Pancreatic neuroendocrine tumors (PNETs) are rare neoplasms representing <5% of all pancreatic malignancies with an estimated incidence of 1-1.5 cases/100,000. PNETs are broadly classified as either functional or nonfunctional. Functional PNETs include insulinomas, gastrinomas, vasoactive intestinal peptideomas, glucagonomas, and somatostatinomas. The clinical manifestations associated with these tumors are the result of excessive hormonal secretion and action. The functional nature of these tumors makes pancreatic hormone testing critical not only for initial diagnosis but also for follow-up, because they are important tumor markers. Nonfunctional PNETs typically remain clinically silent until a substantial mass effect occurs. Although the majority of PNETs occur sporadically, it is important to recognize that these tumors may be associated with a variety of familial syndromes and in many cases genetic testing of PNET patients is warranted. This article familiarizes the reader with the clinical presentation and the biochemical, radiologic, and genetic testing indicated for diagnosis and follow-up of patients with PNET.

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Coronary artery calcification (CAC) is a well-known marker for coronary artery disease and has important prognostic implications. CAC is able to provide clinicians with a reliable source of information related to cardiovascular atherosclerosis, which carries incremental information beyond Framingham risk. However, non-contrast scans of the heart provide additional information beyond the Agatston score. These studies are also able to measure various sources of fat, including intrathoracic (eg, pericardial or epicardial) and hepatic, both of which are thought to be metabolically active and linked to increased incidence of subclinical atherosclerosis as well as increased prevalence of type 2 diabetes. Testing for CAC is also useful in identifying extracoronary sources of calcification. Specifically, aortic valve calcification, mitral annular calcification, and thoracic aortic calcium (TAC) provide additional risk stratification information for cardiovascular events. Finally, scanning for CAC is able to evaluate myocardial scaring due to myocardial infarcts, which may also add incremental prognostic information. To ensure the benefits outweigh the risks of a scanning for CAC for an appropriately selected asymptomatic patient, the full utility of the scan should be realized. This review describes the current state of the art interpretation of non-contrast cardiac CT, which clinically should go well beyond coronary artery Agatston scoring alone.