Autoimmune pancreatitis laboratory findings: Difference between revisions

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==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 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:<ref name="pmid14614606">{{cite journal |vauthors=Kamisawa T, Funata N, Hayashi Y, Eishi Y, Koike M, Tsuruta K, Okamoto A, Egawa N, Nakajima H |title=A new clinicopathological entity of IgG4-related autoimmune disease |journal=J. Gastroenterol. |volume=38 |issue=10 |pages=982–4 |year=2003 |pmid=14614606 |doi=10.1007/s00535-003-1175-y |url=}}</ref><ref name="pmid15044886">{{cite journal |vauthors=Shinji A, Sano K, Hamano H, Unno H, Fukushima M, Nakamura N, Akamatsu T, Kawa S, Kiyosawa K |title=Autoimmune pancreatitis is closely associated with gastric ulcer presenting with abundant IgG4-bearing plasma cell infiltration |journal=Gastrointest. Endosc. |volume=59 |issue=4 |pages=506–11 |year=2004 |pmid=15044886 |doi= |url=}}</ref><ref name="pmid14736977">{{cite journal |vauthors=Takeda S, Haratake J, Kasai T, Takaeda C, Takazakura E |title=IgG4-associated idiopathic tubulointerstitial nephritis complicating autoimmune pancreatitis |journal=Nephrol. Dial. Transplant. |volume=19 |issue=2 |pages=474–6 |year=2004 |pmid=14736977 |doi= |url=}}</ref><ref name="pmid16508232">{{cite journal |vauthors=Saeki T, Saito A, Hiura T, Yamazaki H, Emura I, Ueno M, Miyamura S, Gejyo F |title=Lymphoplasmacytic infiltration of multiple organs with immunoreactivity for IgG4: IgG4-related systemic disease |journal=Intern. Med. |volume=45 |issue=3 |pages=163–7 |year=2006 |pmid=16508232 |doi= |url=}}</ref><ref name="pmid17634963">{{cite journal |vauthors=Umemura T, Zen Y, Hamano H, Kawa S, Nakanuma Y, Kiyosawa K |title=Immunoglobin G4-hepatopathy: association of immunoglobin G4-bearing plasma cells in liver with autoimmune pancreatitis |journal=Hepatology |volume=46 |issue=2 |pages=463–71 |year=2007 |pmid=17634963 |doi=10.1002/hep.21700 |url=}}</ref>
Laboratory findings consistent with the diagnosis of autoimmune pancreatitis include:<ref name="pmid14614606">{{cite journal |vauthors=Kamisawa T, Funata N, Hayashi Y, Eishi Y, Koike M, Tsuruta K, Okamoto A, Egawa N, Nakajima H |title=A new clinicopathological entity of IgG4-related autoimmune disease |journal=J. Gastroenterol. |volume=38 |issue=10 |pages=982–4 |year=2003 |pmid=14614606 |doi=10.1007/s00535-003-1175-y |url=}}</ref><ref name="pmid15044886">{{cite journal |vauthors=Shinji A, Sano K, Hamano H, Unno H, Fukushima M, Nakamura N, Akamatsu T, Kawa S, Kiyosawa K |title=Autoimmune pancreatitis is closely associated with gastric ulcer presenting with abundant IgG4-bearing plasma cell infiltration |journal=Gastrointest. Endosc. |volume=59 |issue=4 |pages=506–11 |year=2004 |pmid=15044886 |doi= |url=}}</ref><ref name="pmid14736977">{{cite journal |vauthors=Takeda S, Haratake J, Kasai T, Takaeda C, Takazakura E |title=IgG4-associated idiopathic tubulointerstitial nephritis complicating autoimmune pancreatitis |journal=Nephrol. Dial. Transplant. |volume=19 |issue=2 |pages=474–6 |year=2004 |pmid=14736977 |doi= |url=}}</ref><ref name="pmid16508232">{{cite journal |vauthors=Saeki T, Saito A, Hiura T, Yamazaki H, Emura I, Ueno M, Miyamura S, Gejyo F |title=Lymphoplasmacytic infiltration of multiple organs with immunoreactivity for IgG4: IgG4-related systemic disease |journal=Intern. Med. |volume=45 |issue=3 |pages=163–7 |year=2006 |pmid=16508232 |doi= |url=}}</ref><ref name="pmid17634963">{{cite journal |vauthors=Umemura T, Zen Y, Hamano H, Kawa S, Nakanuma Y, Kiyosawa K |title=Immunoglobin G4-hepatopathy: association of immunoglobin G4-bearing plasma cells in liver with autoimmune pancreatitis |journal=Hepatology |volume=46 |issue=2 |pages=463–71 |year=2007 |pmid=17634963 |doi=10.1002/hep.21700 |url=}}</ref>
**Increased serum IgG4 levels and hypergammaglobulinemia (>2 times the upper limit of normal in most patients). Using a cutoff of 135 mg/dL, serum IgG4  has following sensitivity and specificity:
*Increased [[serum]] IgG4 levels and [[hypergammaglobulinemia]] (>2 times the upper limit of normal in most patients). Using a cutoff of 135 mg/dL, serum IgG4  has following [[sensitivity]] and [[specificity]]:
