A Case of Cavernous Sinus Syndrome Due to Extranodal Diffuse Large B-Cell Lymphoma.

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin's lymphoma accounting for approximately one-third of all cases. DLBCL can present as a lymph node or extranodal tumor. Cavernous sinus (CS) is a small but complex structure in which various arteries, sympathetic plexuses, and cranial nerves are passing through. Cavernous sinus syndrome (CSS) results from any disease process that affects CS including tumor, vascular disease, infection, or inflammation. Herein, we report a case of extranodal DLBCL diagnosed by skin biopsy presenting as CSS. A 58-year-old male presented with a 3-week-old, gradually growing subcutaneous nodule on the left upper lip. He also suffered from ptosis, ophthalmoplegia, diplopia, and headache confined to the right side for 3 months. Histopathologic examination of the left upper lip showed dense dermal infiltration of atypical large tumor cells resembling centroblasts and immunoblasts. Immunohistochemistry studies revealed that the tumor cells were positive for CD20, BCL2, BCL6, MUM1, and MYC. After additional radiologic evaluation with positron emission tomography-computed tomography (PET-CT), brain magnetic resonance imaging, and orbital CT, he was finally diagnosed with extranodal DLBCL involving the right CS, oculomotor muscles, and left upper lip.

Clinical factors predicting return emergency department visits in chemotherapy-induced febrile neutropenia patients.

BACKGROUND: Although chemotherapy-induced febrile neutropenia (FN) is the most common and life-threatening oncologic emergency, the characteristics and outcomes associated with return visits to the emergency department (ED) in these patients are uncertain. Hence, we aimed to investigate the predictive factors and clinical outcomes of chemotherapy-induced FN patients returning to the ED. METHOD: This single-center, retrospective observational study spanning 14 years included chemotherapy-induced FN patients who visited the ED and were discharged. The primary outcome was a return visit to the ED within five days. We conducted logistic regression analyses to evaluate the factors influencing ED return visit. RESULTS: This study included 1318 FN patients, 154 (12.1%) of whom revisited the ED within five days. Patients (53.3%) revisited the ED owing to persistent fever (56.5%), with no intensive care unit admission and only one mortality case who was discharged hopelessly. Multivariable analysis revealed that shock index >0.9 (odds ratio [OR]: 1.45, 95% confidence interval [CI], 1.01-2.10), thrombocytopenia (<100 × 103/uL) (OR: 1.64, 95% CI, 1.11-2.42), and lactic acid level > 2 mmol/L (OR: 1.51, 95% CI, 0.99-2.25) were associated with an increased risk of a return visit to the ED, whereas being transferred into the ED from other hospitals (OR: 0.08; 95% CI, 0.005-0.38) was associated with a decreased risk of a return visit to the ED. CONCLUSION: High shock index, lactic acid, thrombocytopenia, and ED arrival type can predict return visits to the ED in chemotherapy-induced FN patients.

Use of Gallbladder Width Measurement by Computed Tomography in the Diagnosis of Acute Cholecystitis.

This study aimed to evaluate the diagnostic value of gallbladder width measurement with computed tomography (CT) in patients with acute cholecystitis. This retrospective case−control study was conducted between March 2016 and March 2020 at a tertiary emergency department. Of 310 patients, 254 patients with acute cholecystitis confirmed by surgery were compared with 254 patients diagnosed with other diseases (controls). In the acute cholecystitis group, the number of older patients with underlying illnesses was much higher (64% of men). Upon CT, the median (interquartile range [IQR]) gallbladder width was significantly longer in patients with acute cholecystitis (2.26 [1.82−2.78] cm vs. 3.73 [3.32−4.16] cm, p < 0.001). The optimal cut-off value of gallbladder width for differentiating acute cholecystitis was 3.12 cm, showing a sensitivity of 88% and specificity of 86%. In a multivariable analysis using a logistic regression model for diagnosing acute cholecystitis with CT findings (gallbladder width, length, stone, wall thickening, and pericholecystic fluid), a gallbladder width of ≥3.12 cm was significantly meaningful, even when adjusting for other variables (odds ratio 37.9; p < 0.001). Therefore, an increase in gallbladder width (≥3.12 cm) measured with CT can be a simple and sensitive diagnostic sign of acute cholecystitis, supporting the underlying pathophysiology of bile outflow obstruction.

Echocardiographic Assessment of Patients with Pulmonary Tumor Thrombotic Microangiopathy First Diagnosed in the Emergency Department.

