Amyloid Diabetes Pancreas

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Figure 30 The same pancreas as in Figure 29 has been immunostained to show P-cells: note the destruction of the P-cells in this islet owing to inflammation; compare with Figure 24

Figure 31 This histologic section of pancreas was obtained at autopsy from a patient 5 years after the onset of type 1 diabetes. It shows persistence of an infiltrate of lymphocytes (insulitis) some of which have been indicated by arrows, affecting this islet, immunostained for insulin. This shows that P-cell destruction takes place over years in patients with type 1 diabetes

Cat Pancreas Insulin Immunostaining

Figure 31 This histologic section of pancreas was obtained at autopsy from a patient 5 years after the onset of type 1 diabetes. It shows persistence of an infiltrate of lymphocytes (insulitis) some of which have been indicated by arrows, affecting this islet, immunostained for insulin. This shows that P-cell destruction takes place over years in patients with type 1 diabetes

Insulitis With Lymphocytic Infiltrates
Figure 32 Autopsy section of an islet from a patient who had diabetes for 16 years. Although the islet looks fairly normal on H & E stain (left), insulin staining (right) shows it is devoid of P-cells
Pancreas And Stain

Figure 33 This is a section of pancreas from a 12-year-old boy who died of a cardiomyopathy. He had a family history of type 1 diabetes and was considered to be pre-diabetic because he had high titers of both insulin and islet cell autoantibodies in autopsy blood, but he did not have glycosuria in life. The photograph shows two islets affected by insulitis in his pancreas, confirming that immunologically mediated P-cell destruction takes place in the preclinical period of type 1 diabetes

Figure 33 This is a section of pancreas from a 12-year-old boy who died of a cardiomyopathy. He had a family history of type 1 diabetes and was considered to be pre-diabetic because he had high titers of both insulin and islet cell autoantibodies in autopsy blood, but he did not have glycosuria in life. The photograph shows two islets affected by insulitis in his pancreas, confirming that immunologically mediated P-cell destruction takes place in the preclinical period of type 1 diabetes

Pancreas Affected Diabetes

Figure 35 This section shows that all the endocrine cells (A, B, D, etc.) in this insulin-containing islet hyperexpress class 1 major histocompatibility complex (MHC). Note also that the islet is not inflamed (no lymphocytes). This suggests that hyperexpression of class 1 MHC precedes insulitis within any given islet and is not simply the result of secretion of cytokines by inflammatory cells in the insulitis infiltrate

Figure 35 This section shows that all the endocrine cells (A, B, D, etc.) in this insulin-containing islet hyperexpress class 1 major histocompatibility complex (MHC). Note also that the islet is not inflamed (no lymphocytes). This suggests that hyperexpression of class 1 MHC precedes insulitis within any given islet and is not simply the result of secretion of cytokines by inflammatory cells in the insulitis infiltrate

Figure 34 Circulating cytoplasmic islet-cell antibodies (ICA) can be found in most newly diagnosed type 1 diabetes mellitus (DM) patients, thereby providing evidence of an autoimmune pathogenesis of this disorder. ICA are also seen in the 'prediabetic' period and in siblings of type 1 DM patients, and are a marker of susceptibility to type 1 DM. This high-power view of a cryostat section of human pancreas was incubated with serum from a type 1 DM patient and stained by an indirect immunofluorescence technique using anti-human IgG fluorescinated antiserum. Although ICA are serologic markers of P-cell destruction, the antibodies also stain the entire islet, including glucagon and somatostatin cells (which, unlike the P-cells, are not destroyed). The positive reaction is confined to cell cytoplasm and the nuclei are unstained (seen as black dots)

Black Foot Diabetes

Figure 36 Glucose intolerance occurs in about 30% of cases of cystic fibrosis, although only 1-2% of patients have frank diabetes. This low-power view of the pancreas of a 14-year-old child with cystic fibrosis complicated by diabetes shows complete atrophy of the exocrine pancreas, but with survival of the islets. Some of the islets (lower part of field) are embedded in fibrous tissue. H & E

Figure 36 Glucose intolerance occurs in about 30% of cases of cystic fibrosis, although only 1-2% of patients have frank diabetes. This low-power view of the pancreas of a 14-year-old child with cystic fibrosis complicated by diabetes shows complete atrophy of the exocrine pancreas, but with survival of the islets. Some of the islets (lower part of field) are embedded in fibrous tissue. H & E

