Tropical Pancreatitis Research Articles

Parathyroid scintigraphy, histopathology correlation in patients with tropical pancreatitis and coexisting primary hyperparathyroidism

Purpose:Tropical pancreatitis (TP) is a juvenile, non-alcoholic type of chronic pancreatitis and is highly prevalent in Kerala, India. Increasing prevalence of TP and its varied manifestations prompted us to undertake this retrospective analysis. We attempted to study the incidence of TP in patients with primary hyperparathyroidism (PHPT) and correlate with calcium levels, scintigraphy and histopathology findings.Materials and Methods:Records of 44 hypercalcemic patients with raised parathormone (PTH) were analyzed. Clinical, biochemical and imaging findings were noted to look for diabetes mellitus and pancreatitis. All patients underwent dual phase 99m Technetium methoxy isobutyl isonitrile parathyroid scintigraphy in our department between January 2007 and 2010. Gamma probe assisted minimally invasive parathyroidectomy was performed. Histopathological correlation was obtained in all patients.Results:Our study shows 18% (8/44 patients) incidence of TP in patients with PHPT (compared to 7% reported in 1970's) in Kerala. Results show involvement of middle aged, non-alcoholic males. No direct association between severity of diabetes, pancreatitis and PHPT was noted in our series. Parathyroid adenoma was the most common underlying pathology. All TP patients’ clinical outcome improved post parathyroidectomy. TP patients with PHPT demonstrated adenomas, mainly composed of oxyphilic cells. Non pancreatitis group interestingly showed a varied picture of adenoma, hyperplasia with predominance of chief cells histologically.Conclusion:There is a 2.6 fold increase in the incidence of TP (18%) in patients with PHPT. Hypercalcemia may be the causative factor leading to TP in PHPT patients in our limited series. The data suggests a causal association between pancreatitis and PHPT. Patients presenting with either one or a combination of hypercalcemia, pancreatic dysfunction or raised PTH need to be thoroughly evaluated as their management is interlinked.

Therapeutic Roles of Curcumin: Lessons Learned from Clinical Trials

Extensive research over the past half century has shown that curcumin (diferuloylmethane), a component of the golden spice turmeric (Curcuma longa), can modulate multiple cell signaling pathways. Extensive clinical trials over the past quarter century have addressed the pharmacokinetics, safety, and efficacy of this nutraceutical against numerous diseases in humans. Some promising effects have been observed in patients with various pro-inflammatory diseases including cancer, cardiovascular disease, arthritis, uveitis, ulcerative proctitis, Crohn's disease, ulcerative colitis, irritable bowel disease, tropical pancreatitis, peptic ulcer, gastric ulcer, idiopathic orbital inflammatory pseudotumor, oral lichen planus, gastric inflammation, vitiligo, psoriasis, acute coronary syndrome, atherosclerosis, diabetes, diabetic nephropathy, diabetic microangiopathy, lupus nephritis, renal conditions, acquired immunodeficiency syndrome, β-thalassemia, biliary dyskinesia, Dejerine-Sottas disease, cholecystitis, and chronic bacterial prostatitis. Curcumin has also shown protection against hepatic conditions, chronic arsenic exposure, and alcohol intoxication. Dose-escalating studies have indicated the safety of curcumin at doses as high as 12 g/day over 3 months. Curcumin's pleiotropic activities emanate from its ability to modulate numerous signaling molecules such as pro-inflammatory cytokines, apoptotic proteins, NF-κB, cyclooxygenase-2, 5-LOX, STAT3, C-reactive protein, prostaglandin E(2), prostate-specific antigen, adhesion molecules, phosphorylase kinase, transforming growth factor-β, triglyceride, ET-1, creatinine, HO-1, AST, and ALT in human participants. In clinical trials, curcumin has been used either alone or in combination with other agents. Various formulations of curcumin, including nanoparticles, liposomal encapsulation, emulsions, capsules, tablets, and powder, have been examined. In this review, we discuss in detail the various human diseases in which the effect of curcumin has been investigated.

