Oral anticoagulant therapy is frequently and increasingly prescribed for patients at risk of arterial or venous thromboembolism (VTE). Although elective surgical or invasive procedures have necessitated temporary interruption of anticoagulants, managing these patients has been performed empirically and been poorly investigated. This study was designed to evaluate the adequacy of perioperative anticoagulation using enoxaparin. This was a retrospective, single-center study that evaluated the efficacy and safety of therapeutic-dose enoxaparin for bridging therapy in patients on long-term warfarin at Soonchunhyang University Hospital in Korea between August 2009 and July 2011. Warfarin was discontinued 5 days before surgery, and enoxaparin was administered twice daily by subcutaneous injection at a dose of 1 mg per kg from 3 days before the procedure to the last dose 24 hours before the procedure. Anticoagulation was restarted if proper hemostasis had been confirmed. There were 49 patients, of whom 25 (51%) were men, and the mean age was 63 years. Thirty-four (69%) received warfarin therapy for VTE, and 9 (18%) for atrial fibrillation. Twenty-nine patients (59%) underwent major surgery and 20 (41%) minor surgery. The mean postoperative duration of enoxaparin was 4 days. No patients had thromboembolic complications through 30 days after the procedure. The overall 30-day mortality rate was 0%. In conclusion, our findings demonstrate that bridging therapy with therapeutic-dose enoxaparin is feasible and associated with a low incidence of major bleeding and no thromboembolic complications. However, the optimal approach to managing patients perioperatively is uncertain and requires further evaluation.
Anticoagulants ; Atrial Fibrillation ; Enoxaparin* ; Hemorrhage ; Hemostasis ; Heparin, Low-Molecular-Weight ; Humans ; Incidence ; Injections, Subcutaneous ; Korea ; Male ; Minor Surgical Procedures ; Mortality ; Retrospective Studies ; Thromboembolism ; Venous Thromboembolism ; Warfarin

Interstitial lung disease (ILD) occurs in 15% of patients with collagen vascular disease (CVD), referred to as connective tissue disease (CTD). Despite advances in management strategies, ILD continues to be a significant cause of mortality in patients with CVD-associated ILD (CTD-ILD). There is a lack of randomized, clinical trials assessing pharmacological agents for CTD-ILD, except in cases of ILD-associated systemic sclerosis (SSc). This may be due to the lack of CTD cases available, the difficulty of histological confirmation of ILD, and the various types of CTD and ILD. As a result, evidence-based pharmacological treatment of CTD-ILD is not yet well established. CTD-ILD presents with varying degrees of histology, from inflammation to fibrosis, and a wide spectrum of clinical manifestations, from minimal symptoms to respiratory failure. This renders it difficult for clinicians to make decisions regarding treatment options, observational strategies, optimal timing for interventions, and the appropriateness of pharmacological agents for treatment. There is no specific treatment for reversing fibrosis-like idiopathic pulmonary fibrosis in a clinical setting. This review describes pharmacological interventions for SSc-ILD described in randomized control trials, and presents an overview of recent advances of CTD-ILD-dependent treatments based on the types of CTD.
Autoimmune Diseases ; Collagen ; Connective Tissue Diseases ; Connective Tissue* ; Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis ; Immunosuppressive Agents ; Inflammation ; Lung Diseases, Interstitial* ; Mortality ; Respiratory Insufficiency ; Scleroderma, Systemic ; Vascular Diseases

The majority of colorectal carcinomas (95~100%) are thought to arise from adenomas. Yet colorectal carcinomas may rarely arise de novo. The popular definition of de novo carcinoma is that the lesion should consist exclusively of a carcinoma histologically and contain no adenomatous elements. Without an adenoma-carcinoma sequence, de novo carcinomas have a much higher rate of submucosal invasion, despite their small size. Their speed of growth is thought to be rapid. Some studies have shown that de novo carcinomas might arise as a macroscopically flat or depressed lesion, rather than a protruded one. However, the typical macroscopic findings of de novo carcinomas have not been established. They might be variable macroscopically and include a protruded type. We report a case of de novo colorectal carcinoma that invaded the submucosal layer involving a minute sessile polyp only 3 mm in diameter, which was removed by endoscopic mucosal resection.
Adenoma ; Colorectal Neoplasms ; Polyps

Malignant mesothelioma (MM) is the aggressive tumor of serosal surfaces. There are crude pathogenetic results regarding the biology of MM. Coordinated upregulations of p53 gene expression are shown in malignancies. We believed that there are changes in the p53 expression with transformation from reactive hyperplasia to MM. A 65-year-old male was admitted the hospital because of left pleuritic chest pains in 2004. Chest computed tomography (CT) results showed left pleural effusions with loculation and pleural thickening. Pathologic findings revealed reactive mesothelial hyperplasia. In 2008, the patient again felt left pleuritic chest pains. Chest CT showed progressive thickening of the left pleura. Pathologic diagnosis was atypical mesothelial hyperplasia. In 2011, chest CT showed progressive thickening of his left pleura. He was diagnosed with well-differentiated papillary mesothelioma. Serial change was analyzed by immunohistochemical staining for p53 of pleural tissues. There were no remarkable changes in p53 expressions during the transformation to MM.
Aged ; Biology ; Chest Pain ; Diagnosis ; Follow-Up Studies* ; Genes, p53 ; Humans ; Hyperplasia ; Male ; Mesothelioma* ; Pleura ; Pleural Effusion ; Thorax ; Tomography, X-Ray Computed ; Tumor Suppressor Protein p53

Cytomegalovirus (CMV) is a prevalent pathogen, with 98~100% of Korean adults showing prior exposure by serology. A primary infection, such as CMV infectious mononucleosis, is very rare. CMV infectious mononucleosis often presents an initial diagnostic problem. Patients are often hospitalized with a wide variety of clinical diagnoses including fever of unknown origin without pharyngitis and lymphadenopathy. CMV gastrointestinal infections are rare in previously immunocompetent individuals. The most common sites involved are the colon and rectum, although lesions of the stomach have also been described. It is unusual to see CMV infectious mononucleosis and CMV gastrointestinal infection in the same patient. Our patient received symptomatic treatment and fully recovered. We present a case of CMV infectious mononucleosis with gastric ulcers in a previously healthy adult.
Adult ; Colon ; Cytomegalovirus ; Fever of Unknown Origin ; Humans ; Infectious Mononucleosis ; Lymphatic Diseases ; Pharyngitis ; Rectum ; Stomach ; Stomach Ulcer

Pulmonary siderosis is a pneumoconiosis caused by chronic iron inhalation. A diagnosis of pulmonary siderosis is based on a patient history of iron inhalation, on chest radiographic findings, and on accumulation of iron oxide in macrophages within the lung. A typical radiographic finding of pulmonary siderosis includes ill-defined micronodules that are diffusely distributed in the lung. We experienced a 52-year-woman with a 1.3x1.5-cm mass in the left upper lobe with multiple nodules in both lungs. Because the radiographic findings were atypical, we conducted a video-assisted thorascopic lung biopsy procedure to exclude the diagnosis of metastatic lung cancer. After confirming iron deposition in the lung tissue and knowing the patient's occupational history of welding iron, we concluded that this was a case of pulmonary siderosis.
Biopsy ; Ferric Compounds ; Hemosiderosis ; Humans ; Inhalation ; Iron ; Lung ; Lung Diseases ; Lung Neoplasms ; Macrophages ; Multiple Pulmonary Nodules ; Neoplasm Metastasis ; Pneumoconiosis ; Siderosis ; Thorax ; Welding

Pulmonary siderosis is a pneumoconiosis caused by chronic iron inhalation. A diagnosis of pulmonary siderosis is based on a patient history of iron inhalation, on chest radiographic findings, and on accumulation of iron oxide in macrophages within the lung. A typical radiographic finding of pulmonary siderosis includes ill-defined micronodules that are diffusely distributed in the lung. We experienced a 52-year-woman with a 1.3x1.5-cm mass in the left upper lobe with multiple nodules in both lungs. Because the radiographic findings were atypical, we conducted a video-assisted thorascopic lung biopsy procedure to exclude the diagnosis of metastatic lung cancer. After confirming iron deposition in the lung tissue and knowing the patient's occupational history of welding iron, we concluded that this was a case of pulmonary siderosis.
Biopsy ; Ferric Compounds ; Hemosiderosis ; Humans ; Inhalation ; Iron ; Lung ; Lung Diseases ; Lung Neoplasms ; Macrophages ; Multiple Pulmonary Nodules ; Neoplasm Metastasis ; Pneumoconiosis ; Siderosis ; Thorax ; Welding