Pulmonary tumor thrombotic microangiopathy (PTTM) is a fatal disease that obstructs pulmonary vessels, leading to pulmonary hypertension (PH) and right-sided heart failure causing rapid progressive dyspnea in patients with cancer. This retrospective chart review involved nine patients with PTTM who were first clinically diagnosed in a tertiary emergency department (ED) between January 2015 and June 2021. They underwent laboratory tests, chest radiography, chest computed tomography (CT), and echocardiography. All patients presented with severe and rapidly progressive dyspnea within a few days, a high oxygen demand. The right ventricle (RV): left ventricle ratio was >1 on chest CT, and no life-threatening pulmonary thromboembolism (PTE) was observed. Echocardiographic findings indicated that all patients had moderate-to-severe RV dilatation with a D-shaped LV. The median tricuspid regurgitation maximum velocity was 3.8 m/s, and the median RV systolic pressure was 63 mmHg, indicating severe PH. The median value of tricuspid annular plane systolic excursion was 15 mm, showing a decrease in RV systolic function, and McConnell's sign was observed in five patients. Two patients immediately underwent chemotherapy and are currently alive. PTTM should be suspected and evaluated using echocardiography in patients with cancer presenting to the ED with acute dyspnea and RV failure without PTE.

Ultrasonographic findings of pediatric dermoid cyst.

BACKGROUND: The precise diagnosis of dermoid cysts, which are usually located deeper than other common cysts, is important because dermoid cysts occasionally recur after incomplete excision. Ultrasonography (US) could give useful preoperative information of dermoid cysts but only a few studies have been conducted on US findings related to dermoid cysts. This study aimed to investigate clinical and US findings on pediatric dermoid cysts. METHODS: We retrospectively reviewed the medical records, clinical photographs, and US findings of 31 pediatric patients (≤18 years of age) with histopathologically diagnosed dermoid cysts who visited the Pusan National University Hospital between 2007 and 2016. RESULTS: Of the 31 patients, 25 underwent ultrasonography. The mean long diameter, short diameter, and depth of the cysts were 12.7, 9.0, and 3.8 mm, respectively. Sixteen cysts (64%) were ovoid, 23 (92%) showed hypoechogenicity, 20 (80%) showed heterogeneity, 19 (76%) showed well-demarcated outer margins, and all cysts showed positive posterior acoustic enhancement. All cysts extended to the subcutaneous tissue, and 15 (60%) showed a connection with the underlying muscle. CONCLUSIONS: Ultrasonography may be a useful diagnostic method to visualize the extent and location of the dermoid cyst and make an accurate diagnosis prior to surgical intervention.

Cardiac troponin I predicts clinical outcome of patients with cancer at emergency department.

BACKGROUND: The prognostic ability of cardiac troponin I (TnI) has been demonstrated in general populations and among cardiovascular disease patients, but it has not been evaluated in cancer patients. HYPOTHESIS: This study assumes to have the prognostic ability of cardiac troponin in cancer patients visiting the emergency department. METHODS: Cancer patients visiting the emergency department were enrolled in this retrospective cohort study. Patients with previously known coronary artery disease or clinically indicated coronary angiography were not included. The maximal value from Siemens ADVIA Centaur troponin I Ultra assay within 24 hours was assessed. The primary endpoint was 180-day all-cause death, including cardiovascular and noncardiovascular death. RESULTS: A total of 9135 cancer patients (mean age: 63 years, male gender: 60%) were enrolled. Lowest (0.006 ng/mL), assay-specific <99th % (0.007-0.039 ng/mL), below median ≥ 99th % (0.040-0.129 ng/mL), and above median ≥ 99th % (≥0.130 ng/mL) TnI were found in 4487 (49.1%), 3158 (34.6%), 852 (9.3%), and 638 (7.0%) patients, respectively. There was 3192 (34.9%) all-cause deaths including 137 (1.5%) cardiovascular and 3047 (33.4%) noncardiovascular deaths in the 180-day follow-up period. The risks of all-cause, cardiovascular, and noncardiovascular death increased across higher TnI strata (hazard ratio [HR] = 1.3-2.9; 2.1-9.3; 1.3-1.8; P < .001, all). These findings were consistent within clinical subgroups including solid and hematologic cancers. CONCLUSIONS: Cancer patients visiting the emergency department with elevated troponin I were at increased risk of 180-day death. Cancer patients with elevated TnI may need additional evaluation or careful follow-up even without cardiovascular disease diagnosis.

Epidemiology and Outcome of Powered Mobility Device-Related Injuries in Korea.

