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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paroxystic vasomotor skin manifestations are provoked by various etiologies. Widespread or generalized vasomotor skin manifestations may be induced by a physiological reaction (emotinal flushing), by a drug (vasodilator drugs, antabuse, antidiabetic, sulfonamides), by a discharge of histamine (urticaria, mastocytosis) or by an hypersecretion of serotonin (dumping-syndrome, carcinoid syndrome). They may be caused by an endocrinopathy (menopause, hyperthyroidism, hypoglycaemia, medullary thyroid carcinoma, pheochromocytoma, endocrine pancreas, carcinoma). More rarely vasomotor troubles happen in homocystinuria, inhalation of a toxic (trichlorethylen, calcic cyanamid) and exceptionally in some immunohaematologic diseases. Main localized vasomotor skin manifestations observed are dermographism, facial flushing (Sluder's syndrome, cluster headaches, Frey's syndrome, Riley-Day's syndrome) and acral syndromes (Raynaud's phenomenon, erythromelalgia).
Ann Dermatol Venereol 1978 Dec
PMID:[Paroxystic vasomotor skin manifestations (author's transl)]. 8 21

Scombroid fish poisoning, one of the most common adverse reactions to fish, is also probably one of the most common causes of a flushing syndrome. The reaction usually involves fishes of the Scombridae family but, in Hawaii, the reaction is most often due to mahimahi (Coryphaena hippurus). Onset of the reaction is usually abrupt and commonly associated with a prominent flush resembling a sunburn. Headache, tachye to a toxin with histamine-like properties, which is formed because improper refrigeration enables endogenous bacteria to decarboxylate histidine normally present in dark-meat fishes. Symptoms are usually promptly relieved by parenteral antihistamine therapy.
Arch Dermatol 1979 Aug
PMID:Flushing syndrome due to mahimahi (scombroid fish) poisoning. 57 60

Oral administration of niacin (nicotinic acid) at pharmacologic doses that reduce serum cholesterol levels induces intense flushing in humans. We have recently shown that the vasodilation following ingestion of niacin is due to the release of prostaglandin (PG) D2. However, the site from which PGD2 is released is not known. It has previously been shown that topical application of methylnicotinate causes local cutaneous erythema. Thus, we investigated whether topical methylnicotinate causes a release of PGD2 locally from skin and the possibility that skin may be a major contributor to the release of PGD2 when niacin is administered by mouth. Topical administration of methylnicotinate (10(-1) M) to the forearms of human volunteers resulted in 58- to 122-times increases in levels of PGD2 and 25- to 33-times increases in levels of the metabolite of PGD2, 9 alpha,11 beta-PGF2, in blood drawn from the antecubital vein draining the treated sites. Increased levels of PGD2 and 9 alpha,11 beta-PGF2 were not found in blood drawn simultaneously from veins in the contralateral arm, indicating that the PGD2 was released from the site of methylnicotinate application. The release of PGD2 in response to topically applied methylnicotinate occurred in a dose-dependent manner over the concentration range of 10(-3) to 10(-1) M. The release of PGD2 was not accompanied by a release of histamine, suggesting that the release of PGD2 was not from the mast cell. Following oral ingestion of niacin, levels of PGD2 in superficial venous blood draining the skin were 14 to 1200 times higher than the level in arterial blood supplying the skin of the same arm. This finding indicates that the skin is a major site from which PGD2 is released following oral ingestion of niacin. These studies thus indicate that the cutaneous vasodilation that occurs following oral administration of niacin is primarily due to a release of PGD2 from a niacin responsive cell that resides in the skin.
J Invest Dermatol 1992 May
PMID:Identification of skin as a major site of prostaglandin D2 release following oral administration of niacin in humans. 137 50

Rosacea usually occurs in adults and rarely has been noted in children. We recently observed three children with rosacea, all of whom responded dramatically to systemic and topical antibiotics. Rosacea in childhood must be distinguished from other erythematous facial disorders, most commonly acne, granulomatous perioral dermatitis, and sarcoidosis. The distribution of facial lesions; the presence of telangiectasias, flushing, and pustules; and the appearance of lesional biopsy sections and the ocular lesions, if present, allow differentiation of rosacea from other facial eruptions.
Pediatr Dermatol 1992 Mar
PMID:Childhood rosacea. 153 54

The most frequent site of organ involvement in patients with any form of mastocytosis is the skin. Cutaneous expressions include urticaria pigmentosa, mastocytoma, diffuse and erythrodermic cutaneous mastocytosis, and telangiectasia macularis eruptiva perstans. The cutaneous lesions tend to appear early in life. Although urticaria pigmentosa has been reported in 12 pairs of twins and one set of triplets, the majority of affected individuals have no familial association. Most patients with systemic mastocytosis have skin lesions; however, an occasional patient will have systemic disease with no other skin features than flushing. In lesional cutaneous sites and in non-lesional skin, there is an increase in the number of mast cells. Electron microscopy shows quantitative differences between lesional skin mast cells from patients with and without systemic disease. The mast cells from adult patients with systemic disease have a larger mean cytoplasmic area, nuclear size, and granule diameter. The granules contain predominantly grating/lattice structures. The cutaneous mast cells contain tryptase and chymase. They retain their functional reactivities to relevant secretory stimuli, such as C3a, morphine sulfate, and calcium ionophore A23187. Lesional skin contains histamine, leukotriene B4, prostaglandin D2, 5-hydroxyeicosatetraenoic acid, platelet-activating factor, and heparin. Treatment of the cutaneous manifestations includes the use of H1 and H2 antihistamines, oral disodium cromoglycate, psoralens plus ultraviolet A photochemotherapy, and potent topical corticosteroid preparations.
J Invest Dermatol 1991 Mar
PMID:The skin in mastocytosis. 167 36

