Pancreatic Exocrine Insufficiency Is a Risk Factor for Hepatic Steatosis

New research from Japan indicates that exocrine pancreatic insufficiency after pancreatectomy may be 1 of several factors that indicates an elevated risk of postoperative hepatic steatosis.

Investigators followed 43 patients who underwent total pancreatectomy and used computed tomography to diagnose hepatic steatosis. By the end of the study period, 16 of the patients (37.2%) had developed the condition, which was identified via the attenuation of unenhanced computed tomography values. (All of those patients subsequently experienced negative outcomes associated with hepatic steatosis, outcomes such as marked declines in Controlling Nutritional Status scores and body mass index.)

The investigators compared a variety of baseline characteristics and lab results from patients who did and patients who did not develop hepatic steatosis, looking for variables that predicted which patients faced an elevated risk.

Multiple linear regression analysis found that the tendency to develop hepatic steatosis was correlated with female sex (P = 0.002), early postoperative serum albumin levels (P = 0.003), and pancreatic enzyme replacement therapy with high-dose pancrelipase (P = 0.032).

This last finding, the researchers wrote, suggests that exocrine pancreatic insufficiency (rather than the pancrelipase that is used to treat it) is associated with an elevated risk of hepatic steatosis. Indeed, analysis of patient results suggested that high doses of pancrelipase, started as soon as patients develop exocrine pancreatic insufficiency, may lower the chances that pancreatectomy patients will develop hepatic steatosis.

“The aims of this study were to identify other risk factors in addition to the remnant pancreatic function and elucidate the relationship between postoperative hepatic steatosis and pancreatic exocrine insufficiency in totally pancreatomized patients,” the study authors wrote in Pancreas.

“Postoperative hepatic steatosis after pancreatectomy,” they concluded, “is associated with sex, malnutrition, and pancreatic exocrine insufficiency. High-dose pancreatic enzyme replacement therapy may have preventive effects on hepatic steatosis occurring after pancreatectomy.”

Hepatic steatosis, which is also known as fatty liver disease, is the most common liver disease among people in the U.S. It is most commonly caused by type 2 diabetes and/or obesity and treated, in such cases, with efforts to reduce weight or increase insulin sensitivity. Pancreatectomy is a far less-studied cause of the condition, but prior research does exist.

The new study of hepatic steatosis in pancreatectomy patients strongly resembles a 2012 study that also appeared in Pancreas. The investigators who wrote that paper reported that 31.4% of the 102 pancreatectomy patients in their retrospective study developed postoperative hepatic steatosis. Those investigators, who were also from Japan, also used regression analysis to see which factors were independent predictors of elevated risk.

“Multivariate analysis showed that absence of postoperative insulin use (P < 0.01) and decrease in postoperative body mass index of greater than 3 kg/m² (P < 0.01) were independent risk factors for hepatic steatosis,” they wrote.

The patients in that study underwent pancreatectomy to remove cancer, so the investigators also looked for connections between hepatic steatosis and recurrence-free survival. They found that patients who developed postoperative hepatic steatosis collectively had a poorer rate of recurrence-free survival than those who did not, but the difference did not quite meet the threshold of statistical significance (p=0.053).

“Postoperative hepatic steatosis may affect long-term prognosis after pancreatectomy,” the study authors wrote. “Surgeons should take care of nutritional management including insulin therapy for patients with hepatic steatosis after pancreatectomy.”