By Esen Özkaya, Kurtuluş Didem Yazganoğlu
Adverse cutaneous drug reactions (ACDR) are one of the so much widespread occasions in sufferers receiving drug treatment. Cardiovascular (CV) medicines are an enormous staff of substances with strength possibility of constructing ACDR specially in aged as advertising of extra new medicinal drugs and their prescription proceed to extend. despite the fact that, like with so much different medicinal drugs the precise prevalence of cutaneous unwanted effects from CV medications is tough to estimate because of sporadic reporting. furthermore, a competent designation of a definite drug because the reason for a undeniable form of response can hardly ever be made. except the well known angioedema/urticaria from ACE inhibitors, lichen planus / lichenoid response from beta adrenergic blockers and photosensitivity from thiazid diuretics, ACDR from CV medications may be visible in a large spectrum extending to infrequent yet life-threatening stipulations reminiscent of erythroderma, Stevens-Johnson syndrome, poisonous epidermal necrolysis or drug allergic reaction syndrome. during this complete evaluation, the said forms of ACDR to CV medications could be mentioned in line with drug type and the kind of dermatologic response with specified emphasize on cross-reactions and the position of patch checking out in diagnosis.
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Additional info for Adverse Cutaneous Drug Reactions to Cardiovascular Drugs
The latency period between exposure and onset of a bullous drug eruption may be prolonged, and the diagnosis might be therefore challenging. The in vitro interferongamma (IFN-gamma) release from lymphocyte test  and immunostaining with antibodies to desmoglein were found useful for diagnosing drug-induced pemphigus, the latter suggested as an indicator of a good prognosis . Drug-induced linear IgA dermatosis was found to be more severe than the spontaneous form in a study, with lesions mimicking TEN .
Apart from the well-known hapten concept, the p-i concept is a novel pathomechanism that may be involved in direct recognition of some chemically inert molecules, particularly certain small-sized drugs, by T cells . A distinct clinical variant characterized by acute onset of diffuse bright-red erythema on the gluteal and anogenital area (Figs. 15), usually demarcated by sharp, well-defined borders, resembling the hairless red rump of the baboons (African Old World monkeys belonging to the genus Papio), is known as Baboon syndrome (BS) .
Drug-induced SCLE may present with annular–polycyclic, papulosquamous, or psoriasiform lesions mainly on the upper trunk with involvement of the lower legs that are usually spared in idiopathic SCLE . ANA, anti-Ro/SSA, anti-La/SSB antibodies may be found positive , whereas antihistone antibodies might be absent . Among the cardiovascular drugs, thiazide diuretics, CCBs, and statins have been more commonly implicated to trigger SCLE [67, 68]. Recently, we saw a patient with SCLE-like eruption possibly induced by filgrastim, a granulocyte colony-stimulating factor  (Figs.
Adverse Cutaneous Drug Reactions to Cardiovascular Drugs by Esen Özkaya, Kurtuluş Didem Yazganoğlu