Purpose: The authors aimed to investigate the utility of blood culture (BC) for children with simple febrile seizure (SFS) in the emergency department (ED) in the post-10/13-valent pneumococcal conjugate vaccine (PCV) era. Methods: This study was performed at the ED of a tertiary care university-affiliated women and children’s hospital, and involved 3,237 previously healthy children aged 6-60 months who visited the ED with SFS from January 2013 through December 2017. The SFS was defined according to the International Classification of Diseases, 11th Revision codes related to seizure. The children were divided into 2 groups according to the vaccination rates of the period of their visit: the 70-PCV (70%, 2013-2014) and 97-PCV (97%, 2015-2017) groups. The primary outcome was the yield, defined as a true positivity of BC. In addition, we collected information on baseline characteristics, ED length of stay, inflammatory biomarkers, and ED outcomes. Results: Of the 1,578 children with SFS who underwent BC, 1,357 belonged to the 97-PCV group. The median age of the study population was 22 months (interquartile range, 16.0-30.0), and 935 children (59.3%) were boys. Of the 41 children (2.6%) with positive BC results, 3 had the yield (0.2%): Staphylococcus aureus in 2 children and Streptococcus pneumoniae in the other. All 3 children belonged to the 97-PCV group. There were 38 contaminated BCs (2.4%; 95% confidence interval, 1.6%-3.2%). The 97-PCV group showed a shorter median ED length of stay (166.0 minutes [108.0-279.5] vs. 143.0 [109.5-209.5]; P = 0.010) and a lower rate of hospitalization (39.4% vs. 12.8%; P < 0.001). No differences between the 2 groups were found in the baseline characteristics and biomarkers. Conclusion This study suggests a low utility of BC in previously healthy children with SFS in emergency settings in the post-10/13-valent PCV era.

No abstract available.
Acute Disease ; Biopsy ; Fatal Outcome ; Female ; Fluorescent Antibody Technique ; Glomerulonephritis/*complications/diagnosis/drug therapy/immunology ; Humans ; Immunosuppressive Agents/therapeutic use ; Microscopic Polyangiitis/*complications/diagnosis/drug therapy/immunology ; Middle Aged ; Pancreatitis/diagnosis/drug therapy/*etiology/immunology ; Treatment Outcome

Secondary involvement of the gallbladder by systemic lymphoma is exceedingly rare and relapsed diffuse large B cell lymphoma of the gallbladder has not been reported. A 78-year-old man was admitted to the hospital due to epigastric pain and jaundice. His past medical history was remarkable for diagnosis with diffuse large B-cell lymphoma of the ileum 5 years ago. He underwent right hemicolectomy and three cycles of adjuvant chemotherapy and had complete remission. Abdominal computed tomography showed choledocholithiasis and focal thickening at fundus of the gallbladder. The patient underwent open cholecystectomy. Pathologic examination revealed diffuse large B-cell lymphoma. We report a case of solitary, relapsed diffuse large B-cell lymphoma of the gallbladder with literature review.
Aged ; B-Lymphocytes* ; Chemotherapy, Adjuvant ; Cholecystectomy ; Choledocholithiasis ; Diagnosis ; Gallbladder* ; Humans ; Ileum ; Jaundice ; Lymphoma ; Lymphoma, B-Cell* ; Lymphoma, Non-Hodgkin ; Recurrence

Some parts of published paper were misprinted.

Concurrence of primary gastric adenocarcinoma and lymphoma have been described very rarely in the literature; its incidence is estimated at 0.08%. To our knowledge, there are no reports about a collision tumor comprising early gastric cancer and diffuse large B-cell lymphoma from the same lesion. The term "collision tumor" refers to the coexistence of two or more histologically distinct tumors within the same mass with no histologic admixture. A 76-year-old man complained of a 5-month-history of dyspepsia, and underwent esophagogastroduodenoscopy. Endoscopic findings showed a nodular, round, flat mass lesion in the upper body, therefore we performed endoscopic submucosal dissection (ESD). Pathologic findings revealed a well-differentiated adenocarcinoma accompanied by diffuse large B-cell lymphoma without evidence of Helicobacter pylori infection. Conventional CT and PET-CT scans revealed metastatic lymph nodes in the parotid gland, submandibular gland, maxillary gland and the inguinal regions. The pathogenesis of a collision tumor comprising two different cancers is not well understood. In addition, there are no established treatment guidelines in this series. In the current case, the patient underwent ESD for the removal of adenocarcinoma concomitantly with chemotherapy for the management of metastatic lymphoma.
Adenocarcinoma* ; Aged ; B-Lymphocytes* ; Drug Therapy ; Dyspepsia ; Endoscopy, Digestive System ; Helicobacter pylori ; Humans ; Incidence ; Lymph Nodes ; Lymphoma ; Lymphoma, B-Cell* ; Lymphoma, Large B-Cell, Diffuse ; Parotid Gland ; Stomach Neoplasms ; Submandibular Gland

