scholarly journals ACE Inhibitor-Induced Angioedema of the Intestine: Case Report, Incidence, Pathophysiology, Diagnosis and Management

2001 ◽  
Vol 15 (12) ◽  
pp. 827-832 ◽  
Author(s):  
Gavin Oudit ◽  
Nigel Girgrah ◽  
Johane Allard
Keyword(s):  
Case Report ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Management Strategies ◽  
Angiotensin Ii Receptor ◽  
Radiological Investigation ◽  
Abdominal Symptoms ◽  
Acute Exacerbations ◽  
Gastrointestinal Complaints ◽  
Considerable Morbidity

A case report of fosinopril-induced angioedema of the intestine with a chronic course accompanied by multiple acute exacerbations is described. Angiotensin-converting enzyme (ACE) inhibitor-induced angioedema of the intestine (AIAI) occurs in a minority of patients taking an ACE inhibitor. The clinical presentation encompasses acute abdominal symptoms, pronounced bowel edema and ascites with occasional facial and/or oropharyngeal swelling. AIAI is diagnosed based on the temporal relationship between the symptomatic presentation and drug use, absence of alternative diagnoses including other causes of angioedema, and the prompt resolution of symptoms upon discontinuation of the ACE inhibitor. Prompt radiological investigation (abdominal computerized tomography and/or ultrasound) is critical in making an early diagnosis and in preventing unnecessary surgical intervention. There is a female predominance of AIAI, which may reflect the interaction of estradiol with the various pathways involved in the pathophysiology of AIAI. Management of AIAI consists mainly of conservative measures and discontinuation of the ACE inhibitor. Angiotensin II receptor antagonists should not be considered as appropriate alternatives. Awareness and knowledge of AIAI are important because of the increasing use of ACE inhibitors, current delays in making the diagnosis, obvious management strategies once the diagnosis is made and the dysutility of alternative diagnoses, which may lead to considerable morbidity. AIAI must be considered in patients taking ACE inhibitors who develop gastrointestinal complaints irrespective of the duration of the therapy.

Overcoming Cough and Angioedema: Advocating for the Use of ARBs Over ACE Inhibitors

2021 ◽  
pp. 106002802110299
Author(s):  
Melanie Lam ◽  
Anelsa Beqo ◽  
Ricky Thumar
Keyword(s):  
Angiotensin Ii ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Risk Groups ◽  
Clinical Inertia ◽  
Comparable Efficacy ◽  
Converting Enzyme ◽  
Angiotensin Ii Receptor ◽  
Black Patients ◽  
Receptor Blockers

Angiotensin II receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors have comparable efficacy, but ARBs have a preferential safety profile with particular regard to cough and angioedema. Although guidelines have historically advocated for ACE inhibitor use before ARBs simply because of earlier market entry, data accumulation, and generic availability, updated verbiage advises an “ACE inhibitor or ARB” recommendation, as opposed to the classic “ACE inhibitor then ARB” approach. Despite these updates, clinical inertia in favor of ACE inhibitor use before ARBs overwhelmingly remains. Prescribers and educators should consider an “ARBs only” mentality, especially in high angioedema-risk groups such as black patients.

scholarly journals An unusual presentation of ACE inhibitor-induced visceral angioedema

2019 ◽  
Vol 12 (9) ◽  
pp. e230865 ◽  
Author(s):  
Amanda Jayne Krause ◽  
Naiya Balubhai Patel ◽  
Jennifer Morgan
Keyword(s):  
Abdominal Pain ◽  
Case Report ◽  
Small Bowel ◽  
Ct Scan ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Unusual Presentation ◽  
First Episode ◽  
Ascetic Fluid

ACE inhibitors (ACEi) are common anti-hypertensive drugs that can cause angioedema. Though classic, or facial angioedema is rare, visceral angioedema is even less common. When angioedema occurs, it typically presents early, within 30 days of initiating therapy. Visceral angioedema most commonly presents with nausea, emesis, abdominal pain and diarrhoea, and thus is often mistaken for an episode of gastroenteritis. When a CT scan is obtained, it typically shows characteristic findings, including ascetic fluid, mild mesenteric oedema and thickening of the small bowel. In this case report, we present a patient who did not experience her first episode of visceral angioedema until after she had been on ACEi therapy for 5–7 years. In addition, she experienced recurrent episodes of visceral angioedema that were separated by approximately 4 years at a time. Both of these features make for a particularly unique presentation.

