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Pancreatitis Developing in the Context of Acute Hepatitis: a Literature Review

Pancreatitis Developing in the Context of Acute Hepatitis: a Literature Review

JOP. J (Online) 2015 Mar 20; 16(2):104-109.

REVIEW ARTICLE

Pancreatitis Developing in the Context of : A Literature Review

Hossein Khedmat1, Mohammad Ebrahim Ghamar-Chehreh1, Shahram Agah2, Aghdas Aghaei1

1Baqiyatallah Research Center for & , Baqiyatallah University of Medical Sciences, 2Colorectal Research Center, Iran University of Medical sciences, Tehran, Iran

ABSTRACT Despite strong evidence suggestive of associations between hepatic and pancreas , a potential relationship between acute this review article are: hepatitis failure represents the highest incident rate of hepatitis-related acute ; so a hepatitis and has not been a matter of review; which we focused on in the current paper. Some of the main findings of reported mortality; and a male preponderance in the incidence, with females developing in older ages and having shown the signs of both program might be indicative in these patients. Specific characteristics of HAV- related pancreatitis are that it is a benign condition with no- ed acute pancreatitis was most likely to represent and there was an apparent ethnic-priority with Indian descents, the only conditions simultaneously. The incidence of acute pancreatitis in HBV is the lowest, but the mortality was the highest. HEV-relat and in IFN-induced pancreatitis, cessation of the drug was most effective in treatment, with no catastrophic event reported. reported cases in the literature. Hepatitis-related pancreatitis in liver transplant recipients was most frequent in HBV infected patients;

INTRODUCTION discrepancy when comparing pancreatitis courses and prognosis within similar backgrounds. In this review article

on any evidence of relation between an acute hepatitis intoInflammatory lymphoid follicleshepatic disease[1-4], and incites it has infiltration been demonstrated of B and andwe aimdevelopment to systematically of pancreatitis. review theFor existingthis purpose, literature we thatT , one of the dendritic important cells andcauses inflammatory of pancreatitis is categorized our paper into subsections which discuss any potential relationships between pancreatitis developing in [5]. Acute pancreatitis (AP) is not a rare observation in fulminant hepatic failure (FHF) and has LITERATUREthe context of different REVIEW etiologies of acute hepatitis. been confirmed clinically as well as in autopsy analyses based on histological or serological studies [6]. On the other hand, viral , including , Coxsackie associations between acute hepatitis of any reason and An extensive search for articles was performed concerning hepatitisB virus, Epstein-Barrviruses typically virus have and a measlesstrong tendency virus, have to infect also been implicated as an etiological factor of AP [7]. Although , their have also been detected in forAP usinglevels multipleof evidence sources and includingincluded toPubMed, the review publishers’ article tissues of other organs including the pancreas [8]. It has accordingly.websites and The the Googlefollowing Scholar. keyword All articles or combinations were assessed of also been reported with (HAV), them have been used: acute hepatitis; hepatitis A virus; (HBV), hepatitis non-A non-B or (HCV) and ; non-A non-B hepatitis; ; (HEV) virus infections. hepatitis; transplant patients; drug-induced; ; liver diseases have been largely reported in the literature; hepatitis E virus; fulminant hepatic failure; autoimmune nonetheless,Although pancreatitis its implications episodes are reportedly erupting due different to different when ; HAV; HBV; HCV; HEV; IFN; RBV; pancreatitis; AP; moreetc. When evidence. the search In the was case done of in Google PubMed, Scholar, titles proposedcitations by PubMed as related articles were also screened to find happeningReceived December due to different2nd, 2014 etiologies.– Accepted JanuaryEven, there 26th, 2015is large Keywords Correspondence of the found papers were screened to find more related BaqiyatallahHepatitis Research E; Center Pancreatitis for Gastroenterology & reports. Also, references to the found reports were also Hossein Khedmat searched for more related evidences. Only found papers reported either in English or Persian languages were IranBaqiyatallah Hospital, MullaSadra Str PhoneTehran, PO. Box: 14155-3651 Finallyincluded. in Evidencethe discussion for any section, of the subtypes a conclusion of hepatitis for each and of Fax thetheir reviewed relations subtitles to AP were was reviewedprepared infrom separate their particular subtitles. E-mail [email protected] 21 88934125 features. +98 21 88934125

JOP. Journal of the Pancreas - http://www.serena.unina.it/index.php/jop - Vol. 16 No. 2 – Mar 2015. [ISSN 1590-8577] 104 JOP. J Pancreas (Online) 2015 Mar 20; 16(2):104-109.

