大疱性荨麻疹1例

患者女,16岁。因全身反复出现风团、水疱2年,再次发作3h,于2004年5月12日来我科就诊。患者平时劳累后皮肤上易出现红斑、风团,24h内可消退。有时部分风团表面起水疱,米粒至黄豆大,持续约1周方消退,消退后局部遗留色素沉着斑。     

荨麻疹

20 0 3 3 1 95　咪唑斯汀和氯雷他定起效指数的研究/支玉香 (中国医科院协和医大北京协和医院变态反应科 )…∥中华皮肤科杂志 .-2 0 0 3 ,3 6(7) .-4 0 7起效指数 (O A I)指在服药前后做组织胺点刺试验 ,分别计算风团和红斑的抑制率及计算出服药后某一时间点的起效比率。应用抗组胺药治疗急性荨麻疹 ,起效时间是抗组胺药物药理学重要指标之一。本研究结果显示 ,单次服用咪唑斯汀起效迅速 ,服药后 1 h、2 h分别有 76%、97%的受试者达到起效标准 ;服用氯雷他定的分别为46%、83 % ,二者起效指数差异均有显著性。表 2参 5　 (汤亚娥 )2 0 0 3…     

皮肤血管病及淋巴管病

20 0 4 16 73　 18例荨麻疹性血管炎患者临床分析 /李凌(杭州市一院皮肤性病科 )… / /浙江医学 .- 2 0 0 3,2 5(12 ) .- 75 4～ 75 5均表现为反复发生红斑、风团、自觉灼热或疼痛 ,风团持续时间 >2 4 h,消退过程中出现环状损害、紫癜或色素沉着。伴不规则发热、四肢大关节游走性疼痛、上肢疼痛等 ,部分病例外周血白细胞总数升高 ,中性粒细胞比例升高 ,血沉 18～ 39mm/ h,血 Ig G升高、补体 C3下降 ,有尿蛋白或镜下血尿等。均经组织病理检查确诊。 6例低补体血症患者同时作了直接免疫荧光检查 ,血管壁或基底膜有免疫球蛋白或补体 C3 沉积 …     

扑尔敏致固定型药疹1例

患者男性,24岁,农民。因全身皮肤出现痒性风团,口服扑尔敏8mg,一日三次,连用一周,痒性风团消失。停药第十二天在阴茎龟头处皮肤出现一片紫红斑,瘙痒,经肤轻松软膏外用后红斑消退。两个月后全身皮肤又出现痒性风团,自服扑尔敏8mg(2片),后约两小时在阴茎龟头处皮肤出     

慢性荨麻疹伴发面神经麻痹1例

1　临床资料　患儿男 ,10岁。全身反复起风团伴口眼歪斜 1年。 1年前无明显原因全身起风团 ,剧痒 ,未予治疗 ,风团持续10～ 3 0min可自行消退。 3个月后发作频繁 ,每天发作 2～ 3次并伴发口眼歪斜 ,口眼歪斜一般在风团出现后约 15min发生。自服抗过敏药后 3h风团可消退 ,而口眼     

幼儿色素性荨麻疹1例

1 临床资料 患儿男,6个月.全身反复起红斑、风团伴瘙痒3月余.其母诉患儿出生后3个月时背部有蚕豆大红斑,约3～4天后自行消退,但原皮损处遗留有同样大褐色斑.继之患儿头部、颈部、躯干、四肢及手足部先后出现大小不等的鲜红斑,摩擦后出现风团,少数为水疱, 约4天均可消退,并遗留棕褐色斑,无明显大疱和丘疹,搔抓或摩擦后出现条索状抓痕、风团和片状红斑,可自行消退.     

成人Still病1例

临床资料 患者女,23岁.因全身反复发作风团、红斑3天伴发热39℃,于2008年8月13日就诊我院,3天前无明显诱因出现发热,躯干及双大腿出现大小不等的红斑、风团,微痒.风团反复发作,可自行消退,消退后遗留暗红色斑片.     

