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

Immune complex formation has been recently emphasized as an important pathogenetic mechanism of hepatitis B virus associated glomerulonephritis (HBGN), but little are known on the role of cell- mediated immunity in that disease. In this study, we measured lymphocyte subsets of the blood samples from three groups(HBGN group, healthy control group, hepatitis B group without renal disease) by flow cytometry in order to clarify abnormalities in immune regulatory system of HBGN. The results were as follows: 1) To compare between HBGN and healthy control group, the proportion of CD4+ cells were higher for HBGN than for healthy control but that of B lymphocytes were lower for HBGN than for healthy control. Between HBGN and hepatitis B group without renal disease, the proportion of B lymphocytes were higher for HBGN but that of NK cells were lower for HBGN(P<0.05). 2) To compare the male data of the three groups, the percentage of CD4+ cells in HBGN group were higher and the percentage of B lymphocytes were lower than healthy control. Between HBGN group and hepatitis B group without renal disease, no significant difference were noted in CD4+ cells, CD8+ cells, B lymphocytes, NK cells and CD4/CD8 ratio (P<0.05). 3) HBGN patients with membraneous nephropathy (MN) showed higher proportion of CD4+ cells than those with membranoproliferative glomerulonephritis (MPGN)(P<0.05). But, no difference was observed between HBGN patients with and without nephrotic syndrome. Nor between HBGN patients with and without HBe antigenemia. In conclusion, above result implies the pathogenetic role of cell-mediated immunity in HBGN. Analysis of lymphocyte subsets for each stage of HBGN, together with the assay of lymphocyte activation markers is required in the future.
Antigen-Antibody Complex ; B-Lymphocytes ; Flow Cytometry ; Glomerulonephritis* ; Glomerulonephritis, Membranoproliferative ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis* ; Humans ; Immunity, Cellular ; Killer Cells, Natural ; Lymphocyte Activation ; Lymphocyte Subsets* ; Lymphocytes* ; Male ; Nephrotic Syndrome

Intrathoracic involvement of immunoglobulin G4 (IgG4)-related disease has recently been reported. However, a subset of the disease presenting as interstitial lung disease is rare. Here, we report a case of a 35-year-old man with IgG4-related lung disease with manifestations similar to those of interstitial lung disease. Chest computed tomography showed diffuse ground glass opacities and rapidly progressive pleural and subpleural fibrosis in both upper lobes. Histological findings showed diffuse interstitial lymphoplasmacytic infiltration with an increased number of IgG4-positive plasma cells. Serum levels of IgG and IgG4 were also increased. The patient was diagnosed with IgG4-related lung disease, treated with anti-inflammatory agents, and showed improvement. Lung involvement of IgG4-related disease can present as interstitial lung disease and, therefore, should be differentiated when evaluating interstitial lung disease.
Adult ; Anti-Inflammatory Agents ; Fibrosis ; Glass ; Humans ; Immunoglobulin G ; Immunoglobulins ; Lung ; Lung Diseases* ; Lung Diseases, Interstitial* ; Plasma Cells ; Thorax

BACKGROUND AND PURPOSE: Middle East respiratory syndrome (MERS) has a high mortality rate and pandemic potential. However, the neurological manifestations of MERS have rarely been reported since it first emerged in 2012. METHODS: We evaluated four patients with laboratory-confirmed MERS coronavirus (CoV) infections who showed neurological complications during MERS treatment. These 4 patients were from a cohort of 23 patients who were treated at a single designated hospital during the 2015 outbreak in the Republic of Korea. The clinical presentations, laboratory findings, and prognoses are described. RESULTS: Four of the 23 admitted MERS patients reported neurological symptoms during or after MERS-CoV treatment. The potential diagnoses in these four cases included Bickerstaff's encephalitis overlapping with Guillain-Barré syndrome, intensive-care-unit-acquired weakness, or other toxic or infectious neuropathies. Neurological complications did not appear concomitantly with respiratory symptoms, instead being delayed by 2–3 weeks. CONCLUSIONS: Neuromuscular complications are not rare during MERS treatment, and they may have previously been underdiagnosed. Understanding the neurological manifestations is important in an infectious disease such as MERS, because these symptoms are rarely evaluated thoroughly during treatment, and they may interfere with the prognosis or require treatment modification.
Cohort Studies ; Communicable Diseases ; Coronavirus ; Coronavirus Infections* ; Diagnosis ; Encephalitis ; Guillain-Barre Syndrome ; Humans ; Middle East Respiratory Syndrome Coronavirus ; Middle East* ; Mortality ; Neurologic Manifestations ; Pandemics ; Peripheral Nervous System Diseases ; Prognosis ; Republic of Korea

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

Evans syndrome is a rare complication that develops in adults after liver transplantation. The possible etiologies include ABO mismatch, viral infection, post-transplantation lymphoproliferative disease, graft-versus-host disease, and the use of certain immunosuppressive drugs (e.g., calcineurin inhibitors). Here, we present a case of Evans syndrome that developed after an ABO-matched liver transplant. Glucocorticosteroid, intravenous immunoglobulin, and alternative immunosuppressant therapies all failed. Weekly rituximab (375 mg/m2) was then administered for 4 weeks. The cytopenia improved transiently after the second dose of rituximab, but soon worsened again. However, the cytopenia normalized after a splenectomy.
Adult ; Anemia, Hemolytic, Autoimmune ; Calcineurin ; Graft vs Host Disease ; Humans ; Immunoglobulins ; Liver Transplantation ; Liver* ; Purpura, Thrombocytopenic, Idiopathic ; Splenectomy* ; Rituximab

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

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