In the name of God

1. In the name of God

2. Alopecia areata Dr Giti Sadeghian Dermatologist

3. Introduction: • Alopecia aerata is a chronic inflammatory disorder affecting hair follicles and sometimes the nails that produces non scarring hair loss.

4. Patient typically Develop discrete Arera of complete Hair loss

5. Epidemiology: • The estimated prevalence of alopecia areata is approximately • 1 in 1000 people, with a lifetime risk of approximately 2 percent. Men =women Alopecia areata can started at any age although in most patients the onset is before age 30.

6. Patho physiology: • the hair follicle pathology of AA is probably mediated by auto • reactive T lymphocytes. • Hair follicle auto antibodies are frequently present in sera from AA patients but their pathogenic role is uncertain. • Other autoimmune diseases, such as vitilligo,thyroiditis,and pernicious anemia, may be associated with AA.

8. Approximately 20% of patient have a family history of AA, indicating a genetic predisposition to the disease. this is thought to be polygenic in nature and association with a variety of genes, predominantly immune response genes, have been reported.

9. A variety of factors, such as infections, drugs, and vaccinations, have been implicated in triggering episodes of AA. • Some patients report severe stress, especially emotional stress as a precipitating event, although many patients have no such history.

10. Clinical features: • Patients with AA have smooth, circular, discrete area of complete hair loss that develop over a period of a few weeks, followed by regrowth over several months. These patches may enlarge and coalesce into bizarre patterns. • Short hairs broken off a few millimeters from the scalp are found at the edges of expanding patches .

16. Area overgrowth often are characterized initially by fine , white vellus hairs. • Alopecia most commonly occurs on the scalp, but may be found on any hair bearing area .

17. There also can be nail involvement with fine pitting or roughening of the nail plates.

18. Eye abnormalities, including the rare early development of cataract, may occur in patients with AA

19. Spontaneous regrowth occurs in the majority of patients. • Around 80% of those with limited patchy hair loss will recover within a year, although almost all will experience more than one episode of the disease. • However, alopecia areata may persist for several years and sometimes hair growth never recovers.

20. In a minority of patients there is progression to total loss of scalp hair (alopecia totalis) or loss of the entire scalp and body hair (alopecia universalis).

21. Ikeda,s categories: • Type 1: the common type • 63% • Age 20-40 • Total course les than 3 years • Alopecia totalis develops in only 6%

22. Type2:atopic type • 10% • The onset is in childhood • Disease course is 10 years • Alopecia totalis develops in 75%

23. Type 3:prehypertention type • 4% • Young adults • Disease course is rapid • Alopecia totalis develops in 39%

24. Type 4: combined type • 5% • Patients are over 40 years • Course is prolong • Alopecia totalis develops in 10%

25. Prognosis

26. The following factors are associated with a poor prognosis and /or high likelihood of relapse: • Onset in childhood • Severe disease, specially alopecia totalis or alopecia universalis. • Duration of more than one year. • Involvement of peripheral scalp (ophiasis) • Nail disease • Atopy

27. Diagnosis

28. The diagnosis of AA is suspected in patients with the following: • Smooth, discrete area of hair loss; affected skin may be slightly reddened but show no other changes. • Exclamation point hair at the margins of patches: these are short broken hairs which can be extracted with minimal traction and where the proximal end of the hair is narrower than the distal end. • Exclamation point hair can be difficult to see ;their absence does not exclude AA.

30. Biopsy specimens are usually not necessary to confirm the diagnosis, but may be needed in cases where the diagnosis is uncertain. • If obtained ,it is best to perform two 4mm punch biopsies into the subcutaneous fat and have one specimen processed with routine vertical sectioning and the other with horizontal sectioning.

31. If only a single specimen is obtained, horizontal sections will give a better representation of the histology. • Biopsy taken early in the course of the disease show the majority of follicles in telogen or late catagen. • Some anagen hair bulbs are situated at a higher level in the dermis than normal.

32. A peribulbar lymphocytic infiltration is seen around foliclles, this being more dens in early lesions. • The infiltrater consiss procominantly of Tcells with increases of langerhans cells. • The infiltrate disappears during regrowth.

33. Because of the association between AA and other autoimmune disorders, it is responsible to screen for thyroid disorder or pernicious anemia in the patients with a suggestive history or physical examination.

34. Differential diagnosis:

35. Tinea capitis- • tinea capitis may be associated with pruritus and produces scaling and inflammation in area of hair loss • AA produces smooth area of hair loss, without any scaling . • Adenophaty may be present in tinea capits. • Tinea capitis should always be considered in children presenting with patchy hair loss.

38. Nervous hair pulling (trichotillomania) • Trichotillomania pruduces unusual pattern of broken hair of varying length which lead to a characteristic “Wire brush”, feel, as compared with the smooth hair loss of AA. • However, AA and trichotillomania can co-exist on the same scalp. • A biopsy in the area of alopecia will help differentiate the two conditions.

39. Trichotillomania

40. Trichotillomania

41. Cicatricial Aopecia • Cicatricial alopecia may be the result of diverse pathologies, including lichen plano-pilaris, discoid lupus eryhematosu • and folliculitis decavans. • All are characterized by permanent, distraction of hair follicles. Hair loss is usually patchy and there is loss of follicular orifices. • Additional features are variable and depending on the primary pathology may include erythema scaling follicular plugging and pustulation.

42. Cicatricial Aopecia

43. Androgenic Alopecia • Onset of hair loss is gradual in androgenic alopecia and in a typical distribution patern. • There are no exclamation point hairs. • AA occasionally presents as diffuse hair loss, which may resemble androgenetic alopecia but the progression is most wide spreadand more rapid. • A biopsy may be necessary in doubtful cases.

45. Secondary syphilis • Area of hair loss appear moth- eaten in patients with secondary syphilis rather than the smooth and discrete area seen with AA. Serologic testing may be necessary for differentiation.

46. Counseling • Counseling of patients on the nature of AA its prognosis and the treatment options is essential. • For the majority of patients AA is a cosmetic issue although it can occasionally cause physical disabilities ,where there is eyelash involvement or marked nail dystrophy.

47. Nevertheless the cosmetic importance of hair loss is such that AA can cause sever emotional problem particularly in children • and young women, thought by no means restricted to these groups. • In view of limited efficacy of current forms of treatment the clinician has an important role in helping patients adapt to their lack of hair .

48. This is not an easy task and input from other health professionals, such as a clinical psychologist ,may be needed . • Many patients though not all are helped by involvement in patient support groups. With children it is often the parents whose reaction must be addressed for the child adjust to the hair loss.

49. Treament

50. Treament • Treatment is not mandatory because the condition is benign, and spontaneous remissions and recurrences are common. • Treatments used are believed to stimulate hair growth, but no evidence indicates they can influence the ultimate natural course of alopecia areata. • Treatment modalities usually are considered first according to the extent of hair loss and the patient's age.