Exocrine Pancreatic Function (Serum Immunoreactive Trypsin, Fecal Chymotrypsin, and Pancreatic Isoamylase) in Indian Diabetics

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Abstract
Forty-nine patients with tropical calcific pancreatitis (TCP), 51 insulin- dependent diabetics (IDDMs), 87 non-insulin-dependent diabetics (NIDDMs), and 66 nondiabetic controls were studied to evaluate their exocrine pancreatic function by measurement of serum immunoreactive trypsin (IRT, normal for white Caucasians from the U.K. of 140–414 μg/L), pancreatic isoamylase (PIA, normal of 35–125 U/L), and fecal chymotrypsin (FCT, normal of >6.6 u/g). The majority of patients were studied within 1 year of diagnosis. TCP subjects included 7 nondiabetics, 6 with impaired glucose tolerance (IGT-TCP), and 36 diabetics [fibrocalculous pancreatic diabetes (FCPD)]. There was evidence of active pancreatitis (IRT >800 μg/L) and partial preservation of function in nondiabetic TCP subjects [median IRT of 220 μg/L (range of 102–1,360 μg/L), FCT of 2.2 u/g (range 0.7–12.8 u/g)] and also in IGT-TCP subjects [IRT of 370 pg/L (range of 30–1,360 μg/L), FCT of 4.2 u/g (range of 1–38 u/g)]. FCPDs showed severely diminished exocrine function [IRT of 50 μg/L (range of CL184 μg/L), FCT of 0.23 u/g (range of 0–10.4 u/g)]; none showed IRT > 800 μg/L. IDDMs and NIDDMs also showed diminished exocrine pancreatic function in ∼30 and ∼10%, respectively. Controls showed a wide range of IRT and FCT concentrations; IRT concentrations tended to be higher than those reported in white Caucasians from the U.K. Three controls, one IDDM, and two NIDDMs showed “pancreatitic” IRT concentrations in the absence of symptoms. PIA concentrations were diminished in FCPD but were similar in IDDM and NIDDM subjects compared to controls. Simultaneous measurements showed that IRT concentrations were reduced when PIA concentrations were still normal. Our results suggest that TCP and FCPD (diagnosed by radiographically demonstrable pancreatic calculi) represent advanced disease and that a subclinical “pancreatopathy” appears to be common in tropical subjects (diabetic as well as nondiabetic). Endocrine impairment (hyperglycemia) in TCP parallels exocrine damage.

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