Sex-dependent and race-dependent association of XPNPEP2 C-2399A polymorphism with angiotensin-converting enzyme inhibitor-associated angioedema
Open accessAbstract
XPNPEP2 C-2399A genotype associated with serum APP activity in both men and women. The -2399 A/ genotype was associated with an increased risk of angioedema in men (OR 2.17, p=0.03) in multivariate analysis, especially black men.
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Claims the paper makes
11 of 26 cited sources checked · 7 supported · 0 flagged · accuracy not yet measured
- Premisecitation
Among 20 mixed-gender cases with ACE inhibitor-associated angioedema, the −2399A allele was more common than in 60 ACE inhibitor-exposed controls.
“The frequency of the −2399A allele was also increased in 20 mixed-gender cases of ACE inhibitor-associated angioedema as compared to 60 ACE inhibitor-exposed controls.[11]”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [11] source
The Association section (p. 7) reports a higher −2399A allele frequency in 20 angioedema cases than in 60 controls. However, the Participants section (p. 2) says the Belgian and Canadian controls had no history of ACE inhibitor therapy and the US controls’ medical histories were unknown; it does not support describing the controls as ACE inhibitor-exposed. (LLM, conf=0.92)
Experimental — accuracy not yet measured
- Premisecitation
Reports on serum APP activity in people who previously had angioedema while on ACE inhibitors have been inconsistent.
“Previous studies have provided conflicting data regarding serum APP activity in patients with a history of ACE inhibitor-associated angioedema.”
- Also stated in: § INTRODUCTION · plain
“Because studies have provided conflicting data regarding serum APP concentrations in patients with a history of ACE inhibitor-associated angioedema and because the gene encoding for serum APP is X-linked, we tested the hypothesis that the relationship between XPNPEP2 C-2399A genotype and APP activity or ACE inhibitor-associated angioedema is gender- and/or race-dependent.”
Quote in the paperSubstantial claim1 of 2 sources checked - Also stated in: § INTRODUCTION · plain
- Premisecitation
When ACE is inhibited, aminopeptidase P (APP) is the main enzyme that inactivates bradykinin.
“During ACE inhibition, bradykinin is primarily inactivated by aminopeptidase P (APP).”
- Also stated in: § INTRODUCTION · plain
“During ACE inhibition, BK and substance P are inactivated primarily by aminopeptidase P (APP) and dipeptidyl peptidase IV (DPPIV), respectively.[8, 9]”
Quote in the paperSubstantial claim1 of 2 sources checked- cites [8] source
Section 3.3 (page not available) says APP inactivates bradykinin in human plasma, but identifies it as the major inactivation pathway for des-Arg9-bradykinin, not bradykinin itself. The paper does not establish that APP becomes the primary enzyme inactivating bradykinin during ACE inhibition. (LLM, conf=0.88)
Experimental — accuracy not yet measured - cites [9] source
- Also stated in: § INTRODUCTION · plain
- Findingcitation
Cases had lower serum DPPIV activity than controls.
“Serum DPPIV activity was lower in case subjects as compared to controls, as previously reported for a subset of these subjects.[4]”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [4] source
- Premisecitation
Some patients with ACE inhibitor-associated angioedema have reduced DPPIV activity.
“We have previously reported that DPPIV activity is decreased in some patients with ACE inhibitor-associated angioedema.[4]”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [4] source
- Premisecitation
In hereditary angioedema patients, androgens raise APP activity.
“Androgens increase APP activity in patients with hereditary angioedema, suggesting that increased testosterone concentrations in men cannot account for gender differences.[20]”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [20] source
- Findingown data
Men had lower serum APP activity than women, independent of genotype.
“Serum APP activity was lower in men than in women, independent of genotype.”
- Also stated in: § RESULTS · plain
“Serum APP activity was lower in men compared to women, regardless of genotype.”
Quote in the paperNot a substantial claim - Also stated in: § RESULTS · plain
- Findingown data
Serum APP activity did not differ overall between cases and controls (220.6 ± 162.2 vs 216.9 ± 161.1 pmoles/ml/min, P=0.9).