FULMINANT HEPATIC FAILURE are also some case reports indicating such a relationship. Lopez Morante et al. [16] reported a 12-year-old boy with an 8 day delay between start of icterus and abdominal et al. The association of AP with fulminant hepatic failure (FHF) was first identified by Parbhoo in 1973 [9] et al the of liver disease. Since that time, some studies pain. He completely recovered from the condition. Garty in 44% of their FHF population with no association to after 2 weeks of initiation of symptoms . [17] report a 4-year-old boy who develops severe have investigated the association and clinical profile of features and associations of pancreatitis when developing of hepatitis A virus infection. Medical management also patients with AP and FHF. Recognition of the distinctive Rana et al. [18] report a 10-year-old boy who developed brought him full recovery after 5 days. Sudhir Kumar instruments for clinical management. So, here we review in combination with FHF will provide us more powerful abdominal pain after 6 days of the onset of hepatitis A infection symptoms. He well responded to conservative the existing data in the literature on this subject. The et al has been reported in different studies, which more or less management within 7 days of treatment initiation. Shrier frequency of pancreatitis developing in the context of FHF presented simultaneously with icterus and abdominal pain. Medical. [19] management report from improved a 4 year her oldillnesses Korean thoroughly. girl who Basaranoglu . [20] report from a 20-year-old woman is about one third of all cases. In the A retrospective study et al presenting with icterus and abdominal pain. She recovered of 30 FHF patients ( reason: 9 drug-induced; et al. [10] showed that 10 from both conditions after 5 days of conservative 8 HBV infection; 2 Budd-Chiari Synd.; 11 cryptogenic) . [21] report an 11-year-old with imaging methods by Kuo et al girl who developed of pancreatitis 1 cases developed pancreatitis (diagnosis confirmed by this rate in patients with decompensated chronic liver management.week after icterus. El-Sayed Conservative management brought her radiological studies), comprising to 33% of patients, while full recovery. Moleta et al. [22] report a 26-year-old woman a minimal association between the type of liver disease who simultaneously developed signs and symptoms of disease was 7 out of 30 or 23%. Although authors reported and development of acute pancreatitis, no p value or other icterus and epigastric pain. She improved after 6 days of et al. conservative . Despite the scarcity of large clinical data had been presented [10]. A similar study by Ede [11] on 35 FHF patients ( overdose (27 cases), studies, the existing data is suggestive of a benign course non-A non-B hepatitis (4), hepatitis B (3) and hepatitis A of AP in HAV patients. Future studies are recommended to (one)) also found evidence of AP determined by a distinct HEPATITISconfirm our conclusion. B VIRUS raise in P3 isoenzyme of in 14 (40%) of patients, indicative of AP. 57% of the patients died of the disease course of which included 14 (52%) of patients with