Clinical and morphological characteristics of type 1 and 2 autoimmune pancreatitis

Cover Page


Cite item

Full Text

Abstract

Rationale: In the recent years, an increased interest to autoimmune pancreatitis (AIP) has been seen, related to growing diagnostic potential. In its turn, this leads to an increase in numbers of diagnosed AIP cases. At present, two types of AIP have been described with diverse clinical manifestation and morphology of the pancreas. However, the reproducibility of the differential diagnosis between AIP type 1 and 2 is low even among pancreatic pathologists.

Aim: To identify criteria for the morphologic diagnosis of AIP type 1 and 2.

Materials and methods: A morphological study of biopsy and surgical specimens from 26 patients with AIP was performed. There were 22 cases of AIP type 1 and 4 cases of AIP type 2. In addition to hematoxylin eosin staining of the specimens, immunohistochemistry was used with counting of CD138+ absolute numbers, determination of IgG+ and IgG4+ cells in the inflammatory infiltrates, as well as the ratios of IgG4+/IgG+ and IgG4+/CD138+ cells.

Results: AIP type 1 was characterized by storiform fibrosis of the pancreatic tissue (81.8% cases), involving the parapancreatic fat tissue, by moderateto-severe lymphoplasmocytic infiltration and signs of obliterative/non-obliterative phlebitis. Type 2 AIP was characterized by severe fibrosis with predominantly periductal (centrilobular) fibrosis and mild chronic inflammatory infiltration of the pancreas, while there was no extension of fibrosis and inflammatory infiltration to the parapancreatic tissues in any case. The mean number of CD138+ cell in AIP type 1 was 101.2 ± 27.9 per 1 high-power field (HPF), and in AIP type 2, it was 42.8 ± 20.9 per 1 HPF. The mean absolute number of IgG+ cells in AIP type 1 was 99.6 ± 25.7 per 1 HPF, whereas in AIP type 2, 42.1 ± 20.8 per 1 HPF. In AIP type 1, the mean number of IgG4+ plasmatic cells in the infiltrates was 74.5 ± 27.2 per 1 HPF, whereas in AIP type 2, it was 3.4 ± 2.7 per 1 HPF. The IgG4+/IgG+ ratio was 75 ± 12.6% vs. 8.4 ± 6.2%, and the IgG4+/CD138+ ratio was 72.4 ± 12.3% vs. 8.3 ± 5.9% in AIP type 1 and type 2, respectively.

Conclusion: For the differential diagnosis of type 1 and 2 AIP, it is necessary to take into consideration not only typical histological abnormalities, but also the numbers of CD138+, IgG+ and IgG4+ cells within the inflammatory infiltrate, as well as the IgG4+/IgG+ and IgG4+/CD138+ ratios.

About the authors

S. V. Lishchuk

Research Institute of Human Morphology;
Russian State Research Center – Burnasyan Federal Medical Biophysical Center of the Federal Medical Biological Agency

Author for correspondence.
Email: slishuk@fmbcfmba.ru

Sergey V. Lishchuk – MD, Postgraduate Student, Research Institute of Human Morphology; Head of Department of Pathology, Russian State Research Center – Burnasyan Federal Medical Biophysical Center of the Federal Medical Biological Agency

3 Tsyurupy ul., Moscow, 117418, 46 Zhivopisnaya ul., Moscow, 123182

Russian Federation

Е. A. Dubova

Russian State Research Center – Burnasyan Federal Medical Biophysical Center of the Federal Medical Biological Agency

Email: fake@neicon.ru

Elena A. Dubova – MD, PhD, Pathologist, Department of Pathology

46 Zhivopisnaya ul., Moscow, 123182

Russian Federation

K. А. Pavlov

Russian State Research Center – Burnasyan Federal Medical Biophysical Center of the Federal Medical Biological Agency

Email: fake@neicon.ru

Konstantin A. Pavlov – MD, PhD, Pathologist, Department of Pathology 

46 Zhivopisnaya ul., Moscow, 123182

Russian Federation

Yu. D. Udalov

Russian State Research Center – Burnasyan Federal Medical Biophysical Center of the Federal Medical Biological Agency

Email: fake@neicon.ru

Yuriy D. Udalov – MD, PhD, Head Physician

46 Zhivopisnaya ul., Moscow, 123182

 

