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  Table of Contents    
EDITORIAL  
Year : 2021  |  Volume : 64  |  Issue : 5  |  Page : 6-7
Pancreatic pathology: Emerging issues


Prof and Head, Department of Pathology, M L N Medical College, Prayagraj, Uttar Pradesh, India

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Date of Submission11-May-2021
Date of Decision15-May-2021
Date of Acceptance20-May-2021
Date of Web Publication7-Jun-2021
 

How to cite this article:
Misra V. Pancreatic pathology: Emerging issues. Indian J Pathol Microbiol 2021;64, Suppl S1:6-7

How to cite this URL:
Misra V. Pancreatic pathology: Emerging issues. Indian J Pathol Microbiol [serial online] 2021 [cited 2021 Jul 24];64, Suppl S1:6-7. Available from: https://www.ijpmonline.org/text.asp?2021/64/5/6/317938




Pathology of the pancreas is on the rise with both neoplastic as well as non-neoplastic diseases reported frequently. Diagnosis is important for different prognostic implications and therapeutic interventions. Diseases of the pancreas may vary from inflammatory to non-neoplastic and neoplastic mass lesions. Different types of pancreatitis constitute a large proportion of pancreatic diseases encountered in day-to-day practice.

Idiopathic chronic pancreatitis in the absence of any known precipitating factor especially of family history or alcoholism is termed as chronic pancreatitis (CP). A bimodal age distribution is known with age onset earlier than 35 years termed as early onset, while those later than 35 years are termed as late onset.[1] In 2014, an study from India suggested the cut-off age as 30 years. However, irrespective of the age criteria there exists a clear distinction between both the categories.[2] Pancreatic secretory trypsin inhibitor (SPINK1) mutation in patients suggests an early age onset, more changes of persistent abdominal pain, increased and early chances of pancreatic calcification and pseudocyst formation.[3],[4]

CP is associated with increased levels of bacterial lipopolysaccharide in the plasma. There is reduced acinar cell autophagy in humans with CP suggesting the role of metabolic endotoxemia in its pathogenesis. There is a close possibility that autophagy plays a cytoprotective as well as anti-inflammatory role in pancreatitis.[5]

Over the last two decades our knowledge and understanding regarding the pathogenesis and biology of autoimmune pancreatitis (AIP) has improved tremendously. The term AIP comprises of two clinically and histopathologically distinct forms of steroid responsive CP namely Type 1 AIP or IgG4-related pancreatitis (IgG4-RP) and Type 2 AIP idiopathic duct-centric pancreatitis (IDCP).

Type 1 AIP is now believed to be the prototype of the multisystemic IgG4 related disease, that often clinically mimics pancreatic cancer due to mass forming lesions that are usually seen in elderly males, presenting with obstructive jaundice. Similarly extrapancreatic involvement of the extrahepatic and intrahepatic biliary tree in IgG4 related sclerosing cholangitis (IgG4- SC), which may be seen in 80% of patients need to be distinguished from cholangiocarcinoma. Despite AIP being a steroid responsive condition, many a time these patients may be subjected to Whipple's procedure due to clinically mimicking the carcinoma pancreas.

Histology is characterized by lymphoplasmacytic inflammation, abundant IgG4 positive plasma cell infiltration, storiform fibrosis and obliterative phlebitis. Apart from histology, high serum IgG4 levels, pancreatic parenchymal and duct imaging findings and other organ involvement aid in diagnosis in cases where definitive histology is not evident. Also these parameters lay the foundation of various diagnostic tests criteria proposed over last few years.

Correlation of histopathology with clinic-radiological and serological data, and a close multidisciplinry approach is recommended despite histopathology being gold standard for diagnosis in routine practice, as sometimes the representative features may be difficult to identify in biopsy specimens.

Type 2 autoimmune pancreatitis or the IDCP type is different from Type 1 by being IgG4 negative with no organ other than the pancreas being involved. Also, neither the IgG4 levels in the serum nor the number of IgG4 rich plasma cells are increased. Type 2 autoimmune pancreatitis is lower in incidence than type 1. Histology alone is the mainstay for establishing diagnosis of IDCP as it lacks any specific serological marker or imaging. Since both the types of AIP respond dramatically to corticosteroid, biopsy is crucial to establish the preoperative diagnosis and to exclude malignancy preventing unnecessary surgical intervention.

Hereditary pancreatitis (HP) in majority of the cases is associated with an autosomal dominant inheritance pattern. HP is termed as occurrence of pancreatitis in more than one person in a family for more than two generations or pancreatitis associated with genetic inheritance of a pathogenic mutation in the cationic trypsinogen protease serine 1 (PRSS1) gene.[6]

This special issue contains a nice review. Article on autoimmune pancreatitis by Sakhuja et al.,[7] along with other articles related to gastrointestinal, hepatobiliary and pancreatic pathology dealing with all the aspects of diseases related to these systems. I am sure that the readers would be enlightened after going through these articles.



 
   References Top

1.
Layer PYH, Kalthoff L, Clain JE, Bakken LJ, DiMagno EP. The different courses of early-late-onset idiopathic and alcoholic chronic pancreatitis. Gastroenterology 1994;107:1481-7.  Back to cited text no. 1
    
2.
Rajesh G, Veena AB, Menon S, Balakrishnan V. Clinical profile of early-onset and late-onset idiopathic chronic pancreatitis in South India. Indian J Gastroenterol 2014;33:231-6.  Back to cited text no. 2
    
3.
Chang YT, Weu SC, L PC, Tien YW, Jan IS, Su YN, et al. Association and differential role of PRSS1 and SPINK 1 mutation in early-onset and late-one idiopathic chronic pancreatitis in Chinese subjects. Gut 2009;58:885.  Back to cited text no. 3
    
4.
Bhatia E, Choudhari G, Sikora SS, Landt O, Kage A, Becker M, et al. Tropical calcific pancreatitis: Strong association with SPINK1 trypsin inhibitor mutations. Gastroenterology 2002;123:1020-5.  Back to cited text no. 4
    
5.
Xia L, Xu Z, Zhou X, Bergmann F, Grabe N, Buchler MW, et al. Impaired autophagy increases susceptibility to endotoxin-induced chronic pancreatitis. Cell Death Dis 2020;11:889.  Back to cited text no. 5
    
6.
Hasan A, Moscoso DI, Kastrinos F. The role of genetics in pancreatitis. Gastrointest Endosc Clin N Am 2018;28:587-603.  Back to cited text no. 6
    
7.
Goyal S, Sakhuja P. Autoimmune pancreatitis: Current perspectives. Indian J Pathol Microbiol 2021;64:149-59.  Back to cited text no. 7
  [Full text]  

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Correspondence Address:
Vatsala Misra
Prof and Head, Department of Pathology, M L N Medical College, Prayagraj, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.317938

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