hepatitis. There is also a case report of acute pancreatitis prospectiveAcute hepatitis study, B Jain virus et al (HBV). [14] followed infection 54 has patients also beenwith paracetamol overdose and 6 (75%) of patients with viral reported to be associated with development of AP. In their after FHF (diagnosed by clinical manifestations and raised confirmed diagnosis of acute hepatitis B virus infection ) induced by toxic mushroom (Lepiota for at least 4 weeks, and finally detected 1(2%) of them subincarnata J.E. Lange) toxicity which necessitated a liver patientsdeveloping with signs acute of hepatitis AP, detected B virus by imaginginfection procedures. compared transplantation, and finally patients survived [12]. Overall, The lower percentage of patients diagnosed with AP in AP due to FHF seems to have a high incidence; but due to number of reports in the literature; with the least number patients.the high associated with this condition [13], to infection by other hepatitis almost reflects the no judgment can be made on the fatality of AP in FHF HEPATITIS A VIRUS ofYuen reports et al. for such a relation for HBV infection. [23] report a series of five patients (4 males, 1 To our knowledge, except for one study, all the data from female) with acute exacerbation of chronic HBV infection existence of any association between acute hepatitis A that simultaneously developed AP, and compared their data to 85 cases of AP due to other etiologies and 406 thevirus literature (HAV) infection on the frequencyand AP comes of pancreatitis from case reports developing and patients with an acute HBV exacerbation episode. Finally one case series, and onlyet alone. [14] epidemiological prospectively data followed exists 16 in pancreatitis, while in the controls with pancreatitis, 4 (80%) of the patients in the case (HBV) group died of in HAV infection. Jain the mortality rate was 13(15%), and in those with only thepatients 4 weeks with after confirmed . diagnosis Mishra et ofal . HAV[15] report infection, 5 cases and finally 2 (12.5%) of them developed pancreatitis within andacute B HBVvaccination exacerbation, indicates only developing 9 (2.2%). acute A report necrotizing from a pancreatitis63-year-old following man who vaccination, underwent though combined the hepatitispatient got A of hepatitis A virus infection (1 female, 4 males; age range: 4-20 years) getting complicated with AP. Abdominal pain, icterusas the first & rise symptom in serum of transaminases pancreatitis developed presented after with 10–22 pain, performed,thoroughly recoveredthe rise in [24]. serum In amylase a 32-year-old levels maleindicative liver days from the onset of icterus, except in one case whose transplant recipient in whom serum profile had been hepatitis and pancreatitis with no mortality reported. There simultaneously. All their patients recovered from both of an AP episode was almost overlapping the HBV DNA JOP. Journal of the Pancreas - http://www.serena.unina.it/index.php/jop - Vol. 16 No.profile 2 – Mar [25]. 2015. HBV [ISSN markers 1590-8577] have also been found in chronic105 JOP. J Pancreas (Online) 2015 Mar 20; 16(2):104-109.