“Overall, there was no difference in serum APP activity between cases and controls (220.6 ± 162.2 vs 216.9 ± 161.1 pmoles/ml/min, P=0.9).”
Quote in the paperNot a substantial claim - Findingown data
Among black men, the XPNPEP2 −2399A allele was significantly more common in those with prior angioedema than in ACE inhibitor-exposed controls (31.3% vs. 13.3%, P=0.03).
“This was attributable to a significantly increased frequency of the XPNPEP2 −2399A allele in black males with a history of angioedema compared to ACE inhibitor-exposed black male controls (31.3% vs. 13.3%, P=0.03).”
Quote in the paperSubstantial claim - Findingown data
A significant association was found between XPNPEP2 C-2399A genotype and serum APP activity in both sexes.
“There was a significant association between XPNPEP2 C-2399A genotype and serum APP activity in both men and women (Figure 1).”
Quote in the paperNot a substantial claim - Findingown data
The XPNPEP2 C-2399A genotype explained 9% of serum APP activity variance in women and 13% in men.
“XPNPEP2 C-2399A genotype accounted for 9% of the variability of serum APP activity in women and 13% in men.”
Quote in the paperNot a substantial claim - Findingown data
After adjustment for diabetes, seasonal allergies, and DPPIV activity, the XPNPEP2 −2399 A/ genotype was linked to a 2.2-fold higher angioedema risk in all men (P=0.03).
“In multivariate analysis, the XPNPEP2 −2399 A/ genotype was associated with a 2.2-fold increased risk of angioedema in all males (P=0.03) after controlling for diabetes mellitus, seasonal allergies and DPPIV activity (Table 3).”
Quote in the paperSubstantial claim - Premisecitation
The condition is believed to arise from impaired breakdown of bradykinin and substance P.
“Angioedema is thought to result from decreased degradation of vasoactive peptides.”
- Also stated in: § INTRODUCTION · hedged
“ACE inhibitor-associated angioedema is thought to result from defective degradation of the vasoactive peptides bradykinin (BK) and substance P.[6, 7]”
Quote in the paperSubstantial claim0 of 2 sources checked - Also stated in: § INTRODUCTION · hedged
- Premisecitation
Compared with white Americans, black Americans may be more sensitive to vascular permeability caused by bradykinin.
“Prior studies suggest that black Americans exhibit increased sensitivity to the effects of bradykinin-induced vascular permeability compared to white Americans.[22]”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [22] source
- Interpretationreasoning
Multiple defective pathways might be involved in the development of ACE inhibitor-associated angioedema.
“Mechanistically, defects in multiple pathways may contribute to the pathogenesis of ACE inhibitor-associated angioedema.”
Quote in the paperSubstantial claim - Study design and conductown data
Because of the limited sample size, an effect of XPNPEP2 genotype in white men cannot be ruled out.
“In addition, given the small sample size, we cannot exclude the effect of XPNPEP2 genotype in white men.”
Quote in the paperNot a substantial claim - Premisecitation
Progesterone raises APP activity.
“Progesterone increases APP activity.[19]”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [19] source
- Interpretationreasoning
When APP-mediated bradykinin inactivation is reduced, black American men might be at greater risk for angioedema.
“Thus, black American men may be more susceptible to angioedema when the inactivation of bradykinin by APP is decreased.”
Quote in the paperSubstantial claim - Interpretationreasoning
Variation in XPNPEP2 probably does not explain most ACE inhibitor-associated angioedema cases.
“Thus, while genetic variation in XPNPEP2 associates with angioedema, it is unlikely that variation in this X-linked gene accounts for the majority of cases of ACE inhibitor-associated angioedema.”
Quote in the paperSubstantial claim - Premisecitation
Combined drug inhibition of ACE and NEP raises angioedema risk more than ACE inhibition by itself.
