Post-ERCP pancreatitis: Prevalence of abnormal alpha-1-antitrypsin phenotypes

K. Gottlieb, Stuart Sherman, Evan Fogel, M. Olsson, Glen Lehman

Research output: Contribution to journalArticle

Abstract

BACKGROUND: Alpha-1-antitrypsin (A-1-AT) is an important protease inhibitor which provides approx. 90 % of the serum anti-protease activity. The majority of the population (∼ 90%) have the MM genotype (codominant inheritance). Classic A-1-AT deficiency occurs with the ZZ genotype and is rare. Some of the heterozygote genotypes are associated with relatively lower A-1-AT serum levels. We have previously found that the mean pre-procedure A-1-AT levels were lower in patients who developed post-ERCP pancreatitis. HYPOTHESIS: We postulated that the difference in the group means was related to differences in the prevalence of A-1-AT heterozygotes; the pancreatitis group having more. Alternatively, an acute phase reaction could be responsible for a relative increase in the group of patients who did not develop pancreatitis. METHODS: In a new prospective series A-1-AT phenotypes were determined by a reference laboratory in 295 consecutive patients undergoing ERCP for various indications. C-reactive protein, a marker for the acute phase reaction, and serum A-1-AT levels were determined locally. Pancreatitis was diagnosed as previously described (Gastrointest Endosc 1990:36:462) . Using the z-statistic it was estimated that a sample size of approx. 200 pts would be sufficient to detect a difference of 10% in the incidence of abnormal phenotypes (α=0.05 two-tailed, β=0.20). RESULTS: Pancreatitis No Pancreatitis p-value (two-tailed) n = 26 n = 269 (Fisher's Exact Test) A-1-AT(mg/dl] 186.4±50.1 202.5 ± 59.9 0.19 CRP [mg/dl] 0.23 ± 0.59 1.3 ± 3.38 0.11 Heterozygotes 2/26 (7.8%) 24/269 (8.9%) 0.59 CONCLUSION: This prospective study shows no difference in the incidence of abnormal A-1-AT phenotypes (heterozygotes) between patients who developed post-ERCP pancreatitis and those who did not. This data supports our prior observation that the group of patients without pancreatitis has higher A-1-AT levels. CRP levels are higher in the patients who did not develop pancreatitis. However, the p-values do not reach statistical significance. This is probably due to a type II error and the data will be reanalyzed after more patients have been enrolled. Higher CRP levels suggest that an acute phase reaction may have increased the A-1-AT levels, and this may confer some degree of protection against post-ERCP pancreatitis.

Original languageEnglish
JournalGastrointestinal Endoscopy
Volume45
Issue number4
StatePublished - 1997

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alpha 1-Antitrypsin
Endoscopic Retrograde Cholangiopancreatography
Pancreatitis
Phenotype
Heterozygote
Acute-Phase Reaction
Genotype
Serum
alpha 1-Antitrypsin Deficiency
Incidence
Protease Inhibitors
C-Reactive Protein
Sample Size
Peptide Hydrolases
Prospective Studies

ASJC Scopus subject areas

  • Gastroenterology

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Post-ERCP pancreatitis : Prevalence of abnormal alpha-1-antitrypsin phenotypes. / Gottlieb, K.; Sherman, Stuart; Fogel, Evan; Olsson, M.; Lehman, Glen.

In: Gastrointestinal Endoscopy, Vol. 45, No. 4, 1997.

Research output: Contribution to journalArticle

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abstract = "BACKGROUND: Alpha-1-antitrypsin (A-1-AT) is an important protease inhibitor which provides approx. 90 {\%} of the serum anti-protease activity. The majority of the population (∼ 90{\%}) have the MM genotype (codominant inheritance). Classic A-1-AT deficiency occurs with the ZZ genotype and is rare. Some of the heterozygote genotypes are associated with relatively lower A-1-AT serum levels. We have previously found that the mean pre-procedure A-1-AT levels were lower in patients who developed post-ERCP pancreatitis. HYPOTHESIS: We postulated that the difference in the group means was related to differences in the prevalence of A-1-AT heterozygotes; the pancreatitis group having more. Alternatively, an acute phase reaction could be responsible for a relative increase in the group of patients who did not develop pancreatitis. METHODS: In a new prospective series A-1-AT phenotypes were determined by a reference laboratory in 295 consecutive patients undergoing ERCP for various indications. C-reactive protein, a marker for the acute phase reaction, and serum A-1-AT levels were determined locally. Pancreatitis was diagnosed as previously described (Gastrointest Endosc 1990:36:462) . Using the z-statistic it was estimated that a sample size of approx. 200 pts would be sufficient to detect a difference of 10{\%} in the incidence of abnormal phenotypes (α=0.05 two-tailed, β=0.20). RESULTS: Pancreatitis No Pancreatitis p-value (two-tailed) n = 26 n = 269 (Fisher's Exact Test) A-1-AT(mg/dl] 186.4±50.1 202.5 ± 59.9 0.19 CRP [mg/dl] 0.23 ± 0.59 1.3 ± 3.38 0.11 Heterozygotes 2/26 (7.8{\%}) 24/269 (8.9{\%}) 0.59 CONCLUSION: This prospective study shows no difference in the incidence of abnormal A-1-AT phenotypes (heterozygotes) between patients who developed post-ERCP pancreatitis and those who did not. This data supports our prior observation that the group of patients without pancreatitis has higher A-1-AT levels. CRP levels are higher in the patients who did not develop pancreatitis. However, the p-values do not reach statistical significance. This is probably due to a type II error and the data will be reanalyzed after more patients have been enrolled. Higher CRP levels suggest that an acute phase reaction may have increased the A-1-AT levels, and this may confer some degree of protection against post-ERCP pancreatitis.",
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T2 - Prevalence of abnormal alpha-1-antitrypsin phenotypes

AU - Gottlieb, K.

