The exocrine and endocrine pathophysiology of chronic calcific pancreatitis of the tropics (CCPT) remains elusive. The objective of this study was to evaluate the spectrum and correlates of the exocrine and endocrine pancreatic dysfunction in CCPT. Thirty-seven consecutive patients with a clinico-radiological diagnosis of CCPT were stratified into three subgroups: CCPT-normal glucose tolerance (NGT), CCPT-abnormal glucose tolerance (IGT) and CCPT-diabetes mellitus (DM). Ten ketosis resistant young diabetic (KRDY) patients, 10 classical insulin dependent diabetes mellitus (IDDM) patients and 18 healthy matched controls were included for comparison. Fecal chymotrypsin (FCT) levels and blood C-peptide levels (basal and post i.v. glucagon stimulation) were estimated for assessing the exocrine and endocrine pancreatic functions, respectively. Sonography was performed to evaluate the pancreatic size and ductal diameter. Pancreatic exocrine-endocrine correlation was examined by studying the C-peptide/fecal chymotrypsin ratio ( CP FCT ) ( CP FCT of normal controls = 1). Mean FCT levels in all 3 subgroups of CCPT (NGT: 3.4 μ/g; IGT: 0.82 μ/g; DM: 2.4 μ/g) were very low (87–96% reduction in exocrine pancreatic dysfunction; mean FCT in healthy controls was 22.8 μ/g) ( P < 0.0001). In contrast, KRDY and IDDM patients displayed 50–54% reduction in pancreatic acinar function ( P < 0.001). Basal and stimulated C-peptide levels progressively fell in the 3 CCPT subsets (NGT: 0.23 and 0.46 > IGT: 0.14 and 0.29 > DM 0.10 and 0.14) ( P < 0.01). CCPT patients exhibited pancreatic atrophy and ductal dilatation (> 3 mm). There was a progressive exocrine and endocrine dysfunction in the CCPT patients with appearance of glucose tolerance abnormalities — greater magnitude of acinar cell damage in CCPT-DM/CCPT-IGT patients. Exocrine pancreatic dysfunction is disproportionately severe in CCPT patients ( CP FCT : 2.3–13.3), while KRDY and IDDM patients display dominant endocrine damage ( CP FCT : 0.3–0.7).