Combination ACE Inhibitors and Angiotensin II Receptor Blockers for Hypertension

2003 ◽  
Vol 37 (6) ◽  
pp. 886-889 ◽  
Author(s):  
Patrick M Finnegan ◽  
Brenda L Gleason
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Combination Therapy ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Renin Angiotensin System ◽  
Reduce Blood Pressure ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor

OBJECTIVE: To review data concerning combined angiotensin-converting enzyme (ACE) inhibitor and angiotensin II receptor blocker (ARB) therapy for hypertension. DATA SOURCES: MEDLINE (1966–April 2003), IPA (1970–April 2003), and EMBASE (1974–April 2003) with search terms of ACE inhibitor, angiotensin receptor blocker, essential hypertension, and combination therapy. DATA SYNTHESIS: ACE inhibitors provide incomplete blockade of the renin–angiotensin system, sometimes leading to loss of blood pressure control. Addition of ARBs may in theory further reduce blood pressure. Studies of combined ACE inhibitor and ARB therapy for managing hypertension were evaluated. CONCLUSIONS: While studies have shown statistically significant blood pressure reductions with ACE/ARB combination therapy, clinical significance is lacking. Further trials are needed before routine use of the combination can be recommended.

Malignant Primary Hypertension in Pregnancy Treated with Lisinopril

2000 ◽  
Vol 34 (2) ◽  
pp. 180-182 ◽  
Author(s):  
Antony J Tomlinson ◽  
James Campbell ◽  
James J Walker ◽  
Colin Morgan
Keyword(s):  
Renal Failure ◽  
Case Report ◽  
Necrotizing Enterocolitis ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Neonatal Outcome ◽  
First Trimester ◽  
Successful Outcome ◽  
Chronic Hypertension ◽  
In Pregnancy

OBJECTIVE: To report a case of a patient treated with an angiotensin-converting enzyme (ACE) inhibitor with a good neonatal outcome. CASE REPORT: A 39-year-old African-Caribbean patient who had chronic hypertension presented at 18 weeks' gestation with acute hypertension. She was being treated for chronic hypertension with lisinopril, but had self-discontinued treatment. Attempts to control her hypertension with labetolol, nifedipine, and methyldopa were ineffective. She was therefore offered termination of pregnancy so treatment with lisinopril could be restarted. The patient elected to continue with the pregnancy in spite of the fetal risks associated with the use of an ACE inhibitor. She was delivered of a girl at 26 weeks' gestation. The baby initially had renal failure and also developed acute necrotizing enterocolitis. The renal failure improved simultaneously with the latter complication, and it is postulated that there was enteric excretion of lisinopril. The baby was discharged home on day 102 with no further complications. DISCUSSION: ACE inhibitors are acceptable medications to use in the first trimester of pregnancy; however, fetal malformations and neonatal complications have been associated with their use later in pregnancy, and they have a perinatal mortality rate of 97/1000. Lisinopril is excreted in urine and feces unchanged, and its half-life is prolonged in anuric neonates. Peritoneal dialysis eliminates lisinopril; however, this neonate improved after treatment for necrotizing enterocolitis and simultaneous improvement in bowel function. CONCLUSIONS: ACE inhibitors should not be used in pregnancy beyond the end of the first trimester. In exceptional cases, they may be indicated for the control of severe hypertension when the patient is refractory to other medications. The patient should be fully counseled about the adverse effect profile and neonatal outcome. This case report documents a successful outcome for mother and baby in these circumstances.

