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Benign pancreatic hyperenzymaemia (BPH) is a syndrome characterised by a chronic increase in serum pancreatic enzymes in the absence of pancreatic disease.1,2,3,4,5 In March 2000 we saw a woman who had this form of hyperenzymaemia, whose mother had died of pancreatic cancer. Prompted by this observation, we undertook a prospective study to determine whether there is a familial association between BPH and pancreatic cancer. Between June 2000 and October 2006, we saw 68 subjects with BPH (42 male, 26 female; age range 8 to 72 years, mean age 45.7 years). They were questioned about the presence of pancreatic cancer in members of their families. The subjects who had relatives with pancreatic cancer and their immediate family members were included in the study. In addition to serum pancreatic enzymes, all underwent magnetic resonance imaging (MRI) with secretin stimulation and endoscopic ultrasound for detailed study of the Wirsung duct and pancreatic parenchyma.
Among the 68 subjects who had BPH, six had relatives who had died of pancreatic cancer. The demographic and clinical characteristics of these six subjects are shown in table 11.. MRI was normal in all six, while endoscopic ultrasonography was normal in five; in the sixth (subject 6), parenchymal abnormalities (lobularity and hyperechoic strands) were present in the head of the pancreas. Two of the 10 relatives of these six subjects had pancreatic hyperenzymaemia; in both these subjects, MRI and endoscopic ultrasonography results were normal (table 11).). Among the six study subjects there were nine relatives who had died of pancreatic ductal cancer (table 11).). Four of the six had only one relative; one (subject 2), had two family members with pancreatic cancer, and another (subject 6) had three relatives with pancreatic cancer. The diagnosis of pancreatic cancer was based on histology in seven of the nine subjects, and on clinical and imaging findings in the other two.
Our findings show that there may be a familial association between BPH and pancreatic cancer. The significance of this association is not clear. BPH probably results from a defect in the passage of enzymes from acinar cells into the blood which results in greater than normal quantities in the circulation.4 The anomaly is benign, generally being discovered during a routine blood analysis which includes amylase determination. At this point it is not known whether the occurrence of BPH in a family member or a relative of someone who has pancreatic cancer is incidental or the result of an underlying connection between the two conditions.
In order to see whether there were pancreatic lesions in subjects included in the study, they underwent MRI with secretin stimulation as well as endoscopic ultrasonography, which are generally sensitive for the detection of even small pancreatic lesions.6 MRI was normal in all six subjects, while endoscopic ultrasonography was normal in all but one; this subject had three family members who had died of pancreatic cancer. The parenchymal abnormalities were lobularity and hyperechoic strands in the pancreatic head—lesions that have been seen by other investigators7,8,9 in relatives of patients with pancreatic cancer, primarily subjects who had two or more relatives with the tumour. These changes, together with others,7,8,9 have been shown to be associated with pancreatic dysplasia, a precursor lesion of pancreatic cancer.10 Our study subject who had pancreatic abnormalities on endoscopic ultrasonography will be carefully followed, both clinically and ultrasonographically.
In conclusion, our study shows that persistent pancreatic hyperenzymaemia may be encountered in family members of patients with pancreatic cancer. The significance of this association is not clear, but it is possible that these individuals could be at increased risk of pancreatic cancer.
Conflict of interest: None declared.