Published online Jul 28, 2018. doi: 10.3748/wjg.v24.i28.3120
Peer-review started: April 17, 2018
First decision: June 11, 2018
Revised: June 17, 2018
Accepted: June 27, 2018
Article in press: June 27, 2018
Published online: July 28, 2018
Processing time: 101 Days and 17.5 Hours
In about 42%-66% of patients with autoimmune pancreatitis, hyperglycemia can be observed. Thus, hyperglycemia is a frequent and important complication of this disease. However, it is not known if it merely reflects the severity of pancreatitis or whether it can also influence the progression of autoimmune pancreatitis.
For treating autoimmune pancreatitis in the clinic, guidelines recommend to adjust blood glucose concentration before starting a steroid therapy. However, critical attitudes towards adjusting the blood glucose concentration in these patients have also been published. For example, in one third of all cases, hyperglycemia even worsened after insulin therapy, and treatment of diabetes with insulin sometimes leads to hypoglycemic attacks in patients. In order to decide how important a tight adjustment of blood glucose concentration in patients with autoimmune pancreatitis is, we need to know if hyperglycemia has a positive or negative influence on the progression of this disease.
The purpose of this present study was to address the question of whether diabetes can influence the progression of autoimmune pancreatitis and to analyze which aspects of this disease are affected by hyperglycemia.
We chose to use MRL/MpJ mice, an animal model widely used to study autoimmune pancreatitis. These mice spontaneously develop autoimmune pancreatitis. We induced hyperglycemia by repetitive intraperitoneal (ip) injection of streptozotocin in female mice and compared the extent of inflammation in the pancreas of hyperglycemic and normoglycemic animals. We also analyzed the number of immune cells in the blood. In addition, we determined the percentage of T-cells, especially regulatory T-cells in the spleen.
Surprisingly, experimental hyperglycemia did not cause an aggravation of autoimmune pancreatitis, but moderately improved autoimmune pancreatitis. We noticed an increased percentage of regulatory T-cells in the spleen, as well as an increased number of leukocytes in the blood of hyperglycemic mice. These findings suggest that hyperglycemia might rather influence the overall immune system and only indirectly affect autoimmune pancreatitis itself.
Our preclinical study on mice supports the idea that an aggressive adjustment of blood glucose concentration might not be necessary as a prerequisite for the treatment of patients with autoimmune pancreatitis.
A clinical study that evaluates whether a tight adjustment of blood glucose is beneficial or harmful to patients should be pursued.