ACE Inhibitor—Induced Bronchial Reactivity in Patients with Respiratory Dysfunction

2002 ◽  
Vol 36 (6) ◽  
pp. 1058-1067 ◽  
Author(s):  
Kathleen A Packard ◽  
Richard L Wurdeman ◽  
Amy J Arouni
Keyword(s):  
Heart Failure ◽  
Chronic Obstructive Pulmonary Disease ◽  
Congestive Heart Failure ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Chronic Obstructive ◽  
Angiotensin Ii Receptor ◽  
Obstructive Pulmonary Disease ◽  
Bronchial Responsiveness ◽  
Increased Risk

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors are often associated with an increased incidence of cough and bronchial responsiveness that may cause further deterioration of patients with impaired pulmonary function. OBJECTIVE: To review the available literature on the incidence of cough and bronchial responsiveness associated with ACE-inhibitor therapy in patients with asthma, chronic obstructive pulmonary disease (COPD), and congestive heart failure (CHF). DATA SOURCES: Literature was accessed through MEDLINE (1985–September 2001). Key search terms included cough, bronchospasm, asthma, congestive heart failure, chronic obstructive pulmonary disease, ACE inhibitors, and angiotensin II receptor blockers. DATA SYNTHESIS: The literature reports several cases of increased bronchial responsiveness associated with ACE inhibitors. Larger, controlled studies evaluating the increased risk in patients with pulmonary dysfunction are limited. Data from these trials are summarized in this article. CONCLUSIONS: The literature shows that patients with primary airway disease such as asthma and COPD are not at an increased risk of developing cough or bronchoconstriction as a result of ACE-inhibitor therapy. Despite the ability of ACE inhibitors to improve exercise tolerance, perfusion, and gas transfer, patients with CHF may be at higher risk of developing cough than the general population. Whether this cough is attributed to ACE inhibition or increased left-ventricular dysfunction remains uncertain. If increased bronchial responsiveness does occur, angiotensin II receptor antagonists are another reasonable option.

scholarly journals A clinical dose of angiotensin-converting enzyme (ACE) inhibitor and heterozygous ACE deletion exacerbate Alzheimer's disease pathology in mice

2019 ◽  
Vol 294 (25) ◽  
pp. 9760-9770 ◽  
Author(s):  
Shuyu Liu ◽  
Fujiko Ando ◽  
Yu Fujita ◽  
Junjun Liu ◽  
Tomoji Maeda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Angiotensin Converting Enzyme ◽  
Amyloid Precursor Protein ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Precursor Protein ◽  
Causative Role ◽  
Converting Enzyme ◽  
Clinical Dose

Inhibition of angiotensin-converting enzyme (ACE) is a strategy used worldwide for managing hypertension. In addition to converting angiotensin I to angiotensin II, ACE also converts neurotoxic β-amyloid protein 42 (Aβ42) to Aβ40. Because of its neurotoxicity, Aβ42 is believed to play a causative role in the development of Alzheimer's disease (AD), whereas Aβ40 has neuroprotective effects against Aβ42 aggregation and also against metal-induced oxidative damage. Whether ACE inhibition enhances Aβ42 aggregation or impairs human cognitive ability are very important issues for preventing AD onset and for optimal hypertension management. In an 8-year longitudinal study, we found here that the mean intelligence quotient of male, but not female, hypertensive patients taking ACE inhibitors declined more rapidly than that of others taking no ACE inhibitors. Moreover, the sera of all AD patients exhibited a decrease in Aβ42-to-Aβ40–converting activity compared with sera from age-matched healthy individuals. Using human amyloid precursor protein transgenic mice, we found that a clinical dose of an ACE inhibitor was sufficient to increase brain amyloid deposition. We also generated human amyloid precursor protein/ACE+/− mice and found that a decrease in ACE levels promoted Aβ42 deposition and increased the number of apoptotic neurons. These results suggest that inhibition of ACE activity is a risk factor for impaired human cognition and for triggering AD onset.

scholarly journals Pneumatosis intestinalis in a radioactive iodine-refractory metastasic thyroid papillary carcinoma with BRAFV600E mutation treated with dabrafenib–trametinib: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
M. C. Martín-Soberón ◽  
S. Ruiz ◽  
G. De Velasco ◽  
R. Yarza ◽  
A. Carretero ◽  
...  
Keyword(s):  
Case Report ◽  
Papillary Carcinoma ◽  
Radioactive Iodine ◽  
Specific Treatment ◽  
Pneumatosis Intestinalis ◽  
Thyroid Papillary Carcinoma ◽  
Intestinal Pneumatosis ◽  
Abdominal Symptoms ◽  
Positron Emission ◽  
Thyroid Papillary