et al. whomalcoholic the pancreatitis patient represented [26]. An interesting by repetitive case episodes of chronic of conservativeicterus and epigastrictreatment. pain, Makharia with finalet al. diagnosis of HEV HBV infection has been reported by Chen [27] in frominfection a 45-year-old and AP; heIndian recovered man who his represent disease course with acute with therapy, and while the patient was on , he [33] also reportet al. wouldAP which have would remained have in been remission. controlled Nonetheless, with lamivudine shortly after cessation of lamivudine, pancreatitis episodes would peopleHEV infection of Indian and ethnicity AP with who benign completely course. recovered Bhagat from return that shows the effects of lamivudine therapy in their[34] reportillnesses a series with medical of 4 acute management. HEV-infection Thapa related et al. AP in

[35] rarecontrol entity of HBVwhich associated can be controlled pancreatitis. by lamivudine Studies reviewed therapy. report an Indian boy as young as 7-year-old with Nonetheless,in this section that suggest same that issue AP is developing thoroughly post different HBV is in a 6 phosphate dehydrogenase deficiency who present with comingacute HEV from infection prospective and AP,studies which that well investigates responded this to review article. issue,conservative and we therapy.recommend Again, future literature tries directing lacks enough at it, with data transplant context which will be discussed latter in this NON-A NON-B HEPATITIS/ HEPATITIS C VIRUS as the virus type. Due to the chronic nature of hepatitis C virus infection, some focus on genetic specifications of the patients as well to the best of our knowledge, there is limited data in the IN TRANSPLANT PATIENTS current literature supportive of any connection between infection has also been reported in transplant AP developing in the context of acute hepatitis virus this infection and development of AP. Nonetheless, there is a case report from a 33-year-old man who developed recipients. A retrospective study of 1832 liver transplant AP concomitant to non-A non-B hepatitis virus infection recipients at a center, 55 (3%) of them had a confirmed infected[28]. Although by hepatitis no specific C virus diagnostic infection. test In was another performed case diagnosis of AP during their follow up, in 17/114 (14.9%) report,at that time,Álvares-da-Silva patient’s data et al.suggests that he probably was of them, hepatic failure was due to HBV ,et al.15/340 [25] old woman presenting with signs and symptoms of icterus (4.4%) due to non-A non-B hepatitis, and 1/59 (1.7%) [29] report from a 70-year- due to [36]. Cavallari and pancreatitis. She was treated and was report from a 32-year-old Italian man who developed liver atand the pancreatitis; 10th month finalafter diagnosisdiagnosis. was To our acute knowledge HCV infection these failure due to fulminant HBV infection. After orthotopic , he experienced an acute reactivation of HBV infection which, according to the HBV-DNA load two reports are the only evidence existing in the literature withprofile, complaint it started fromon day severe 40 post-transplantation abdominal pain which and reach was supportive of any potential role for HCV infection in the to its peak level on day 70. On day 60, the patient came developmentHEPATITIS Eof VIRUS AP. intensive treatment [25]. In a series of 5 kidney transplant In the prospective follow up of 54 patients with documented finally confirmed as AP diagnosis. The patient died despite et al. [14] Sinha et al patients who represented AP after acute viral infections, diagnosis of acute hepatitis E virus infection, Jain . [37] report a 49-year-old Indian renal recipient reported 4(7.4%) caseset al. developed [15] report AP a in 14-year-old their infection boy who developed symptoms and signs of AP and acute HEV presentingcourse. In with a series jaundice of and six severe cases epigastric with hepatitis-virus- pain, after 2 organinfection. failure. He alsoLimited represented data from with the infectedliterature review in associated AP, Mishra thiswhich section then is get suggestive drained, of and a catastrophic finally died consequence of multiple recoveredweeks of . from both Final conditions. diagnosis Deniel was acute et al. HEV infection transplant patients; while future studies with large patient for AP occurring in the context of acute hepatitis in aand 26-year-old AP; he received man presentedconservative with treatment intense andepigastric thoroughly pain populations are needed for more detailed investigations. [30] report AUTOIMMUNE HEPATITIS/PANCREATITIS 3 weeks after developing signs and symptoms of acute hepatitis including jaundice which was confirmed as acute has also been reported to be related to the occurrence HEV infection. Computed tomography confirmed diagnosis Autoimmune involvement of either liver or pancreas Theof necrotizingpatient recurred pancreatitis after gradeconservative E in themanagement. Ranson– considered the same as acute disease, we felt that to have of the other. Although may not be Balthazar radiological classification with a et pseudocyst. al. a perfect view on the relation of these two conditions, it is also necessary to discuss autoimmune diseases as well. We afterAnother about similar 1 week case of presentingwas reported with by signs Somani of icterus. [31]; Final a found two case reports in the current literature indicating 35-year-old Indian man developed severe epigastric pain any relation between these two conditions. The second pancreatitis developing pseudocyst; he developed acute report is from a 44-year-old Brazilian white woman who renaldiagnosis failure was and acute hemodynamic HEV infection instability and acute that necrotizing led to his demise. Jaroszewicz et al. was a confirmed case of autoimmune hepatitis type I [32] also report a 28-year-old and developed AP which had been well managed with conservative treatment [38]. Pakistani-originJOP. Journal of the Pancreas French - http://www.serena.unina.it/index.php/jop male patient who represent with - Vol. 16 No. 2 – Mar 2015. [ISSN 1590-8577] 106 JOP. J Pancreas (Online) 2015 Mar 20; 16(2):104-109.