45 Years of experience in the surgical treatment of pancreatic insulinoma

Background: Chronic pancreatitis (CP) has a heterogeneous aetiology. In the Western world, the predominant cause is alcoholism, while in India tropical chronic pancreatitis (TCP) is thought to be common. TCP has been defined as a form of idiopathic chronic pancreatitis (ICP), with unique epidemiological and clinical features. However, the clinical profile of ICP in India is changing. The aim of our study was to investigate the phenotype of ICP in India compared to the phenotype of ICP in the Western World. Methods: We included CP patients from 3 registries from India, Germany and the Netherlands. We compared data regarding age, age of onset, cause of CP and the presence of CP complications between the 3 cohorts. Results: We included 1919 CP patients; (India n1⁄41033; Germany n1⁄4528; Netherlands n1⁄4358). The majority (68%) of patients were male. Relative to the Western cohorts Indian CP patients were younger, had a younger age of onset and smoked less frequently. The majority of Indian subjects were diagnosed with ICP (65%) (Netherlands 40%, Germany 23%). Endocrine insufficiency and pancreatic calcifications were more frequently seen in Indian ICP patients. Pain was present in the large majority (> 85%) of all CP patients. Conclusions: The phenotype of Indian ICP patients used to be dominated by TCP, but our analysis demonstrates that most of Indian patients now have a form of CP that can be labeled as ICP. Indian patients have younger onset of CP with more endocrine insufficiency and pancreatic calcifications, and there is a shift towards the phenotype of ICP in the Western world.

Spectrum of pancreatitis in children and adolescents

Very little is known about the early stages of tropical chronic pancreatitis except that many patients give history of childhood abdominal pain. To examine whether tropical chronic pancreatitis may initially present clinically as recurrent acute pancreatitis. Children and adolescents with acute, recurrent acute and chronic pancreatitis were prospectively followed up from 2003 to 2010. Seventy-three consecutive patients were analyzed for progression from acute to recurrent and recurrent acute to chronic pancreatitis. Of the 36 acute, 28 were recurrent acute pancreatitis patients. Similarly of the 37 chronic pancreatitis patients 27 were de novo and 10 had progressed to chronicity from recurrent acute. The mean age of patients was not significantly different between the different groups. Majority of patients in all groups were of idiopathic etiology. The progression of recurrent acute to chronic took 1 to 5 years. Minimum number of episodes of acute pancreatitis before progression to chronicity was 2 and minimum period was 1 year. In 11 of the 27 de novo chronic pancreatitis patients, the age of first pain and diagnosis were identical, in the remaining 16, there were varying intervals between the first pain and diagnosis (1-12 years). There was a continuum of acute pancreatitis to recurrent acute pancreatitis, some of the recurrent acute pancreatitis patients further progressed to chronic. In some instances tropical chronic pancreatitis may initially present clinically as recurrent acute pancreatitis.

Chronic calcific pancreatitis of tropics

Chronic calcific pancreatitis of tropics

Su1246 Evidence of Chronic Pancreatitis in Patients With Unexplained Recurrent Acute Pancreatitis: Implications to Understanding the Early Stages of Tropical Chronic Pancreatitis

Su1246 Evidence of Chronic Pancreatitis in Patients With Unexplained Recurrent Acute Pancreatitis: Implications to Understanding the Early Stages of Tropical Chronic Pancreatitis

Chronic Pancreatitis in India and Asia

Chronic pancreatitis (CP) is widely prevalent in Asian countries much more so in India and Japan. The phenotype of CP is somewhat similar to that reported from western countries. The prevalent types of CP are mainly idiopathic and alcohol related. Current evidence suggests that the term "tropical pancreatitis" used for idiopathic CP from India is a misnomer. Gallstones' association with CP reported from China remains controversial. There has been ample evidence that mutations in the SPNIK1 and CFTR genes are strongly associated with idiopathic CP in patients from different ethnic backgrounds. Oxidative stress is important in the pathophysiology and antioxidants have been shown to result in significant pain relief with CP. Home-made balanced diet is effective for treating malnutrition in patients with CP. Endoscopic therapy combined with ESWL may provide significant relief in patients with pancreatic ductal calculi/stricture. Surgery is quite effective in CP and may be better than endotherapy.