“Pharmacologic inhibition of both ACE and NEP increases the risk of angioedema when compared to ACE inhibition alone.[24]”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [24] source
- Interpretationreasoning
ACE inhibitor-associated angioedema pathogenesis probably involves a combination of genetic and environmental factors that alter vasoactive peptide breakdown and action during ACE inhibition.
“The combination of multiple genetic and environmental factors that affect the degradation and action of vasoactive peptides during ACE inhibition likely contribute to ACE inhibitor-associated angioedema pathogenesis.”
Quote in the paperSubstantial claim - Premisecitation
Most people who develop ACE inhibitor-associated angioedema are women.
“This is likely because, as reported previously [6], the majority of patients with ACE inhibitor-associated angioedema are women.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [6] source
- May combine two claims. 13
- Classified as probably not a substantial claim. 20
May combine two claims.
PremisecitationAngioedema linked to ACE inhibitors is more frequent among women and black Americans.
“Angioedema is a rare adverse effect of angiotensin converting enzyme (ACE) inhibitors that occurs more commonly in women and black Americans.”
- Also stated in: § INTRODUCTION · plain
“Clinical risk factors for ACE inhibitor-associated angioedema include black American race, female gender, smoking, seasonal allergies, and immunosuppressant therapy.[3-5]”
Quote in the paperSubstantial claim1 of 3 sources checked- Also stated in: § INTRODUCTION · plain
Classified as probably not a substantial claim.
PremisecitationA reported link exists between the XPNPEP2 C-2399A variant and APP activity.
“A single nucleotide polymorphism, −2399C>A (rs3788853, C-2399A), in XPNPEP2, the X-linked gene that encodes membranous APP, has been reported to associate with APP activity.”
- Also stated in: § INTRODUCTION · plain
“A previous study investigating the role of genetic factors in the regulation of APP activity identified a single nucleotide polymorphism (SNP), C-2399A (rs3788853), in XPNPEP2, an X-linked gene that encodes for membranous APP.[11]”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [11] source
- Also stated in: § INTRODUCTION · plain
Classified as probably not a substantial claim.
PremisecitationIn families where the proband had either ACE inhibitor-associated angioedema or an anaphylactoid reaction during dialysis, the C-2399A variant tracked with lower serum APP activity.
“This variant segregated with reduced serum APP activity in families in which the proband had ACE inhibitor-associated angioedema or anaphylactoid reaction during dialysis.[11]”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [11] source
The Measured Genotype Analysis (p. 7) links C-2399A to lower plasma APP activity in seven pedigrees. But the family whose proband had an anaphylactoid reaction during hemodialysis carried a different XPNPEP2 variant—a coding deletion—and was excluded from that SNP analysis (Mutation Screening, p. 6; Measured Genotype Analysis, p. 7). The paper measured plasma, not serum, APP activity. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationByrd and colleagues found lower DPPIV antigen and activity in serum from 50 patients with prior ACE inhibitor-associated angioedema than in 176 ACE inhibitor-exposed controls, but they saw no link between case-control status and APP activity.
“Byrd et al. reported decreased DPPIV antigen and activity levels in the sera of 50 patients with a history of ACE inhibitor-associated angioedema as compared to 176 ACE inhibitor-exposed controls, but did not observe a relationship between case-control status and APP activity.[4]”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [4] source
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationDuring ACE inhibition, bradykinin-mediated vasodilation is affected by genetic variation in the B2 receptor.
“Genetic variation in the bradykinin B2 receptor influences bradykinin-mediated vasodilation during ACE inhibition.[25]”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [25] source
Probably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataWomen made up 56% of the case group.
“Fifty-six percent of cases were women.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataSeasonal allergies were significantly more common among cases than controls.
“The prevalence of seasonal allergies was significantly higher in cases compared with control subjects.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataControls had a median ACE inhibitor exposure of 42 months, whereas cases had a median of 5 months, a significant difference (P<0.001).
“The median ACE inhibitor exposure time for controls was 42 months. Only 16 controls took an ACE inhibitor for less than one year. The median exposure time for cases was 5 months (P<0.001).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataIn the multivariate model, both a history of seasonal allergies and DPPIV activity were associated with higher angioedema risk in men and women.