依巴斯汀抗组胺活性的随机、双盲、安慰剂对照研究

目的:研究单次口服依巴斯汀10mg的药效动力学特点。方法:60名健康受试者随机、双盲口服依巴斯汀10mg或安慰剂1片,于服药前和服药后2、4、24h,对全部受试者行组胺皮肤点刺滴定试验。在揭盲后,对依巴斯汀组的受试者于服药后48h再做一次组胺皮肤点刺滴定试验。以剂量-反应曲线下面积(AUDRC)和痒觉积分为参数,评价依巴斯汀的抗组胺活性。结果:服药前两组数据无统计学差异。依巴斯汀组的风团和红晕AUDRC于服药后2h即明显低于安慰剂组,而痒觉积分于服药后4h才明显低于安慰剂组(P<0.01)。服用依巴斯汀后24h,AUDRC和痒觉积分均降至最低;48h上述两者均有所升高,但仍明显低于服药前(P<0.01)。结论:依巴斯汀的抗组胺作用起效较慢,作用较强,持续时间较长。     

掌跖脓疱型银屑病伴荨麻疹1例

患者,男,５２岁。６年前因外伤而致右手掌部出现花生米大片状红斑、丘疹,渐面积扩大至整个掌面,并出现脓疱,不久右手掌部、双足掌部也出现类似皮疹,自觉轻度痒感。皮疹反复发作,新出现之皮损一般７～１０天可吸收变干燥、脱屑。二月后背部、胸、大腿部出现片状红斑、风团,时起时消,瘙痒显著。自觉红斑、风团随掌跖部脓疱的出现而加重,脓疱消退,荨麻疹也很快消退。无发热、畏寒,无关节疼痛史,无腹痛、胸闷史。入院查：掌跖部散在红斑、丘疹、脓疱、疱壁紧张,躯干、四肢散在片状淡红色红斑、风团,皮肤划痕症（＋）。掌部皮损病…     

以荨麻疹性血管炎为临床表现的多菌性麻风1例

正1临床资料患者,男,31岁,因全身反复水肿性红斑、风团伴痒20天入院。20天前无明显诱因在躯干、四肢部位出现大小不一的水肿性红斑、风团,自觉轻度瘙痒,皮损约3日可消退,消退后遗留色素沉着,受热后可诱发皮损出现,无明显皮肤感觉异常。曾于10天前在当地医院就诊,具体诊治不详,病情无明显     

Topically applied aspirin decreases histamine-induced wheal and flare reactions in normal and SLS-inflamed skin,but does not decrease itch. A randomized,double-blind and placebo-controlled human study

Topically applied aspirin has recently been reported to decrease histamine-induced itch in human volunteers. Our aim is to confirm this and to study the antipruritic ability of topical aspirin in inflamed skin. In 24 non-atopic volunteers, an inflammatory skin reaction was induced in forearm skin at 5 different sites by sodium lauryl sulphate contained in Finn Chambers. Aspirin 10%, aspirin 1%, mepyramine 5% and vehicle were applied to the inflamed and corresponding non-inflamed areas 20 min before itch induction with intradermal histamine injection. Itch and pain were scored on a visual analogue scale at regular intervals. Wheal and flare areas were measured. No difference in itch intensities was found after application of aspirin, mepyramine and vehicle, but more itch was induced in aspirin and mepyramine pretreated sites in inflamed skin compared to normal skin (p<0.05). In normal skin, flare areas were smaller after pretreatment with aspirin 10% (p<0.05) and mepyramine (p<0.001), as were wheal areas after mepyramine (p<0.01), compared to vehicle pretreatments. In inflamed skin, flare areas were smaller after pretreatment with aspirin 10% (p<0.01) and mepyramine (p<0.001), as were wheal areas after aspirin 10% (p<0.01), aspirin 1% (p<0.05) and mepyramine (p<0.001). We conclude that despite a significant skin penetration as measured by the influence on wheal and flare reactions, topically applied aspirin did not decrease histamine-induced itch in the model used.     