Cyclosporine is known to be effective in the treatment of psoriasis. In this study, we have used oral cyclosporine (6 mg/kg per day) given for 5 to 30 weeks to 24 patients for the treatment of 12 different dermatoses. Patients with the following diseases demonstrated a marked response or total clearing: 1 patient each with pyoderma gangrenosum, pityriasis lichenoides chronica, and psoriasis of the acrodermatitis continua of Hallopeau type. Moderate to marked response occurred in both patients with epidermolysis bullosa acquisita and the patient with hidradenitis suppurativa. Minimal to moderate responses were obtained in both patients with granuloma annulare, 1 of 2 with acrodermatitis continua of Hallopeau, both patients with Darier's disease, and 1 of 6 patients with vitiligo. Little or no response was noted in both patients with sarcoidosis, all 3 patients with pityriasis rubra pilaris, 5 of 6 patients with vitiligo, 1 patient with pemphigus foliaceous, and 1 with pemphigus vulgaris. Clinical side effects were mild and transient and included dysesthesia, fatigue, hypertrichosis, nausea, and flushing. The most frequent clinically significant abnormalities were hypertension and renal dysfunction, with all factors normalizing within 1 month of discontinuation of cyclosporine therapy.
Arch Dermatol 1990 Mar
PMID:Oral cyclosporine in the treatment of inflammatory and noninflammatory dermatoses. A clinical and immunopathologic analysis. 217 58

We studied four patients (a mother, her two daughters, and her son) with bullous mastocytosis, or diffuse cutaneous mastocytosis, whose genetic inheritance suggested an autosomal dominant pattern. The clinical characteristics included extensive bullae, numerous urticaria, pruritus, flushing, and pseudolichenified skin over all body surfaces without systemic organ involvement. The histopathologic findings disclosed a pronounced accumulation of mast cells in the dermis. Electron microscopic studies of lesional skin obtained in infancy showed round or spindle-shaped mast cells with numerous fingerlike villous protrusions. The cytoplasmic granules varied in size and shape, and the appearance of degranulation was markedly noted. In the adult, most mast cells had markedly decreased numbers of granules and cytoplasmic villi. Some cells displayed degenerative or necrotic appearances. These findings correlated well with the clinical course of these cases, which improved spontaneously over time.
Arch Dermatol 1990 Nov
PMID:The familial occurrence of bullous mastocytosis (diffuse cutaneous mastocytosis). 224 Dec 1

A 43-year-old miner of the Donetsk coal fields is described, who developed in a month after a microinjury of the skin of the thoracic left side an intumescence and skin reddening. Later an agglomeration of nodules formed there with small ulcers regularly appearing, that did not heal for a long time. Histologic and bacteriologic analysis confirmed chromomycosis. The disease focus was resected. No recurrences were recorded in the following 8 months. This observation points to a wider prevalence of chromomycosis in a nonendemic area, the European part of the USSR, than it is reported in literature.
Vestn Dermatol Venerol 1990
PMID:[A case of chromomycosis in a nonendemic region]. 228 67

We have recently shown that the novel neuropeptide calcitonin gene-related peptide, CGRP, is a potent vasodilator. In this paper we report a detailed study of the effects of CGRP in human skin. CGRP induces a clearly defined, long-lasting erythema. We have measured the effect of CGRP on blood flow in human skin using a laser Doppler technique and have demonstrated increased local blood flow that persists for a number of hours. We compared the response of CGRP with other known vasodilators [histamine, prostaglandin (PG) E2, PGI2, substance P, and vasoactive intestinal peptide (VIP)] in the skin, and in all subjects the erythema induced by CGRP was more persistent than that induced by the other mediators tested. Except at high doses the local vasodilatation induced by CGRP was not associated with a wheal and flare as seen with histamine, substance P, and VIP. CGRP is an extremely potent vasodilator and if released into the circulation, or locally from peripheral nerve endings, it could have a role in the regulation of blood flow in both physiologic and pathologic conditions; CGRP may be the endogenous mediator of the flare in the triple response. A deficiency in CGRP secretion or action could be an important component of peripheral vascular disease. Some flushing reactions (e.g., those associated with medullary thyroid carcinoma) may result from circulating CGRP.
J Invest Dermatol 1986 Oct
PMID:Potent vasodilator activity of calcitonin gene-related peptide in human skin. 242 85

The effect of nadolol versus placebo on both flushing provoked in a laboratory setting and spontaneous flushing was studied in 15 patients with erythematous telangiectatic rosacea. The intensity of the flushing reactions was assessed in the laboratory by the cutaneous perfusion index method with laser-Doppler velocimetry. No effect of nadolol on the flushing reactions provoked in the laboratory was detected.
J Am Acad Dermatol 1989 Feb
PMID:Effect of nadolol on flushing reactions in rosacea. 252 41


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