneficial effects in terms of in-hospital outcomes. Further studies concerning the long term outcomes of such cases are needed.
Angina Pectoris ; Creatine Kinase ; Echocardiography ; Electrocardiography* ; Heart Failure ; Hospitalization ; Humans ; Incidence ; Infarction ; Ischemic Preconditioning ; Models, Animal ; Myocardial Infarction* ; Myocardium ; Thrombolytic Therapy