Urologic Aspects of AIDS and HIV Infection

       HIV : retrovirus, replicates and kills T-helper cells
       HIV-1
       HIV-2 : less transmitted, less virulent
       AIDS : development of opportunistic infections, neoplasms, other life-threatening conditions resulting from immunosuppression caused by HIV infection
       HIV transmission
       Unprotected intercourse (semen, vaginal discharge) : men à female, circumcision decrease risk
       Contact with blood
       Mother to child transmission
       Screening : anti HIV-1 and anti HIV-2 antibodies
       Infection phase :
       Primary infection
       Chronic asymptomatic : slow progress à > 15 yrs (5-15 % pts)
       Overt AIDS : rapid progress à < 5 yrs (10-20 % pts)
       Tissue sanctuary :
       Lymphoid system
       Urogenital organ
       Nervous system
TESTS TO DIAGNOSE AND MONITOR HIV INFECTION
       History : first isolated HIV 1983, first diagnostic test marketed 1985
       Detection :
       2 days in lymphoid system
       12 days in RNA HIV
       21 days in antibody
        Predictor of disease progress : RNA HIV viral load ↑ à treatment failure
UROLOGIC MANIFESTATIONS OF HIV INFECTION
       Nonmalignant Conditions
       Primary HIV Infection
       Sexually Transmitted Infections : Herpes simplex virus (HSV), Human Papillomavirus, Syphilis, Chancroid, Urethritis, Molluscum Contagiosum.
        HIV-Related Genitourinary Tract Infections : Renal Infections, Prostatitis, Epididymitis and Orchitis à testicular atrophy, Impetigo, Abscesses, Cellulitis, Lymphadenitis, and Necrotizing Fasciitis. Therapy : antibiotics + HAART
       Voiding Dysfunction ß infection, obstruction, neurologic disorders
       Urinary retention (54%)
       Detrusor hyperreflexia (27%)
       Outflow obstruction (18%)
       Urolithiasis :
       Indinavir : protease inhibitor à minimal finding in NCCT, developing at pH 7
                                   conservative : hydration, analgesics, temporary cessation of indinavir
  
       HIV-Associated Nephropathy (10-30% on patients with HIV)
       More common in black patients
       Oedem, hypertension, anemia
       Renal insufficiency
       Massive proteinuria in the nephrotic range (>3.5 g/day)
       Ultrasound : echogenic kidney with preserved size
       Neoplasms
       Kaposi’s Sarcoma : co-infection HIV + Human Herpes Virus 8
       Non-Hodgkin Lymphoma
       Squamous Genital Cancers
       Testicular Cancer (seminoma)
OCCUPATIONAL RISKS FOR HIV INFECTION IN UROLOGY
       Exposures on seroconverted worker :
       84% percutaneous (puncture/cut injury) à needle stick injury
       9% mucocutaneous (mucous membrane and/or skin)
       4% both percutaneous and mucocutaneous
       4% unknown route
       Risk factors for occupational infection
       deep + superficial exposure (P < .0001)
       blood visible on the device causing the exposure (P = .0014)
       placement of the device in a source-patient’s vein or artery (P = .0028)
       death of the source-patient within 60 days of the exposure (P = .0011),
       and no post exposure chemoprophylaxis with zidovudine
Interventions to Decrease Occupational Risk
       Wounds should be washed with soap and water and then irrigated with sterile saline, a disinfectant, or other suitable solution
       Postexposure chemoprophylaxis 
       Severe : 3 drug regimens (zidovudine, lamivudine, other drug)
       Lesser exposure : 2 drug regimens (zidovudine + lamivudine, or zidovudine + other drug)
        Vaccines to Prevent HIV Infection : in progress

