Nakamura T, Imamura K, Takebe K, Terada A, Arai Y, Tandoh Y, Yamada N, Ishii M, Machida K, Suda T
Third Department of Internal Medicine, Hirosaki University School of Medicine, Aomori, Japan.
Int J Pancreatol. 1996 Dec;20(3):169-75. doi: 10.1007/BF02803765.
Pancreatic endocrine capacities are remarkably disturbed in patients with pancreatic diabetes owing to calcific pancreatitis as opposed to those owing to noncalcific pancreatitis. Insulin secretion in calcific pancreatitis resembled that in insulin-dependent diabetes mellitus (IDDM), whereas insulin secretion in noncalcific pancreatitis resembled that in non-IDDM (NIDDM). The involvements of acinar cell and ductal cell function closely correlate with endocrine function (insulin and glucagon secretions) in chronic pancreatitis (pancreatic diabetes).
We sought to clarify the differences of pancreatic endocrine function between pancreatic diabetes and primary diabetes, and to verify the correlations between pancreatic exocrine and endocrine dysfunction in patients with chronic pancreatitis.
Urinary C-peptide (CPR) excretion and fasting plasma glucagon levels in patients with pancreatic diabetes owing to calcific pancreatitis (19 cases) and owing to noncalcific pancreatitis (14 cases) were studied in comparison with those in patients with insulin-dependent diabetes mellitus (IDDM, 23 cases), noninsulin-dependent diabetes (NIDDM, 18 cases), and in healthy controls (11 cases). In addition, pancreatic exocrine function was investigated in patients with chronic pancreatitis (calcific and noncalcific) and in healthy controls. The correlation between pancreatic exocrine and endocrine function was studied.
The urinary CPR excretion in controls was 94.9 +/- 20.5 micrograms/d. The urinary CPR excretion in calcific pancreatitis was 12.8 +/- 7.4 micrograms/d and it resembled that in IDDM (9.4 +/- 5.8 micrograms/d). The urinary CPR excretion in noncalcific pancreatitis was 41.5 +/- 30.1 micrograms/d, being similar to that in NIDDM (49.3 +/- 21.0 micrograms/d). The plasma glucagon level in calcific pancreatitis was 64.1 +/- 15.9 rho g/mL, which was significantly lower than the values in IDDM (111.2 +/- 50.2 rho g/mL) and NIDDM (96.7 +/- 21.9 rho g/mL). The plasma glucagon level in calcific and noncalcific pancreratitis (88.4 +/- 29.6 rho g/mL) were significantly lower than that in controls (129.8 +/- 21.6 rho g/mL). The residual capacities of acinar cells and ductal cells were strongly correlated with urinary CPR excretion and plasma glucagon concentration.
与非钙化性胰腺炎所致胰腺糖尿病患者相比，钙化性胰腺炎所致胰腺糖尿病患者的胰腺内分泌功能明显紊乱。钙化性胰腺炎中的胰岛素分泌类似于胰岛素依赖型糖尿病（IDDM）中的胰岛素分泌，而非钙化性胰腺炎中的胰岛素分泌类似于非IDDM（NIDDM）中的胰岛素分泌。在慢性胰腺炎（胰腺糖尿病）中，腺泡细胞和导管细胞功能的受累与内分泌功能（胰岛素和胰高血糖素分泌）密切相关。
我们试图阐明胰腺糖尿病与原发性糖尿病之间胰腺内分泌功能的差异，并验证慢性胰腺炎患者胰腺外分泌和内分泌功能障碍之间的相关性。
研究了钙化性胰腺炎（19例）和非钙化性胰腺炎（14例）所致胰腺糖尿病患者的尿C肽（CPR）排泄和空腹血浆胰高血糖素水平，并与胰岛素依赖型糖尿病（IDDM，23例）、非胰岛素依赖型糖尿病（NIDDM，18例）患者及健康对照者（11例）进行比较。此外，还对慢性胰腺炎（钙化性和非钙化性）患者及健康对照者的胰腺外分泌功能进行了研究。研究了胰腺外分泌和内分泌功能之间的相关性。
对照组尿CPR排泄量为94.9±20.5微克/天。钙化性胰腺炎患者尿CPR排泄量为12.8±7.4微克/天，与IDDM患者（9.4±5.8微克/天）相似。非钙化性胰腺炎患者尿CPR排泄量为41.5±30.1微克/天，与NIDDM患者（49.3±21.0微克/天）相似。钙化性胰腺炎患者血浆胰高血糖素水平为64.1±15.9纳克/毫升，显著低于IDDM患者（111.2±50.2纳克/毫升）和NIDDM患者（96.7±21.9纳克/毫升）的值。钙化性和非钙化性胰腺炎患者的血浆胰高血糖素水平（88.4±29.6纳克/毫升）显著低于对照组（129.8±21.6纳克/毫升）。腺泡细胞和导管细胞的残余能力与尿CPR排泄和血浆胰高血糖素浓度密切相关。
