PURPOSE: We reviewed the treatment outcomes and prognostic factors for patients with anal canal carcinoma who were treated with curative intent chemoradiotherapy (CRT) at Severance Hospital from 2005 to 2011. MATERIALS AND METHODS: Data for 38 eligible patients treated during this period were reviewed. All patients were treated with curative intent using radiotherapy (RT) with (n = 35) or without concomitant chemotherapy (n = 3). Among 35 patients who received CRT, most of the chemotherapeutic regimens were either 5-fluorouracil (5-FU) plus mitomycin C (23 patients) or 5-FU plus cisplatin (10 patients). Recurrence-free survival (RFS), colostomy-free survival (CFS), overall survival (OS), and locoregional control (LRC) rates were calculated using the Kaplan-Meier method and survival between subgroups were compared using the log-rank test. Cox's proportional hazard model was used for multivariate analysis. RESULTS: Over a median follow-up period of 44 months (range, 11 to 96 months), 3-year RFS, CFS, OS, and LRC were 80%, 79%, 85%, and 92%, respectively. In multivariate analysis, tumor size >4 cm was an independent predicting factor for poorer RFS (hazard ratio [HR], 6.35; 95% confidence interval [CI], 1.42 to 28.5; p = 0.006) and CFS (HR, 6.25; 95% CI, 1.39-28.0; p = 0.017), while the presence of external iliac lymph node metastasis was an independent prognosticator for poorer OS (HR, 9.32; 95% CI, 1.24 to 70.3; p = 0.030). No treatment-related colostomies or deaths occurred during or after treatment. CONCLUSION: Curative intent CRT resulted in excellent outcomes that were comparable to outcomes in previous randomized trials. No severe treatment-related toxicities were observed.
Anal Canal ; Anus Neoplasms ; Carcinoma, Squamous Cell ; Chemoradiotherapy ; Cisplatin ; Colostomy ; Fluorouracil ; Follow-Up Studies ; Humans ; Lymph Nodes ; Mitomycin ; Multivariate Analysis ; Neoplasm Metastasis ; Proportional Hazards Models

BACKGROUND: Acute kidney injury (AKI) is a risk factor for progression to chronic kidney disease, with even subclinical AKI episodes progressing to chronic kidney disease. Several risk factors such as preexisting kidney disease, hyperglycemia, and hypertension may aggravate renal disease after AKI. However, mechanisms underlying the progression of AKI are still unclear. This study identified the effect of human cluster of differentiation 36 (CD36) overexpression on the progression of folic acid-induced AKI. METHODS: Pax8–rtTA/tetracycline response element–human CD36 transgenic mice were used to elucidate the effect of human CD36 overexpression in the proximal tubules on folic acid-induced AKI. RESULTS: Results of histological analysis showed severely dilated tubules with casts and albuminuria in folic acid-treated transgenic mice overexpressing human CD36 compared with folic acid-treated wild-type mice. In addition, analysis of mRNA expression showed a significant increase in the collagen 3a1 gene in folic acid-treated transgenic mice overexpressing human CD 36 compared with folic acid-treated wild type mice. CONCLUSION: Human CD36-overexpressing transgenic mice showed severe pathological changes and albuminuria compared with wild-type mice. Moreover, mRNA expression of the collagen 3a1 gene increased in folic acid-treated transgenic mice. These results suggest that human CD36 overexpression is a risk factor of AKI and its progression to chronic kidney disease.
Acute Kidney Injury* ; Albuminuria ; Animals ; Collagen ; Fibrosis ; Folic Acid ; Humans* ; Hyperglycemia ; Hypertension ; Kidney Diseases ; Mice* ; Mice, Transgenic ; Renal Insufficiency ; Renal Insufficiency, Chronic ; Risk Factors ; RNA, Messenger