Gastric Volvulus

The clinical presentation of patients with gastric volvulus depends upon the speed of the onset. In 1904 Borchardt described the classic triad of acute or localized distention of the epigastrium associated with pain, inability to pass a nasogastric tube, and nonproductive attempts at vomiting; a recent literature review described 581 cases in infants and children (Coran, 2012).
The presenting symptoms can be intermittent or complete gastric obstruction, ischemia, pain, and/or bleeding. The most common signs and symptoms of gastric volvulus in children include acute abdominal pain, intractable retching, and the inability to pass a nasogastric tube into the stomach lumen (George W., 2014).
The principal symptoms include cyanosis (11%), acute respiratory distress (10%), abdominal pain (34%), non-bilious emesis (75%), and epigastric distention (47%). In contrast to the acute presentation, 75% of chronic volvulus was of primary etiology. The vast majority of chronic cases are organoaxial (85%). Non-bilious emesis remains the most common symptom. Feeding problems or growth failure (30%) was seen more prominently in chronic cases (Coran, 2012). In this case, the symptoms include non-bilious emesis, coughing, chocking and then admitted to the hospital after suffered from the respiratory problem/ pneumonia.
Gastric volvulus is classified according to the plane of rotation. In organoaxial volvulus, the stomach rotates on its long axis; the greater curvature passes anteriorly but may be displaced posteriorly. The less common mesenteroaxial volvulus, rotation is on an axis from greater to lesser curvature (the pylorus or cardia commonly rotates anteriorly). The opposite rotation may also occur. The torsion may be total, involving the entire stomach, or partial, limited to the pyloric end. The rotating section usually passes anteriorly (Coran, 2012) .
Gastric volvulus is a rare condition that is seldom considered in the first as in this case, the patient initially treated with pneumonia for almost 1 month of hospitalization. Further investigation such as esophagus-stomach-duodenum imaging with barium and endoscopy was done and gastric volvulus was identified. The imaging with contrast that held to the patient showed partial mesenteroaxial volvulus, fundus appeared to be rotated toward inferior anteromedial and some fundus in caudal. The part of gatser that rotated was partial, and limited to the fundus of gaster. Therefore, the symptoms are not so typical.
The patient had been coughing and chocking followed by vomiting while breast feeding since the age of 3 months. The reflux of gastric contains could irritate esophagus and surrounding structure including respiratory tract, and in the long term emerged symptoms of pneumonia.
Treatment consists of patient resuscitation, nasogastric decompression, and surgical correction. The volvulus is reduced. Any diaphragmatic defects are repaired in secondary gastric volvulus. A gastropexy is then performed. This has traditionally been accomplished with a gastrostomy tube or button. However, there have been several recent reports of successful laparoscopic gastropexy in which the anterior stomach, along the greater curvature, is sutured to the abdominal wall (George W., 2014).
Reference
Coran, Arnol, Adzick, N. Scott, Krummel, Thomas, Laberge, Jean-Martin, Shamberger, Robert, Caldamone, Anthony. 2012. Peptic Healing and Other Conditions of the Stomach in pediatric Surgery Volume3, Seventh edition. Elsevier: Philadelphia.
Holcom, George W., Murphy, J. Patrick, Ostile, Daniel J. 2014. Lesions of the stomach in Ashcraft’s Pediatric Surgery. Elsevier: Philadelphia

Rashif, F., Thangarajah, T., Mulvey, D., Larvin, M., Iftikhar, S.Y. A review article on gastric volvulus: A challenge to diagnosis and management. International Journal of Surgery 2009;8:18-24.

