Nonalcoholic Fatty Pancreas Disease: Role in Metabolic Syndrome, "Prediabetes," Diabetes and Atherosclerosis.

Fat accumulation in the pancreas associated with obesity and the metabolic syndrome (MetS) has been defined as "non-alcoholic fatty pancreas disease" (NAFPD). The aim of this review is to describe the association of NAFPD with obesity, MetS, type 2 diabetes mellitus (T2DM) and atherosclerosis and also increase awareness regarding NAFPD. Various methods are used for the detection and quantification of pancreatic fat accumulation that may play a significant role in the differences that have been observed in the prevalence of NAFPD. Endoscopic ultrasound provides detailed images of the pancreas and its use is expected to increase in the future. Obesity and MetS have been recognized as NAFPD risk factors. NAFPD is strongly associated with non-alcoholic fatty liver disease (NAFLD) and it seems that the presence of both may be related with aggravation of NAFLD. A role of NAFPD in the development of "prediabetes" and T2DM has also been suggested by most human studies. Accumulation of fat in pancreatic tissue possibly initiates a vicious cycle of beta-cell deterioration and further pancreatic fat accumulation. Additionally, some evidence indicates a correlation between NAFPD and atherosclerotic markers (e.g., carotid intima-media thickness). Weight loss and bariatric surgery decreases pancreatic triglyceride content but pharmacologic treatments for NAFPD have not been evaluated in specifically designed studies. Hence, NAFPD is a marker of local fat accumulation possibly associated with beta-cell function impairment, carbohydrate metabolism disorders and atherosclerosis.

A case of severe hyponatremia due to linezolid-induced SIADH.

WHAT IS KNOWN AND OBJECTIVE: Hyponatremia is the most common electrolyte disorder. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the main cause of euvolemic hyponatremia and is often associated with medications or underlying diseases. Linezolid is a potent antibiotic against resistant Gram-positive microorganisms that has been associated with mild hyponatremia, yet with a mechanism different from SIADH. CASE SUMMARY: We present the case of a patient who developed severe hyponatremia during treatment with linezolid for an ampicillin-resistant E. faecium bacteremia. A thorough work-up during the hyponatremia, as well as after it resolved, firmly identified SIADH as its cause. Importantly, SIADH occurred after linezolid was started and resolved after it was stopped, and a work-up for another cause of SIADH was negative, suggesting that linezolid was the cause of SIADH in this patient. WHAT IS NEW AND CONCLUSION: This is the second case of a linezolid-induced SIADH, diagnosed with a thorough work-up so to correctly differentiate between SIADH from other causes of hyponatremia.