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Autoimmune pancreatitis laboratory findings

Introduction

Overview

Overview

Laboratory findings consistent with the diagnosis of autoimmune pancreatitis may include increased serum IgG4 levels and hypergammaglobulinemia (>2 times the upper limit of normal in most patients), antilactoferrin antibody, anticarbonic anhydrase II antibody, other autoantibodies (ANA), rheumatoid factor (RF), IgG4-positive plasma cells, elevated serum alkaline phosphatase levels (ALP), elevated serum aminotransferases, ESR, and CA19-9.

Laboratory Findings

Laboratory Findings

Laboratory findings consistent with the diagnosis of autoimmune pancreatitis include:[1][2][3][4][5]

Fecal tests:

(a) Sudan staining of feces:
  • A non-specific, qualitative test that is no longer used for the diagnosis of steatorrhea.
(b) 72-hour quantitative fecal fat (Gold standard):
  • A quantitaive test that determines fecal fat excretion for over 24hrs.
  • Fecal fat excretion of >7g/day is diagnostic of malabsorption.
  • Patients with steatorrhea usually have an excretion of >10g of fat per day.
(c) Faecal elastase measurement (Test of choice):
  • The most sensitive and specific test for pancreatic exocrine dysfunction.
  • It can be done with a single random stool sample.
  • The results are independent of pancreatic enzyme replacement therapy.
  • A value of less than 200 ug/g indicates pancreatic insufficiency.[7][8][9][10]

Pancreatic function tests:

(a) Direct/ Invasive tests:
  • Direct tests are used to assess pancreatic insufficiency in the early course of disease when patient has clinical symptoms but no radiology findings.
  • Direct tests involve pancreatic stimulation via meal or hormonal secretagogues and assessment of pancreatic secretions in the duodenal fluid.
  • Direct tests along with radiographic findings (pancreatic calcifications) are stll considered to be the gold standard for the diagnosis of chronic pancreatitis.[11][12][13][14]
  • The limitation of direct tests is that they are costly and cumbersome.[11][12][13][14]
  • Direct tests include:
    • Secretin stimulation test
    • Pancreozymin-secretin test

Secretin stimulation test is considered the gold standard functional test for diagnosis of chronic pancreatitis.

The observation that bi-carbonate production is impaired early in chronic pancreatitis has led to the rationale of use of this test in early stages of disease:

  • Sensitivity – 82%[15]
  • Specificity- 86%[15]
(b) Indirect/ Non-invasive tests:

Indirect tests are used to assess the complications of chronic pancreatitis.

  • Indirect tests include:
    • Faecal chymotrypsin, PABA, pancreolauryl
    • Faecal elastase test

Indirect tests are not sensitive to assess pancreatic insufficiency in the early course of disease.[14][16]