***Sensitivity 95%
**[[Sensitivity]] 95%
***Specificity 97%
**[[Specificity]] 97%
**Antilactoferrin antibody
*Antilactoferrin antibody
**Anticarbonic anhydrase II antibody
*Anticarbonic anhydrase II [[antibody]]
**Anti-plasminogen-binding protein (PBP) peptide antibodies<ref name="pmid19940298">{{cite journal |vauthors=Frulloni L, Lunardi C, Simone R, Dolcino M, Scattolini C, Falconi M, Benini L, Vantini I, Corrocher R, Puccetti A |title=Identification of a novel antibody associated with autoimmune pancreatitis |journal=N. Engl. J. Med. |volume=361 |issue=22 |pages=2135–42 |year=2009 |pmid=19940298 |doi=10.1056/NEJMoa0903068 |url=}}</ref>
*Anti-plasminogen-binding protein (PBP) peptide antibodies<ref name="pmid19940298">{{cite journal |vauthors=Frulloni L, Lunardi C, Simone R, Dolcino M, Scattolini C, Falconi M, Benini L, Vantini I, Corrocher R, Puccetti A |title=Identification of a novel antibody associated with autoimmune pancreatitis |journal=N. Engl. J. Med. |volume=361 |issue=22 |pages=2135–42 |year=2009 |pmid=19940298 |doi=10.1056/NEJMoa0903068 |url=}}</ref>
**Rheumatoid factor (RF)
*[[Rheumatoid factor]] (RF)
**IgG4-positive plasma cells
*IgG4-positive [[plasma cells]]
**Elevated serum alkaline phosphatase levels (ALP)
*Elevated [[serum]] [[alkaline phosphatase]] levels (ALP)
**Elevated serum aminotransferases
*Elevated [[serum]] [[aminotransferases]]
**Elevated ESR
*Elevated [[ESR]]
**Elevated CA19-9
*Elevated [[CA19-9]]
==== 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.<ref name="UpTo">{{cite web |author=Freedman SD |url=http://www.uptodate.com/patients/content/topic.do?topicKey=~EzkfCtNwumVrg |title=Clinical manifestations and diagnosis of chronic pancreatitis in adults |format= |work=UpToDate  |accessdate=}}</ref><ref name="pmid15285176">{{cite journal |vauthors=Keim V, Teich N, Moessner J |title=Clinical value of a new fecal elastase test for detection of chronic pancreatitis |journal=Clin. Lab. |volume=49 |issue=5-6 |pages=209–15 |year=2003 |pmid=15285176 |doi= |url=}}</ref><ref name="pmid12093988">{{cite journal |vauthors=Walkowiak J, Herzig KH, Strzykala K, Przyslawski J, Krawczynski M |title=Fecal elastase-1 is superior to fecal chymotrypsin in the assessment of pancreatic involvement in cystic fibrosis |journal=Pediatrics |volume=110 |issue=1 Pt 1 |pages=e7 |year=2002 |pmid=12093988 |doi= |url=}}</ref><ref name="pmid15343184">{{cite journal |vauthors=Borowitz D, Baker SS, Duffy L, Baker RD, Fitzpatrick L, Gyamfi J, Jarembek K |title=Use of fecal elastase-1 to classify pancreatic status in patients with cystic fibrosis |journal=J. Pediatr. |volume=145 |issue=3 |pages=322–6 |year=2004 |pmid=15343184 |doi=10.1016/j.jpeds.2004.04.049 |url=}}</ref>
=== 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.<ref name="pmid11276375">{{cite journal |vauthors=Boeck WG, Adler G, Gress TM |title=Pancreatic function tests: when to choose, what to use |journal=Curr Gastroenterol Rep |volume=3 |issue=2 |pages=95–100 |year=2001 |pmid=11276375 |doi= |url=}}</ref><ref name="pmid12641496">{{cite journal |vauthors=Chowdhury RS, Forsmark CE |title=Review article: Pancreatic function testing |journal=Aliment. Pharmacol. Ther. |volume=17 |issue=6 |pages=733–50 |year=2003 |pmid=12641496 |doi= |url=}}</ref><ref name="pmid15508057">{{cite journal |vauthors=Siegmund E, Löhr JM, Schuff-Werner P |title=[The diagnostic validity of non-invasive pancreatic function tests--a meta-analysis] |language=German |journal=Z Gastroenterol |volume=42 |issue=10 |pages=1117–28 |year=2004 |pmid=15508057 |doi=10.1055/s-2004-813604 |url=}}</ref><ref name="pmid16633964">{{cite journal |vauthors=Ammann RW |title=Diagnosis and management of chronic pancreatitis: current knowledge |journal=Swiss Med Wkly |volume=136 |issue=11-12 |pages=166–74 |year=2006 |pmid=16633964 |doi=2006/11/smw-11182 |url=}}</ref>