Russian Federation

References

  1. Щеголев АИ, Павлов КА, Дубова ЕА, Егоров ВИ. Аутоиммунный панкреатит. Архив патологии. 2008;5(70): 46–51.
  2. Shimosegawa T, Kanno A. Autoimmune pancreatitis in Japan: overview and perspective. J Gastroenterol. 2009;44(6): 503–17. doi: 10.1007/s00535-009-0054-6.
  3. Kim KP, Kim MH, Song MH, Lee SS, Seo DW, Lee SK. Autoimmune chronic pancreatitis. Am J Gastroenterol. 2004;99(8): 1605–16. doi: 10.1111/j.1572-0241.2004.30336.x.
  4. Umehara H, Okazaki K, Masaki Y, Kawano M, Yamamoto M, Saeki T, Matsui S, Sumida T, Mimori T, Tanaka Y, Tsubota K, Yoshino T, Kawa S, Suzuki R, Takegami T, Tomosugi N, Kurose N, Ishigaki Y, Azumi A, Kojima M, Nakamura S, Inoue D; Research Program for Intractable Disease by Ministry of Health, Labor and Welfare (MHLW) Japan G4 team. A novel clinical entity, IgG4-related disease (IgG4RD): general concept and details. Mod Rheumatol. 2012;22(1): 1–14. doi: 10.1007/s10165-011-0508-6.
  5. Егоров ВИ, Павлов КА, Дубова ЕА, Шевченко ТВ, Мелехина ОВ, Свитина КА. Аутоиммунный панкреатит. Хирургическая или терапевтическая проблема? Хирургия. Журнал им. Н.И. Пирогова. 2008;(1): 62–5.
  6. Vasile D, Ilco A, Popa D, Belega A, Pana S. The surgical treatment of chronic pancreatitis: a clinical series of 17 cases. Chirurgia (Bucur). 2013;108(6): 794–9.
  7. Okazaki K, Uchida K. Autoimmune pancreatitis: the past, present, and future. Pancreas. 2015;44(7): 1006–16. doi: 10.1097/MPA.0000000000000382.
  8. Cai O, Tan S. From pathogenesis, clinical manifestation, and diagnosis to treatment: an overview on autoimmune pancreatitis. Gastroenterol Res Pract. 2017;2017:3246459. doi: 10.1155/2017/3246459.
  9. Kawa S, Ota M, Yoshizawa K, Horiuchi A, Hamano H, Ochi Y, Nakayama K, Tokutake Y, Katsuyama Y, Saito S, Hasebe O, Kiyosawa K. HLA DRB10405-DQB10401 haplotype is associated with autoimmune pancreatitis in the Japanese population. Gastroenterology. 2002;122(5): 1264–9. doi: 10.1053/gast.2002.33022.
  10. Zhang L, Chari S, Smyrk TC, Deshpande V, Kloppel G, Kojima M, Liu X, Longnecker DS, Mino-Kenudson M, Notohara K, RodriguezJusto M, Srivastava A, Zamboni G, Zen Y. Autoimmune pancreatitis (AIP) type 1 and type 2: an international consensus study on histopathologic diagnostic criteria. Pancreas. 2011;40(8): 1172–9. doi: 10.1097/MPA.0b013e318233bec5.
  11. Majumder S, Takahashi N, Chari ST. Autoimmune Pancreatitis. Dig Dis Sci. 2017;62(7): 1762–9. doi: 10.1007/s10620-017-4541-y.
  12. Zamboni G, Luttges J, Capelli P, Frulloni L, Cavallini G, Pederzoli P, Leins A, Longnecker D, Kloppel G. Histopathological features of diagnostic and clinical relevance in autoimmune pancreatitis: a study on 53 resection specimens and 9 biopsy specimens. Virchows Arch. 2004;445(6): 552–63. doi: 10.1007/s00428004-1140-z.
  13. Wu L, Li W, Huang X, Wang Z. Clinical features and comprehensive diagnosis of autoimmune pancreatitis in China. Digestion. 2013;88(2): 128–34. doi: 10.1159/000353597.
  14. Manfredi R, Graziani R, Cicero C, Frulloni L, Carbognin G, Mantovani W, Mucelli RP. Autoimmune pancreatitis: CT patterns and their changes after steroid treatment. Radiology. 2008;247(2): 435–43. doi: 10.1148/radiol.2472070598.
  15. Notohara K, Nishimori I, Mizuno N, Okazaki K, Ito T, Kawa S, Egawa S, Kihara Y, Kanno A, Masamune A, Shimosegawa T. Clinicopathological Features of Type 2 Autoimmune Pancreatitis in Japan: Results of a Multicenter Survey. Pancreas. 2015;44(7): 1072–7. doi: 10.1097/MPA.0000000000000438.

Supplementary files

Supplementary Files
Action
1. JATS XML

Copyright (c) 2018 Lishchuk S.V., Dubova Е.A., Pavlov K.А., Udalov Y.D.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies