Tropical Calcific Pancreatitis

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Tropical Calcific Pancreatitis

R. SUBHASH, V. A. IYOOB, and BONNY NATESH

A38-year-old woman was admitted with complaints of recur-rent episodes of upper abdominal pain. The pain was severe,

ontinuous, and of a dull aching type, radiating to her back. Shelso had a history of steatorrhea and diabetes mellitus of 8 years’uration. There was also a gradual weight loss over the past fewears. She had multiple hospital admissions in the past for acutexacerbations of abdominal pain, starting in her early 20s. Thelinical examination was unremarkable except for mild tendernessn the epigastrium on deep palpation. Laboratory investigationsevealed high serum amylase and lipase values, suggesting pancre-titis. She was not an alcoholic or a smoker. Her serum calciumevel also was normal. The ultrasonogram showed evidence ofcute exacerbation of chronic calcific pancreatitis, and there waso evidence of gallstone disease. The patient was managed con-ervatively, to which she responded well. Later, a computed tomog-aphy was performed that revealed multiple, large, chunky calculin the entire length of the dilated pancreatic duct, from head to tailegion, with atrophy of the pancreatic parenchyma (Figure A and). The clinical and imaging features were suggestive of a type ofhronic pancreatitis that is very common in tropical countries ands known as chronic calcific pancreatitis of the tropics or tropicalalcific pancreatitis (TCP). Subsequently, she underwent surgicalreatment in the form of lateral pancreaticojejunostomy with re-

oval of all intraductal stones (Figure C). Postoperative recoveryas uneventful, and at 1 year of follow-up evaluation she remainssymptomatic.

TCP is a form of idiopathic, nonalcoholic chronic pancreatitisith characteristic clinical and imaging features.1 The disease is

ndemic in several tropical countries, including India.2 TCP isharacterized by recurrent episodes of upper abdominal pain,teatorrhea, malnutrition, and the development of diabetes melli-us, occurring in young adults. The disease slowly progresses overears and is associated with a high risk of pancreatic cancer.3

Imaging features are characteristic with multiple large intraductal

calculi in the pancreas and gross atrophy and fatty replacement ofpancreatic parenchyma. The etiopathogenesis of TCP is still un-clear, but genetic, toxic, and environmental factors are implicatedin its causation.1 The disease seems to have a multifactorial etiol-ogy, with environmental factors acting on genetic predisposition.Individuals with certain genetic abnormalities, such as serine pro-tease inhibitor kazal type 1, cystic fibrosis transmembrane conduc-tance regulator gene mutations, or cathepsin B polymorphism, aresusceptible to develop the disease. Acute episodes of TCP aremanaged conservatively similar to other forms of pancreatitis.Patients then are followed up with analgesics and enzyme supple-ments. Surgical treatment is indicated when there are recurrentand intractable episodes of abdominal pain or when complicationsof pancreatitis arise. The surgical options are directed mainlytoward pancreatic ductal decompression and drainage of dilatedducts with clearance of the calculi in the form of lateral pancrea-ticojejunostomy.

References1. Tandon RK, Sato N, Garg PK, et al. Consensus study group.

Chronic pancreatitis: Asia-Pacific consensus report. J GastroenterolHepatol 2002;17:508–518.

2. Balaji LN, Tandon RK, Tandon BN, et al. Prevalence and clinicalfeatures of chronic pancreatitis in Southern India. Int J Pancreatol1993;15:29–34.

3. Chari ST, Mohan V, Pitchumoni CS, et al. Risk of pancreatic carci-noma in tropical calcifying pancreatitis: an epidemiologic study. Pan-creas 1994;9:62–66.

Conflicts of interestThe authors disclose no conflicts.

© 2012 by the AGA Institute1542-3565/$36.00

http://dx.doi.org/10.1016/j.cgh.2012.03.012

CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2012;10:xxx