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

Coccidioidomycosis is a fungal infection caused by Coccidioides immitis. The endemic area is mostly south-western United States. As increasing in overseas travel to endemic areas, the incidence rate has been recently increased in non-endemic areas. The diagnosis may be delayed in non-endemic area. It is important to elicit traveling histories and to differentiate lung consolidation with eosinophilia, for timely diagnosis of coccidioidomycosis. Recently, we experienced a case with pulmonary coccidioidomycosis in a Korean American who visited Korea showed consolidation in right lower lobe on chest X-ray and prolonged eosinophilia. In the case, a confirmatory diagnostic method was percutaneous transthoracic needle biopsy of lung. We report acute pulomonary coccidioidomycosis case and review previous published reports with pulmonary manifestation in Korea.
Asian Americans ; Biopsy, Needle ; Coccidioides ; Coccidioidomycosis* ; Diagnosis ; Endemic Diseases ; Eosinophilia ; Humans ; Incidence ; Korea* ; Lung Diseases, Fungal ; Lung* ; Thorax ; United States

Smoking-related interstitial fibrosis (SRIF) is characterized by marked alveolar septal fibrosis seen as distinct thick collagen bundles, along with emphysema and respiratory bronchiolitis. In 2010, SRIF was deemed a new entity that differed from idiopathic pulmonary fibrosis (IPF) clinically, pathologically, and radiologically. No case of SRIF has been reported in Korea and it is rare worldwide. Here, we report the 1-year follow-up of three cases of SRIF.
Bronchiolitis ; Collagen ; Emphysema ; Fibrosis* ; Follow-Up Studies* ; Idiopathic Pulmonary Fibrosis ; Korea ; Smoking

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

A 52-yr-old male with alcoholic liver cirrhosis was hospitalized for hematochezia. He had undergone small-bowel resection due to trauma 15 yr previously. Esophagogastroduodenoscopy showed grade 1 esophageal varices without bleeding. No bleeding lesion was seen on colonoscopy, but capsule endoscopy showed suspicious bleeding from angiodysplasia in the small bowel. After 2 weeks of conservative treatment, the hematochezia stopped. However, 1 week later, the patient was re-admitted with hematochezia and a hemoglobin level of 5.5 g/dL. Capsule endoscopy was performed again and showed active bleeding in the mid-jejunum. Abdominal computed tomography revealed a varix in the jejunal branch of the superior mesenteric vein. A direct portogram performed via the transhepatic route showed portosystemic collaterals at the distal jejunum. The patient underwent coil embolization of the superior mesenteric vein just above the portosystemic collaterals and was subsequently discharged without re-bleeding. At 8 months after discharge, his condition has remained stable, without further bleeding episodes.
Embolization, Therapeutic/*methods ; Gastrointestinal Hemorrhage/etiology/therapy ; Humans ; Jejunum/*blood supply ; Liver Cirrhosis, Alcoholic/complications ; Male ; Middle Aged ; Varicose Veins/diagnosis/etiology/*therapy

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

BACKGROUND/AIMS: Diesel exhaust particles (DEPs) lead to elevation of reactive oxygen species, which can activate the nucleotide-binding oligomerization domain-like receptor (NLR) family members containing the pyrin domain 3 (NLRP3)-inf lammasome. In this study, we elucidated whether NLRP3 -inf lammasome is activated by DEPs and whether antioxidants (N-acetylcysteine [NAC]) could inhibit such activation. METHODS: RAW 264.7 cells and ex vivo lung tissues explants obtained from elastase-induced emphysema animal models were stimulated with cigarette smoking extract (CSE), DEPs, and lipopolysaccharide, and levels of interleukin-1β (IL-1β), caspase-1 and nucleotide-binding oligomerization domain-like receptor (NLR) family members containing the pyrin domain (NLRP3)-inflammasome were assessed by Western blotting and immunohistochemistry. RESULTS: NAC and caspase-1 inhibitor suppressed CSE- and DEP-induced secretion of IL-1β in RAW 264.7 cells. The expression levels of the NLRP3-inflammasome and caspase-1 were upregulated in RAW 264.7 cells by stimulation with CSE and DEPs and were inhibited by NAC. CSE and DEPs increased the secretion of IL-1β in lung tissues from both the normal and elastase-induced emphysema groups. The secretion of IL-1β by CSE and DEPs was increased in the elastin-induced emphysema group more than that in the normal group (CSE: 309 ± 19 pg/mL vs. 151 ± 13 pg/mL, respectively, p < 0.05; DEP: 350 ± 24 pg/mL vs. 281 ± 15 pg/mL, respectively, p < 0.05). NAC inhibited CSE- and DEP-induced IL-1β secretion in both the normal and elastase-induced emphysema groups. NLRP3-inflammasome expression as determined by immunohistochemistry was increased by CSE and DEPs in both the normal and elastin-induced emphysema groups, and was suppressed by NAC. CONCLUSIONS: The NLRP3-inf lammasome is activated by DEPs in ex vivo tissue explants from elastase-induced emphysema animal model, and this activation is inhibited by NAC.
Antioxidants ; Blotting, Western ; Emphysema* ; Humans ; Immunohistochemistry ; Lung* ; Models, Animal ; Pancreatic Elastase ; Pulmonary Disease, Chronic Obstructive ; RAW 264.7 Cells* ; Reactive Oxygen Species ; Smoking ; Vehicle Emissions*