Abstract Background Pneumatosis intestinalis (PI) is a rare entity which refers to the presence of gas within the wall of the small bowel or colon which is a radiographic sign. The etiology and clinical presentation are variable. Patients with PI may present either with chronic mild non-specific symptoms or with acute abdominal pain with peritonitis. Some cases of intestinal pneumatosis have been reported as adverse events of new oncological treatments such as targeted therapies that are widely used in multiple tumors. Case presentation A 59-year-old caucasian female with radioactive iodine-refractory metastatic thyroid papillary carcinoma with BRAFV600E mutation was treated with dabrafenib and trametinib as a compassionate use. After 4 months treatment, positron emission tomography–computed tomography (PET–CT) showed PI. At the time of diagnosis, the patient was asymptomatic without signs of peritonitis. The initial treatment was conservative and no specific treatment for PI was needed. Unfortunately, after dabrafenib–trametinib withdrawal, the patient developed tumor progression with significant clinical worsening. Conclusions This case report is, in our knowledge, the first description of PI in a patient treated with dabrafenib–trametinib. Conservative treatment is feasible if there are no abdominal symptoms.

The role of cardio-protective agents in breast cancer patients to prevent anthracycline induced cardiotoxicity: a systematic review and network meta-analysis

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P Jeyaprakash ◽  
S Sangha ◽  
K Robeldo ◽  
K Ellenberger ◽  
S Sivapathan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
High Risk ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Beta Blockers ◽  
Meta Analysis ◽  
Risk Of Bias ◽  
Breast Cancer Patients ◽  
Protective Agents ◽  
Cardio Protection

Abstract Background Anthracycline (ANT)-based chemotherapy for breast malignancies have significantly improved cancer outcomes. However, the cardiotoxicity induced by ANTs in the breast cancer population has increased major adverse cardiac events. While randomised controlled trials (RCTs) have explored different primary preventative agents to confer cardio-protection pre chemotherapy, comparisons between agents has been limited. It is unclear which drug is the most efficacious in preserving Left Ventricular Ejection Fraction (LVEF) amongst this population. Purpose To perform a network meta-analysis of RCTs comparing the impact on LVEF of various prophylactic cardio-protective agents, when prescribed to breast cancer patients prior to ANT-based chemotherapy. Methods Two independent authors performed a literature search as per the PRISMA guidelines using four databases (CENTRAL, Cochrane Reviews, MEDLINE, SCOPUS), to find RCTS evaluating cardio protective agents. The trial population was limited to patients with breast cancer without prior ANT exposure. Trials were only included if the cardio-protective agents were commenced prior to ANT dosing. The assessed outcome was a mean change in LVEF pre and post ANT dosing, compared to placebo prevention. Extracted data included age, ANT dose, and LVEF pre and post chemotherapy. The Cochrane Risk of Bias tool was used to appraise included RCTs. Results From 2807 search results, we identified twelve RCTs which evaluated 1126 patients. Seven studies assessed beta-blockers alone and two assessed combination ACE inhibitors and beta blockers. Individual studies assessing ACE inhibitors, spironolactone or rosuvastatin alone were also included. All patients were female with an average age of 50.5 and average ANT dose of 412 mg/m2. Our network meta-analysis showed beta-blockers showed significant protection with higher LVEF than placebo by 2.38% [0.52, 4.25]. ACE inhibitors showed a similar magnitude of LVEF preservation 2.59% [−0.20, 5.38] but not statistically significant due to wider CI because of lower sample size (n=250). Spironolactone showed a statistically significant preservation in LVEF by 12.80% [3.44, 22.16], however this was based on a single study (n=83), with marked measurement bias and deviations from intended intervention. All included trials had an intermediate or high risk of bias, with marked heterogeneity in ANT dosing and LVEF monitoring. Conclusion Beta-blockers minimise LVEF decline when administered prior to anthracycline chemotherapy, compared against alternate agents. Data may be underpowered to demonstrate the benefit of ACE inhibitor and combination beta blocker/ACE inhibitor prescription. The quality of RCT data to date is limited by a high risk of bias and significant heterogeneity between RCA reporting. This analysis is likely to inform clinical practice, and allow clinicians to prescribe primary cardio-protection in patients at high risk of cardiotoxicity. Funding Acknowledgement Type of funding source: None

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