Video-optical monitoring of wheal and flare reactions

Background/aims: In order to monitor the dynamics of experimentally-induced cutaneous inflammation in humans, we developed an objective, computerized video-optical method for wheal and flare area determination.
Methods: The method was used for evaluation of PAF-acether-induced experimental inflammations on the volar aspect of the forearms of human volunteers. The study design was double-blind, randomized, placebo-controlled. Repeated measurements can be performed, e.g., with intervals of 1 min to reveal the time-course of the inflammatory reaction. In the present study, the effect of topical application of creams containing 3 different concentrations of the putative anti-inflammatory drug sodium sucrose-sulphate (SoS) on cutaneous inflammation was investigated.
Results: 30 min after intracutaneous PAF-acether injection, a statistically significantly increased (p<0.05) wheal area was found in skin sites treated by either 1%, 3% and 9% SoS cream, whereas no influence of sucrose-sulphate could be demonstrated on the flare area. The reduction of the wheal area was significantly faster in the SoS-treated areas than in the placebo (p<0.05).
Conclusions: Computerized video-optical quantification of acute skin inflammatory reactions may be a suitable experimental tool for objective dynamic monitoring of both wheal and flare reactions and hence for quantification of the effect of anti-inflammatory drugs in humans. Topical application of SoS surprisingly increased PAF-acether-induced skin oedema (wheal), significantly whereas no effect was found on the flare reaction. No concentration-related effect of SoS could be shown.     

Effects of acrivastine, loratadine and cetirizine on histamine-induced wheal and flare responses

It is accepted that studies evaluating histamine-induced wheal and flare reactions in the skin represent a simple and reliable method for demonstrating pharmacodynamic activity and pharmacokinetics of the H1-receptor antagonists. In this study, the effects of single oral doses of acrivastine (8 mg), loratadine (10 mg) and cetirizine (10 mg) on the histamine-induced wheal and flare reactions were compared in 60 healthy volunteers. The wheal and flare responses were produced by prick test using 1% histamine solution. Measurements were performed before the ingestion of antihistamines (baseline values) and afterwards at 15, 30, 90, 240, 360 min and 24 h. The values obtained for each antihistamine were compared with each other and with baseline values. Cetirizine was found to be superior to acrivastine and loratadine for the suppression of wheal and flare responses at 240, 360 min and 24 h (P < 0.05) and acrivastine was superior to the other two antihistamines for the suppression of flare response at 30 min (P < 0.05). Our results indicate that a single dose of cetirizine provides a more effective and long acting suppression on wheal and flare reactions in urticaria when compared to acrivastine and loratadine.     

Some effects of calcitonin gene-related peptide in human skin and on histamine release

Calcitonin gene-related peptide (CGRP) produced a dose-related wheal and flare reaction in human skin at doses of 12.5 to 50 pmol. The flare response but not the wheal response to CGRP and substance P were inhibited by prior treatment of the subject with oral chlorpheniramine, 16 mg. CGRP, but not substance P, was potent in producing a delayed erythema and surrounding pallor in human skin, which peaked at 1 h and persisted for more than 3 h after injection, when wheal and flare responses had subsided. The delayed response was accompanied by infiltration of polymorphonuclear leukocytes. The delayed erythema and pallor produced in response to CGRP were not inhibited by oral chlorpheniramine, or by 4% prilocaine injected locally. CGRP released histamine from rat peritoneal mast cells over the concentration range 2.5-10 microM. CGRP was about fourfold less potent than substance P in releasing histamine. The substance P analogue, [D-Pro4, D-Trp7,9,10]SP4-11 10 microM, and benzalkonium chloride 10 microM inhibited histamine release from rat mast cells stimulated by either CGRP or substance P.     

