​  ​中環鍾經略醫生【皮膚學碩士 x 美容醫學碩士】(課程研究)

此蕁麻疹/風疹/風爛/風癩的皮膚科醫學相片由鍾經略醫生於診所拍攝,版權所有。



本文之中文翻譯本只作參考,如與原文有差異,應以英文版本為準。



【病    史】

38歲男士因為痕癢的皮疹幾個月前來看我. 該些皮疹時消時現, 每次出現維持不超過24小時.病因和誘因不明.

【診    治】

皮膚檢查發現明顯的風團,大(>8cm)小(<1cm) 不等, 紅色或皮色(邊緣紅色) 形狀不一: 圓形,卵圓形,半圓形,環狀或匍行狀, 這是由於在某一區域皮疹互相融合或正在消散,而在另一區域皮疹正處於進展期. 皮疹痕癢, 一過性(即不超過24小時), 全身性, 誘因不明. 按照定義,本例診斷為慢性原發性蕁麻疹. 很幸運,患者口服cetrizine有效,同時,我囑咐他避免精神壓力,酒精和某些止痛葯. 此症很可能持續1~3年後自然消失.

【討    論】

急性蕁麻疹

診斷標準

1. 痕癢.

2. 風團維持不足24小時.

3. 皮疹消散後不留痕迹.

4. 無脫皮現像.

5. 病程少於6星期.

約15%急性蕁麻疹轉化為慢性. 兒童病例全身症狀(發熱,腸胃症狀及關節痛)常見.

病因

1. 過敏性(傳遞皮膚肥大細胞的致敏作用的IgE)

a. 食物例如貝類,蟹,雞等.

b.葯物,例如盤尼西林, 造影劑等.

c. 免疫接種.

d. 植物的膠乳. 等等.

2. 非過敏性:

a. 病毒感染(尤其在小孩).

b. 葯物,例如嗎啡,阿士匹靈,Ibuprofen等.

c. 組織胺(腐壞的魚).

診斷

1. 從病史找出原因.

2. 檢查血清中特異性IgE 或 致敏原皮試(在醫院內進行).

3. 檢查可能介入的病毒感染.

4. 查詢药物史.

治療

1. 短療程的Prednisolone.

2. 每日口服一次無睡意的抗組胺葯物.

3. 外用Calamine lotion, 含1%menthol的Aqueous cream.

慢性蕁麻疹 (原發性,佔50% ; 免疫性,佔30~50% ; 非免疫性 三種類型)

1. 慢性原發性蕁麻疹

病因不明(有可能是幽門螺旋菌引致). 非特異性的加重因素有: 精神壓力; 酒精飲料; 非類固醇消炎止痛葯; ACE inhibitor類葯物; 病毒感染; 經期影响等.

2. 自體免疫性蕁麻疹

甲狀腺自體抗體  /  30~50%患者有IgG自體抗體  /  ASST(自體血清皮膚試驗)

3. 非免疫性慢性蕁麻疹  致病因或加重因素有: 嗎啡; 阿士匹靈及其他非類固醇消炎止痛葯; ACE Inhibitor類葯物.

治療

1. 避免致病或加重疾病的因素(如上所述).

2. 急性發作的治療: 温水淋浴; 外用含Menthol 的Aqueous cream; 口服Chlorpheniramine; 必要時口服Prednisolone.

3. 長期治療: 抗組織胺葯, H2-抗組織胺葯.

4. 難治病例: 抗組織胺药, Montelukast, Cyclosporin.

其他類型蕁麻疹(不在本文討論之列)

A. 物理性蕁麻疹

皮膚划痕症

遲發壓力性蕁麻疹

胆碱能性蕁麻疹

寒冷性蕁麻疹

日光性蕁麻疹

熱蕁麻疹

浸水性蕁麻疹

B. 血管神經性水腫

CASE HISTORY:

The above 38 year old gentleman came to see me for itchy skin rash which had lasted for a few months. The skin rash came and went. Each of the rash will not last longer than 24 hours. No aetiological factors/triggering factors were identified.