Tropical Pancreatitis presented as early onset Diabetes Mellitus

Tropical pancreatitis (TP) is a special form of chronic pancreatitis seen in tropical countries and has been less commonly reported from Nepal. We present a young non alcoholic female with early onset Diabetes Mellitus whose further investigations revealed pancreatic duct stones and was diagnosed as a case of tropical pancreatitis and underwent modified puestow’s procedure.

Chronic pancreatitis.

We review important new clinical observations in chronic pancreatitis made in the past year. Tropical pancreatitis associates with SPINK1 and/or CFTR gene mutations in approximately 50% of patients, similar to the frequency in idiopathic chronic pancreatitis. Corticosteroids increase secretin-stimulated pancreatic bicarbonate concentrations in autoimmune pancreatitis (AIP) by restoring mislocalized CFTR protein to the apical ductal membrane. Most patients with asymptomatic hyperenzymemia have pancreatic lesions of unclear significance or no pancreatic lesions. Common pitfalls in the use of diagnostic tests for exocrine pancreatic insufficiency (EPI) confound interpretation of findings in irritable bowel syndrome and severe renal insufficiency. Further study is needed to improve the accuracy of endoscopic ultrasonography (EUS) to diagnose chronic pancreatitis. Celiac plexus block provides short-term pain relief in a subset of patients. Results of this year's investigations further elucidated the genetic associations of tropical pancreatitis, a reversible mislocalization of ductal CFTR in AIP, the association of asymptomatic pancreatic hyperenzymemia with pancreatic disorders, limitations of diagnostic tests for EPI, diagnosis of chronic pancreatitis by EUS and endoscopic pancreatic function testing and treatment of pain.

Anthropometric measurements of nutritional status in chronic pancreatitis in India: comparison of tropical and alcoholic pancreatitis

Undernutrition is considered to be a cause of tropical pancreatitis (TP) since this disease is commonly seen in the underprivileged populations of the world. This study was done to compare the nutritional status in patients with TP and alcoholic chronic pancreatitis (ACP) using anthropometric measurements. Anthropometric measurements were done in patients with TP and ACP aged >18 years and matched healthy controls. Presence of pain, recent dietary restriction, diabetes mellitus (DM), calcification, serum prealbumin (PAB), and quantitative fecal elastase (FE) was assessed. Premorbid body mass index (BMI) was determined from weight before the onset of illness as reported by the patients. Of 54 patients (47 male), 39 (72.2%) had TP and the rest had ACP. Patients with TP were younger than those with ACP; the frequency of pain, DM, calcification, and exocrine insufficiency was similar in the two groups. Compared to control subjects, patients had lower BMI, triceps skin fold thickness (TSFT) and mid-arm circumference (MAC) (p < 0.01), but waist-to-hip ratio (W/H) was similar. Undernutrition was equally common in TP and ACP (15 [38.5%] vs. 6 [40%]). The BMI, TSFT, MAC, and W/H were similar in TP and ACP. The premorbid BMI was higher than that at presentation (20.2 [3.8] kg/m² vs. 19.1 [3.3] kg/m², p < 0.01). There was no association between BMI and features contributing to undernutrition (DM, pain, recent dietary restriction, FE level, and calcification) on univariate analysis. Energy undernutrition occurs equally commonly in TP and ACP and this appears to develop after the onset of illness.

Assessment of oxidative status in chronic pancreatitis and its relation with zinc status