References

References

  1. ↑ Kamisawa T, Funata N, Hayashi Y, Eishi Y, Koike M, Tsuruta K, Okamoto A, Egawa N, Nakajima H (2003). “A new clinicopathological entity of IgG4-related autoimmune disease”. J. Gastroenterol. 38 (10): 982–4. doi:10.1007/s00535-003-1175-y. PMIDΒ 14614606.
  2. ↑ Shinji A, Sano K, Hamano H, Unno H, Fukushima M, Nakamura N, Akamatsu T, Kawa S, Kiyosawa K (2004). “Autoimmune pancreatitis is closely associated with gastric ulcer presenting with abundant IgG4-bearing plasma cell infiltration”. Gastrointest. Endosc. 59 (4): 506–11. PMIDΒ 15044886.
  3. ↑ Takeda S, Haratake J, Kasai T, Takaeda C, Takazakura E (2004). “IgG4-associated idiopathic tubulointerstitial nephritis complicating autoimmune pancreatitis”. Nephrol. Dial. Transplant. 19 (2): 474–6. PMIDΒ 14736977.
  4. ↑ Saeki T, Saito A, Hiura T, Yamazaki H, Emura I, Ueno M, Miyamura S, Gejyo F (2006). “Lymphoplasmacytic infiltration of multiple organs with immunoreactivity for IgG4: IgG4-related systemic disease”. Intern. Med. 45 (3): 163–7. PMIDΒ 16508232.
  5. ↑ Umemura T, Zen Y, Hamano H, Kawa S, Nakanuma Y, Kiyosawa K (2007). “Immunoglobin G4-hepatopathy: association of immunoglobin G4-bearing plasma cells in liver with autoimmune pancreatitis”. Hepatology. 46 (2): 463–71. doi:10.1002/hep.21700. PMIDΒ 17634963.
  6. ↑ Frulloni L, Lunardi C, Simone R, Dolcino M, Scattolini C, Falconi M, Benini L, Vantini I, Corrocher R, Puccetti A (2009). “Identification of a novel antibody associated with autoimmune pancreatitis”. N. Engl. J. Med. 361 (22): 2135–42. doi:10.1056/NEJMoa0903068. PMIDΒ 19940298.
  7. ↑ Freedman SD. “Clinical manifestations and diagnosis of chronic pancreatitis in adults”. UpToDate.
  8. ↑ Keim V, Teich N, Moessner J (2003). “Clinical value of a new fecal elastase test for detection of chronic pancreatitis”. Clin. Lab. 49 (5–6): 209–15. PMIDΒ 15285176.
  9. ↑ Walkowiak J, Herzig KH, Strzykala K, Przyslawski J, Krawczynski M (2002). “Fecal elastase-1 is superior to fecal chymotrypsin in the assessment of pancreatic involvement in cystic fibrosis”. Pediatrics. 110 (1 Pt 1): e7. PMIDΒ 12093988.
  10. ↑ Borowitz D, Baker SS, Duffy L, Baker RD, Fitzpatrick L, Gyamfi J, Jarembek K (2004). “Use of fecal elastase-1 to classify pancreatic status in patients with cystic fibrosis”. J. Pediatr. 145 (3): 322–6. doi:10.1016/j.jpeds.2004.04.049. PMIDΒ 15343184.
  11. ↑ 11.0 11.1 Boeck WG, Adler G, Gress TM (2001). “Pancreatic function tests: when to choose, what to use”. Curr Gastroenterol Rep. 3 (2): 95–100. PMIDΒ 11276375.
  12. ↑ 12.0 12.1 Chowdhury RS, Forsmark CE (2003). “Review article: Pancreatic function testing”. Aliment. Pharmacol. Ther. 17 (6): 733–50. PMIDΒ 12641496.
  13. ↑ 13.0 13.1 Siegmund E, LΓΆhr JM, Schuff-Werner P (2004). “[The diagnostic validity of non-invasive pancreatic function tests–a meta-analysis]”. Z Gastroenterol (in German). 42 (10): 1117–28. doi:10.1055/s-2004-813604. PMIDΒ 15508057.
  14. ↑ 14.0 14.1 14.2 Ammann RW (2006). “Diagnosis and management of chronic pancreatitis: current knowledge”. Swiss Med Wkly. 136 (11–12): 166–74. doi:2006/11/smw-11182 Check |doi= value (help). PMIDΒ 16633964.
  15. ↑ 15.0 15.1 Ketwaroo G, Brown A, Young B, Kheraj R, Sawhney M, Mortele KJ, Najarian R, Tewani S, Dasilva D, Freedman S, Sheth S (2013). “Defining the accuracy of secretin pancreatic function testing in patients with suspected early chronic pancreatitis”. Am. J. Gastroenterol. 108 (8): 1360–6. doi:10.1038/ajg.2013.148. PMCΒ 5388854. PMIDΒ 23711627.
  16. ↑ Etemad B, Whitcomb DC (2001). “Chronic pancreatitis: diagnosis, classification, and new genetic developments”. Gastroenterology. 120 (3): 682–707. PMIDΒ 11179244.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]