Pulmonary Hemorrhage Following Percutaneous Computed Tomography-Guided Lung Biopsy: Retrospective Review of Risk Factors, Including Aspirin Usage.

BACKGROUND: To evaluate the significance of aspirin, as well as, other potential confounding risk factors, on the incidence and volume of pulmonary hemorrhage in patients undergoing percutaneous computed tomography-guided lung biopsy. METHODS: This retrospective study was approved by the institutional review board. Between September 2013 and December 2014, 252 patients taking aspirin underwent transthoracic computed tomography-guided lung biopsy. Patient, technical, and lesion-related risk factors were evaluated. Univariate analysis was performed with a Student's t test, chi-square test, or Fisher's exact test, as appropriate followed by multivariate logistic regression. RESULTS: Of 252 patients, 49 (19.4%) continued or stopped aspirin ≤4 days prior to biopsy and 203 (80.6%) patients stopped aspirin ≥5 days prior to biopsy. Pulmonary hemorrhage occurred in 174 cases (69.0%). The median volume of hemorrhage was 3.74 cm3 (range, 0-163.5 cm3). Multivariate analysis revealed that lesion size (P < 0.0001) and lesion depth (P < 0.0001) were independent risk factors for the incidence of pulmonary hemorrhage, while lesion size (P = 0.0035), transgression of intraparenchymal vessels (P < 0.0001), and lesion depth (P = 0.0047) were independent risk factors for severity of hemorrhage. Aspirin stopped ≤4 days from a percutaneous lung biopsy was not associated with pulmonary hemorrhage. CONCLUSION: Aspirin taken concurrently or stopped within 4 days of transthoracic lung biopsy is not an independent risk factor for pulmonary hemorrhage. The incidence of hemorrhage following lung biopsy is associated with lesion size and depth, while the severity of hemorrhage is associated with lesion size, depth, as well as traversal of intraparenchymal vessels.

Prevalence of Pancreatic Steatosis at a Pediatric Tertiary Care Center.

OBJECTIVES: Pancreatic steatosis in adults has been proposed to be associated with obesity; however, data on pancreatic steatosis in children are lacking. Our study aimed to measure the prevalence of pancreatic steatosis in children and to examine its association with obesity and nonalcoholic fatty liver disease. METHODS: This is a retrospective chart review study of 232 patients 2 to 18 years old who underwent abdominal computed tomographic imaging in the emergency department or inpatient ward within a 1-year time span and from whom demographics, anthropometrics, and medical history were obtained. Our radiologist determined mean Hounsfield unit (HU) measurements for the pancreas, liver, and spleen. A difference of -20 between the pancreas and spleen (psHU) and between the liver and spleen was used to determine fatty infiltration. RESULTS: Of the 232 patients, 11.5% had a psHU less than -20. The prevalence of pancreatic steatosis was more than double among obese children (19%) than that in nonobese groups (8%). There is a significant correlation between the psHU and liver-spleen HU (r = 0.50, P < 0.001). CONCLUSIONS: Pancreatic steatosis was identified in 10% of the study population and is associated with obesity. Also, pancreatic steatosis is significantly associated with nonalcoholic fatty liver disease. This is the first study assessing the prevalence of pancreatic steatosis in children.

Increased FDG activity in a dermatofibroma in esophageal cancer patient.

PET using the radiotracer (18)F-FDG is used for staging patients with esophageal cancer. Nonmalignant conditions, mainly inflammation and some benign tumors, however, can cloud the clinical picture by taking up FDG and producing a false-positive result. We report the case of a 46 year-old man with squamous cell carcinoma of the thoracic esophagus who underwent combined PET/CT and had false-positive uptake in a chest wall dermatofibroma. Dermatofibroma is a benign skin lesion with a characteristic large presence of fibroblasts and macrophages. Macrophage uptake of FDG is likely responsible for the false-positive result on PET/CT.

Functional characterization of human Cd33+ and Cd11b+ myeloid-derived suppressor cell subsets induced from peripheral blood mononuclear cells co-cultured with a diverse set of human tumor cell lines.

BACKGROUND: Tumor immune tolerance can derive from the recruitment of suppressor cell populations, including myeloid-derived suppressor cells (MDSC). In cancer patients, MDSC accumulation correlates with increased tumor burden, but the mechanisms of MDSC induction remain poorly understood. METHODS: This study examined the ability of human tumor cell lines to induce MDSC from healthy donor PBMC using in vitro co-culture methods. These human MDSC were then characterized for morphology, phenotype, gene expression, and function. RESULTS: Of over 100 tumor cell lines examined, 45 generated canonical CD33+HLA-DR(low)Lineage- MDSC, with high frequency of induction by cervical, ovarian, colorectal, renal cell, and head and neck carcinoma cell lines. CD33+ MDSC could be induced by cancer cell lines from all tumor types with the notable exception of those derived from breast cancer (0/9, regardless of hormone and HER2 status). Upon further examination, these and others with infrequent CD33+ MDSC generation were found to induce a second subset characterized as CD11b+CD33(low)HLA-DR(low)Lineage-. Gene and protein expression, antibody neutralization, and cytokine-induction studies determined that the induction of CD33+ MDSC depended upon over-expression of IL-1ß, IL-6, TNFα, VEGF, and GM-CSF, while CD11b+ MDSC induction correlated with over-expression of FLT3L and TGFß. Morphologically, both CD33+ and CD11b+ MDSC subsets appeared as immature myeloid cells and had significantly up-regulated expression of iNOS, NADPH oxidase, and arginase-1 genes. Furthermore, increased expression of transcription factors HIF1α, STAT3, and C/EBPß distinguished MDSC from normal counterparts. CONCLUSIONS: These studies demonstrate the universal nature of MDSC induction by human solid tumors and characterize two distinct MDSC subsets: CD33+HLA-DR(low)HIF1α+/STAT3+ and CD11b+HLA-DR(low)C/EBPß+, which should enable the development of novel diagnostic and therapeutic reagents for cancer immunotherapy.