Diabetes Fat Wasting

Figure 37 This is a coronal section of the tail of the pancreas from a patient with hemochromatosis. Note the brown color of the pancreas compared with the surrounding fat. Normal pancreas tissue appears pale. The smaller piece of pancreas has been stained with Prussian blue to show the presence of iron deposits

Figure 37 This is a coronal section of the tail of the pancreas from a patient with hemochromatosis. Note the brown color of the pancreas compared with the surrounding fat. Normal pancreas tissue appears pale. The smaller piece of pancreas has been stained with Prussian blue to show the presence of iron deposits

Diabetes Type Amyloid

Figure 39 The characteristic histologic abnormality in type 2 diabetes mellitus (DM) is amyloid deposition in the islets, which is significant in around two-thirds of cases. Increasing amounts of amyloid deposition are associated with progressive islet cell damage, which probably contributes to the insulin deficiency of type 2 DM. In this pancreas from a patient who had type 2 DM of long standing, two islets containing large deposits of amorphous pink-staining amyloid can be seen

Figure 39 The characteristic histologic abnormality in type 2 diabetes mellitus (DM) is amyloid deposition in the islets, which is significant in around two-thirds of cases. Increasing amounts of amyloid deposition are associated with progressive islet cell damage, which probably contributes to the insulin deficiency of type 2 DM. In this pancreas from a patient who had type 2 DM of long standing, two islets containing large deposits of amorphous pink-staining amyloid can be seen

Hemosiderin Staining Urinary Deposits
Figure 38 Hemochromatosis. Hemosiderin deposits in this low-power view of pancreas are stained blue. Note the accumulation of iron in the endocrine cells of the islet (center) as well as in the acinar cells of the exocrine pancreas. Prussian blue staining

Mumps

Viruses implicated in the

Viruses implicated in the

Pancreatic Amyloid Deposits

Figure 40 Viruses have been suggested to be a cause or factor in the development of type 1 diabetes mellitus (DM), and are thought to be the most likely agents to trigger the disease, probably on the basis of genetic predisposition, in some cases. Evidence comes from epidemiologic studies and the isolation of viruses from the pancreas of a few recently diagnosed type 1 DM patients. Mumps and Coxsackie viruses can cause acute pancreatitis, and Coxsackie virus can cause P-cell destruction

Histology Acute Pancreatitis

Figure 41 Autopsy sample of histology of Coxsackie B viral pancreatitis in a neonate. Coxsackie B viral infection may cause inflammatory destruction of the P-cells and Coxsackie B viruses have been isolated from the pancreas of patients with new-onset type 1 diabetes. Injection of such isolates into mice causes insulitis and P-cell damage. The similarity between this picture and the previous one of insulitis is obvious. Nevertheless, although Coxsackie B virus may be diabetogenic in men, its precise etiologic importance in the development of type 1 diabetes remains unclear

Figure 41 Autopsy sample of histology of Coxsackie B viral pancreatitis in a neonate. Coxsackie B viral infection may cause inflammatory destruction of the P-cells and Coxsackie B viruses have been isolated from the pancreas of patients with new-onset type 1 diabetes. Injection of such isolates into mice causes insulitis and P-cell damage. The similarity between this picture and the previous one of insulitis is obvious. Nevertheless, although Coxsackie B virus may be diabetogenic in men, its precise etiologic importance in the development of type 1 diabetes remains unclear

Normal Pancreatic Side
Figure 42 This endoscopic retrograde cholangiopancreato-gram shows a normal pancreatic duct
Dilated Pancreatic Duct
Figure 43 This endoscopic retrograde cholangiopancreato-gram shows the typical appearances of chronic pancreatitis. There is a dilated pancreatic duct with amputation and beading of the side branches
Normal Pancreatic Side

Figure 45 This CT scan shows cancer of the pancreas. An association between adenocarcinoma of the pancreas and diabetes has long been recognized. Pancreatic cancer may precede the diagnosis of diabetes, but some epidemiologic studies suggest that there is an increased risk of pancreatic cancer in diabetic patients. Unexplained weight loss or back pain in a patient with type 2 diabetes must always raise the suspicion of underlying pancreatic cancer

Figure 45 This CT scan shows cancer of the pancreas. An association between adenocarcinoma of the pancreas and diabetes has long been recognized. Pancreatic cancer may precede the diagnosis of diabetes, but some epidemiologic studies suggest that there is an increased risk of pancreatic cancer in diabetic patients. Unexplained weight loss or back pain in a patient with type 2 diabetes must always raise the suspicion of underlying pancreatic cancer

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