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)

Recombinant gamma interferon (IFN-gamma) was employed to treat adult-type atopic dermatitis. Eight cases received subcutaneous injections of 500,000 JRU of IFN-gamma for 8 weeks. They responded relatively well to this treatment; however, the overall response to the treatment was not significantly better than that to conventional therapy in the control group. There was no significant suppression of itch or erythema. Swelling was reduced at the 8th week in the treatment group. Frequency of flushing attacks on the face was reduced and disappeared within four weeks in 6 of these patients; however, a similar reduction of frequency was observed in the control group. Papular and lichenified lesions on the trunk and extremities responded significantly to the treatment later than 5 weeks after its initiation. Serum IgE level was not affected by the treatment. Seven had the same level of serum IgE before and after the treatment. The serum cytokine level in the treated patients was also unaltered. Therefore, although IFN-gamma treatment has some benefit in the treatment of severe cases of atopic dermatitis, it should be applied to limited cases because of its high cost.
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PMID:Gamma-interferon therapy for severe cases of atopic dermatitis of the adult type. 773 73

There is increasing evidence that neuropeptides may be involved in the pathogenesis of atopic dermatitis (AD). This study examines whether neuropeptide distribution in the skin of patients with AD differs from normal controls. The distribution and density of several neuropeptides were examined in lesional and non-lesional skin of AD patients (n = 5) and in normal controls (n = 4) using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Staining with the general neuronal marker protein gene product 9 x 5 showed a subepidermal network of nerves with fibres penetrating the epidermis, and nerves around blood vessels, sweat glands and hair follicles. Image analysis of nerves around sweat glands showed a significantly higher nerve density in non-lesional compared with both normal controls and lesional skin (P < 0.05); lesional compared with control skin showed no significant difference. In the epidermis the density of nerves was not significantly greater in non-lesional compared with lesional skin and controls. Calcitonin gene-related peptide immunoreactivity was similar in all subjects except in three of the AD patients, where more nerves appeared to penetrate the epidermis. Substance P immunoreactivity in the papillary dermis was seen in all AD patients but no controls. Vasoactive intestinal polypeptide and neuropeptide Y staining were similar in all groups. Acetylcholinesterase-positive nerves were found around sweat glands in all subjects, the staining being greatest in non-lesional and least in lesional skin. Occasional nerves were seen in the papillary dermis in lesional skin of two out of the four patients. We have demonstrated quantitative differences in nerve growth in clinically normal skin of AD patients, and altered cutaneous neuropeptide expression in these patients which may contribute to the pathogenesis of AD. The cause of atopic dermatitis (AD) has not been fully established but it is believed that there is a complex interaction between genetic susceptibility, precipitating environmental factors and disordered immune responsiveness. There is increasing evidence that neuropeptides may be involved in the pathogenesis of AD. Exacerbations of the disease can be provoked by stress, scratching and sweating which may be the result of neurogenic inflammation. One of the first features of an exacerbation is flushing of the affected skin and pruritus. Several neuropeptides that have been identified in human skin are potent inducers of vasodilation and may induce pruritus. Substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) all cause vasodilation when injected intradermally, and SP and CGRP have been shown to be mediators of the weal and flare reaction. Spantide, a competitive antagonist of SP, has been shown to inhibit immediate and delayed-type hypersensitivity reactions. Part of these responses may be due to release of histamine and indeed elevated concentrations of histamine have been found in vivo in the skin and plasma of patients with AD. In this study the distribution and density of several neuropeptides were examined in lesional and nonlesional skin of AD patients and in normal controls using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Because many afferent fibres do not express CGRP or SP, the general neuronal marker protein gene product (PGP 9 x 5) was used to assess the overall nerve supply to the skin.
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PMID:Neuropeptides in the skin of patients with atopic dermatitis. 885 37

A 15 year old female with uterus bicornis bicollis was admitted for operation. She had a history of atopic dermatitis and allergy to buckwheat, raw egg and latex. Two months previously she had developed whole body flushing during dental treatment, and latex glove used by the dentist had been suspected as the cause. Prior to the operation she underwent internal examination and intrauterine echogram in which a latex glove was carelessly used by another gynecologist who had not confirmed her past history. After 30 minutes, dyspnea and urticaria without itching, appeared suddenly. Blood pressure decreased to 80/50 mmHg and heart rate increased to 120 beats.min-1. She was then transferred to our ICU. Methylprednisolone was administered intravenously for dyspnea and circulatory collapse. After 3 hours, the patient made an uneventful recovery. The increased plasma latex protein-specific IgE levels confirmed anaphylaxis to latex. The increasing incidence of potentially life-threatening allergic reactions to latex has caused mounting concern over recent years. We may suspect latex allergy when an anaphylaxic reaction or shock of unknown origin occurs. In hospitals, latex free products must be prepared for use with latex allergic patients and for protection of medical staff with this allergy.
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PMID:[A case of anaphylaxic shock due to latex glove used on internal examination and on the probe of intrauterine echogram]. 1102 62

