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Tropical Calcific Pancreatitis
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Image of the Month Tropical Calcific Pancreatitis R. SUBHASH, V. A. IYOOB, and BONNY NATESH Department of Surgical Gastroenterology, Government Medical College Thiruvananthapuram, Thiruvananthapuram, Kerala, India A 38-year-old woman was admitted with complaints of recur- rent episodes of upper abdominal pain. The pain was severe, continuous, and of a dull aching type, radiating to her back. She also had a history of steatorrhea and diabetes mellitus of 8 years’ duration. There was also a gradual weight loss over the past few years. She had multiple hospital admissions in the past for acute exacerbations of abdominal pain, starting in her early 20s. The clinical examination was unremarkable except for mild tenderness in the epigastrium on deep palpation. Laboratory investigations revealed high serum amylase and lipase values, suggesting pancre- atitis. She was not an alcoholic or a smoker. Her serum calcium level also was normal. The ultrasonogram showed evidence of acute exacerbation of chronic calcific pancreatitis, and there was no evidence of gallstone disease. The patient was managed con- servatively, to which she responded well. Later, a computed tomog- raphy was performed that revealed multiple, large, chunky calculi in the entire length of the dilated pancreatic duct, from head to tail region, with atrophy of the pancreatic parenchyma (Figure A and B). The clinical and imaging features were suggestive of a type of chronic pancreatitis that is very common in tropical countries and is known as chronic calcific pancreatitis of the tropics or tropical calcific pancreatitis (TCP). Subsequently, she underwent surgical treatment in the form of lateral pancreaticojejunostomy with re- moval of all intraductal stones (Figure C). Postoperative recovery was uneventful, and at 1 year of follow-up evaluation she remains asymptomatic. TCP is a form of idiopathic, nonalcoholic chronic pancreatitis with characteristic clinical and imaging features. 1 The disease is endemic in several tropical countries, including India. 2 TCP is characterized by recurrent episodes of upper abdominal pain, steatorrhea, malnutrition, and the development of diabetes melli- tus, occurring in young adults. The disease slowly progresses over years 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 of pancreatic parenchyma. The etiopathogenesis of TCP is still un- clear, but genetic, toxic, and environmental factors are implicated in 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, are susceptible to develop the disease. Acute episodes of TCP are managed 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 recurrent and intractable episodes of abdominal pain or when complications of pancreatitis arise. The surgical options are directed mainly toward pancreatic ductal decompression and drainage of dilated ducts with clearance of the calculi in the form of lateral pancrea- ticojejunostomy. References 1. Tandon RK, Sato N, Garg PK, et al. Consensus study group. Chronic pancreatitis: Asia-Pacific consensus report. J Gastroenterol Hepatol 2002;17:508 –518. 2. Balaji LN, Tandon RK, Tandon BN, et al. Prevalence and clinical features of chronic pancreatitis in Southern India. Int J Pancreatol 1993;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 interest The authors disclose no conflicts. © 2012 by the AGA Institute 1542-3565/$36.00 http://dx.doi.org/10.1016/j.cgh.2012.03.012 CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2012;10:xxx
Transcript of Tropical Calcific Pancreatitis
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Image of the Month
Tropical Calcific Pancreatitis
R. SUBHASH, V. A. IYOOB, and BONNY NATESH
Department of Surgical Gastroenterology, Government Medical College Thiruvananthapuram, Thiruvananthapuram, Kerala, IndiaA38-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
