scholarly journals ACE-inhibitor induced angioedema masked by nephrotic syndrome

2016 ◽  
Vol 4 (16) ◽  
pp. 67
Author(s):  
Kenneth Iwuji ◽  
Hezekiah Sobamowo ◽  
James Tarbox ◽  
Rose Egbe

Angiotensin-converting enzyme (ACE) inhibitors are the leading cause of drug-induced angioedema in the United States because these drugs are widely prescribed for several common medical disorders. Angiotensin-converting enzyme inhibitors cause angioedema in 0.1 to 0.7 percent of recipients. When prescribing ACE-inhibitors to patients, angioedema should always be considered as a potential adverse reaction during treatment.

1993 ◽  
Vol 27 (3) ◽  
pp. 344-350 ◽  
Author(s):  
Wayne R. Melchior ◽  
Vinita Bindlish ◽  
Linda A. Jaber

OBJECTIVE: Diabetic nephropathy (DN) is a leading cause of kidney disease in the US. At least four factors influence whether people with diabetes will develop DN: (1) hypertension, (2) hyperglycemia, (3) dietary protein intake, and (4) intrarenal hemodynamics. The angiotensin-converting enzyme (ACE) inhibitors are known to affect blood pressure (BP) and intrarenal hemodynamics; thus, they may prevent the onset of DN or slow the decline in renal function once DN has been diagnosed. DATA SOURCES: English-language, controlled, and crossover studies published between 1973 and 1991 and indexed in MEDLINE under the headings diabetic nephropathies and angiotensin-converting enzyme inhibitors. MAIN OUTCOME MEASURES: The primary outcome indicators of interest were the effects of the ACE inhibitors captopril, enalapril, and lisinopril on BP control and urinary albumin excretion rate. CONCLUSIONS: ACE inhibitors delay the onset and slow the progression of DN in people with diabetes independent of BP effects. They also slow the progression of DN in people with diabetes who have poorly controlled hyperglycemia. The proper dose and time at which to initiate ACE inhibitor therapy to prevent the appearance of DN is not known. It is also not known how long the beneficial effects of ACE-inhibitor therapy persists as only two studies have followed patients for more than one year. Finally, large, long-term, controlled clinical trials are needed before ACE inhibitors can be considered for prophylactic use to prevent the onset and/or progression of DN.


2010 ◽  
Vol 1 (1) ◽  
pp. 62-64
Author(s):  
A. S Galyavich

The paper analyzes the use of angiotensin-converting enzyme (ACE) inhibitors in patients after prior myocardial infarction. It presents the data of controlled studies, which indicate that it is warranted to use ACE inhibitors to improve prognosis in patients. It is concluded that it is unreasonable for a physician not to prescribe ACE inhibitors to post-myocardial infarction patients with obvious or asymptomatic left ventricular dysfunction and to diabetic patients (if no contraindications).


Author(s):  
Suleiman Aminu ◽  
Mohammed Auwal Ibrahim ◽  
Abdullahi Balarabe Sallau

Abstract Background Recent COVID-19 outbreak has prompted the search of novel therapeutic agents to treat the disease. The initial step of the infection involves the binding of the virus through the viral spike protein with the host angiotensin converting enzyme 2 (ACE2). In this study, the interaction of some ACE or ACE2 inhibitors and their analogues as well as selected compounds with the viral spike protein as a strategy to hinder viral-ACE2 interaction were investigated. SARS-CoV-2 spike protein as well as the ligands were retrieved from protein databank and ChEBI database respectively. The molecules were prepared before initiating the virtual screening using PyRx software. Discovery studio was used to further visualize the binding interactions between the compounds and the protein. Results The ACE inhibitors and their analogues fosinopril (1-), fosinopril and moexipril have the best binding affinity to the protein with binding energies < − 7.0 kcal/mol while non-flavonoid stilben-4-ol binds with free binding energy of − 7.1 kcal/mol. Others compounds which belong to either the flavonoids, terpenes and alkaloid classes also have binding energies  < − 7.0 kcal/mol. Such high binding energies were enhanced via hydrogen bond (h-bond) interactions in addition to other interactions observed between the compounds and the amino acid residues of the protein. Conclusions The ACE inhibitors and their analogues as well as the selected compounds could serve as inhibitors of the spike protein as well as lead in drug discovery processes to target the SARS-CoV-2 virus.