Diagnosis and Management of Pancreatolithiasis

Pancreatic duct stone is a rare disease. Defined as stone or calcification in the pancreatic duct, the pathogenesis of the disease remains unknown, but many theories are available for its formation. 1, 2  Chronic pancreatitis, pancreatic duct fibrosis, malnutrition, alcohol abuse, spontaneous pancreatic duct stone, dysthyroid, etc are associated with the formation. These conditions cause pancreatic exocrine dysfunction and intraductal proteinaceous deposits which subsequently lead to calcification, thus inducing chronic pancreatitis and pancreatic duct stone formation. Meanwhile, pancreatic duct stones in patients with chronic pancreatitis usually result from chronic inflammation or altered metabolism. The stones perpetuate the cycle of ductal obstruction and contribute to pain, worsening of pancreatic inflammation, ductal disruption, and deterioration of the exocrine and endocrine function of the gland. Pancreatic duct stone has been considered a marker of chronic pancreatitis. 3
 Pancreatic duct stone is difficult to diagnose in its early stage for the absence of specific clinical manifestations. Clinical manifestaion of pancreatolithiasis differ because it is complicated by chronic pancreatitis, bile duct stone or pancreatic cancer. The main manifestations of this disease include upper abdominal pain, fat diarrhea, diabetes mellitus, obstructive jaundice and abdominal mass. With the advancement of radiological techniques in diagnosis and in-depth study the incidence of the disease has appeared to be rising in recent years. Currently, laboratory test for pancreatic duct stone has no specific indices. To confirm the diagnosis, radiological examinations, ultrasonography, computed tomography (CT), endoscopic retrograde cholangiopancreatography (ERCP) and magnetic resonance cholangiopancreatography (MRCP) are used. 3
The principle of operation is to remove pathogeny, take out stones, unchain the obstruction and relax drainage. Operation is a major treatment of pancreatic duct stone. 4 Currently, surgical intervention is recommended for all patients with pancreatic stones, while individual treatment is emphasized and microinvasive surgery may be a developing option for treating pancreatic stone. 3
Surgical therapy results in complete or partial relief of the symptoms of the disease. Different surgical procedures can be chosen according to the location of the stones in the pancreatic duct. 5 When the stones are mainly located in the head of pancreas, endoscopic drainage and removal of the stones is usually the first choice of treatment. If it fails, surgical procedure should be applied. If the stones are mainly located in the body of the pancreas, they can be treated with Pusetow-Gillesby procedure (pancreaticojejunostomy), Lateral pancreaticojejunostomy is suitable for most patients with this disease. 6 Because the pathogenesis of pancreatic stone is unknown, improvement of symptoms is a major goal. However, the management of pancreatic duct stones continue to evolve, and it is dependent on the available facilities. 7, 8, 9
Peustow procedure (pankreaticojejunostomi longitudinal) were performed in both cases this is the action of pancreatic drainage by means of pancreatic opened later retrieved the stones there and done between pancreatic jejunal anastomosis side to side with retrocolic Roux en Y, so that the product can flow to the pancreas jejunum. Decompression of pressure in the pancreatic duct produces cleaning all stone and give good results at postoperative. With this procedure, the morbidity is also not increased. After surgery, upper abdominal pain on both the patient becomes lost. In the post-operative laboratory tests obtained alpha amylase and lipase was decrease. This procedure is a safe procedure with morbidity and mortality of less than 2%. Peustow procedures can relieve pain in the long time more than 70% of patients. 10, 11
Pancreatic duct stone is a rare disease. With the advancement of radiological techniques in diagnosis and in-depth study the incidence of the disease has appeared to be rising in recent years, especially in the Western world. Defined as stone or calcification in the pancreatic duct, the pathogenesis of the disease remains unknown, but many theories are available for its formation.1,2Chronic pancreatitis, pancreatic duct fibrosis, malnutrition, alcohol abuse, spontaneous pancreatic duct stone, dysthyroid, etc are associated with the formation. These conditions cause pancreatic exocrine dysfunction and intraductal proteinaceous deposits which subsequently lead to calcification, thus inducing chronic pancreatitis and pancreatic duct stone formation. Meanwhile, pancreatic duct stones in patients with chronic pancreatitis usually result from chronic inflammation or altered metabolism. The stones perpetuate the cycle of ductal obstruction and contribute to pain, worsening of pancreatic inflammation, ductal disruption, and deterioration of the exocrine and endocrine function of the gland. Pancreatic duct stone has been considered a marker of chronic pancreatitis. 3

Formation of pancreatic stone
Bibulosity is the main cause of pancreatic stone, which was followed by bile duct diseases, recurrent pancreatitis, inherited factors, hyperfunction of the parathyroid, lack of protein 12 , and annular pancreas. 13 In 1979 De Caro separated a kind of protein from pancreatic stone or P-glycoprotein possesing 133 kinds of amino acid peptide with a molecular weight of 14.000. it is synthesized in the endoplasmic reticulum of gland and is secreted in to pancreatic fluid, thus is named as pancreatic stone protein (PSP). 14 It is bbelieved that the formation of pancreatic stone is due to the decrease of PSP in pancreatic fluid. 15 Alkohol, chronic pancreatitis, and cacotrophia decrease the secretion of PSP, which cause the crystalication and depotition of calcium carbonate, and further the formation of stone. 16 Another important factor is fortoferrin. High concentration fortoferrin, dropped epithelium, mucous membrane and pancreatic enzyme can form the ner-like structure of pancreatic stone. It is presumed that high secretion of fortoferrin may be related to the occurrence of pancreatic stone. Clinically inflammatory stricture of the pancreatic duct causes the stagnation of pancreatic fluid and the formation of pancreatic stone. In patiens with hyperfunction of the parathyroid, hypercalciumenia causes the rise of calcium in pancreatic fluid, which acceralates the formation of pacreatic stone. 17