This paper reviews a wide range of somatization-related symptoms that are encountered in dermatology. These include the unexplained cutaneous sensory syndromes especially the cutaneous dysesthesias associated with pain, numbness and pruritus; traumatic memories in post-traumatic stress disorder (PTSD) which are experienced on a sensory level as 'body memories' and may present as local or generalized pruritic states, urticaria and angioedema; and unexplained flushing reactions and profuse perspiration, in addition to unexplained exacerbations of stress-reactive dermatoses such as psoriasis and atopic eczema secondary to the autonomic hyperarousal in PTSD; classic 'pseudoneurologic' symptoms associated with dissociation including unexplained loss of touch or pain, in addition to the self-induced dermatoses such as dermatitis artefacta and trichotillomania that are encountered with dissociative states; and body dysmorphic disorder where the patient often presents with a somatic preoccupation involving the skin or hair.
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PMID:Somatization disorders in dermatology. 1645 79

Cutaneous reactions to foods represent one of the most common presentations of food allergy in children. IgE-mediated (urticaria, angioedema, flushing, pruritus), cell-mediated (contact dermatitis, dermatitis herpetiformis), mixed IgE- and cell-mediated (atopic dermatitis), and nonimmune-mediated (irritant contact dermatitis, Frey's syndrome) reactions to foods have all been reported. It is important for the pediatrician to recognize the variety of skin reactions potentially related to food allergy and to consider timely referral to an allergy specialist for further evaluation and definitive diagnosis.
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PMID:Dermatologic food allergy. 1704 15

Myristyl nicotinate is an ester prodrug under development for delivery of nicotinic acid to skin for treatment and prevention of conditions that involve skin barrier impairment such as chronic photodamage and atopic dermatitis or for mitigating skin barrier impairment that results from therapy such as retinoids or steroids. The formulation stability of myristyl nicotinate is crucial because even small amounts of free nicotinic acid cause skin flushing, an effect that is not harmful but would severely limit tolerability. We report here reversed-phase HPLC methods for the rapid analysis of myristyl nicotinate and nicotinic acid in dermatological preparations. Because of the large differences in polarity, myristyl nicotinate and nicotinic acid were analyzed by different chromatographic conditions, but they can be rapidly extracted from cream formulations using HPLC mobile phase as a solvent followed by HPLC analysis in less than 10 min. The methods were validated in terms of linearity, precision and accuracy and mean recovery of myristyl nicotinate from topical creams ranged from 97.0-101.2%. Nicotinic acid at levels of 0.01% in the formulations could be quantified. Stability studies show that myristyl nicotinate formulations are stable at room temperature for 3 years with less than 0.05% conversion to nicotinic acid. These methods will be effective for routine analysis of myristyl nicotinate stability in dermatological formulations.
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PMID:Analysis and stability study of myristyl nicotinate in dermatological preparations by high-performance liquid chromatography. 1704 29

We report a case of allergic contact dermatitis due to alcamphor present in a flushing solution used by a 58-year-old woman. It is the first case described in our Division of Allergy and the second one reported in the literature. Alcamphor is a chemical substance present in many products that may have been underestimated as the causative agent of contact allergic dermatitis as the allergen is not available in the standard patch test batteries.
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PMID:[Contact dermatitis by camphor present in a flushing solution]. 1755 77

Red face syndrome is characterized by an erythematous dermatitis that is produced by different entities. These include rosacea, seborrheic dermatitis, contact dermatitis, atopic dermatitis, psoriasis, cutaneous lupus, photodermatosis, post-topical steroid dermatosis, demodicosis, borderline borderline (BB) leprosy, mastocytosis, carcinoid, postneoplasia flushing, cutaneous lymphoma, tineas, ulerythema ophryogenes, and psychosomatic flushing. Red face is a relatively common dermatologic manifestation. Our goal is to review tinea corporis and other fungi that affect this region causing facial erythema and its therapeutic management.
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PMID:Red face and fungi infection. 2544 65

Head-and-neck dermatitis is a variant of atopic dermatitis (AD) often seen in children and is challenging to diagnose, as it frequently overlaps with other eczematous dermatoses. Successful head-and-neck dermatitis (HND) treatment requires identification of common triggers and clinical mimickers, such as airborne dermatitis, periorificial dermatitis, and steroid-induced rosacea. Head-and-neck involvement negatively impacts quality of life and is often harder to treat than other body parts, as long-term topical corticosteroid use carries higher risks for skin atrophy on the face. Heating and flushing associated with HND further exacerbate the itch-and-scratch-cycle and disrupt sleep. We aim to address diagnostic gaps, identify clinical mimickers, and share clinical pearls in managing HND, including cooling pillows, thermal water sprays, rice starch paper facial masks, and tips to minimize food and saliva-induced facial irritation.
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PMID:Head-and-neck dermatitis: Diagnostic difficulties and management pearls. 3015 60