INDUCED BY ANTI-HEPATITIS DRUGS area of research would be the increased pancreatic

in any liver conditions [47], but a potential Drug-induced AP has also been reported in patients with a matter of concern in the current literature; and we did relationship between acute hepatitis and AP has not been therapyviral hepatitis. in a single In a center, review Chaudhari of data of et 1706 al. HCV-infected patients under interferon-α2b (IFN) and ribavirin (RBV) not find any comprehensive review article systematically [39] reported efforts. So, we prepared this paper that comprehensively who have developed pancreatitis during a mean time of searching the literature in our searches, despite extensive 7 (0.4%) cases (4 males, 3 females; mean age: 51±5 years) potential relationship between acute hepatitis of any type than the incidence rate in the general population [40, 41]. and systematically reviews the existing evidence on 13.4 months after treatment initiation, which is quite higher and AP development. wereIFN and hospitalized RBV were discontinuedand one refused in all hospitalpatients atadmission. the time of diagnosis of AP. Six out of the seven patients (85.7%) FHF was the first hepatic condition attended in this review none of these individuals had recurrent pancreatitis during article. The existing literature indicates astonishingly high Pancreatitis was finally resolved in all seven patients and rates of AP (up to 44% [9]) developing in the context of FHF, and this rate was not largely dissimilar in different There are also some case reports indicating similar effects a median follow-up of 18 months (range, 3–27 months). itreports seems (33% very necessaryin one survey to implement [10] and 40% a screening in another program [11]). et al. [42] whichSo, with puts the highunexpectedly levels of alertnesshigh incidence for the rate of AP in FHF; and in a report from a 45-year-old man with chronic hepatitis for pharmaceutical agents in inducing AP. Tahan the health system. The limitation of our findings in FHF- C virus infection with positive RNA who were put on therapy, he came with severe epigastric pain indicative of related AP is mostly related to the very divergent causes of treatment with IFN-α2b plus RBV, and after 5 weeks of drug FHF as well as high mortality rate of FHF itself, irrespective therapy brought him full recovery, with no recurrence of development of an AP course, which might provoke AP. Cessation of pharmaceutical treatment and supportive some bias to our findings. within 1 year of follow up. A series of two patients withet mostAcute of HAV the infection evidence has on also this been association repetitively comes reported from chronical. HCV infection who were under therapy with IFN- caseas a causativereports and factor small in theseries; development nonetheless, of AP.there Although is one α2bvery (andinteresting RBV in becauseone case) of has the been very reported meticulous by Elandconduct of the[43] authors from Netherlands to their patients who developed that showed AP. detailsThis study of the is et al. [14] prospective study investigating the rate of AP developing within 4 weeks of the diagnosis of acute HAV; Jain whichpharmaceutical resulted in side complete effects remission on the development of the acute ofphase AP. in their study of 124 patients with acute (16 pancreatitis;In the first case, nonetheless, after cessation 5 days ofafter both hospital the IFN admission, and RBV HAV) have reported 12.5% (2 males) of people who catch acute HAV infection have been diagnosed with AP, within return of the signs and symptoms and laboratory results the follow up time. In fact, from 124 patients (94 males, indicativeIFN was readministered of the acute illness, without just RBV within which hours. resulted In the in could30 females) be suggestive diagnosed of a male with preponderance acute HAV, HBV in this and relation HEV infections, finally 7 (5.6%), all males, developed AP which following IFN therapy, drug treatment was discontinued in a series of 6 reported by Mishra et al. [15] could also be second case, after physical and laboratory evidence for AP (7 out of 94 (7.4%)). The higher frequency of males (83%) administered, and within two and a half hour, serum amylaseand the patientsand got levels recovery. increased Again, several treatment times, was and re- confirmative to this conclusion; although in this study, the within 2 weeks, he developed epigastric pain that was showsoverall thatincidence the only has cases not beensimultaneously reported. Adeveloping careful review both of the reports from HAV infection and AP development report by Cecchi et al. [44] described disease course of a 52- older than males at the time of diagnosis. In none of the confirmed as not related to pancreas [43]. Another case- year-old Italian Caucasian man who got under treatment reportsthe conditions or series, are any females. incident As mortality well, females has been seemed reported, to be