BACKGROUND: This study described and analysed the features of powered mobility device (PMD)-related injuries and compared elderly and younger adult injuries. METHODS: Data from Korea Emergency Department-based Injury In-depth Surveillance (EDIIS) database involving eight emergency departments in 2011-2016 were analysed. The inclusion criteria were injuries sustained during the use of PMDs. The variables were compared between adults aged ≥ 65 years and younger adults. Primary and secondary outcomes were severe trauma and poor clinical course accordingly. The logistic regression analysis was used to identify risk factors for study outcomes. RESULTS: A total of 231 adults were enrolled, of whom 150 were ≥ 65 years of age. The total number of PMD-related injuries and the proportion of elderly injured patients increased annually, and most injuries occurred on the roadway and did not involve crash opponents. By multivariate analysis, patients aged ≥ 65 years had a higher injury severity score (adjusted odds ratio [AOR], 2.78; 95% confidence interval [CI], 1.50-5.40) and had a higher incidence of intensive care unit admissions, surgery, and death (AOR, 2.42; 95% CI, 1.16-5.28). CONCLUSION: Given the higher number and severity of injuries sustained among elderly adults ≥ 65 years of age shown in this study, we recommend that safety educations, such as the use of protective equipment and the safe driving on the roadway, are considered for PMD users ≥ 65 years of age.

Hypoxia-inducible transgelin 2 selects epithelial-to-mesenchymal transition and γ-radiation-resistant subtypes by focal adhesion kinase-associated insulin-like growth factor 1 receptor activation in non-small-cell lung cancer cells.

Microenvironment, such as hypoxia common to cancer, plays a critical role in the epithelial-to-mesenchymal transition (EMT) program, which is a major route of cancer metastasis and confers γ-radiation resistance to cells. Herein, we showed that transgelin 2 (TAGLN2), an actin-binding protein, is significantly induced in hypoxic lung cancer cells and that Snail1 is simultaneously increased, which induces EMT by downregulating E-cadherin expression. Forced TAGLN2 expression induced severe cell death; however, a small population of cells surviving after forced TAGLN2 overexpression showed γ-radiation resistance, which might promote tumor relapse and recurrence. These surviving cells showed high metastatic activity with an increase of EMT markers including Snail1. In these cells, TAGLN2 activated the insulin-like growth factor 1 receptor ß (IGF1Rß)/PI3K/AKT pathway by recruitment of focal adhesion kinase to the IGF1R signaling complex. Activation of the IGF1Rß/PI3K/AKT pathway also induced inactivation of glycogen synthase kinase 3ß (GSK3ß), which is involved in Snail1 stabilization. Therefore, both the IGF1Rß inhibitor (AG1024) and the PI3K inhibitor (LY294002) or AKT inactivation with MK2206 lower the cellular level of Snail1. Involvement of GSK3ß was also confirmed by treatment with lithium chloride, the inducer of GSK3ß phosphorylation, or MG132, the 26S proteasomal inhibitor, which also stabilized Snail1. In conclusion, the present study provides important evidence that hypoxia-inducible TAGLN2 is involved in the selection of cancer cells with enhanced EMT properties to overcome the detrimental environment of cancer cells.

Nitric oxide induces BNIP3 expression that causes cell death in macrophages.

Nitric oxide (NO) is involved in many physiological processes and also causes pathological effects by inducing apoptosis. It can enhance or suppress apoptosis depending on its concentration and the cell type involved. In this report, we used cDNA microarray analysis to show that SNAP, an NO donor, strongly induces Bcl-2/adenovirus E1B 19kDa-interacting protein 3 (BNIP3) in macrophages. BNIP3 is a mitochondrial pro-apoptotic protein that contains a Bcl-2 homology 3 domain and a COOH-terminal transmembrane (TM) domain. Macrophages activated by LPS/IFN-gamma produce nitric oxide synthase 2 (NOS2) and release endogenous NO. Expression of BNIP3 was also induced in macrophages by LPS/IFN-gamma, and the induction was blocked by a NOS2 inhibitor, S-methyl-isothiourea. Peritoneal macrophages from NOS2-null mice failed to produce BNIP3 in response to LPS/IFN-gamma. We conclude that BNIP3 expression in macrophages is controlled by the intracellular level of nitric oxide. Overexpression of BNIP3 but not of BNIP3 deltaTM, a BNIP3 mutant without the TM domain and C-terminal tail, led to apoptosis of the cells. Promoter analysis showed that the region between -281 and -1 of the 5'-upstream enhancer region of murine BNIP3 was sufficient for NO-dependent expression of BNIP3.

LPS-induced CD53 expression: a protection mechanism against oxidative and radiation stress.

The CD53 antigen is a member of the tetraspanin membrane protein family that is expressed in the lymphoid-myeloid lineage. Its biological role remains unknown. Using microarrays, we identified CD53 as one of the principal genes up-regulated by exposure of macrophages to LPS. Northern blot analysis confirmed the induction of CD53 in RAW264.7 macrophages treated with LPS or SNAP (a nitric oxide donor). Cells stably transfected with sense CD53 cDNA had increased levels of intracellular GSH and lower levels of peroxide, and were more resistant to H2O2 and to UVB irradiation. Cells harboring antisense CD53 had the opposite properties. We propose that the induction of CD53 is a major mechanism by which macrophages protect themselves against LPS-induced oxidative stress and UVB irradiation.