15-Hydroxyeicosatetraenoic acid (15-HETE) specifically inhibits the LTB4-induced skin response

Summary 15-Hydroxyeicosatetraenoic acid (15-HETE), a 15-lipoxygenase product of arachidonic acid, inhibits leukotriene B₄ (LTB₄)-induced chemotaxis of polymorphonuclear leukocytes (PMNs) in vitro. In this study the effects of intradermal injections of LTB₄ were determined in the absence or presence of 15-HETE. For comparison intradermal injections of purified human complement split product C5a were performed in the absence or presence of 15-HETE. The skin response was evaluated by measuring the diameter of the wheal, the area of the flare and by intensity of the erythema (erythema index). LTB₄ and C5a were injected at the concentration of 200 ng/ml. At this concentration the maximal skin response of LTB₄ and C5a were equivalent. In contrast to C5a reaction, which resolved within 1 h, LTB₄-induced skin response lasted up to 18 h. In all subjects the skin response was significantly decreased when LTB₄ was injected together with 300 ng of 15-HETE. The decrease of wheal, flare, and erythema index averaged 81.9%, 56.6%, 53.6%, respectively, when all parameters were obtained at the maximal skin response. In contrast, the C5a-induced skin response was not affected by addition of 15-HETE, even when the final dose of 15-HETE was increased 10 times to 3 g. The LTB₄-induced reaction could last up to 18 h after injection. After the addition of 300 ng of 15-HETE the skin response resolved after 1 h. The present results demonstrate that 15-HETE is a specific inhibitor of the LTB₄-induced skin response and brings additional evidence in support of the ability of 15-HETE to regulate the proinflammatory effects of LTB₄ in vivo.     

Regulation of wheal and flare by tea tree oil: complementary human and rodent studies

When applied 20 min after injection of histamine into human forearm skin, tea tree oil (TTO) reduces the developing cutaneous vascular response. In this study, the effect of TTO on inflammatory microvascular changes was dissected at the base of an experimental blister on rat skin. 1,8-Cineole, representing 2% of TTO, reduced vascular changes induced by sensory neuropeptides released when the distal portion of a cut sciatic nerve was electrically stimulated. The pre-terminal modulatory effect of 1,8-Cineole was confirmed in tests in sensory-denervated rats. Terpinen-4-ol (approximately 40% TTO) reduced substance P-induced microvascular changes and protein extravasation by a direct nitric oxide-mediated effect on the microvasculature, without sensory nerve involvement. alpha-Terpineol (3% of TTO) regulated both pre- and post-sensory nerve terminals. In human skin, terpinen-4-ol applied 10 min after histamine injection, but not alpha-terpineol or 1,8-cineole, regulated the developing wheal and flare suggesting that the histamine-induced responses in humans (at the dose used in this study, 50 microL of 330 microM histamine) are in large part determined by histamine directly affecting the vasculature via post-terminal-mediated events. The underlying strength of these studies is the use of a well-established rat physiologic model to differentiate the mechanism of regulation of microvascular changes by modulatory agents.     

Reactions to intradermally injected substance P and topically applied mustard oil in atopic dermatitis patients.

Skin reactions and itch or burning pain sensations following intradermal injection of the neuropeptide substance P and topical application of the substance P releasing agent mustard oil were studied in 20 atopic dermatitis patients and 20 healthy controls. Changes in skin blood flow were measured with a Laser Doppler flowmeter. Areas of wheal and flare reactions were evaluated planimetrically. Simultaneous with Laser Doppler flowmeter measurements, subjective itch and burning pain ratings were verbally reported on a category partitioning scale at 10-second intervals. Substance P evoked dose-dependent wheal, flare, and itch reactions in both patients and controls. However, substance P doses of 10(-9) -10(-11) mol elicited smaller flares in patients than in the controls whereas the wheal sizes were similar in both groups. Substance P-induced itch ratings were lower in patients at a dose of 10(-10) mol, and the onset of itching was delayed at all substance P levels applied. Mustard oil elicited similar neurogenic inflammatory reactions in both groups, although pain sensations were significantly delayed in atopic dermatitis patients at two mustard oil concentrations, which is further indication of a desensitization of afferent nerve endings contributing to the neurogenic inflammatory reactions in the skin of these patients.     