has a benign course. with IFN-α2b and RBV for chronic HCV infection just from so we can conclude that AP in the context of HAV infection after8 days cessation before the of signs the started,pharmaceutical which was treatment, finally diagnosed and no The number of reports studying an association between reoccurrenceas AP. His symptoms of pancreatitis were thoroughly was observed remitted in justa 6 onemonths day follow-up. by Jain et al. HBV infection and AP is limited. In the prospective study DISCUSSION et al. [14], only one out of 54 (<2%) of the HBV Literature is strongly indicative of associations between pancreatitis,patients developed suggestive AP; whileof very in aggressive the series and report fatal by course Yuen hepatic diseases and pancreas injury [45]. Nevertheless, [23], 80% of patients with both conditions died of such a relationship is most evident in neoplastic conditions, by Chen et al. and most of the literature has focused on this issue [46]. onlyof AP curative developing in these in the patients, course of it HBV.also Moreover,brings remission the study in [27] showed that lamivudine therapy is not

MaybeJOP. Journal the of second the Pancreas most - http://www.serena.unina.it/index.php/jopinvestigated topic on this extended - Vol. 16 casesNo. 2 – Marwith 2015. recurring [ISSN 1590-8577] episodes of AP.

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2. interleukin-12 and soluble interleukin-2 receptor in Kitaoka S, Shiota G, Kawasaki H. Serum levels of interleukin-10, Nonetheless,In the case of acuteboth ofHCV the or cases non-A reported non-B hepatitis in the literature infection hadand relationa benign to courseAP development, of illness datawith is complete extremely recovery limited. type C. Hepatogastroenterology. 2003; 50:1569-74. [PMID: 14571788] 3. Jie Z, Liang Y, Hou L, Dong C, Iwakura Y, Soong L, Cong Y, Sun J. Intrahepatic innate lymphoid cells secrete IL-17A and IL-17F that are after conservative treatment. On the other hand, data crucial for T cell priming in viral infection. J Immunol 2014; 192:3289- prospective study, Jain et al. 4. on HEV infection and AP is immensely available. In their 300. [PMID: 24600029] record among all types of acute [14] viral reported hepatitis. 7.4% It also of seems their Seki E, Schwabe RF. Hepatic and : Functional Links5. and Key Pathways. 2014. [PMID: 25066777] HEV infected patients developing AP, which hits the highest pancreatitis: histo- and immunopathological features. J Gastroenterol pseudocysts, with both of the two cases reported with Klöppel G, Sipos B, Zamboni G, Kojima M, Morohoshi T. Autoimmune that AP after HEV infection is most likely to represent with 2007;6. 18:28-31. [PMID: 17520220] this condition in this review having acute HEV infection. Sass DA, Shakil AO. Fulminant hepatic failure. Liver Transpl 2005; ethnic predominance in this relation with all cases being 11:594-605. [PMID: 15915484] Another interesting observation in HEV related AP is the pancreatitis - a distinct entity, or merely a type of ? 7. Balakrishnan V, Nair P, Radhakrishnan L, Narayanan VA. Tropical In transplant recipients also, hepatitis has been associated from Indian/Pakistani ethnicity. Indian8. J Gastroenterol 2006; 25:74-81. [PMID: 16763335]