BACKGROUND: Most patients with influenza recover spontaneously or following treatment with an anti-viral agent, but some patients experience pneumonia requiring hospitalization. We conducted a retrospective review to determine the incidence and risk factors of pneumonia in hospitalized patients with influenza A or B. METHODS: A total of 213 patients aged 18 years or older and hospitalized with influenza between January 2012 and January 2015 were included in this study. A reverse-transcriptase polymerase chain reaction assay was used to detect the influenza A or B virus in the patients' sputum samples. We collected demographic and laboratory data, combined coexisting diseases, and radiologic findings. RESULTS: The incidence of pneumonia was higher in patients in the influenza A group compared to those in the influenza B group (68.6% vs. 56.9%), but this difference was not statistically significant. The presence of underlying respiratory disease was significantly associated with pneumonia in the influenza A group (adjusted odds ratio [OR], 3.975; 95% confidence interval [CI], 1.312–12.043; p=0.015). In the influenza B group, the white blood cell count (adjusted OR, 1.413; 95% CI, 1.053–1.896; p=0.021), platelet count (adjusted OR, 0.988; 95% CI, 0.978–0.999; p=0.027), and existence of an underlying medical disease (adjusted OR, 15.858; 95% CI, 1.757–143.088; p=0.014) were all significantly associated with pneumonia in multivariate analyses. CONCLUSION: The incidence of pneumonia was 65.7% in hospitalized patients with influenza A or B. The risk factors of pneumonia differed in hospitalized patients with influenza A or B.
Comorbidity ; Herpesvirus 1, Cercopithecine ; Hospitalization ; Humans ; Incidence* ; Influenza, Human* ; Leukocyte Count ; Multivariate Analysis ; Odds Ratio ; Platelet Count ; Pneumonia* ; Polymerase Chain Reaction ; Retrospective Studies ; Risk Factors* ; Seasons* ; Sputum

BACKGROUND: Vitamin D can translocate a vitamin D receptor (VDR) from the nucleus to the cell membranes. The meaning of this translocation is not elucidated in terms of a role in pathogenesis of chronic obstructive pulmonary disease (COPD) till now. VDR deficient mice are prone to develop emphysema, suggesting that abnormal function of VDR might influence a generation of COPD. The blood levels of vitamin D have known to be well correlated with that of lung function in patients with COPD, and smoking is the most important risk factor in development of COPD. This study was performed to investigate whether cigarette smoke extracts (CSE) can inhibit the translocation of VDR and whether mitogen activated protein kinases (MAPKs) are involved in this inhibition. METHODS: Human alveolar basal epithelial cell line (A549) was used in this study. 1,25-(OH2)D3 and/or MAPKs inhibitors and antioxidants were pre-incubated before stimulation with 10% CSE, and then nucleus and microsomal proteins were extracted for a Western blot of VDR. RESULTS: Five minutes treatment of 1,25-(OH2)D3 induced translocation of VDR from nucleus to microsomes by a dose-dependent manner. CSE inhibited 1,25-(OH2)D3-induced translocation of VDR in both concentrations of 10% and 20%. All MAPKs inhibitors did not suppress the inhibitory effects of CSE on the 1,25-(OH2)D3-induced translocation of VDR. Quercetin suppressed the inhibitory effects of CSE on the 1,25-(OH2)D3-induced translocation of VDR, but not in n-acetylcysteine. CONCLUSION: CSE has an ability to inhibit vitamin D-induced VDR translocation, but MAPKs are not involved in this inhibition.
Animals ; Antioxidants ; Blotting, Western ; Cell Membrane ; Emphysema ; Epithelial Cells ; Humans ; Lung ; Mice ; Microsomes ; Mitogen-Activated Protein Kinases ; Proteins ; Pulmonary Disease, Chronic Obstructive ; Quercetin ; Receptors, Calcitriol ; Risk Factors ; Smoke ; Smoking ; Tobacco Products ; Vitamin D ; Vitamins

BACKGROUND/AIMS: The mortality rate following massive and submassive pulmonary embolism (PE) remains high despite thrombolytic therapy. Although thrombolytic therapy is considered a life-saving intervention in massive PE, it is only selectively indicated in patients without hypotension who are at high risk of developing hypotension. Little is known about its clinical outcome in Korea. METHODS: We retrospectively reviewed the records of patients given thrombolytics for massive and submassive PE objectively confirmed with chest computed tomography at Soon Chun Hyang University Hospital, Seoul, Korea, from 1 January 2004 to 1 August 2011. The primary outcome of this study was 30-day mortality. Secondary outcomes were the incidence of major bleeding at 30 days, mortality at 90 days, and recurrent venous thromboembolism (VTE) at 90 days. RESULTS: Thrombolytic therapy was performed in 21 patients: nine with massive and 12 with submassive PE. The overall 30-day mortality rate was 24% (5/21). The mortality rate in patients with massive PE was higher than that in patients with submassive PE (44% vs. 8%, respectively; p = 0.010). Mortality rates at 90 and 30 days were identical. The estimated causes of death were right ventricular failure in four patients and fatal bleeding in one patient. The median time to death from thrombolysis was 1 day (0-13 days). Major bleeding episodes occurred in three patients (14%), including fatal bleeding in one patient. There was no recurrent VTE at 90 days. CONCLUSIONS: Patients who underwent thrombolytic therapy for massive PE showed a higher 30-day mortality compared with patients with submassive PE.
Cause of Death ; Hemorrhage ; Humans ; Hypotension ; Incidence ; Korea ; Pulmonary Embolism ; Retrospective Studies ; Thorax ; Thrombolytic Therapy ; Venous Thromboembolism