* The limitation of direct tests is that they are costly and cumbersome.<ref name="pmid11276375">{{cite journal |vauthors=Boeck WG, Adler G, Gress TM |title=Pancreatic function tests: when to choose, what to use |journal=Curr Gastroenterol Rep |volume=3 |issue=2 |pages=95–100 |year=2001 |pmid=11276375 |doi= |url=}}</ref><ref name="pmid12641496">{{cite journal |vauthors=Chowdhury RS, Forsmark CE |title=Review article: Pancreatic function testing |journal=Aliment. Pharmacol. Ther. |volume=17 |issue=6 |pages=733–50 |year=2003 |pmid=12641496 |doi= |url=}}</ref><ref name="pmid15508057">{{cite journal |vauthors=Siegmund E, Löhr JM, Schuff-Werner P |title=[The diagnostic validity of non-invasive pancreatic function tests--a meta-analysis] |language=German |journal=Z Gastroenterol |volume=42 |issue=10 |pages=1117–28 |year=2004 |pmid=15508057 |doi=10.1055/s-2004-813604 |url=}}</ref><ref name="pmid16633964">{{cite journal |vauthors=Ammann RW |title=Diagnosis and management of chronic pancreatitis: current knowledge |journal=Swiss Med Wkly |volume=136 |issue=11-12 |pages=166–74 |year=2006 |pmid=16633964 |doi=2006/11/smw-11182 |url=}}</ref>
* 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%<ref name="pmid23711627">{{cite journal |vauthors=Ketwaroo G, Brown A, Young B, Kheraj R, Sawhney M, Mortele KJ, Najarian R, Tewani S, Dasilva D, Freedman S, Sheth S |title=Defining the accuracy of secretin pancreatic function testing in patients with suspected early chronic pancreatitis |journal=Am. J. Gastroenterol. |volume=108 |issue=8 |pages=1360–6 |year=2013 |pmid=23711627 |pmc=5388854 |doi=10.1038/ajg.2013.148 |url=}}</ref>
*Specificity- 86%<ref name="pmid23711627">{{cite journal |vauthors=Ketwaroo G, Brown A, Young B, Kheraj R, Sawhney M, Mortele KJ, Najarian R, Tewani S, Dasilva D, Freedman S, Sheth S |title=Defining the accuracy of secretin pancreatic function testing in patients with suspected early chronic pancreatitis |journal=Am. J. Gastroenterol. |volume=108 |issue=8 |pages=1360–6 |year=2013 |pmid=23711627 |pmc=5388854 |doi=10.1038/ajg.2013.148 |url=}}</ref>
===== (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.<ref name="pmid16633964">{{cite journal |vauthors=Ammann RW |title=Diagnosis and management of chronic pancreatitis: current knowledge |journal=Swiss Med Wkly |volume=136 |issue=11-12 |pages=166–74 |year=2006 |pmid=16633964 |doi=2006/11/smw-11182 |url=}}</ref><ref name="pmid11179244">{{cite journal |vauthors=Etemad B, Whitcomb DC |title=Chronic pancreatitis: diagnosis, classification, and new genetic developments |journal=Gastroenterology |volume=120 |issue=3 |pages=682–707 |year=2001 |pmid=11179244 |doi= |url=}}</ref>


==References==
==References==

Latest revision as of 14:46, 19 January 2018

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

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 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

  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. PMID 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. PMID 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. PMID 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. PMID 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. PMID 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. PMID 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. PMID 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. PMID 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. PMID 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. PMID 11276375.
  12. ↑ 12.0 12.1 Chowdhury RS, Forsmark CE (2003). "Review article: Pancreatic function testing". Aliment. Pharmacol. Ther. 17 (6): 733–50. PMID 12641496.
  13. ↑ 13.0 13.1 Siegmund E, Löhr 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. PMID 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). PMID 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. PMC 5388854. PMID 23711627.
  16. ↑ Etemad B, Whitcomb DC (2001). "Chronic pancreatitis: diagnosis, classification, and new genetic developments". Gastroenterology. 120 (3): 682–707. PMID 11179244.

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