On dermatological examination, I found sharply defined wheals, some of them were small (<1cm), some of them were large (>8cm) They were erythematous or white (skin coloured) with an erythematous rim. Their shape were round, oval, acriform, annular, and serpiginous – this was due to confluence and resolution in one area and progression in another. These lesions were pruritic and transient (ie last less than 24 hours). Distribution – generalized. No triggering factors were identified.

By definition, his was suffering from chronic idiopathic urticaria. Luckily, he responded very well to oral cetirizine. He was also advised to avoid the exacerbating factors eg stress, alcohol, and some painkillers. Chronic idiopathic urticaria is very likely to last for 1 – 3 years before clearing spontaneously.

DISCUSSION:

Acute urticaria and chronic urticaria

Diagnostic criteria for acute urticaria:

1. itching

2. duration of weals – less than 24 hr

3. No residual skin staining

4. No desquamation

5. duration of the condition – less than 6 weeks

About 15% of acute urticaria turn into chronic urticaria.

Systemic symptoms are frequent in children – fever, GI upset, arthralgia.

Cause:1. Allergic (IgE mediated sensitisation of dermal mast cells) –

a. food eg shellfish, crab, chicken

b. drugs eg penicillin, radiocontrast media

c. immunisation

d. Latex

2. Non-allergic –

a. virus infections (esp in children)

b. drugs eg morphine, aspirin, ibuprofen

c. Histamine (spoiled fish)

Investigation:

History to identify the culprit ( eg food)

RAST – measurement of specific IgE in serum or Allergen Prick Test (to be done in a hospital)

Look for intercurrent virus infection

Drug history

Management:

1. a short tapering course of prednisolone

2. once daily non sedating anti histamine

3. calamine lotion, aqueous cream containing 1% menthol

Chronic spontaneous urticaria

1. idiopathic >50% cases

2. immunological >30-50%

3. non-immunological

1. Chronic idiopathic urticaria (CIU)

No contributory factors identified – H. pylori might be possible

Non-specific exacerbating factors:a. stress

b. alcohol

c. NSAIDs

d. ACE inhibitor

e. viral illness

f. menstruation

2. Autoimmune urticaria (IU)

a. increased frequency of thyroid autoantibodies.

b. 30 – 50% of chronic urticaria patients have IgG autoantibodies directed against the high affinity IgE receptor, FceRI on mast cell surfaces or an autoantibody to IgE.

c. ASST – autologous serum skin test

3. Non-immunological / allergic urticaria (causes or exacerbating factors)

a. Morphine – both a histamine and non-histamine dependent component are involved , thought to act directly on the mast cell

b. aspirin and other NSAIDs – act via alteration of the leukotriene pathways.

c. ACE inhibitor – cause angio-edema. Via alteration of the kinin pathway.

Management of chronic spontaneous urticaria:

1. avoid exacerbating factors: stress,alcohol, aspirin, NSAIDs, ACEI

2. Treat acute flare-ups: tepid shower, menthol in aqueous cream, oral chlorpheniramine, oral steroid

3. Long term treatment: low sedating and sedating antihistamine, H2 antihistamine

4. Resistant cases: antihistamine, montelukast, cyclosporin.

Other forms of urticaria (not discussed in this article):

A. PHYSICAL URTICARIA:

1. symptomatic dermatographism

2. delayed pressure urticaria

3. cholinergic urticaria

4. cold urticaria

5. solar urticaria

6. heat urticaria

7. aquagenic urticaria

8. vibratory urticaria

9. exercise induced anaphylaxis/urticaria

B. Angio-edema

主診醫生:鍾經略醫生


監督及指導機構: 英國威爾斯大學/卡的夫大學臨床皮膚專科部門。

皮膚科醫生常見皮膚疾病 – 蕁麻疹  (風疹,風爛,風癩)。