Isolated Pancreatic Metastasis from a Lung Adenocarcinoma Primary: A Case Report and Literature Review.

Isolated pancreatic metastasis is a rare occurrence and is commonly misdiagnosed as primary pancreatic malignancy. We present a case of a 65-year-old female patient with a history of stage IIIA lung adenocarcinoma, who developed significant epigastric pain 27 months after diagnosis and treatment of a primary lung adenocarcinoma. This patient was found to have a pancreatic head lesion initially suspected to be a primary pancreatic neoplasm but eventually discovered to be a metastatic lesion from the previously treated primary lung adenocarcinoma.

Metastatic adenocarcinoma of the pancreas presents as metastases to the axillary/supraclavicular region as the first sign of the disease.

Mucinous tumors of the pancreas are rare and the diagnosis of invasive carcinoma can be a dilemma. While metastatic disease from mucinous cystadenocarcinoma (MCAC) and invasive intraductal papillary mucinous neoplasms (IPMN) have been reported, no extraperitoneal mucinous cystic metastatic disease has been described. When metastatic, the overall survival rates for invasive adenocarcinoma, mucinous cystadenocarcinoma (MCAC) and invasive intraductal papillary mucinous neoplasms (IPMN) are similar. The best improvement in the overall and progression free survival has been demonstrated with FOLFIRINOX (folinic acid - fluorouracil - irinotecan - oxaliplatin) for metastatic adenocarcinoma and Gemcitabine based regimens for MCAC. However, the variable responses of metastatic mucinous lesions have been observed and the overall prognosis remains poor. We describe a case of a patient who presented with metastatic adenocarcinoma of the pancreas as cystic masses in the supraclavicular and axillary regions. Additionally, this patient was initially treated with FOLFIRINOX and continues to have stable primary and metastatic disease after 18 months from the diagnosis.

Correlates of D-dimer in older persons.

BACKGROUND AND AIMS: D-dimer is a marker of active fibrinolysis. Understanding how age-related factors affect D-dimer levels may help the interpretation of high D-dimer levels in older individuals. METHODS: 776 Baltimore Longitudinal Study on Aging (BLSA) participants (mean age 68.4+/-13.9 yrs) were divided into three groups according to baseline D-dimer levels >200 ng/mL; 100-200 ng/mL and <100 ng/mL. RESULTS: D-dimer level increased with age (p<0.0001). Using polychotomous logistic regression models, we found that age, cholesterol, triglycerides, creatinine, erythrocyte sedimentation rate, hemoglobin and body mass index were independently associated with D-dimer level. CONCLUSIONS: Rising levels of D-dimer with age can be explained in part by the high prevalence of pro-inflammatory conditions and increasing burden of lipid abnormalities, anemia and obesity. These factors compromise the specificity of D-dimer levels as a diagnostic aid to thrombosis in older individuals.