pancreaticJin Y, Gaocancer H, Chentissues H, and Wang adjacent J, Chen non-cancerous M, Li G, Wang tissues. L, Gu J, Tu H. with AP episodes. In liver transplant recipients, incidence of Identification and impact of hepatitis B virus DNA and antigens in AP was most high in patients whose hepatic failure was due Lett9. 2013; 335:447-54. [PMID: 23499889] to HBV infection with about 15% of all patients, followed Parbhoo SP, Welch J, Sherlock S. Acute pancreatitis in patients with by non-A non-B hepatitis (4%) and the least frequency for fulminant10. hepatic failure. Gut 1973; 14: 428. [PMID: 4716531] autoimmune hepatitis (<2%) [36]. Moreover, it has been liver transplant recipients is directly associated with the Kuo PC, Plotkin JS, Johnson LB. Acute pancreatitis and fulminant shown that development of an AP episode in HBV infected hepatic11. failure. J Am Coll Surg 1998; 187: 522-8. [PMID: 9809570] this subsection was that just like patients in non-transplant Ede RJ, Moore KP, Marshall WJ, Williams R. Frequency of pancreatitis HBV-DNA load [25]. An interesting observation in in fulminant hepatic failure using isoenzyme markers. Gut 1988; 29:778- 81.12. [PMID: 2454877] induced fulminant hepatic failure presenting with pancreatitis. J Med context, the only transplant recipient who was reportedly Mottram AR, Lazio MP, Bryant SM. Lepiota subincarnata J.E. Lange developed pseudocyst was infected by HEV infection. has also been broadly reported in the literature. In a large Toxicol 2010; 6:155-7. [PMID: 20532846] AP induced by pharmaceutical therapy for HCV infection series, Caudhari et al. [40] reported 0.4% incidence of 13. Lee WM. . Semin Respir Crit Care Med 2012; 33:36- 45.14. [PMID: 22447259] Jain P, Nijhawan S, Rai RR, Nepalia S, Mathur A. Acute pancreatitis AP during anti-HCV treatment. Similar observation has in acute viral hepatitis. World J Gastroenterol 2007; 13:5741-4. [PMID: also been reported by other authors, as well [43, 45]. 17963301]15. ofInterestingly, IFN therapy evidence seems suggeststo be a benignthat it isdisorder, IFN and withnot RBV full Mishra A, Saigal S, Gupta R, Sarin SK. Acute pancreatitis associated recoverythat induces after pancreatitis cessation of [45].the drugs. Finally AP in the context with viral hepatitis: a report of six cases with review of literature. Am J Gastroenterol16. 1999; 94:2292-5. [PMID: 10445566] CONCLUSION Lopez Morante A, Rodriguez de Lope C, San Miguel G, Pons Romero F. In conclusion, substantial evidence is suggestive of Acute pancreatitis in hepatitis A infection. Postgrad Med J 1986; 62:407- 8. [PMID: 3763554] 17. Garty BZ, Kanner D, Danon YL. Pancreatitis associated with hepatitis A18. viral infection. J Pediatr 1995; 127:669. [PMID: 7562301] associatedstrong associations with the betweenreason of acute hepatitis. hepatitis Nonetheless, and AP. wePrognosis should and have features in mind of suchthat athis relation conclusion is also hasdistinctly been Rana SK, Singh R, Aggarwal B, Kumar S. Acute pancreatitis in hepatitis A19. infection in a 10-year-old boy. Ped Infect Dis 2013; 5:172-174. made based on data coming from resources of limited study populations; and therefore, future studies of large Shrier LA, Karpen SJ, McEvoy C. Acute pancreatitis associated with acute hepatitis A in a young child. J Pediatr 1995; 126: 57-9. [PMID: patient populations with strong methodological approach 7815225]20. . Basaranoglu M, Balci NC, Klör HU. sludge and acute pancreatitis induced by acute hepatitis A. Pancreatology 2006; 6: 141-4. are needed for confirming and extending our findings 21. Conflict of Interest [PMID: 16354962] El-Sayed R, El-Karaksy H. Acute pancreatitis complicating acute hepatitis A virus infection. Arab J Gastroenterol. 2012; 13: 184-5. [PMID: 23432988]22. Authors declare to have no conflict of interest. pancreatitis associated with acute viral hepatitis: case report and review References Moleta DB, Kakitani FT, Lima AS, França JC, Raboni SM. Acute

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JOP. Journal of the Pancreas - http://www.serena.unina.it/index.php/jop - Vol. 16 No. 2 – Mar 2015. [ISSN 1590-8577] 109

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