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PubMed · 14758392

Amlodipine associated hyperpigmentation.

Zulal Erbagci
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Abstract

Amlodipine is a potent peripheral and coronary vasodilator with high selectivity for vascular smooth muscle, and is widely used in mild to moderate hypertension, chronic stable angina and vasospastic angina. Its most prevalent side effects are peripheral edema, flushing and headache. Cutaneous adverse reactions associated with amlodipine have been rarely reported. Herein, a male patient is described to develop oral mucosal and cutaneous hyperpigmentation one year after starting amlodipine, which became more noticeable with time. Although cutaneous hyperpigmentation was most prominent on the photoexposed areas, there was no history of previous photosensitivity, pruritus or flushing. To our knowledge, no case of oral and cutaneous hyperpigmentation associated with amlodipine has been formally reported up to date.

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AmlodipineBiopsy, NeedleCalcium Channel BlockersHumansHyperpigmentationHypertensionImmunohistochemistryMaleMiddle AgedMouth MucosaPrognosisRare DiseasesRisk AssessmentSeverity of Illness IndexTurkeyCase ReportsJournal Article

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Zulal Erbagci. 2004. Amlodipine associated hyperpigmentation.. https://pubmed.ncbi.nlm.nih.gov/14758392/

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PubMed2004

Influence of serum cholesterol on atherogenesis and intimal hyperplasia after angioplasty: inhibition by amlodipine.

The objectives of the present study were to determine whether serum hypercholesterolemia (HC) promotes the development of spontaneous and angioplasty-induced lesions and whether amlodipine inhibits these lesions and cellular processes underlying their genesis. Rabbits were fed normal, 0.5%, or 2% cholesterol diets for 9 wk, which resulted in the development of increasing HC. After week one, balloon dilation of the abdominal aorta was performed while the thoracic aorta was not disturbed and monitored for the development of spontaneous lesions. Lesion size increased with the degree of HC and was accompanied by increased collagen synthesis and smooth muscle cell (SMC) proliferation at each site. Amlodipine (5 mg/kg p.o.) inhibited lesion size by 50% (P < 0.01) at both sites in cholesterol-fed animals but not at angioplasty sites in animals on a normal diet. Local collagen synthesis was inhibited at both sites by amlodipine in the diet animals. The increase in HC was accompanied by a 1.7-fold increase in basal Ca2+ uptake in SMCs in the thoracic aorta, which was not altered by amlodipine, nifedipine, Ni2+, or La3+, revealing an uninhibitable calcium leak during atherogenesis. In culture, cholesterol enrichment increased SMC proliferation, collagen synthesis, and the secretion of a soluble SMC mitogen, which were inhibited by amlodipine (10(-9) M). Finally, in SMC membranes, amlodipine uniquely restored the cholesterol-expanded membrane bilayer width without any effect on membrane fluidity. This study establishes a causal role between serum HC and the development of spontaneous and angioplasty-induced lesions and the ability of amlodipine to disrupt this action by a novel remodelling action on the SMC membrane.

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