Cardiac tamponade and purulent pericarditis secondary to an oesophageal pericardial fistula as an initial presentation of squamous cell carcinoma of the oesophagus.

Pericardial effusions resulting in a cardiac tamponade have previously been reported with oesophageal cancers. However, most of these cases have been reported in association with radiation and chemotherapy. Rarely as oesophageal pericardial fistuls (OPF) have been reported as the culprits in causing pericardial effusions in patients with oesophageal cancers. Here we present the case of a 61-year-old woman who presented clinically with cardiac tamponade. She was found to have an OPF due to oesophageal squamous cell cancer that resulted in a purulent pericardial effusion. She underwent a median sternotomy, pericardial decompression, and mediastinal debridement. An oesophageal stent was attempted unsuccessfully. The patient refused any more aggressive treatments and was discharged to a hospice where she passed away 13 days after presentation. This case and the associated literature review highlights an unusual presentation of oesophageal cancer and an uncommon cause of cardiac tamponade.

Ultrastructure of islet microcirculation, pericytes and the islet exocrine interface in the HIP rat model of diabetes.

CONTEXT: The transgenic human islet amyloid polypeptide (HIP) rat model of type 2 diabetes mellitus (T2DM) parallels the functional and structural changes in human islets with T2DM. OBJECTIVE: The transmission electron microscope (TEM) was utilized to observe the ultrastructural changes in islet microcirculation. METHODS: Pancreatic tissue from male Sprague Dawley rats (2, 4, 8, 14 months) were used as controls (SDC) and compared to the 2-, 4-, 8- and 14-month-old HIP rat models. RESULTS: The 2-month-old HIP model demonstrated no islet or microcirculation remodeling changes when compared to the SDC models. The 4-month-old HIP model demonstrated significant pericapillary amyloid deposition and diminution of pericyte foot processes as compared to the SDC models. The 8-month-old model demonstrated extensive islet amyloid deposition associated with pericyte and beta-cell apoptosis when compared with SDC. The 14-month-old HIP model demonstrated a marked reduction of beta-cells and intra-islet capillaries with near complete replacement of islets by amyloidoses. Increased cellularity in the region of the islet exocrine interface was noted in the 4- to 14-month-old HIP models as compared to SDC. In contrast to intra-islet capillary rarefaction there was noticeable angiogenesis in the islet exocrine interface. Pericytes seemed to be closely associated with collagenosis, intra-islet adipogenesis and angiogenesis in the islet exocrine interface. CONCLUSION: The above novel findings regarding the microcirculation and pericytes could assist researchers and clinicians in a better morphological understanding of T2DM and lead to new strategies for prevention and treatment of T2DM.

Ultrastructural islet study of early fibrosis in the Ren2 rat model of hypertension. Emerging role of the islet pancreatic pericyte-stellate cell.

CONTEXT: Type 2 diabetes mellitus is a multifactorial disease with polygenic and environmental stressors resulting in multiple metabolic toxicities and islet oxidative stress. We have integrated the role of the islet renin-angiotensin system (RAS) in the pathogenesis of early islet fibrosis utilizing the transgenic (mRen2)27 rodent model of hypertension and tissue RAS overexpression. OBJECTIVE: The Ren2 pancreatic islet tissue was evaluated with transmission electron microscopy to study both early cellular and extracellular matrix remodeling. ANIMALS: Four 9- to 10-week-old male Ren2 untreated models and four Sprague Dawley sex and age matched controls were used. DESIGN: Ultrastructural study to compare pancreatic islet tissue. MAIN OUTCOME MEASURES: Only qualitative and observational transmission electron microscopy findings are reported. RESULTS: Major remodeling differences in the Ren2 model were found to be located within the islet exocrine interface, including deposition of early fibrillar-banded collagen (fibrosis) and cellular remodeling of the pericyte suggesting proliferation, migration, hypertrophy and activation as compared to the Sprague Dawley controls. CONCLUSION: This study points to the possibility of the pericyte cell being one of many contributors to the fibrogenic pool of cells important for peri-islet fibrosis as a result of excess angiotensin II at the local tissue level in the Ren2 model. These findings suggest that the pericyte may be capable of differentiating into the pancreatic stellate cell. This islet ultrastructure study supports the notion that pericyte cells could be the link between islet vascular oxidative stress and peri-islet fibrosis. Pericyte-endothelial-pancreatic stellate cell associations and morphology are discussed.