Oxidative stress-induced free radicals have been implicated in the pathology of chronic pancreatitis (CP). We aimed to estimate oxidative stress and antioxidant status in tropical chronic pancreatitis (TCP) and alcoholic chronic pancreatitis (ACP) and correlate with zinc status. One hundred and seventy-five CP patients (91 TCP, 84 ACP) and 113 healthy subjects were prospectively studied. Disease characteristics and imaging features were recorded. Erythrocyte reduced glutathione, glutathione peroxidase (GPx), superoxide dismutase (SOD), plasma vitamin C, and erythrocyte thiobarbituric acid reactive substance (TBARS) were estimated by spectrophotometry. Erythrocyte zinc was estimated by flame atomic absorption spectrophotometry. Enhanced lipid peroxidation with concomitant decrease in antioxidant status was observed in both TCP and ACP patients (p < 0.05). The findings were comparable in both diabetic and non-diabetic CP patients. Significantly, lower plasma vitamin C and elevated levels of erythrocyte TBARS was noted in TCP as compared to ACP patients. The erythrocyte zinc significantly correlated with SOD activity (r = 0.450, p < 0.001). Our study corroborates the role of oxidative stress in CP and suggests some differences in oxidative status in TCP and ACP patients. Zinc deficiency appears to affect oxidative status in CP patients.

Asian chronic pancreatitis: The common and the unique

Chronic pancreatitis (CP) is a disabling condition worldwide that presents as pain, maldigestion, and diabetes. It is usually perceived as alcohol related, or classified as idiopathic otherwise. However, this is true only for Western countries. Asian CP comprises not only alcohol-related CP but also tropical pancreatitis (TP). Tropical pancreatitis is a unique entity commonly found in South Asia. It shares similar presentations with other CPs for pain and maldigestion. However, its diabetes is more ketosis resistant. Non-surgical approach like endoscopic therapy plus extracoporeal shock wave lithotripsy provides better outcome for TP than other CPs, because of its less strictured pancreatic duct that is more amenable to endoscopic stone clearance. Diagnosis of CP in Asia mainly relies on image studies such as ultrasonography ± computed tomography (CT) scan, and non-invasive tests on fecal chymotrypsin, serum trypsin, and serum pancreatic isoamylase. Endoscopic ultrasonography and intestinal tubing tests are used mainly in some research centers. Autoimmune pancreatitis (AIP) is another CP originated from Asia in large series and subsequently being recognized in the West. AIP patients seldom present with maldigestion until the disease progresses to a very late stage and this occurs in less than one third of patients. In contrast, AIP is usually presented as pseudotumor of the pancreatic head, causing obstructive jaundice. Immunoglobulin G4 level is typically elevated in AIP and can be used as a marker for responsiveness. Without a need of surgery, steroids are the standard treatment. Those who relapse and are resistant to steroids should be placed on long-term immunosuppressive agents.

Extracorporeal shock wave lithotripsy (ESWL) for large pancreatic stones: are these shocks worth while?

Chronic pancreatitis is characterized by irreversible damage to the pancreas that leads to pain and/or exocrine and endocrine insufficiency [1–3]. Abdominal pain is the most common and distressing symptom and is the most common indication for endoscopic or surgical intervention [1, 4, 5]. One of the mechanisms responsible for pain in chronic pancreatitis is obstruction to the pancreatic duct by strictures or calculi and relief of this obstruction by surgical or endoscopic drainage relieves pain in a majority of patients [6–8]. Endoscopic drainage procedures for relief of pain include pancreatic sphincterotomy, dilation of pancreatic strictures, removal of pancreatic stones and the placement of pancreatic stents to overcome the obstruction [8]. On plain X-ray of the abdomen, pancreatic calcification can be seen in up to 30% of patients with chronic pancreatitis [4]. The advent of newer imaging modalities like computed tomography (CT) has improved the ability to detect pancreatic calcification [9]. Up to 70% of patients with alcohol-related chronic pancreatitis can have pancreatic calcification after 10 years of disease [10]. The calcification can be either due to parenchymal or ductal calculi. Pancreatic duct calculi have been reported in 50% to 90% of patients with chronic pancreatitis and there is higher incidence of ductal calculi in patients with tropical pancreatitis [2, 11]. The ductal calculi cause obstruction leading to an increase in intraductal as well as parenchymal pressure and ischemia, thus causing pain [12]. The factors correlating with pain are the stone size and the diameter of the pancreatic duct. The goal of endoscopic treatment for chronic painful pancreatitis with ductal calculi is complete clearance of calculi from the duct, thus relieving the obstruction and pain [13–16]. Endoscopic extraction of pancreatic duct calculi is usually more difficult than extraction of bile duct stones because pancreatic stones are generally spiculated, hard and multiple, and on many occasions are impacted behind strictures. Endoscopic sphincterotomy followed by balloon or Dormia-assisted stone extraction is usually successful when the stones are of small size and are located in the head or body of the pancreas, and there is no ductal stricture [17]. The presence of ductal stricture or large calculi creates difficulty in endoscopic clearance and requires either decrease in the size of calculi by breaking them into small pieces or enlarging the ampullary orifice so as to successfully deliver intact large stones. Endoscopic balloon sphincteroplasty of the papilla has been used to enlarge the papillary orifice and to successfully extract intact ductal calculi >1 cm, especially radiolucent stones [18]. However, this technique is technically demanding, and has potentially serious complications including bleeding, retroduodenal perforation and pancreatitis [18]. An alternative method is to break the large stones into small pieces so that they can be easily extracted through the papilla. This can be done by using mechanical lithotripsy, intraductal electrohydraulic lithotripsy (EHL) and extracorporeal shock wave lithotripsy (ESWL). Mechanical lithotripsy using a throughthe-scope mechanical lithotripter is technically difficult and is not successful in all cases with large pancreatic calculi, especially when there is difficulty in grasping large stones [19]. Intraductal EHL is cumbersome and requires specialized D. K. Bhasin : S. S. Rana Department of Gastroenterology, Post Graduate Institute of Medical Education and Research (PGIMER), Sector 12, Chandigarh 160 012, India

