Endocrine pathology


Pancreatic mass.


A 44-year-old woman presented with pancreatic mass. Blood chemistries were normal.

Distal pancreatomy was performed. The spleen and the lymph nodes from the base of the mesocolon, right gastric artery node ,node from the greater curvature of stomach, peripancreatic node, node from margin of the splenic vein were also removed.


A tan-white well circumscribed, firm mass was identified 0,5 cm away from the surgical margin. The entire mass measures 2 x 2x 1,5cm.


Microscopic examination.


Microscopic examination  revealed that the tumor consists of ralatively monomorphous population of cells arranged in cords and nests (Fig-1, Fig-2). The individual cells range from cuboidal to columnar with eosinophilic cytoplasm. The nucleoli are incnspicious. Chromatin has characteristic salt and pepper appearence. Mitotic figures are rare to absent (Fig-3). No tumor are identified within the vascular spaces but perineural invasion is present (Fig-4). Adjasent pancreatic parenchima shows chronic pancreatitis, fibrosis (Fig-6). Lymphnodes from the base of the mesocolon, peripancreatic lymphnode and node from the margin of the splenic vein are positive for metastatic tumor (Fig-5).Tumor cells are strongly positive for panendocrine markers- synaptophysin (Fig-7), NSE, chromogranin. Tumor cells are negative for somatostatin, insulin, glucagons, gastrin.






              Fig-1                                 Fig-2                                 Fig-3


            Fig-4                                    Fig-5                                Fig-6




Final diagnosis:


Pancreatic islet cell tumor  (nonfunctioning).




Islet cell tumors are nearly always located within the pancreatic parenchima, and only rarely in the duodenum. These are rare tumors. Most occures in adults. Most common location is the body and the tail of the pancreas, correlating with the greater islet concentration in these locations, The endocrine component of the pancreas is comprised of four types of hormone - producing islet cells: glucagon(A-cells), insulin(B-cells), somatostatin (D-cells), and pancreatic polypeptide. It has been established that islet cell tumors arise from a primitive neuroendocrine stem cells with the capacity to differentiate in to various secreting cells.

Studies of islet cell tumors have shown that multihormonal examples are common and these can occur in a variety of forms as a single tumor with multiple cell types; as multiple tumors, each being of a single cell type; and as multiple tumors, each of multiple cell types. Sometimes two different peptide hormones have been found within the same tumor cell and even within the same secretory granule.

The nature of the predominant cells determines the type of clinical syndrome and the name given to tumor. Examination of hematoxilin-eosin sections allows the generic diagnosis of islet cell tumor. Electron microscopy demonstrates cytoplasmic secretory granules of endocrine type in all but most undifferentiated members of these groups.

The immunohistochemical markers can be divided into two types - pan endocrine (NSE, cromogranin, synaptophysin, opioid peptides). Second group of markers have demonstrated that these tumors can secrete hormones present in the pancreatic islets including insulin, glucagon, somatostatin, pancreatic polypeptide.                                   


The correlation between morphologic features and their clinical behavior is poor. Features that correlate with a greater metastasis potential are- stoma invasion, tumor emboli in pancreatic vessels, glandular or solid rather then gyriform pattern of growth.

Beta cell tumors are malignant in about 7-10 % of the cases, whereas almost all the other types including nonfunctioning tumors are malignant in the large majority of cases. DNA ploidy analysis and cell prolipheration markers do not allow a distinction between benign and malignant tumors but show correlation with clinical aggressiveness.