Relation of pancreatic stone to chronic pancreatitis
Pancreatolithiasis is not a kind of independent disease. It co-exsist with chronic pancreatitis. Pancreatic stone formation is characterized by chronic pancreatitis. Chronic pancreatitis is characterized by irreversible damage to the pancreas that leads to pain and/or exocrine and endocrine insufficiency. 18  Abdominal pain is the most common and distressing symptom and is the most common indication for endoscopic or surgical intervention. 19,20  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. 21,22,23 The obstruction of the pancreatic tube not only accelerated the development of chronic pancreatitis but also speeds up the formation of pancreatic stone, which is defined as one of the diagnostic guidelines for this disease. Recent studies have shown normal pancreatic functions and infrequent abdominal pain in some patient. Hence the occurence of pancreatic stone is not always the late manifestation ond the clinical symptoms of pancreatolithiasis is mainly due to the second pathologic change. Clinical manifestaion of pancreatolithiasis differ because it is complicated by chronic pancreatitis, bile duct stone or pancreatic cancer. The main manifestations of this disease include upper abdominal pain, fat diarrhea, diabetes mellitus, obstructive jaundice and abdominal mass.

Diagnostic procedure for pancreatic duct stone
Pancreatic duct stone is difficult to diagnose in its early stage for the absence of specific clinical manifestations. Currently, laboratory test for pancreatic duct stone has no specific indices. To confirm the diagnosis, radiological examinations, ultrasonography, computed tomography (CT), endoscopic retrograde cholangiopancreatography (ERCP) and magnetic resonance cholangiopancreatography (MRCP) are used.  
On plain X-ray of the abdomen, pancreatic calcification can be seen in up to 30% of patients with chronic pancreatitis. 19 The advent of newer imaging modalities like computed tomography (CT) has improved the ability to detect pancreatic calcification. 24  Up to 70% of patients with alcohol-related chronic pancreatitis can have pancreatic calcification after 10 years of disease. 25 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. 26
The ductal calculi cause obstruction leading to an increase in intraductal as well as parenchymal pressure and ischemia, thus causing pain. 27 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. 28  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. 23  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. 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. However, this technique is technically demanding, and has potentially serious complications including bleeding, retroduodenal perforation and pancreatitis. 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). 29
ESWL, which works by concentrating focused short waves on stones and causing their disruption, was first used in the field of gastroenterology by Sauerbruch et al. in Germany for fragmentation of gall bladder stones. 29 Thereafter the same authors used it for fragmentation of pancreatic duct stones. Subsequently a number of investigators have used it for fragmentation of pancreatic stones. Radiopaque stones can be easily targeted by ESWL under fluoroscopy. Radiolucent stones can be targeted using ultrasound-guided shock wave lithotripsy or by injection of contrast through the nasopancreatic catheter. The authors concluded that ESWL is a safe and effective preferred treatment for selected patients with painful calcified chronic pancreatitis and combining endoscopy with ESWL adds to the cost of patient care without improving the outcome of pancreatic pain. All these studies have demonstrated that ESWL is a safe technique with low complication rates. The minor complications of ESWL include skin or duodenal contusion, exacerbation of pancreatitis, mild abdominal discomfort and asymptomatic hyperamylasemia. Serious complications reported include hepatic sub-capsular hematoma, splenic rupture, splenic abscess, cholangitis, pancreatitisrelated sepsis, hemosuccus pancreaticus and fluid collections with complication rates ranging from 0% to 20% . 30

Treatment of pancreatic duct stone
The principle of operation is to remove pathogeny, take out stones, unchain the obstruction and relax drainage. Currently, surgical intervention is recommended for all patients with pancreatic stones, while individual treatment is emphasized and microinvasive surgery may be a developing option for treating pancreatic stone.
Operation is a major treatment of pancreatic duct stone 4  Surgical therapy results in complete or partial relief of the symptoms of the disease. Different surgical procedures can be chosen according to the location of the stones in the pancreatic duct. 13  When the stones are mainly located in the head of pancreas, endoscopic drainage and removal of the stones is usually the first choice of treatment. If it fails, surgical procedure should be applied. If the stones are mainly located in the body of the pancreas, they can be treated with Pusetow-Gillesby procedure (pancreaticojejunostomy), Lateral pancreaticojejunostomy is suitable for most patients with this disease. 6 Resection of the tail of the pancreas or combined resection with splenectomy is done if the stones are located in the tail of the pancreas. Sometimes the stones are found in the head or the tail of the main duct of the pancreas. The Pusetow-Gillesby procedure or dividing of the neck of the pancreas while removing stones from both ends of the pancreatic duct is the choice of management.
Successful removal of pancreatic duct stones can reduce pain and improve pancreatic function, and patients have regressed ductographic changes of chronic pancreatitis and decreased diameter of the pancreatic duct. By retrospective analysis of the management of patients with pancreatic duct stone, Li et al 31  have also suggested that surgical therapy is the most curative method for pancreatic duct stone in patients with severe symptoms or suspected pancreatic carcinoma. A prospective, randomized trial 32 ,  ompared endoscopic and surgical therapy for chronic pancreatitis showed that surgery is superior to endotherapy for long-term pain reduction in patients with painful obstructive chronic pancreatitis and concluded that endotherapy could be offered as a first line treatment with surgery being performed in case of failurre and/or recurrence. But therapeutic ERCP is safe in pediatric patients with pancreatitis. Significant clinical improvement is achieved in patients with billiary or pancreatic stone disease.

