Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hereditary variations in the handling of a drug (pharmacogenetics) may result in adverse reactions in the skin. Such reactions could result from: (1) an inherited defect in enzymes responsible for drug metabolism (formation or detoxification of potentially toxic metabolites); (2) altered susceptibility of an endogenous metabolic pathway to inhibition by a drug. Increased alcohol-dehydrogenase activity or decreased aldehyde-dehydrogenase activity will predispose an individual to ethanol-induced flushing. Decreased uroporphyrinogen decarboxylase may result in porphyria cutanea tarda. Slow acetylators are more susceptible to developing drug-induced lupus erythematosus. A hypersensitivity syndrome may result if a patient is unable to detoxify the toxic metabolites of a drug such as phenytoin. A pharmacogenetic defect should alert the clinician to the possibility of cross-reactivity with other drugs or potential drug reactions in relatives of the patient.
Pediatr Dermatol 1983 Oct
PMID:Pharmacogenetics and adverse drug reactions in the skin. 623 48

A 49-year-old man was observed to have a strong flushing reaction in both the epigastric and facial areas after drinking wine. He had severe facial erythematous telangiectatic rosacea. Similar prominent intense changes in the epigastric skin probably represent extrafacial erythematous telangiectatic rosacea.
Arch Dermatol 1980 May
PMID:Epigastric rosacea. 644 9

The effects of caffeine and coffee, agents widely alleged to provoke flushing in patients with erythematotelangiectatic rosacea, were investigated. Neither caffeine nor coffee at 22 degrees C led to flushing reactions. Both coffee at 60 degrees C and water at 60 degrees C led to flushing reactions with similar temporal characteristics and of similar intensities. It is concluded that the active agent causing flushing in coffee at 60 degrees C is heat, not caffeine.
J Invest Dermatol 1981 Jan
PMID:Oral thermal-induced flushing in erythematotelangiectatic rosacea. 645 Aug 9

A patient with symptomatic urticaria pigmentosa who responded to nifedipine therapy is reported. Relief from cold-induced urtication and flushing was obtained with 10 mg taken orally three times daily. Calcium influx is an early step in the degranulation of mast cells. We hypothesize that the beneficial effect of nifedipine was due to calcium-channel blockade causing elevation of the mast cell threshold for degranulation.
J Am Acad Dermatol 1984 Oct
PMID:Urticaria pigmentosa responsive to nifedipine. 649 Oct

Increasing numbers of chemotherapeutic agents are being used to treat patients with cancer and various immunologically mediated and inflammatory disorders. Many of the drugs used have distinctive cutaneous side effects that range from relatively common ones, such as alopecia, stomatitis, and hyperpigmentation, to more unusual ones, such as radiation enhancement and recall phenomena, photosensitivity and hypersensitivity reactions, and phlebitis or chemical cellulitis. In addition, there are some rare complications such as diffuse sclerosis of the hands and feet, Raynaud's phenomenon, sterile folliculitis, and flushing reactions. By being aware of which drug may have caused a particular cutaneous reaction, dermatologists will be able to contribute to the care of patients with complex problems in a meaningful way.
J Am Acad Dermatol 1983 Nov
PMID:Cutaneous complications of chemotherapeutic agents. 664 64

A patient with cutaneous mastocytosis had intractable pruritus but no visible skin lesions. Skin biopsies and urinary histamine and prostaglandin D2 metabolite assays confirmed the diagnosis. Adding therapy with psoralens and ultraviolet A to the antihistamine regimen markedly decreased the patient's pruritus. In patients with pruritus, flushing, syncope, or other symptoms associated with mastocytosis, this diagnosis should be considered even in the absence of specific skin lesions.
J Am Acad Dermatol 1984 May
PMID:Cutaneous mastocytosis without clinically obvious skin lesions. 672 77

A patient with the carcinoid syndrome had flushes provoked by the ingestion of water at 60 degrees C, red wine, and milk chocolate. The patient was given sequential courses of clonidine hydrochloride, chlorpheniramine maleate, cimetidine, and a combination of chlorpheniramine and cimetidine. No flushes followed ingestion of red wine or milk chocolate during treatment courses with cimetidine (alone or in combination with chlorpheniramine) or clonidine. Chlorpheniramine alone did not affect flushing. None of the pharmacologic agents altered the flushing response to the ingestion of water at 60 degrees C.
Arch Dermatol 1982 Feb
PMID:Blockade of carcinoid flush with cimetidine and clonidine. 705 11