In randomized phase 3 clinical trials azacitidine has been shown to prolong survival in patients with higher-risk myelodysplastic syndrome (MDS). Therefore, azacitidine therapy should be considered for treating MDS patients with higher-risk disease. A 78-year-old male was administered the first cycle of azacitidine treatment for higher-risk MDS. On day three of chemotherapy he complained of fever and dyspnea, and radiographic findings revealed bilateral perihilar-peribronchial infiltration and a small amount of pleural effusion. Considering the possibility of pneumonia, intravenous broad-spectrum antibiotics were administered and azacitidine therapy was discontinued. Upon improvement of the patient's subjective symptoms and radiographic abnormalities, azacitidine therapy was resumed. However, fever and dyspnea developed again upon recommencement of azacitidine therapy. A diagnosis was made of azacitidine-induced lung injury and corticosteroid treatment was administered. Although lung injury is a rare complication induced by azacitidine, physicians should be aware of this life-threatening side effect.
Aged ; Anti-Bacterial Agents ; Azacitidine ; Diagnosis ; Drug Therapy ; Dyspnea ; Fever ; Humans ; Lung Injury* ; Male ; Myelodysplastic Syndromes* ; Pleural Effusion ; Pneumonia

Heterotopic gastric mucosa (HGM) is a rare anomaly in the small bowel and may be the cause of intussusception when it gets a lead point in the jejunum. All cases of intussusception due to intestinal HGM have been treated with surgical resection. A 5-year-old girl presented with chief complaints of vomiting and abdominal pain for 2 weeks. A computed tomography scan of the abdomen showed intussusception at the proximal jejunal loops. Three air reductions and one saline reduction were attempted without success. She continued to be symptomatic, and endoscopic evaluation was performed. Enteroscopy revealed some variable-sized polypoid mucosal lesions with erosions on the proximal jejunum. Endoscopic mucosal resection was performed using a snare. The resected tissues histologically showed a hyperplastic polyp arising from the HGM. Her symptoms did not recur within 1 year after the treatment. Our case showed that enteroscopy could be useful for the diagnosis and management of jejunal intussusception caused by HGM.
Abdomen ; Abdominal Pain ; Child, Preschool ; Diagnosis ; Female ; Gastric Mucosa* ; Humans ; Intussusception* ; Jejunum ; Polyps ; SNARE Proteins ; Vomiting

OBJECTIVE: To compare the image quality of shoulder CT arthrography performed using 120 kVp and 140 kVp protocols. MATERIALS AND METHODS: Fifty-four CT examinations were prospectively included. CT scans were performed on each patient at 120 kVp and 140 kVp; other scanning parameters were kept constant. Image qualities were qualitatively and quantitatively compared with respect to noise, contrast, and diagnostic acceptability. Diagnostic acceptabilities were graded using a one to five scale as follows: 1, suboptimal; 2, below average; 3, acceptable; 4, above average; and 5, superior. Radiation doses were also compared. RESULTS: Contrast was better at 120 kVp, but noise was greater. No significant differences were observed between the 120 kVp and 140 kVp protocols in terms of diagnostic acceptability, signal-to-noise ratio, or contrast-to-noise ratio. Lowering tube voltage from 140 kVp to 120 kVp reduced the radiation dose by 33%. CONCLUSION: The use of 120 kVp during shoulder CT arthrography reduces radiation dose versus 140 kVp without significant loss of image quality.
Adult ; Aged ; Contrast Media/diagnostic use ; Female ; Humans ; Male ; Middle Aged ; Prospective Studies ; Radiation Dosage ; Radiographic Image Interpretation, Computer-Assisted ; Shoulder/*radiography/surgery ; Shoulder Dislocation/pathology/radiography ; Signal-To-Noise Ratio ; *Tomography, X-Ray Computed