AU - Sherman, Stuart

AU - Fogel, Evan

AU - Olsson, M.

AU - Lehman, Glen

PY - 1997

Y1 - 1997

N2 - BACKGROUND: Alpha-1-antitrypsin (A-1-AT) is an important protease inhibitor which provides approx. 90 % of the serum anti-protease activity. The majority of the population (∼ 90%) have the MM genotype (codominant inheritance). Classic A-1-AT deficiency occurs with the ZZ genotype and is rare. Some of the heterozygote genotypes are associated with relatively lower A-1-AT serum levels. We have previously found that the mean pre-procedure A-1-AT levels were lower in patients who developed post-ERCP pancreatitis. HYPOTHESIS: We postulated that the difference in the group means was related to differences in the prevalence of A-1-AT heterozygotes; the pancreatitis group having more. Alternatively, an acute phase reaction could be responsible for a relative increase in the group of patients who did not develop pancreatitis. METHODS: In a new prospective series A-1-AT phenotypes were determined by a reference laboratory in 295 consecutive patients undergoing ERCP for various indications. C-reactive protein, a marker for the acute phase reaction, and serum A-1-AT levels were determined locally. Pancreatitis was diagnosed as previously described (Gastrointest Endosc 1990:36:462) . Using the z-statistic it was estimated that a sample size of approx. 200 pts would be sufficient to detect a difference of 10% in the incidence of abnormal phenotypes (α=0.05 two-tailed, β=0.20). RESULTS: Pancreatitis No Pancreatitis p-value (two-tailed) n = 26 n = 269 (Fisher's Exact Test) A-1-AT(mg/dl] 186.4±50.1 202.5 ± 59.9 0.19 CRP [mg/dl] 0.23 ± 0.59 1.3 ± 3.38 0.11 Heterozygotes 2/26 (7.8%) 24/269 (8.9%) 0.59 CONCLUSION: This prospective study shows no difference in the incidence of abnormal A-1-AT phenotypes (heterozygotes) between patients who developed post-ERCP pancreatitis and those who did not. This data supports our prior observation that the group of patients without pancreatitis has higher A-1-AT levels. CRP levels are higher in the patients who did not develop pancreatitis. However, the p-values do not reach statistical significance. This is probably due to a type II error and the data will be reanalyzed after more patients have been enrolled. Higher CRP levels suggest that an acute phase reaction may have increased the A-1-AT levels, and this may confer some degree of protection against post-ERCP pancreatitis.

AB - BACKGROUND: Alpha-1-antitrypsin (A-1-AT) is an important protease inhibitor which provides approx. 90 % of the serum anti-protease activity. The majority of the population (∼ 90%) have the MM genotype (codominant inheritance). Classic A-1-AT deficiency occurs with the ZZ genotype and is rare. Some of the heterozygote genotypes are associated with relatively lower A-1-AT serum levels. We have previously found that the mean pre-procedure A-1-AT levels were lower in patients who developed post-ERCP pancreatitis. HYPOTHESIS: We postulated that the difference in the group means was related to differences in the prevalence of A-1-AT heterozygotes; the pancreatitis group having more. Alternatively, an acute phase reaction could be responsible for a relative increase in the group of patients who did not develop pancreatitis. METHODS: In a new prospective series A-1-AT phenotypes were determined by a reference laboratory in 295 consecutive patients undergoing ERCP for various indications. C-reactive protein, a marker for the acute phase reaction, and serum A-1-AT levels were determined locally. Pancreatitis was diagnosed as previously described (Gastrointest Endosc 1990:36:462) . Using the z-statistic it was estimated that a sample size of approx. 200 pts would be sufficient to detect a difference of 10% in the incidence of abnormal phenotypes (α=0.05 two-tailed, β=0.20). RESULTS: Pancreatitis No Pancreatitis p-value (two-tailed) n = 26 n = 269 (Fisher's Exact Test) A-1-AT(mg/dl] 186.4±50.1 202.5 ± 59.9 0.19 CRP [mg/dl] 0.23 ± 0.59 1.3 ± 3.38 0.11 Heterozygotes 2/26 (7.8%) 24/269 (8.9%) 0.59 CONCLUSION: This prospective study shows no difference in the incidence of abnormal A-1-AT phenotypes (heterozygotes) between patients who developed post-ERCP pancreatitis and those who did not. This data supports our prior observation that the group of patients without pancreatitis has higher A-1-AT levels. CRP levels are higher in the patients who did not develop pancreatitis. However, the p-values do not reach statistical significance. This is probably due to a type II error and the data will be reanalyzed after more patients have been enrolled. Higher CRP levels suggest that an acute phase reaction may have increased the A-1-AT levels, and this may confer some degree of protection against post-ERCP pancreatitis.

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