Nonalcoholic, Nonbiliary Pancreatitis: Cross-Sectional Imaging Spectrum

The purpose of this review is to describe the epidemiologic, etiopathogenetic, clinical, and imaging characteristics of various nonalcoholic, nonbiliary pancreatitis syndromes. The spectrum of nonalcoholic, nonbiliary pancreatitis includes autoimmune pancreatitis, groove pancreatitis, hereditary pancreatitis, tropical pancreatitis, tuberculous pancreatitis, and metabolic pancreatitis. Advances in genetics and molecular pathology have shed new light on the etiopathogenesis and course of these syndromes. Accurate diagnosis aided by imaging findings allows optimal management.

Tropical Chronic Pancreatitis (TCP): A Cytogenetic Study in Patients Residing in and around Coimbatore City, Tamil Nadu

KEYWORDS Tropical. Pancreatitis. Karyotype. Chromosomal Aberrations ABSTACT Tropical chronic pancreatitis (TCP) is a juvenile form of chronic calcific non- alcoholic pancreatitis found almost exclusively in tropical countries. This study was performed to find out the chromosomal aberrations in chronic pancreatitic patients of Coimbatore city, south India. 41 tropical chronic pancreatitis patients were examined for chromosome abnormalities using standard procedure of analysis from peripheral blood leukocyte culture using trypsin G – banding. The patients and the control set of individuals displayed different types of chromosomal abnormalities such as deletions, translocations, inversions and mosaicism. Familial transmission of chromosomal aberration was detected in 6 TCP patients and abnormalities in chromosome 7 were found in seven patients including the familial cases. The etiology of the disease needs to be studied, taking geographical location of Coimbatore city also into consideration.

Pancreatic cancer in chronic pancreatitis; aetiology, incidence, and early detection

Acute pancreatitis, chronic pancreatitis and pancreatic cancer are responsible for most of the burden of exocrine pancreatic disease. Glandular damage from recurrent bouts of acute pancreatitis can lead to irreversible changes characteristic of chronic pancreatitis. In recent decades accumulating evidence has defined longstanding pre-existing chronic pancreatitis as a strong risk factor for pancreatic cancer. The lag period between diagnosis of chronic pancreatitis and pancreatic cancer is usually one or two decades: pancreatitis appearing a year or two before the diagnosis of pancreatic cancer is often the result of tumour-related ductal obstruction. The risk of developing pancreatic cancer appears to be highest in rare types of pancreatitis with an early onset, such as hereditary pancreatitis and tropical pancreatitis. Even though there is a strong link between chronic pancreatitis and pancreatic cancer, over a 20 year period only around five percent of patients with chronic pancreatitis will develop pancreatic cancer. Until the development of more sophisticated screening procedures, screening is not recommended for patients with chronic pancreatitis.

