Gastropericardial fistula: radiologic findings and literature review.

BACKGROUND: Gastropericardial fistula, a rare condition characterized by an abnormal communication between the stomach and the pericardium, is an emergency as sequelae such as cardiac tamponade and sepsis may lead to hemodynamic instability and death. We aimed to summarize the surgical and radiologic findings of the reported cases published to date, describe their pertinent surgical history, and present an algorithm for diagnosis. METHODS: The Pubmed database was searched using the terms: gastropericardial, pericardiogastric, pneumopericardium, pericardial, and pneumopericardium with the term "fistula" added to each term. The search was limited to January 2000-October 2015 and English language publications. RESULTS: Thirty five cases were identified. The most common etiology was prior esophageal and/or gastric surgery (80% of cases; esophagectomy = 26%/gastrointestinal reflux disease associated surgery = 23%/bariatric surgery = 11%/partial gastrectomy = 6%/other = 20%). The average duration between presentation and surgery was 7.3 ± 6.2 years (SD). Radiology typically played a crucial role in diagnosis with computed tomography most commonly demonstrated to be the most appropriate modality to demonstrate the fistula and assist in surgical planning. Contrast studies were frequently helpful to confirm the diagnosis. Chest x-ray findings including pneumopericardium and pericardial thickening were contributory but nonspecific. Esophagoduodenoscopy characterized the fistula in cases where imaging was equivocal and may provide therapeutic options. CONCLUSIONS: We present the clinical radiologic findings of the 35 cases of gastropericardial fistula reported. This is the first literature review of gastropericardial fistula to focus on the effectiveness of these various diagnostic modalities and to present an algorithm for diagnosis.

Vitamin D3 Produced by Skin Exposure to UVR Inhibits Murine Basal Cell Carcinoma Carcinogenesis.

The effect of UVR on human basal cell carcinoma (BCC) epidemiology is complex-the incidence rises until approximately 30,000 hours of lifetime sunlight exposure and then plateaus. We hypothesize that UVR has opposing effects on BCC carcinogenesis-stimulatory via mutagenesis and inhibitory via production of hedgehog-inhibiting vitamin D3 (D3). We find that UVR exposure of ionizing radiation-treated Ptch1+/- mice accelerates BCC carcinogenesis in male mice, in which UVR does not produce D3. By contrast, in female mice, in which UVR does produce D3, UVR fails to accelerate BCC carcinogenesis, thus mirroring the plateauing in humans. However, if D3 production is attenuated in female mice by deletion of keratinocyte lathosterol 5-desaturase, then UVR accelerates ionizing radiation-induced BCC carcinogenesis. Congruently, chronic topical application of D3 inhibits ionizing radiation-induced BCC tumorigenesis. These findings confirm that UVR-induced production of D3 in keratinocytes significantly restrains murine BCC tumorigenesis and demonstrate the counterintuitive conclusion that UVR has anti-BCC carcinogenic effects that can explain, at least in part, the complex relationship between exposure to UVR and BCC incidence.

Establishment of murine basal cell carcinoma allografts: a potential model for preclinical drug testing and for molecular analysis.

Dysregulated hedgehog (HH) signaling has been found in numerous cancers, suggesting that therapeutic targeting of this pathway may be useful versus a wide range of cancers. Basal cell carcinoma (BCC) is an excellent model system for studying the influence of the HH pathway on carcinogenesis because aberrant activation of HH signaling is crucial not only for the development of but also the maintenance of BCC. Genetically engineered BCC mouse models provide one important tool for the study of the biology of human BCCs and for evaluating therapeutic interventions, as these mice produce multiple genetically defined tumors within a relatively short period of time. However, these models remain expensive and cumbersome to use for large-scale preclinical drug testing. Here we report a method for growing allografts from murine BCC tumors in NOD/SCID mice. These allografts develop faster and reproduce the histology, immunophenotypes, and response to at least one anti-BCC drug of the parental autochthonous tumors from which they arise. Therefore, the allograft model provides a practical model for (i) studying BCC carcinogenesis and (ii) initial preclinical screening for anti-HH pathway and other anti-BCC drugs.