Treatment of pancreatic stones complicated by pancreatic cancer
The high incidence of pancreatic stone complicated with pancreatic cancer has been varied. 33, 34 Some scientists, 17 favored Whipple as the first choice for pancreatic stone complicated with pancreatic cancer. Foe patients with pancreatolithiasis associated with pancreatic cancer, surgical treatment should follow the principles of individualized therapy. Tumors in the head or neck can be removed by Whipple’s procedure, those in the body or tail be resected by removal of the pancreatic body and neck. If they invilved the spleen, the spleen can be resected. If tumors metastatic to the abdominal cavity, extended radical incision of the pancreatic is necessary.

Abdominal X-ray is the first choice in diagnosing pancreatic stone. CT scan of the abdomen is still the main choice in Indonesia, although in some centers, MRCP has taken over the role of CT scanning in the diagnosis of pancreatic stone. Surgery remains the primary treatment and techniques Peustow (longitudinal pancreaticojejunostomy) is still the procedure of choice for pancreatolithiasis, which is relatively safe, with morbidity and mortality are low.

References
1. Etemad B, Whitcomb DC. Chronic pancreatitis: diagnosis, classification, and new genetic developments. Gastroenterology. 2001;120:682–707.
2. Ammann RW, Muench R, Otto R, Buehler H, Freiburghaus AU, Siegenthaler W. Evolution and regression of pancreatic calcification in chronic pancreatitis. A prospective long-term study of 107 patients. Gastroenterology. 1988;95:1018–28.
3. Li L and Zhang SN. Management of pancreatic duct stone. Hepatobiliary Pancreat Dis Int, 2008; 7: 1: 9-10.
4. Chen J, Li NG, Ho Y. The diagnosis and treatment of pancreatic duct stone. Chin J Hepatobiliary Surg. 2011;7:564-565.
5. Kozarek RA, Patterson DJ, Ball TJ, Traverso LW. Endoscopic placement of pancreatic stents and drains in the management of pancreatitis. Ann Surg. 1989;209:261–6.
6. Laca CE, Paley D, Lechgerwood AM, Vlahos A. Surgical decompression of ductal obstruction in patients with chronic pancreatitis. Surgery 1999; 126: 790-795: discussion 795-797.
7. Bhasin DK, Singh G, Rana SS, et al. Clinical profile of idiopathic chronic pancreatitis in North India. Clin Gastroenterol Hepatol. 2009;7:594–9.
8. Sean JM. Pancreas, in Basic Science and Clinical Evidence. Springer. 2001. 529-533.
9. Haile TD. Chronic pancreatitis, in Gastrointestinal Surgery, Pathophysiology and Management. Springer.2004. 115-127.
10. Liu BN, Zhang TP, Zhao YP, Liao Q, Dai MH, Zhan HX. Pancreatic duct stones in patients with chronic pancreatitis : surgical outcomes. Hepatobiliary Pancreat Dis Int. 2010. Aug; 9(4): 423-7.
11. Oscar JH, Howard AR. Chronic pancreatitis , in Maingot’s Abdominal Operations. McGraw Hill. 2007. 983-997.
12. Dhing ZM. Pancreatolithiasis. Foreing medicine. (Fascicale of Digestive diseases). 1985;3;144-148
13. Yogi Y, Kossi S, Higashi S, Iwamura T. Annular pancreas associated with pancreatolithiasis; a case report, Hepatogastroenterology. 1999;46:527-530.
14. Bimmler D, Schisser M, Perren A. Coordinate regulation of PSP/ reg and PAP isoforms as a family of secretory stress proteins in an animal model of chronic pancreatitis. J Surg Res 2004;118: 122-135.
