Alopecia Totalis - Oorzaken, Symptomen en Behandeling van Haarverlies

Alopecija areata – dijagnoza

Dijagnozu ove bolesti lako je postaviti i samim kliničkim pregledom zahvaćenog područja bez dlaka i noktiju.

Liječnik će Vas poslati na neke pretrage kako bi otkrili mogući uzrok alopecije (krvna slika za otkrivanje upale i anemije, jetreni enzimi za stanje jetre, temeljit pregled zubala…) Detaljan razgovor o Vašim tegobama postavit će sumnju na dodatnu bolest kao što je npr. celijakija, tireoiditis te će Vas liječnik možda poslati na pretrage koje to dokazuju (antitijela na gluten i antitiroidna antitijela).

Krvne pretrage u bolesnika s alopecijom areatom će pokazati ubrzanu sedimentaciju eritrocita.

Biopsija kože i patohistološki nalaz daju dijagnozu alopecije areate. U nalazu se vidi smanjen broj ili nedostatak folikula dlake te upalni infiltrat mononukleara, najčešće T limfocita i eozinofila. Mogu biti prisutne i promjene na žlijezdama znojnicama i lojnicama u koži. Metodom direktne imunofluorescentne tehnike vide se depoziti C3-komponente komplementa u folikulima dlake.

Diagnosis Alopecia Areata

Untuk menegakkan diagnosis dan memastikan penyebab kerontokan rambut, perlu dilakukan pemeriksaan penunjang, seperti:

Biopsi kulit kepala

Biopsi dilakukan dengan mengambil sampel dari kulit kepala untuk diperiksa dengan bantuan mikroskop. Biopsi dilakukan untuk mendeteksi ketidaknormalan sel dan jaringan di kulit kepala serta memastikan penyebab kerontokan atau kebotakan yang dialami.

Tes darah

Tes ini dilakukan jika dicurigai pasien menderita penyakit autoimun atau penyakit lain yang bisa menyebabkan kebotakan dan kerontokan rambut. Beberapa hal yang akan dinilai dan dideteksi pada saat tes darah adalah:

• Antinuclear antibody (ANA)
• C-reactive protein
• Sedimentasi eritrosit
• Zat besi
• Hormon tiroid
• Testosterone
• Follicle stimulating hormone (FSH)
• Luteinizing hormone (LH)

Evaluation

The history and physical examination are often sufficient for making the diagnosis. In most cases, the patient will have a history of patchy hair loss, which has progressed to complete loss of hair on the scalp, with the physical exam findings described above. Dermatoscopy can aid in examination. Trichoscopy, a term for dermoscopic evaluation of hair, reveals perifollicular yellow dots, black dots, tapering hairs, and vellus hairs.[16][17]

In certain patients, lab work may be indicated. Thyroid testing, such as thyroid-stimulating hormone (TSH) with reflex to free thyroxine (T4), is the most important screening laboratory test. Other tests sometimes ordered with alopecia, in general, include a complete blood count (CBC), vitamin and mineral levels, rapid plasma reagin (RPR), plasma testosterone, dehydroepiandrosterone sulfate (DHEA-S), and antinuclear antibody (ANA).

Epidemiology

There are multiple theories on the pathogenesis of AA. Central to these is the loss of the immune privilege of the hair follicle, leading to an attack of the follicle by the immune system. The loss of immune privilege may occur secondary to an environmental insult such as a virus, or it may be a spontaneous autoimmune phenomenon. In normal conditions, healthy anagen hair follicles express major histocompatibility complex (MHC) class I at low levels, which prevents molecular presentation as autoantigens. When this process is disturbed, and MHC expression is increased, immune privilege is lost, as previously hidden antigens may be presented to T-cells.[4]

CD8 + T-cells, in particular, are known to play a key role in the pathogenesis. These T-cells produce interferon (IFN)-gamma, which activates interleukin (IL)-2, IL-7, IL-15, and IL-21 cytokines. IL-15 suppresses regulatory T cells, promoting the proliferation of natural killer cells. Downstream, these cytokines signal the Janus kinase/ signal transducer and activator of the transcription (JAK/STAT) pathway. JAK3 is overexpressed in patients with AA.[12]