Lobulitis in nonneoplastic breast tissue from breast cancer patients: association with phenotypes that are common in hereditary breast cancer.

Lobular inflammation (lobulitis) has been demonstrated in benign breast tissue adjacent to in situ and invasive breast cancers and, more recently, in nonneoplastic tissue from prophylactic mastectomy specimens for hereditary high-risk breast carcinoma. The aim of this study is to investigate the incidence of lobulitis in benign breast tissue of patients with breast cancer and associated clinicopathologic features. We reviewed nonneoplastic breast tissue sections from 334 patients with invasive breast carcinoma to study lobulitis in normal breast tissue and to correlate its presence with clinicopathologic features of the associated tumor. Clinical information (age, menopausal status, and follow-up), tumor characteristics (type, grade, size, lymph node status, stage, estrogen and progesterone receptor, HER2), and survival were recorded. Characteristics of women with and without lobulitis were cross-classified with categories of clinical, pathologic, and histologic characteristics, and differences in distributions were tested in univariate and multivariate analysis. Lobulitis was found in 26 (8%) of 334 patients. The lymphocytic infiltrate was predominantly T-cell type. In a multivariate model, lobulitis in patients with breast cancer was significantly associated with younger age, triple (estrogen receptor, progesterone receptor, HER2)-negative cancers, and medullary phenotypes. Lobulitis in nonneoplastic breast tissue, away from tumor, is associated with clinicopathologic features more commonly seen in hereditary breast cancer.

Free oxycodone concentrations in 67 postmortem cases from the Hennepin County medical examiner's office.

Heart blood free oxycodone concentrations in oxycodone-related and mixed drug overdose deaths were compared with those found incidentally at autopsy in medical examiner cases. Between 2000 and 2005, 67 oxycodone-positive postmortem cases were identified. Thirty of 67 cases (44.8%) were determined to be drug overdoses. Oxycodone alone was responsible for 7 of the 30 (23.3%) overdose deaths. Mean (median) oxycodone concentrations were 1.060 mg/L (0.824 mg/L) with a range of 0.270-3.390 mg/L. Three cases were accidents, three were suicides, and one was undetermined. The remaining 23 were mixed drug overdoses. Mean (median) oxycodone concentrations in these cases were 0.820 mg/L (0.470 mg/L) with a range of 0.014-3.800 mg/L. Sixteen mixed drug overdoses were accidental, and seven were suicidal. Where oxycodone was an incidental finding, 24 were natural, 6 accident, 4 suicide, 1 homicide, and 2 undetermined. The mean (median) concentrations in the incidental finding group were 0.330 mg/L (0.150 mg/L) with a range of 0.017-1.300 mg/L. In conclusion, the findings substantiate the considerable overlap that exists with blood oxycodone concentrations in cases where oxycodone alone was determined to be the cause of death compared with mixed drug overdoses and incidental findings. Free oxycodone concentrations in postmortem cases must be interpreted in the context of the deceased's past medical history and autopsy findings.