Diabetic ketoacidosis (DKA) is a complex medical disorder characterized by abnormalities in electrolyte, acid-base, and volume status. Metabolic acidosis in mild and moderate DKA is corrected with insulin therapy. Bicarbonate therapy may be indicated in cases of severe metabolic acidosis, however the use of bicarbonate in severe DKA is controversial due to a lack of prospective randomized studies. Renal replacement therapy can be used for correction of systemic acidemia. Continuous renal replacement therapy (CRRT) is used in patients who are too hemodynamically unstable to tolerate conventional hemodialysis, but has also been used in treatment of patients with severe DKA. CRRT has never been used previously in DKA patients with refractory metabolic acidosis in Korea. Here, we describe the successful treatment of a DKA patient with refractory metabolic acidosis with CRRT.
Acidosis* ; Diabetic Ketoacidosis* ; Hemodiafiltration* ; Humans ; Insulin ; Korea ; Prospective Studies ; Renal Dialysis ; Renal Replacement Therapy

PURPOSE: Sclerostin, an inhibitor of Wnt/beta-catenin signaling, exerts negative effects on bone formation and contributes to periodontitis-induced alveolar bone loss. Recent studies have demonstrated that serum sclerostin levels are increased in diabetic patients and that sclerostin expression in alveolar bone is enhanced in a diabetic periodontitis model. However, the molecular mechanism of how sclerostin expression is enhanced in diabetic patients remains elusive. Therefore, in this study, the effect of hyperglycemia on the expression of sclerostin in osteoblast lineage cells was examined. METHODS: C2C12 and MLO-Y4 cells were used in this study. In order to examine the effect of hyperglycemia, the glucose concentration in the culture medium was adjusted to a range of levels between 40 and 100 mM. Gene expression levels were examined by quantitative reverse transcription-polymerase chain reaction and Western blot assays. Top-Flash reporter was used to examine the transcriptional activity of the beta-catenin/lymphoid enhanced factor/T-cell factor complex. Tumor necrosis factor-alpha (TNFalpha) protein levels were examined with the enzyme-linked immunosorbent assay. The effect of reactive oxygen species on sclerostin expression was examined by treating cells with 1 mM H2O2 or 20 mM N-acetylcysteine. RESULTS: The high glucose treatment increased the mRNA and protein levels of sclerostin. High glucose suppressed Wnt3a-induced Top-Flash reporter activity and the expression levels of osteoblast marker genes. High glucose increased reactive oxygen species production and TNFalpha expression levels. Treatment of cells with H2O2 also enhanced the expression levels of TNFalpha and sclerostin. In addition, N-acetylcysteine treatment or knockdown of TNFalpha attenuated high glucose-induced sclerostin expression. CONCLUSIONS: These results suggest that hyperglycemia increases sclerostin expression via the enhanced production of reactive oxygen species and TNFalpha.
Acetylcysteine ; Alveolar Bone Loss ; Blotting, Western ; Enzyme-Linked Immunosorbent Assay ; Gene Expression ; Glucose ; Humans ; Hyperglycemia* ; Necrosis* ; Osteoblasts ; Osteogenesis ; Oxygen* ; Periodontitis ; Reactive Oxygen Species ; RNA, Messenger ; Tumor Necrosis Factor-alpha

Rothia muciliaginosa (R. mucilaginosa) is a facultative, Gram-positive coccus that is considered to be part of the normal flora of the mouth and respiratory tract. There are sporadic reports of the organism causing endocarditis in patients with heart valve abnormalities, as well as meningitis, septicemia, and pneumonia associated with intravenous drug abuse. However, it is an unusual pathogen in cases of peritoneal dialysis (PD)-associated peritonitis. Although R. mucilaginosa is generally susceptible to penicillin, ampicillin, cefotaxime, imipenem, rifampicin, and glycopeptides, there are no guidelines for the treatment of PD-associated peritonitis. Herein, we report a case of PD-associated peritonitis due to R. mucilaginosa that was resolved with intraperitoneal antibiotic treatment.
Ampicillin ; Cefotaxime ; Endocarditis ; Glycopeptides ; Heart Valves ; Humans ; Imipenem ; Meningitis ; Mouth ; Penicillins ; Peritoneal Dialysis ; Peritoneal Dialysis, Continuous Ambulatory ; Peritonitis* ; Pneumonia ; Respiratory System ; Rifampin ; Sepsis ; Substance Abuse, Intravenous

