Diabetes mellitus and Exocrine Pancreatic Function

Abstract

lary circulation and thereby reduces islet perfusion. Interestingly, in tropical countries and India a special form of non-alcoholic tropical calcifying pancreatitis leads to DM. Although little is known about the exact etiology of this form of diabetes it has been found that the -cell function is damaged whereas the  cells are preserved [6, 7] . This is in contrast to the non-tropical chronic pancreatitis where both cell populations are altered. In any case, two different pathogenic mechanisms have been proposed, one eliciting CP and the other selective pancreatic -cell impairment and subsequent DM. DM caused by chronic infl ammation of the exocrine pancreas develops typically in 80% of the patients within the fi rst 10 years after the initial diagnosis of chronic pancreatitis [8] . Chronic calcifying pancreatitis (60–70%) leads to diabetes more often than non-calcifying pancreatitis (15–30%) [2, 9] . The duration of CP plays an important role: the continuing infl ammatory-fi brotic disturbance of exocrine and endocrine tissue, with a signifi cant loss of
cells and hence a progressive decrease in insulin-secretion, triggers overt DM. DM occurs when approximately 80% of the cells are destroyed [10] . One can try to explain the occurrence of pancreatic exocrine dysfunction as a complication of preexisting diabetes . However, only in a few patients do overt DM symptoms precede a later fi nding of chronic pancreatitis. It is rather questionable whether DM is the reason for CP rather than CP being oligosymptomatic and allowing DM to become overt somewhat earlier. Anyway, this may lead to an initial misclassifi cation [11, 12]. Overall, it seems About one million endocrine islets are scattered throughout the human exocrine pancreas. An islet is composed of about fi ve thousand endocrine cells and the whole body of islets accounts for 1–2% of the volume of the pancreas. An islet contains four major types of endocrine cells, a majority of insulin-producing
cells, less glucagon-producing  cells, and fewer  (somatostatin) and pancreatic polypeptide cells. It has a certain tradition that gastroenterologists study the exocrine pancreas whereas endocrinologists study the endocrine pancreas. This goes so far that the pancreas is often regarded as two separate organs. However, clinical observations clearly show that disturbances of the exocrine gland impact on endocrine cells. Patients with chronic pancreatitis (CP) often suffer from endocrine pancreatic dysfunction. This even leads to a distinct secondary type of diabetes [1] . Diabetes mellitus (DM) secondary to CP accounts for ! 1% of all diabetes cases, which is probably the reason why it is not of that much interest to most diabetologists. On the other hand, 80% of patients with CP develop an overt DM in the long run and DM is an independent risk factor for mortality in patients with CP [2–4] . This makes this form of DM relevant to the gastroenterologist. The most frequent cause of secondary DM in patients with pancreatic diseases in the Western hemisphere is chronic alcoholic pancreatitis [5] . Its occurrence is attributed to the close anatomical and functional links between the exocrine and endocrine pancreas. It is believed that CP, progressively developing fi brosis and sclerosis, alters pancreatic capilPublished online: August 19, 2005