Aspek Histologi
On histology, the classical fleeting wheal demonstrates edema of the upper and mid dermis, with dilatation of the postcapillary venules and lymphatic vessels of the upper dermis. In angioedema, similar changes occur primarily in the lower dermis and the subcutis. Skin affected by wheals virtually always exhibits upregulation of endothelial adhesion molecules and a mixed inflammatory perivascular infiltrate of variable intensity, consisting of neutrophils and/or eosinophils, macrophages, and T-cells Pada histologi, wheal sekilas klasik menunjukkan edema atas dan pertengahan dermis, dengan dilatasi postcapillary terjadi pada venula dan pembuluh limfaik dermis atas. Di angioedema, perubahan serupa terjadi terutama di dermis lebih rendah dan subcuis. Kulit yang terkena bercak hampir selalu pameran upregulaion molekul endotel adhesi dan menyusup campuran inlamasi perivascular intensitas variabel, terdiri dari neutroil dan/atau eosinoil, makrofag, dan T-sel
(3). A mild to moderate increase of mast cell numbers has also been reported by some authors. In delayed pressure urticaria, the infiltrate is typically located in the mid to lower dermis. In some subtypes of urticaria, upregulation of adhesion molecules (4) and altered cytokine expression are also seen in uninvolved skin (5). These findings underline the complex nature of the pathogenesis of urticaria which has many features in addition to the release of histamine from dermal mas cells (6, 7). These changes are also seen in a wide variety of inflammatory reactions and are thus not specific or of diagnostic value. A search for more specific histological markers for different subtypes of urticaria is desirable.
Sebuah ringan hingga sedang iang kenaikan jumlah sel juga telah dilaporkan oleh beberapa penulis. Dalam tekanan urikaria, tertunda yang menyusup biasanya terletak di pertengahan untuk menurunkan dermis. Dalam beberapa subtypes dari urikaria, upregulaion adhesi molekul ( 4 ) dan diubah cytokine ekspresi juga terlihat di uninvolved kulit ( 5 ). Penemuan-penemuan ini menggarisbawahi kompleks sifat pathogenesis dari urikaria yang memiliki banyak itur selain pelepasan histamin dari sel ( 6, dermal mas 7 ). Perubahan ini juga terlihat pada berbagai reaksi inlamasi dan dengan demikian idak spesiik atau tes diagnosik nilai. Mencari lebih spesiik histological penanda untuk berbagai subtypes dari urikaria yang diinginkan
Parofisiologi Urtikaria Hal yang mendasari terjadinya urtikaria adalah triple respon dari lewis yaitu eritema akibat dilatasi kapiler, timbulnya flare akibat dilatasi arteriolar yang diperantarai refleks akson saraf dan timbulnya wheal, akibat ekstravasasi cairan karena meningkatnya permeabilitas vaskuler. (Buku imunologi anak).
EXAMINATIONS There are two aims of clinical examinations for urticaria. One is to make a solid diagnosis, and the other one is to explore causes of the disease. They may vary according to subtypes of urticaria, suspected by clinical observations. In general, the former may be important for urticaria developed by type I allergy and physical urticarias. On the other hand, the latter may be more important for idiopathic urticaria. Clinical examinations that may be taken for urticaria subtypes are listed in Table 4 TREATMENTS General Principles There are two principles for treating urticaria; the first one being to remove or avoid causes and_or aggravating factors of urticaria, and the second one being to use medications, including antihistamines. The former is more important than the latter in the management of inducible types of urticaria, whereas the latter is more important in spontaneously occurring urticaria (Fig. 1). Another important message of this algorithm is aims of the treatments for urticaria. Namely, the first one is to achieve a symptom-free condition by continuous use of medications as the first stage, and the second one is to achieve both symptom and drug-free condition, as the final stage. The third point for the treatment is the balance of disease severity and burdens of the treatments. The guideline classified disease severities of urticaria into six levels with necessities of further treatments (Table 5). Regarding medications for the treatment of urticaria, it is widely accepted that oral antihistamines may be used as a mainstay for virtually all subtypes of urticaria. However, the efficacies of medications including antihistamines on urticaria are largely variable among subtypes, or individuals. Therefore, the aims and nature of the treatment for urticaria should be planned, taking into the subtype and severity of urticaria as well as specific conditions of individual patients.
Medications Many of the studies about pharmaceutical treatments for urticaria have been conducted for idiopathic urticaria and angioedema. Medications for idiopathic urticaria have been classified into four steps in the Japanese guidelines (Fig. 2). The first one is the use of standard dose of antihistamines among a list of nonor low-sedative antihistamines in Figure 4. If it is not sufficiently effective, change to other antihistamines or an increase up to twice the dose of non- or low sedative antihistamines are recommended (recommendation level B-C1, evidence level II, V). The medications grouped in the second step, as supplementary treatments, include histamine H2-receptor antagonists, antileukotrienes, extracts of inflammatory rabbit skin inoculated with vaccinia virus, glycyrrhizinic acid, dapsone, anti-anxiety drugs, tranexamic acid, and Chinese herbs. The third step is the use of steroid equivalent to 5-15 mg_day prednisolone. The fourth step includes immunological treatments, such as ciclosporin, and prednisolone at 20 mg_day or more. The fourth step treatments are still experimental, and may be tried only if symptoms are very severe and refractory. Treatments to take after full suppression of symptoms are indicated in Figure 3. Medications for other subtype of urticaria were described in the original guideline,8 but have not been included in the present article, because of the limited space. Most of them are, however, included in step 1 and 2 for idiopathic urticaria.
Terapi urtikaria pada anak An H1 antihistamine such as diphenhydramine (Benadryl) should be given at once. It is preferable to use the liquid or rapid-dissolving tablet form with their rapid onset of action, because a capsul may take much longer to achieve an effective blood level. H2 histamine blockers have also been recommended for the treatment of anaphylactic reactions, but their use in cases of acute urticaria has not been studied. A dose of epinephrine will resolve urticaria quickly but, because of its short half-life, a second dose may be required. If the urticaria does not fade within 2 hours, or if other symptoms develop, it is advisable to add an oral corticosteroid (prednisone at a dose of 1 mg/kg/day) in an undivided dose for a total of 5 days. Lengthy treatment with corticosteroids should be accompanied by a warning about possible side effects. It is interesting to note that in a recent survey,10 general emergency room physicians were 2.6 times more likely to use H2 antagonists and more than three times as likely to use corticosteroids to treat severe
urticaria then primary care physicians. It is unclear why there are such distinctive differences in the approach to treating these patients.
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