Rapid effects of olopatadine hydrochloride on the histamine-induced skin responses

Olopatadine hydrochloride is one of the second-generation nonsedating antihistamines that are used for treating allergic disorders such as urticaria, rhinitis, and atopic dermatitis. We examined the inhibitory effects of this drug on the flare and wheal responses induced by histamine iontophoresis at 30, 60, and 90 min after oral administration in a double-blind, cross-over, and placebo-controlled study. Olopatadine hydrochloride significantly inhibited the histamine-induced flare and wheal responses as early as 60 min after oral administration when compared with placebo. Significant inihibitory effects of olopatadine hydrochloride on the itch responses were seen at 90 min after administration. Thus, olopatadine hydrochloride exhibited a very rapid and potent antihistamine effect on the histamine-induced skin responses.     

Effects of cetirizine and epinastine on the skin response to histamine iontophoresis

Epinastine and cetirizine are second-generation, nonsedating and long-lasting antihistamines that are now frequently used for the allergic disorders. We have examined the inhibitory effects of these two drugs on the histamine-induced flare and wheal responses using iontophoresis at 1, 2, 4, 8 and 24 h after the oral administration by a double-blind, cross-over and placebo-controlled study. Both cetirizine and epinastine significantly inhibited the histamine-induced flare and wheal responses at 2 h after the oral administration when compared with placebo. The inhibitory effects of cetirizine and epinastine on the flare response lasted long until at 24 h, however, epinastine was less potent than cetirizine. The inhibitory effects on the wheal response was also clearly and significantly evident at 2-8 h by cetirizine and epinastine. At 24 h cetirizine only showed the significant inhibition on the histamine-induced wheal response. In contrast, epinastine seemed to exhibit the inhibitory capacity earlier than did cetirizine. The inhibitory action of the drugs on the histamine-induced wheal response peaked at 4 h after the oral administration. The histamine-induced itch sensation was also markedly or completely suppressed at 2-8 h by the drugs. Thus, both drugs exhibited the potent and long-lasting antihistamine activity on the skin responses induced by histamine iontophoresis.     

Histamine is released following aminolevulinic acid-photodynamic therapy of human skin and mediates an aminolevulinic acid dose-related immediate inflammatory response

Acute skin inflammation occurs following topical aminolevulinic acid-photodynamic therapy (ALA-PDT), but its nature and mediation are ill defined. As we observed an urticarial response, a potential role for histamine was explored. In 13 healthy volunteers, we assessed the time course and dose-response of the acute cutaneous response(s) to ALA-PDT, the impact of H(1) antihistamine blockade, and measured dermal histamine release. An ALA dose series was iontophoresed into ventral forearm skin and exposed to red light. All participants exhibited an immediate urticarial response, both wheal and flare correlating with log ALA dose. Subsequently, a dose-related erythema developed at treatment sites by 3 hours and persisted at 24 hours. H(1) blockade with oral cetirizine doubled the median minimal urticating dose of ALA and reduced the slope of dose-response for wheal and flare, whereas at the highest ALA dose, mean wheal and flare areas reduced by 68 and 60%, respectively. In contrast, cetirizine did not influence the 24 hour minimal phototoxic dose or erythema dose-response. Histamine release after ALA-PDT mirrored the urticarial response, levels peaking within 30 minutes and returning to baseline by 24 hours. Thus, two discrete acute inflammatory responses to topical ALA-PDT occur in human skin; histamine mediates the immediate response, but does not appear involved in the delayed phototoxicity.