benazepril and Hyperplasia

We report the case of a 42 year old patient who developed chronic hyperplastic laryngitis during treatment with the angiotensin converting enzyme-inhibitor Cibacen 10. A severe cough and vocal restrictions with hoarseness were only incompletely cured after changing this anti-hypertensive medication to a adrenergic blocker, combined with a vocal rest and anti-inflammatory inhalation. Therefore we performed a laryngoscopy under general anesthesia and excised the swelling of the vocal cords. Additionally, voice therapy was prescribed and complete restitution achieved. Although hoarseness is documented as a potential side effect of angiotensin converting enzyme-inhibitors, morphological alterations in the vocal cords have not been linked to this type of drug. In our case, prolonged medication with Cibacen 10 led to chronic hyperplastic laryngitis. Initial coughing might have induced the trauma of the epithelium of the vocal cords. Due to the morphological alterations to the vocal cords the patient developed additional functional dysphonia.

Topics: Adult; Angiotensin-Converting Enzyme Inhibitors; Benzazepines; Chronic Disease; Humans; Hyperplasia; Hypertension; Laryngitis; Male; Treatment Outcome; Vocal Cords

We investigated the role of vascular angiotensin-converting enzyme (ACE) activity, cell proliferation, and the effect of different doses of benazepril on intimal hyperplasia after angioplasty in rabbits. Angioplasty was performed in all left iliac arteries in 28 rabbits. Benazepril was administrated to treatment groups in low (1 mg/kg/day) and high (10 mg/kg/day) doses. Two weeks after angioplasty, vascular ACE activity of the angioplasty subgroup was significantly higher than that of the nonangioplasty subgroup (from 0.44 to 1.19 nmol His-Leu/mg/min; p < 0.01). Strong correlation was demonstrated between vascular ACE activity and intimal area (r = 0.708; p < 0.01). Suppression of vascular ACE activity (59% decrease) and inhibition of intimal hyperplasia (43% decrease) was observed in the high-dose subgroup compared with the angioplasty subgroup without drug intervention (p < 0.01). But in the low-dose subgroup, the level of vascular ACE activity decreased moderately (24.4%; p < 0.05), and the intimal area did not alter significantly. Both the low and high dosage of benazepril resulted in a significant decrease in blood pressure (31 and 44 mm Hg, respectively). Striking correlation was displayed between proliferating-cell nuclear antigen (PCNA)-positive cell percentage and intimal area (r = 0.716; p < 0.01). These results indicated that with excessive expression of vascular ACE, intimal cellular proliferation may play a potential role in restenosis after angioplasty. Benazepril could inhibit intimal hyperplasia by suppressing vascular-tissue ACE.

Topics: Analysis of Variance; Angioplasty, Balloon, Coronary; Angiotensin-Converting Enzyme Inhibitors; Animals; Benzazepines; Biomarkers; Blood Pressure; Cell Division; Coronary Disease; Coronary Vessels; Disease Models, Animal; Hyperplasia; Male; Peptidyl-Dipeptidase A; Proliferating Cell Nuclear Antigen; Rabbits; Tunica Intima