1990 ◽  
Vol 18 (6) ◽  
pp. 1184-1185 ◽  
Author(s):  
MRIDULA CHOPRA ◽  
JOHN McMURRAY ◽  
JENNIFER STEWART ◽  
HENRY J. DARGIE ◽  
W. EWEN SMITH

Summary Free radical (FR) scavenging may be a therapeutically useful adjunctive property of angiotensin converting enzyme (ACE) inhibitors. In this study we have shown that SH-containing ACE inhibitors (captopril, epicaptopril, zofenopril) are potent FR scavengers at a concentration of 4 × 10-5m whereas non-SH ACE inhibitors (enalaprilat, quinaprilat and perindoprilat) have no FR-scavenging activity at this concentration. Furthermore, the SH-containing agents preferentially scavenged general radicals rather than superoxide radicals, i.e. suggesting that these drugs would be effective in quenching the culprit FR in ischaemia/reperfusion injury.


Author(s):  
Gawade Sonba. C ◽  
G.K. Dyade ◽  
Dr.S.G. Jadhav

A simple, economical and rapid by UV detector and PDA Detector was used for Estimation of Trandolapril and Verapamil in combination and other drugs in various Pharmaceutical formulation. Calcium channel blockers(CCBs) and angiotensin- converting enzyme (ACE) inhibitors  has been developed and fully validated by High performance liquid Chromatographic Methods. Calcium channel blockers (CCBs) or Calcium antagonists are among the most widely used drugs in cardiovascular medicine and hypertension also in angina. CCBs promote vasodilator activity by reducing calcium influx into vascular smooth muscle cells by interfering with calcium channels in the cell membrane. Trandolapril is a potent nonsulfhydryl and dicarboxyl containing Angiotensin converting inhibitor (ACE). Trandolapril used to treatment of hypertension appears to result the inhibition of tissue ACE activity and to improve survival myocardial infarction thereby reduce angiotensin II formation. It includes drugs like Trandolapril, Norverapamil, Nifedipine, Verapamil. This Review enlists different method Developed, Validated and determination of Calcium channel blockers and angiotensin- converting enzyme inhibitors Like, RP-HPLC, LC-MS/MS and HPLC UV- Spectophotometric method. This method was also validated for various validation terms indicates that precise, accurate, linearly, and limit of Detection and limit of Quantitation as per ICH guidelines. Keywords: HPLC Chromatography, Calcium Channel blocker, angiotensin- converting enzyme (ACE) inhibitors, Hypertension, Validation etc.


1996 ◽  
Vol 30 (11) ◽  
pp. 1242-1245 ◽  
Author(s):  
Peter V Dicpinigaitis

OBJECTIVE: To determine whether baclofen can suppress the cough induced by angiotensin-converting enzyme (ACE) inhibitors. DESIGN: Prospective, open-label, clinical trial of a 4-week course of low-dose oral baclofen (5 mg tid days 1–7, 10 mg tid days 8–28). SUBJECTS: Seven patients with severe, persistent ACE inhibitor-induced cough. SETTING: University-affiliated teaching hospital. MAIN OUTCOME MEASURES: Study participants kept daily diaries monitoring the frequency of cough during and after completion of baclofen therapy. RESULTS: All subjects demonstrated diminution of cough after initiation of baclofen. Initial improvement was noted by a mean of 4.0 days (range 3–6), and maximal improvement during treatment was achieved by a mean of 10.7 days (range 5–15). In addition, all subjects demonstrated persistent suppression of cough (range 25–74 d) after discontinuation of the study drug. CONCLUSIONS: Low-dose oral baclofen therapy caused a prolonged antitussive effect in all subjects without inducing any adverse reactions. Baclofen may offer an alternative to the discontinuation of ACE inhibitor therapy in patients for whom these drugs are required.


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