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I read with interest the paper by Midha et al 1 which brings a new perspective on non-alcoholic chronic pancreatitis in India which raises some concerns. The term ‘tropical pancreatitis’ was used to denote a form of chronic pancreatitis unassociated with alcohol abuse which occurred in the tropics and subtropics. The subtropics, by definition, denote geographic areas adjacent to the tropical zone (usually 20–40° latitude) where daytime temperatures remain above 10°C for >8 months of the year. India's geographic latitudinal extent is 6.74678°N to 37.09681°N and daytime temperatures do exceed 10°C for >8 months, and hence qualifies as being ‘tropical’. In the study, the definition for chronic pancreatitis is vague. Our own preference is to use four criteria: …

I read the article on idiopathic chronic pancreatitis (ICP) in India in which there was reference to tropical chronic pancreatitis (TCP).1 TCP was a form of ICP first described in the 1960s in the south-western state of Kerala in India.2 Even though the aetiology of this new condition was unknown, the clinical features of the new entity of chronic pancreatitis (CP) in young malnourished non-alcoholic subjects in poor tropical countries was so distinctive that, to distinguish it from alcoholic chronic pancreatitis (ACP), the term ‘TCP’ came into usage without much thought into its aetiological connotation and was accepted by the medical community. …

Clinical research into patients with idiopathic chronic pancreatitis points to a possible immunopathogenetic process in a number of cases. In order to examine the behaviour between the exocrine pancreas under the influence of anti-rat-pancreas immune serum produced in rabbits, a 1.00 ml immune serum is administered once a week over a maximum 26 week period into Wistar-rats by intraperitoneal injection. By electrone-microscopy a much reduced production of enzymes apparently takes place, though to differing extent. There is also destruction of the basal membrane of acinocytes: the production of interstitial oedema, the new formation of collagen fibres and the proliferation of connective tissue cells. Under a conventional light microscope the first changes become noticeable after 8-12 weeks of study. These take the form of localised cell decay, deterioration and lysis of acinocytes; and an increasing non-specific inflammation. There is also the new formation of connective tissue. After 20-26 weeks the exocrine pancreas is characterised by reduction of parenchyma, acino-ductal metaplasia, chronic inflammatory infiltrates of differing density, fibrous and irregular calibres of the smaller and larger ducts. The findings are almost identical to the structural changes of chronic idiopathic pancreatitis in human beings. The results support the view of an immuno-pathologic aetiology for human chronic idiopathic pancreatitis.

Among 192 cases of chronic pancreatitis, 51 (27%) were classifed as idiopathic after exclusion of all known aetiological factors. The age distribution of idiopathic chronic pancreatitis suggests that there are two separate entities, a "senile" (n = 38) (ISCP) and a "juvenile" form (n = 13) (IJCP). IJCP seems to represent a new nosological entity characterized by a low mean age at onset (25.6 years), a preponderance of males (n = 12), typical recurrent episodes of pancreatitis (n = 13), and a very high incidence of calcifications (n = 10). The course of IJCP seems to be rather benign but protracted. Despite lacking direct evidence, IJCP seems to be due to a genetic factor. The postulated causes of IJCP and ISCP may be identical with the primary factors which are considered to be responsible in combination with high alcohol intake, for the development of alcohol-induced chronic pancreatitis.

ROENTGENOGRAPHIC evidence of pancreatic calcification has been noted in approximately 25 per cent of patients with idiopathic chronic pancreatitis and in 50 per cent of cases of recurrent pancreatitis associated with alcoholism.1 , 2 Calcification developing within a primary pancreatic carcinoma is relatively rare. However, the converse does not appear to be true, and indeed, the reported incidence of pancreatic carcinoma in patients with chronic calcific pancreatitis has been 9.4 and 25 per cent.1 , 3 The case reported below was considered unique because during the course of chronic calcific pancreatitis, roentgenographic evidence of pancreatic decalcification was observed and post-mortem examination revealed a primary . . .

Six patients with idiopathic chronic pancreatitis are described in whom a pancreatogram showed an unusual morphology, being irregularly narrowed throughout. This "shrunken" appearance differs from the classic irregular dilatation usually seen in chronic pancreatitis. Two of the patients had inflammatory bowel disease, none had a history of alcoholism and only one had gallstones.

Organ- and nonorgan-specific autoantibodies (AA) have been investigated in 49 patients affected by alcoholic or idiopathic chronic pancreatitis (CP) to evaluate their prevalence and correlation with the clinical features of the disease. AA have been found in about 50% of CP and their recurrence rate was similar to that of alcoholic or cryptogenic liver cirrhosis (LC); age- and sex-matched healthy subjects (C) showed only about 8% positive sera (C vs. CP, p less than 0.001). Quite different IFL patterns between CP and LC have been detected. Antibrush border, antireticulin and antigastric parietal cell antibodies alone or combined prevailed in CP, while antinuclear and antismooth muscle AA prevailed in LC. No correlation with sex, age, etiology, presence of pancreatic stones, diabetes, symptoms and years of CP was found for one or more AA. In conclusion, the detection of AA in CP is a quite common finding of still unclear clinical significance.

The endoscopic cannulation records of two medical centers (Niigata, Japan and NEMCH, Boston, Mass.) were studied for evidence of pancreatic cancer. Of a total group of 483 pancreatic ductograms, 33 were characteristically abnormal and fell into 4 patterns: stenotic, tapering, obstructed, or unclassified. Three causes of false-positive patterns emerged: idiopathic chronic pancreatitis, surgical mobilization of the head of the pancreas, and traumatic pancreatitis. No false-negative results have been found in this brief followup period. The endoscopic method remains valid for preoperative diagnosis of pancreatic cancer, keeping in mind these sources of false-positive results.