“A history of seasonal allergies and DPPIV activity were associated with an increased risk of angioedema in both males and females in the multivariate analysis.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataIn race-stratified multivariate analysis, the XPNPEP2 −2399 A/ genotype was associated with higher ACE inhibitor-associated angioedema risk in black men (P=0.01) but not white men (P=0.53).
“When multivariate analysis was further stratified by race, the XPNPEP2 −2399 A/ genotype was associated with increased risk of ACE inhibitor-associated angioedema in black males (P=0.01) but not white males (P=0.53).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataIn men overall (black and white combined), the −2399 A/ genotype was more frequent in cases than in ACE inhibitor-exposed controls, with a trend toward significance (P=0.07 univariate).
“In contrast, among men, the frequency of the −2399 A/ genotype tended to be increased in cases compared to ACE inhibitor-exposed controls (P=0.07 for univariate analysis) for black and white males combined (Table 2).”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataBlack men showed a trend toward higher serum APP activity than white men (P=0.058).
“Serum APP activity trended higher in black men compared to white men (P=0.058).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataIn white men, the −2399A allele frequency was 23.1% in angioedema cases and 20.6% in ACE inhibitor-exposed controls, a nonsignificant difference.
“The frequency of the −2399A allele was 23.1% in white males with angioedema versus 20.6% with ACE inhibitor-exposed controls, but this difference was not significant.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataThe distribution of XPNPEP2 C-2399A genotypes was similar across white and black women and across white and black men.
“XPNPEP2 C-2399A genotype frequencies were similar in white and black women and in white and black men (Table 2).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataNo association was found between XPNPEP2 C-2399A genotype and ACE inhibitor-associated angioedema in women, whether all women, white women, or black women were analyzed, and whether heterozygotes were treated as intermediate or the −2399A allele was treated as dominant.
“There was no association between XPNPEP2 genotype and case-control status, in all women (P=0.7), in white women (P=0.9) or in black women (P=0.6) when heterozygote was treated as intermediate (Table 2).”
- Also stated in: § RESULTS · plain
“There was also no association between XPNPEP2 genotype and angioedema in women when the −2399A allele was treated as dominant (i.e. A/A + C/A vs C/C).”
Quote in the paperSubstantial claim- Also stated in: § RESULTS · plain
Classified as probably not a substantial claim. May combine two claims.
Study design and conductown dataThe control group was designed in advance to be half black American and half white American, and half female and half male.
“Controls were pre-specified to be 50% black American, 50% white American and 50% female, 50% male.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenTo correct for quenching by serum and substrate, an internal standard was routinely added to every well.
“After the 3h reading, 1nmol of internal standard, Abz-Gly (Bachem, Torrance, CA), was routinely added to each well to normalize for serum and substrate quenching effects.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataThe month when ACE inhibitor treatment began did not differ between cases and controls (P=0.26).
“Month of ACE inhibitor initiation was similar in the two groups (P=0.26).”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenA research nurse verified medical history, including any angioedema history, with a detailed case report form.
“Medical history, including the history of angioedema, was confirmed by a research nurse using a detailed case report form.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
PremisecitationAdam and colleagues found lower APP activity in serum from 39 white individuals with prior ACE inhibitor-associated angioedema than in 39 ACE inhibitor-exposed controls.
“Adam et al. have previously reported decreased APP activity in the sera of 39 white patients with a history of ACE inhibitor-associated angioedema, as compared to 39 ACE inhibitor-exposed controls.[10]”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [10] source
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenAge and smoking status were used to group-match cases with controls.
“Cases and controls were group-matched by age and smoking status.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningAngioedema could be influenced by variation in enzymes that break down bradykinin (ACE, APP, NEP) or substance P (ACE, DPPIV, NEP), as well as in bradykinin receptors (B1, B2) and the substance P receptor (NK1).