Genetic factors in chronic pancreatitis; implications for diagnosis, management and prognosis

Chronic pancreatitis (CP) is a clinical situation with persisting inflammation leading to destruction of the pancreas ensuing endocrine and exocrine failure. There are 4 subtypes: hereditary, idiopathic, alcoholic and tropical pancreatitis. Genetic factors can explain a significant proportion of CP cases. The PRSS1 gene, encoding cationic trypsinogen, was found to be correlated with hereditary CP. This signalled the extensive search for other candidate genes within the trypsin pathway. Genes like SPINK1 and CTRC are associated with CP and should be considered as important contributing factors rather than causative. The search for candidate genes not part of the trypsin pathway has been less successful and the only gene consistently associated with CP is the Cystic Fibrosis Transmembrane Regulator. In this review we will discuss the various CP subtypes in relation to the respective genetic variants. This review will also address the implications of genetic testing in daily clinical practise.

Tropical Chronic Pancreatitis (TCP): A Cytogenetic Study in Patients Residing in and around Coimbatore City, Tamil Nadu

KEYWORDS Tropical. Pancreatitis. Karyotype. Chromosomal Aberrations ABSTACT Tropical chronic pancreatitis (TCP) is a juvenile form of chronic calcific non- alcoholic pancreatitis found almost exclusively in tropical countries. This study was performed to find out the chromosomal aberrations in chronic pancreatitic patients of Coimbatore city, south India. 41 tropical chronic pancreatitis patients were examined for chromosome abnormalities using standard procedure of analysis from peripheral blood leukocyte culture using trypsin G – banding. The patients and the control set of individuals displayed different types of chromosomal abnormalities such as deletions, translocations, inversions and mosaicism. Familial transmission of chromosomal aberration was detected in 6 TCP patients and abnormalities in chromosome 7 were found in seven patients including the familial cases. The etiology of the disease needs to be studied, taking geographical location of Coimbatore city also into consideration.

Tropical or Idiopathic Chronic Pancreatitis: What Is in a Name?

Tropical or Idiopathic Chronic Pancreatitis: What Is in a Name?

Endoscopic treatment as first‐line therapy for pancreatic ascites and pleural effusion

Ascites and pleural effusion are well recognized complications of pancreatic diseases. Drug therapy of these is limited by high cost, prolonged hospitalization and failure rates; surgery is invasive and is associated with considerable morbidity and mortality. To analyze the data on patients with pancreatic ascites and/or pleural effusion treated endoscopically over a ten-year period. Patients with symptomatic ascites/pleural effusion for at least 3 weeks with a fluid amylase level of > 1000 S units/dl and underlying pancreatic disease were included. The interventions were a 5 mm sized pancreatic sphincterotomy and placement of a 7 Fr pancreatic stent. Somatostatin/octreotide and parenteral nutrition were not used after endoscopic therapy. Of the 28 patients included (22 men), 17 (60.7%) had chronic pancreatitis. The causes were tropical pancreatitis (13, 46.4%), alcohol abuse (10, 35.7%), idiopathic acute pancreatitis (4, 14.3%) and resective surgery for gastric cancer (1, 3.6%). Ascites alone was seen in 15, pleural effusion alone in 6 and both in 7 patients. Ten patients (35.7%) had 14 pseudocysts. Endotherapy was successful in 27 (96.4%). Twenty-six (92.8%) patients had complete resolution of ascites/effusion over a median 5 weeks. The stents were removed 3-6 weeks later without any recurrence over the next 6-36 (median = 17) months. Complications (7, 25%) included severe pain in 2 (7.1%) and fever in 5 (17.8%) of which 3 (10.7%) had infection of residual fluid collections. No patient died. Endoscopic therapy offers an excellent therapeutic alternative in patients with pancreatic ascites and pleural effusion.