15. Rao KN, Thiel VD. Pancreatic stone protein: what is it and what does it do? Dig Dis Sci 1991; 36: 1505-1508.
16. Tanaka T, Miura Y, Ichiba Y, Itoh H, Dohi K. Experimental pancreatolithiasis: association with chronic alcoholic pancreatitis. Am J Gastroenterol1992; 87: 1061.
17. Shen K, Zhong SX, Zhang Sd. Pancreatic surgery. Publication of Demotic Health 2000; 377.
18. Narasimhulu KV, Gopal NO, Rao JL, Vijayalakshmi N, Natarajan S, Surendran R, et al. Structural studies of the biomineralized species of calcified pancreatic stones in patients suffering from chronic pancreatitis. Biophys Chem 2005;114:137-147.
19. Midha S, Khajuria R, Shastri S, Kabra M, Garg PK. Idiopathic chronic pancreatitis in India: phenotypic characterization and strong genetic susceptibility due to SPINK1 and CFTR gene mutations. Gut. 2010;59:800–7.
20. Witt H, Apte MV, Keim V, Wilson JS. Chronic pancreatitis: challenges and advances in pathogenesis, genetics, diagnosis, and therapy. Gastroenterology. 2007;132:1557–73.
21. Ebbehoj N, Borly L, Bulow J, Rasmussen SG, Madsen P. Evaluation of pancreatic tissue fluid pressure and pain in chronic pancreatitis. A longitudinal study. Scand J Gastroenterol. 1990;25:462–6.
22. Kozarek RA, Patterson DJ, Ball TJ, Traverso LW. Endoscopic placement of pancreatic stents and drains in the management of pancreatitis. Ann Surg. 1989;209:261–6.
23. Warshaw AL, Banks PA. Fernandes-Del Castillo C. AGA technical review: treatment of pain in chronic pancreatitis. Gastroenterology. 1998;115:765–76.
24. Luetmer PH, Stephens DH, Ward EM. Chronic pancreatitis: reassessment with current CT. Radiology. 1989;171:353–7.
25. Ammann RW,Muellhaupt B. The natural history of pain in alcoholic chronic pancreatitis. Gastroenterology. 1999;116:1132–40.
26. Chari ST, Mohan V, Jayanthi V, et al. Comparative study of the clinical profiles of alcoholic chronic pancreatitis and tropical chronic pancreatitis in Tamil Nadu, South India. Pancreas. 1992;7:52–8.
27. Di Sebastiano P, Friess H, Di Mola FF, Innocenti P, Buechler MW. Mechanisms of pain in chronic pancreatitis. Ann Ital Chir. 2000;71:11–6.
28. Adamek HE, Jakobs R, Buttmann A, Adamek MU, Schneider AR, Riemann JF. Long-term follow-up of patients with chronic pancreatitis and pancreatic stones treated with extracorporeal shock wave lithotripsy. Gut. 1999;45:402–5.
29. Sauerbruch T, Delius M, Paumgartner G, et al. Fragmentation of gallstones by extracorporeal shock waves. N Engl J Med. 1986;314:818–22.
30. Ong WC, Tandon M, Reddy V, Rao GV, Reddy DN. Multiple main pancreatic duct stones in tropical pancreatitis: Safe clearance with extracorporeal shockwave lithotripsy. J Gastroenterol Hepatol. 2006;21:1514–8.
31. Li JS, Zhang ZD, Tang Y, Jiang R. Retrospective analysis of 88 patients with pancreatic duct stone. Hepatobiliary Pancreat Dis Int 2007;6:208-212.
32. Dite P, Ruzicha M, Zboril V, Novotiry I. A prospective randomized trial comparing endoscopic and surgical therapy for chronic pancreatitis. Endoscopy 2003;35: 553-558.
33. Mariani A, Bernard JPCheylan PM. Differences of pancreatic stone morfology and content in patient with pancreatic lithiasis. Dig Dis Sci. 1991;36:1509-1516.

34. Yang W, Ding SQ, Wu Sl et al. Diagnosis and treartment of pancreatolithiasis complicated with pancreatic cancer. J Hepatobiliopancreatic Surg. 2002;8: 87-89.