“Thus, variation in enzymes responsible for the inactivation of bradykinin (ACE, APP, neutral endopeptidase P (NEP)) or substance P (ACE, DPPIV, NEP), or for the receptor targets of bradykinin (B1 and B2) and substance P (NK1) could contribute to angioedema.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataAge did not differ across genotype groups in either women or men.
“Age was similar among genotype groups (58.2 ± 13.3, 59.2 ± 11.7, 58.1 ± 12.2 years in C/C, C/A and A/A) women and (56.5 ± 11.7, 54.8 ± 10.9 years in C/ and A/) men.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductown dataXPNPEP2 C-2399A genotype was not associated with diabetes or smoking prevalence (both P>0.2).
“There was no association between XPNPEP2 C-2399A genotype and the prevalence of diabetes or smoking (both P>0.2).”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataAmong women, genotype frequencies conformed to Hardy-Weinberg equilibrium.
“Genotypes were in Hardy-Weinberg equilibrium among women.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationAnimal studies show that ACE inhibitor-associated angioedema can be prevented by blocking either B2 or NK1 receptors.
“In animal models, blocking either B2 or NK1 receptors prevents ACE inhibitor-associated angioedema.[7]”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [7] source
Probably not a substantial claim: may not pass S3 (load-bearing).
InterpretationreasoningSex hormones might regulate APP and thereby help explain why enzyme activity differs by gender.
“Regulation of APP by sex hormones could contribute to gender differences in enzyme activity.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
PremisecitationBradykinin raises vascular permeability through B2 receptor stimulation.
“Bradykinin increases vascular permeability by stimulating its B2 receptor.[23]”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [23] source
May combine two claims.
PremisecitationBradykinin causes nerve terminals to release substance P, which then raises vascular permeability by activating NK1 receptors.
“Bradykinin also stimulates the release of substance P from nerve terminals, and substance P increases vascular permeability via NK1 receptor stimulation.[23]”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [23] source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationXPNPEP2 is not subject to X-inactivation.
“In addition, a prior study suggests XPNPEP2 escapes X-inactivation.[21]”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [21] source
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Results attribute the control sampling plan to cases
MinorThe methods say controls were pre-specified to have a 50% female composition, whereas the results attribute that specification to cases. The results also report that 56% of cases were women.
“As specified in the methods, cases were pre-specified to be 50% black American and 50% female and matched for age and smoking status. Fifty-six percent of cases were women.”
“Controls were pre-specified to be 50% black American, 50% white American and 50% female, 50% male. Cases and controls were group-matched by age and smoking status.”
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- Authors
- Woodard-Grice, A. V., Lucisano, A. C., Byrd, J. B., Stone, E. R., Simmons, W. H., & Brown, N. J.
- Affiliations
- Vanderbilt University (US)
- Loyola University Chicago (US)
- Venue
- Pharmacogenetics and Genomics
- Published
- 2010-09
- Volume
- 20
- Issue
- 9
- Pages
- 532-536
- ISSN
- 1744-6872 (ISSN-L)
- PMC
- PMC2945219
- OpenAlex
- W1964792142
- Semantic Scholar
- 9cc2cde5712dc64f8ebf883d2a187769bb0ab594
- Cited by
- 92
- References
- 25
- Citations by year
- 2025: 3 · 2024: 4 · 2023: 5 · 2022: 7 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 5 · 2017: 11 · 2016: 13 · 2015: 7 · 2014: 8 · 2013: 6 · 2012: 5
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pharmacogenetics and Genomics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL079184, R01HL079184)
- National Institute of General Medical Sciences (GM007569, T32GM007569)
- National Center for Research Resources (UL1RR024975)
- Topics
- Health Sciences › Medicine › Genetics › Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
- Keywords
- ACE inhibitors, aminopeptidase P, sex differences, racial differences, bradykinin, genetic susceptibility, pharmacogenetics
- MeSH terms
- Aminopeptidases, Angioedema, Angiotensin-Converting Enzyme Inhibitors, Female, Gene Frequency, Humans, Male, Middle Aged, Sex Characteristics, Multivariate Analysis, Logistic Models, Case-Control Studies, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Genetic Association Studies
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