Non-Alcoholic Fatty Pancreas Disease: A Diagnosis of Increasing Importance

Abstract

In this issue of Angiology, Sahin and Karadeniz report the results of their study involving 183 patients with hepatic steatosis (HS) diagnosed by transabdominal ultrasonography. 1 Among these patients, 85 (46.5%) also had non-alcoholic fatty pancreas disease (NAFPD). Patients with both HS and NAFPD exhibited significantly greater carotid intima media thickness (cIMT), a marker of early atherosclerosis, compared with patients with HS only. Age, hypertension and the presence of NAFPD were independent predictors of increased cIMT in multivariate analyses. Thus, the study of Sahin and Karadeniz 1 suggests that the presence of increased fat in the pancreas may be associated with the development of atherosclerosis in patients who also have HS.Abnormal peri-organ or intra-organ fat (APIFat) deposition has been recognized as a possible risk factor for metabolic and vascular diseases. 2 The term APIFat generally describes an increase in the fat that normally surrounds organs or the increase in intra-organ fat. Such changes may be observed in several organs (e.g. liver, epicardium, muscle, kidney, vascular wall and pancreas). 3,4 A well-studied abnormal APIFat deposition is nonalcoholic fatty liver disease (NAFLD) and its more advanced form, non-alcoholic steatohepatitis (NASH). The prevalence of these conditions is rapidly increasing worldwide due to the obesity and diabetes pandemic. 5 Indeed, NAFLD is considered as a hepatic manifestation of metabolic syndrome (MetS), which is a cluster of CVD risk factors that, in combination, significantly increase the risk of type 2 diabetes (T2DM) and cardiovascular disease (CVD). Although NAFLD and NASH are risk factors for liver cirrhosis and hepatocellular carcinoma, atherosclerotic disease is the main aetiology of death in patients with these conditions. Consequently, NAFLD and NASH predict an increased atherosclerotic risk. [6][7][8] The term NAFPD is used to define the accumulation of fat in pancreatic tissue (located within adipocytes). 9,10 Its prevalence is estimated to be 10-35% in the general population and increases in parallel with age and obesity. 10 The wide interval in NAFPD prevalence is notable and denotes significant differences between populations with different ethnic background, age and comorbidities. It should also be noted that the

Pathophysiological Mechanisms and Clinical Associations of Non-Alcoholic Fatty Pancreas Disease

“…In general, fat deposition is linked to multiple diseases like metabolic syndrome, diabetes, and atherosclerosis. 2,76 In a large cross-sectional study where NAFPD and its risk factors were examined, authors compared pancreatic echogenicity with that of the liver and demonstrated that fatty pancreas and fatty liver composition were found in combination in almost 26% of patients, whereas fatty pancreas alone was found in 16%. 11 In a prospective study almost 68% of the included patients with fatty pancreas presented with fatty liver, but 97% of patients initially diagnosed with fatty liver presented concurrently with a fatty pancreas, making fatty liver a strong predictive factor of fatty pancreas disease.…”

“…Pancreatic fat deposition in the absence of excessive alcohol intake, described as non-alcoholic fatty pancreas disease (NAFPD), 1 is an emerging clinical entity. 2 Despite the higher susceptibility to fat deposition of the pancreas compared to the liver, 3,4 the clinical relevance and underlying pathophysiological mechanisms of pancreatic fat infiltration remain unclear in the medical literature. Robertson F. Ogilvie was the first to describe pancreatic fat deposition in obese cadavers, reporting 17% of pancreatic fat storage, as compared to 9% in lean ones.…”

Fatty Pancreas: Linking Pancreas Pathophysiology to Nonalcoholic Fatty Liver Disease

“…In the presence of oxidative stress, an increase in free fatty acid transport to the pancreas by very-low-density lipoprotein and changes in various adipokines such as adiponectin, 36 lipocalin-2, 37 and hepatokine fetuin-A 38 via the serine/threonine-protein kinase 25 (STK-25) pathway may contribute to this type of pancreatic fat accumulation. 39…”

“…Available evidence from experimental models and human studies suggests a bidirectional relationship between fatty pancreas and NAFLD. 6,19,24,39…”