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

PURPOSE: Acute myocardial infarction (AMI) concomitant with acute aortic syndrome (AAS) is rare but prompt recognition of concomitant AAS is critical, particularly in patients with ST-segment elevation myocardial infarction (STEMI) because misdiagnosis with early thrombolytic or anticoagulant treatment may result in catastrophic consequences. This study examined the clinical features of patients of STEMI concomitant with AAS that may be a diagnostic clue. METHODS: Between January 1, 2010 and December 31, 2014, 22 patients who had the initial diagnosis of acute coronary syndrome (AMI and unstable angina) and AAS (aortic dissection, intramural hematoma, and ruptured thoracic aneurysm) in our emergency department were reviewed. Among them, 10 patients who were transferred from other hospitals and 4 patients with non-STEMI were excluded, leaving 8 patients of STEMI concomitant with AAS for analysis. RESULTS: The mean age of study patients was 57.5+/-16.31 years and five patients were Stanford type A and three patients were type B aortic dissection. Six patients had ST-segment elevation in anterior leads and 2 patients in inferior leads. Most patients had acute onset and severe chest pain, but none had dissecting nature chest pain. Serum troponin I was elevated in three patients but all patients had Ddimer elevation. Aortic regurgitation or regional wall motion abnormality was detected in four patients, and widened mediastinum was observed in all study patients. CONCLUSION: Concomitant AAS might be suspected in patients with STEMI who have elevated D-dimer and widened mediastinum.
Acute Coronary Syndrome ; Aortic Valve Insufficiency ; Chest Pain ; Diagnosis ; Diagnostic Errors ; Emergency Service, Hospital ; Hematoma ; Humans ; Mediastinum ; Myocardial Infarction* ; Troponin I

PURPOSE: The purpose of this study is to examine the causes of Pleural effusion (PE) in cancer patients and to compare the clinical characteristics between malignant PE (MPE) and non-MPE. METHODS: All consecutive cancer patients with PE who underwent diagnostic thoracentesis from January 1, 2008 to March 31, 2011 were analyzed retrospectively. RESULTS: A total of 719 patients were included; mean age was 58.4+/-13.6 years and 44.5% were female. The most common cause of PE was MPE (57.7%), followed by parapneumonic or empyema in 16.3%. However, the etiology was significantly different according to primary tumor origin and subtypes of lung cancer. While MPE was most common in lung, breast, and gynecologic cancer, hepatic hydrothorax was the main cause in Hepatocellular carcinoma (HCC). MPE accounted for 85.2% in adenocarcinoma, and 30.2% and 58.8% in squamous cell and small cell carcinomas, respectively. Patients with MPE were younger (57.0 vs. 60.2 years) and female-dominant (55.4% vs. 29.6%) compared to those with non-MPE. MPE had the large size (53.5% vs. 34.9%) and left location of PE (31.3% vs. 19.4%) more frequently than non-MPE, and fewer neutrophils (15.4% vs. 30.6%) and more lymphocytes (32.2% vs. 28.2%), higher levels of pH (7.33 vs. 7.29), and lower levels of glucose (111.5 vs. 129.7 mg/dL) than non-MPE (p<0.001 for all). CONCLUSION: Overall, MPE was the most common cause of PE in cancer patients. However the etiology of PE was significantly different according to primary tumor origin and subtypes of lung cancer. A difference in age, gender, size and location of PE, cell count, pH, and glucose was observed between MPE and non-MPE.
Adenocarcinoma ; Breast ; Carcinoma, Hepatocellular ; Carcinoma, Small Cell ; Cell Count ; Empyema ; Female ; Glucose ; Humans ; Hydrogen-Ion Concentration ; Hydrothorax ; Liver Neoplasms ; Lung ; Lung Neoplasms ; Lymphocytes ; Neutrophils ; Pleural Effusion* ; Retrospective Studies

Graves' ophthalmopathy occurs in 25-50% of patients with Graves' disease. Although patients with Graves' ophthalmopathy mostly present with hyperthyroidism, a minority of patients have euthyroid or hypothyroid characteristics, which may delay a correct diagnosis. Here, we report a case of euthyroid Graves' ophthalmopathy that was initially negative for thyroid autoantibodies, but later changed to positivity.
Autoantibodies* ; Diagnosis ; Graves Disease ; Humans ; Hyperthyroidism ; Thyroid Gland