A new method for the characterization of flushing reactions is established based on the curvilinear relationship between malar skin temperature and an index of cutaneous blood flow in the face. Previous studies relied on the absolute change in malar temperature which overlooks the curvilinear aspect of this relationship. The change in malar thermal circulation index (delta MTCI) is derived from the mathematical model of this curvilinear relationship. There were 71 positive flushing reactions in 162 challenges to a variety of agents. The peak malar temperature, change in malar temperature, and delta MTCI significantly correlated with flushing (p less than 0.001). For the commonly used threshold values for change in malar temperature of 1.1 degrees C and 1.2 degrees C, sensitivity was only 63.4 and 54.9, respectively. The sensitivity, specificity, and predictive value of a positive result for the delta MTCI were 90.1, 95.6 and 94.1, respectively. delta MTCI did not appear to be related to the baseline malar temperature, suggesting that a low malar temperature did not predispose to flushing. Thus, the inverse relationship between change in malar temperature and baseline malar temperature results solely from the curvilinear relationship between malar skin temperature and cutaneous blood flow in the face. Data from 2 previously reported studies are reevaluated employing the delta MTCI method; in both studies the new method is more sensitive without loss in specificity. The results indicate that delta MTCI may be useful as an accurate, noninvasive method for the quantitative characterization of flushing reactions.
J Invest Dermatol 1982 Apr
PMID:A quantitative, non-invasive method for the characterization of flushing reactions. 706 5

Iloprost, a stable prostacyclin analogue, is known to have beneficial effects on the disturbed microcirculation. To develop a topical application for venous leg ulcers it is necessary to know the extent to which iloprost might be absorbed through the ulcer base. The aim of this study was to measure the absorption kinetics of iloprost solutions in increasing concentrations and doses (0.004% [15 micrograms]-0.006% [30 micrograms]) in 23 patients. There was considerable variation amongst the patients in the amount of iloprost absorbed. In 40% of patients no iloprost could be detected in the plasma, whereas in others up to 82% of the iloprost applied was absorbed through the ulcer base. High iloprost plasma levels provoked flushing in two patients. The highest plasma levels were always reached during the first hour after application. There was no direct relation between the ulcer size and the amount of iloprost absorbed. Iloprost concentrations up to the highest concentration applied (0.006%) were well tolerated locally.
Br J Dermatol 1993 Nov
PMID:Absorption of the stable prostacyclin analogue iloprost through the ulcer base in chronic venous insufficiency. 750 5

Although cyclosporin A is a highly effective treatment for several skin disorders, particularly psoriasis, its use in dermatology appears limited due to drug-induced hypertension and nephrotoxicity. Newer, similar-acting anti-T-cell agents such as FK-506 and rapamycin may be more effective; therefore a comparison was made with cyclosporin A to assess their inhibitory action on T-cell responses and keratinocyte proliferation. Using a guinea-pig model of delayed-type hypersensitivity to dinitrofluorobenzene (DNFB), drugs were given systemically (25 mg/kg cyclosporin A, rapamycin; 2.5 mg/kg FK-506) and topically (0.02% and 2%) at the time of DNFB challenge or several hours after and were assessed with respect to erythema and the numbers of infiltrating T lymphocytes entering skin-challenge sites. FK-506, at all concentrations, significantly inhibited both T-cell infiltration and skin reddening when used by both routes. Rapamycin displayed no inhibitory effect, whereas cyclosporin A only suppressed the erythema response when given systemically. The inhibition of normal human keratinocyte growth by the drugs was assessed using a protein dye-binding assay. After 2 weeks, FK-506 had no effect, whereas cyclosporin A and rapamycin both inhibited keratinocyte growth in a dose-dependent fashion and almost equivalently in serum-containing and serum-free keratinocyte growth medium. The findings showed that in vivo only FK-506 suppressed T-cell involvement in sensitized animals. In contrast, it failed to have any effect on keratinocyte growth, whereas rapamycin was more potent than cyclosporin A in inhibiting their proliferation. The future benefit of these drugs in dermatology may ultimately lie in their combined use.
J Invest Dermatol 1994 Jan
PMID:Differential inhibition of cutaneous T-cell-mediated reactions and epidermal cell proliferation by cyclosporin A, FK-506, and rapamycin. 750 55


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