Alpha-1-antitrypsin (A1AT) and post-ERCP pancreatitis: Final results

K. Gottlieb, Stuart Sherman, Evan Fogel, C. Choudari, Glen Lehman

Research output: Contribution to journalArticle

Abstract

Our previous abstracts (95-97) show that pre-procedure serum A1AT levels are significantly lower in patients who develop post-ERCP pancreatitis (PERP) compared to those who do not. Recently another group has published similar findings (Gastro 112:A6, 1997). What are the reasons? Hypotheses: 1. The difference is related to genetic heterogeneity, i.e., pts with PERP are more likely to be heterozygous for the A1AT gene and heterozygotes (hetZ) have lower A1AT levels. HetZs are therefore at higher risk for PERP. 2. The difference is due to selection bias. Pts who have an acute phase reaction (APR) have higher A1AT levels than those who do not. These patients have low risk for PERP conditions (dilated bile ducts) or are less likely to undergo higher risk procedures. Methods: Prior to ERCP serum A1AT, C-reactive protein, and A1AT phenotyping was obtained. PERP was diagnosed according to the published consensus criteria. A CRP > 5 mg/dl indicated an APR. Results: Total Patients (n=599) n A1AT Level (mb/dl) PERP% Mean SD Heterozygotes 66 159 52 3.2%, Homozygotes 534 207*63 8.0%, APResponders 42 272*112 0% Acute Phase Non-Responders (n=557) n A1AT Level (mg/dl) Mean SD Heterozygotes 63 154*45 Homozygotes (normal) 494 201*54 Pancreatitis 42 189**47 No Pancreatitis 515 196**56*p<.005**NS. Pancreatitis incidence in controls was 8.1%, and in hetZs was 3.2%. Summary: The average A1AT level for hetZs is significantly lower (p<0.005) than for controls. In contrast, patients in acute phase response have significantly higher A1AT levels (p<0.005). When patients in acute phase response are excluded from the analysis, there is no difference between serum A1AT levels of patients who later develop pancreatitis and those who do not. The hetZ state does not predispose to pancreatitis. Spontaneous APR appears to be protective for PERP. Conclusion: Further studies are needed to determine if therapeutically induced APR are protective against PERP.

Original languageEnglish
JournalGastrointestinal Endoscopy
Volume47
Issue number4
StatePublished - 1998

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alpha 1-Antitrypsin
Endoscopic Retrograde Cholangiopancreatography
Pancreatitis
Acute-Phase Reaction
Heterozygote
Homozygote
Serum
Genetic Heterogeneity
Selection Bias
Bile Ducts
C-Reactive Protein

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Alpha-1-antitrypsin (A1AT) and post-ERCP pancreatitis : Final results. / Gottlieb, K.; Sherman, Stuart; Fogel, Evan; Choudari, C.; Lehman, Glen.

In: Gastrointestinal Endoscopy, Vol. 47, No. 4, 1998.

Research output: Contribution to journalArticle

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abstract = "Our previous abstracts (95-97) show that pre-procedure serum A1AT levels are significantly lower in patients who develop post-ERCP pancreatitis (PERP) compared to those who do not. Recently another group has published similar findings (Gastro 112:A6, 1997). What are the reasons? Hypotheses: 1. The difference is related to genetic heterogeneity, i.e., pts with PERP are more likely to be heterozygous for the A1AT gene and heterozygotes (hetZ) have lower A1AT levels. HetZs are therefore at higher risk for PERP. 2. The difference is due to selection bias. Pts who have an acute phase reaction (APR) have higher A1AT levels than those who do not. These patients have low risk for PERP conditions (dilated bile ducts) or are less likely to undergo higher risk procedures. Methods: Prior to ERCP serum A1AT, C-reactive protein, and A1AT phenotyping was obtained. PERP was diagnosed according to the published consensus criteria. A CRP > 5 mg/dl indicated an APR. Results: Total Patients (n=599) n A1AT Level (mb/dl) PERP{\%} Mean SD Heterozygotes 66 159 52 3.2{\%}, Homozygotes 534 207*63 8.0{\%}, APResponders 42 272*112 0{\%} Acute Phase Non-Responders (n=557) n A1AT Level (mg/dl) Mean SD Heterozygotes 63 154*45 Homozygotes (normal) 494 201*54 Pancreatitis 42 189**47 No Pancreatitis 515 196**56*p<.005**NS. Pancreatitis incidence in controls was 8.1{\%}, and in hetZs was 3.2{\%}. Summary: The average A1AT level for hetZs is significantly lower (p<0.005) than for controls. In contrast, patients in acute phase response have significantly higher A1AT levels (p<0.005). When patients in acute phase response are excluded from the analysis, there is no difference between serum A1AT levels of patients who later develop pancreatitis and those who do not. The hetZ state does not predispose to pancreatitis. Spontaneous APR appears to be protective for PERP. Conclusion: Further studies are needed to determine if therapeutically induced APR are protective against PERP.",
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N2 - Our previous abstracts (95-97) show that pre-procedure serum A1AT levels are significantly lower in patients who develop post-ERCP pancreatitis (PERP) compared to those who do not. Recently another group has published similar findings (Gastro 112:A6, 1997). What are the reasons? Hypotheses: 1. The difference is related to genetic heterogeneity, i.e., pts with PERP are more likely to be heterozygous for the A1AT gene and heterozygotes (hetZ) have lower A1AT levels. HetZs are therefore at higher risk for PERP. 2. The difference is due to selection bias. Pts who have an acute phase reaction (APR) have higher A1AT levels than those who do not. These patients have low risk for PERP conditions (dilated bile ducts) or are less likely to undergo higher risk procedures. Methods: Prior to ERCP serum A1AT, C-reactive protein, and A1AT phenotyping was obtained. PERP was diagnosed according to the published consensus criteria. A CRP > 5 mg/dl indicated an APR. Results: Total Patients (n=599) n A1AT Level (mb/dl) PERP% Mean SD Heterozygotes 66 159 52 3.2%, Homozygotes 534 207*63 8.0%, APResponders 42 272*112 0% Acute Phase Non-Responders (n=557) n A1AT Level (mg/dl) Mean SD Heterozygotes 63 154*45 Homozygotes (normal) 494 201*54 Pancreatitis 42 189**47 No Pancreatitis 515 196**56*p<.005**NS. Pancreatitis incidence in controls was 8.1%, and in hetZs was 3.2%. Summary: The average A1AT level for hetZs is significantly lower (p<0.005) than for controls. In contrast, patients in acute phase response have significantly higher A1AT levels (p<0.005). When patients in acute phase response are excluded from the analysis, there is no difference between serum A1AT levels of patients who later develop pancreatitis and those who do not. The hetZ state does not predispose to pancreatitis. Spontaneous APR appears to be protective for PERP. Conclusion: Further studies are needed to determine if therapeutically induced APR are protective against PERP.

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