TNF-alpha, a proinflammatory cytokine, inhibits osteoblast differentiation under diverse inflammatory conditions; however, the underlying mechanisms in terms of the TNF-alpha signaling pathway remain unclear. In this study, we examined the role of Msx2 in TNF-alpha-mediated inhibition of alkaline phosphatase (ALP) expression and the signaling pathways involved. TNF-alpha down-regulated ALP expression induced by bone morphogenetic protein 2 (BMP2) in C2C12 and Runx2-/- calvarial cells. Over-expression of Msx2 suppressed BMP2-induced ALP expression. Furthermore, TNF-alpha induced Msx2 expression, and the knockdown of Msx2 by small interfering RNAs rescued ALP expression, which was inhibited by TNF-alpha. TNF-alpha activated the NF-kappaB and the JNK pathways. Inhibition of NF-kappaB or JNK activation reduced the inhibitory effect of TNF-alpha on ALP expression, whereas TNF-alpha-induced Msx2 expression was only suppressed by the inhibition of the NF-kappaB pathway. Taken together, these results indicate that Msx2 mediates the inhibitory action of TNF-alpha on BMP2-regulated osteoblast differentiation and that the TNF-alpha-activated NF-kappaB pathway is responsible for Msx2 induction.
Alkaline Phosphatase/genetics/metabolism ; Animals ; Animals, Newborn ; Bone Morphogenetic Protein 2/pharmacology ; Cell Culture Techniques ; Cell Differentiation/*drug effects/genetics ; Cell Proliferation/drug effects ; Cells, Cultured ; Core Binding Factor Alpha 1 Subunit/genetics ; Down-Regulation/drug effects ; Gene Expression Regulation/drug effects ; Homeodomain Proteins/antagonists & inhibitors/genetics/*physiology ; Mice ; Mice, Inbred ICR ; Mice, Transgenic ; Osteoblasts/*drug effects/metabolism/physiology ; RNA, Small Interfering/pharmacology ; Tumor Necrosis Factor-alpha/*pharmacology

BACKGROUND AND OBJECTIVES: Endothelial dysfunction and increased vascular inflammation may be associated with variant angina (VA). However, their exact roles remain to be clarified. The aim of the presents study is to investigate whether the level of inflammation markers and the flow-mediated dilation (FMD) are related to VA. SUBJECTS AND METHODS: The study included 46 patients (VA group: 53.9+/-12.0 years, 20 males) with positive spasm provocation tests and they were without significant coronary stenosis, and 14 patients (control group: 46.6+/-13.5 years, 7 males) with negative spasm provocation tests and they were without significant coronary stenosis. The clinical characteristics and inflammatory markers, including the high sensitive C-reactive protein (hsCRP) level, the monocyte count and the von Willebrand factor (vWF) level, and the FMD were compared between the two groups. The FMD and inflammatory markers were measured in the morning before performing the ergonovine provocation coronary angiogram. RESULTS: The level of vWF was significantly higher in the VA group than in the control group (166.5+/-41.9% vs. 118.0+/-65.3%, respectively, p=0.029). The FMD was significantly decreased in the VA group compared with the control group (9.2+/-4.3% vs. 12.4+/-4.2%, respectively, p=0.021). Nitrate-mediated dilation did not differ between the two groups. The levels of the monocyte count, hs-CRP and homocysteine were higher in the VA group than in the control group (554.7+/-261.0/mm3 vs. 440.7+/-136.0/mm3, respectively, p=0.039; 0.3+/-0.4 mg/dL vs. 0.1+/-0.1 mg/dL, respectively, p=0.029; 7.54+/-4.0micronmol/L vs. 5.92+/-1.6micronmol/L, respectively, p=0.033). CONCLUSION: The results of this study suggested that increased inflammatory markers and endothelial dysfunction may be associated with variant angina.
Angina Pectoris ; C-Reactive Protein ; Coronary Stenosis ; Endothelium ; Ergonovine ; Homocysteine ; Humans ; Inflammation ; Monocytes ; Spasm ; von Willebrand Factor