1.Moderator Dr Puneet Bhargava

2. INTRODUCTION Women presenting with diffuse hair loss is a very commonand challenging problem for dermatologists. Telogen effluvium (TE) is the most common cause, followed by female pattern hair loss (FPHL) and chronic telogen effluvium (CTE); the rest of the causes are not so common and can be relatively easily diagnosed through history and examination. The problem arises in differentiating between TE, FPHL, and CTE, which account for the majority of diffuse alopecia cases in females. 3. Hair follicle cycling Hair follicle is subjected to constant turn over. Different phases of hair cycle are-ANAGENphase of active hair growth Responsible for final length of hair 80-90% of scalp hair at any one time 3 year or more in scalp 1-3 month in other area 2. CATAGEN At the end of anagen, the follicle enters an involutionary phase known as catagen. 1. 4. phase of regression Proximal end of hair shaft keratinizes to form club shapedstructure The lower part of follicle involutes by apoptosis Base of follicle, together with its dermal papilla move upwards to lie just below the level of arrector pili Lasts about 3 weeks. Approximately 2% of hair of scalp 3. TELOGEN resting phase period between completion of follicular regression & onset of next anagen phase The club hair lies within an epithelial sac to which it is attached by tricholemmal keratin Lasts about 3 months 8 to 10% of scalp hair 5. 4. EXOGEN It is a highly controlled active process of shedding of the hair fiber ,unlike the previous assumption that the newly formed hair fiber pushes the resting shaft outward to effect shedding. 5. KENOGENThe interval of hair cycle in which the hair follicle remains empty after the telogen hair has been extruded and before a new anagen hair emerges. 6. ` 7. PATHOLOGIC DYNAMICS OF HAIR LOSS Dystrophic anagen effluvium Results from a direct insult to the rapidly dividing bulbmatrix cells. Abrupt cessation of mitotic activity leads to weakening of the partially keratinized, proximal portion of the hair shaft, its narrowing, and subsequent breakage within the hair canal. Thus Shedding of the hair from anagen phase of growth. Morphological consequence- tapered proximal end and lack of root sheeth. 8. Telogen effluvium Headington proposed classification of telogen effluviuminto 5 functional types1. Immediate anagen release the follicle that would normally complete a longer cycle by remaining in anagen, prematurely enters telogen. Most common type. Occurs after periods of physiological stress, fever etc. Shedding is dependent on transition from anagen through catagen and telogen, with subsequent release of telogen hair, hair loss occurs 3-4 months after the inciting event. 9. 2. Delayed anagen release Hair follicle remain in prolonged anagen rather than cycling into telogen. When finally release from anagen ,clinical sign of increased shedding of telogen hair is found. Seen in post partum hair loss3. Immediate telogen release Hair follicle normally programmed for release of the club hair after an interval of usually 100 days after the end of anagen, are prematurely stimulated to cycle into anagen. Premature teloptesis. Seen in initiation of therapy with topical minoxidil. 10. 4. Delayed telogen release hair follicle remain in prolonged telogen rather than being shed and recycled into anagen, when finally teloptesis sets in, increased shedding of club hair is observed. Seen in moutling in mammals. 5. Short anagen phase Slight but persistent telogen effluvium in association with decrease hair length. Seen in androgenetic alopecia or female pattern hair loss. 11. Causes of diffuse hair loss in females 1. Anagen effluvium(a)Dystrophic (b)Loose anagen hair2. Telogen effluvium (a)acute telogen effluvium (b)Chronic telogen effluvium 3. Female pattern hair loss 12. Loose anagen hair This condition features anagen hairs that are loosely anchored and easily pulled from the scalp . The majority of cases are fairhaired children, aged 29 years, mostly girls. Autosomal dominant inheritance. They typically have slightly unruly hair, which is of uneven length and patchy in quality. Hair is usually easily and painlessly plucked with the hairpull test. 13. There have been isolated reports of loose anagen syndromeassociated with hypohidrotic ectodermal dysplasia and ocular coloboma. Histological examination shows premature keratinizationof the inner root sheath layers of Huxley and Henle. Trichograms show 98100% anagen hairs. 14. Dystrophic Anagen effluvium It is the hair loss that result from the shedding of largenumber of hairs from anagen phase of growth. Causes-Anti neoplastic drugs (chemotherapy induced alopecia). 2. Radiation (radiation induced alopecia). 3. Toxins (toxic alopecia). 1. 15. chemotherapy induced alopecia Begins at 1-3wks and is complete at 1-2 month after initiation of chemotherapy. Normally upto 90% of scalp hairs are in anagen ,hair loss is usually copious and the resulting alopecia is quite obvious. Drugs are(a) antimicrotubule agents eg paclitaxel (b)topoisomerase inhibitors eg doxorubicin (c) alkylators eg cyclophosphamide (d) antimetabolites eg 5 fluorouracil plus leucovorin 16. This type of alopecia is usually reversible with hairregrowth typically occurring after a delay of 2-3 months. In some patients the regrown hair shows changes in colour,structure and texture.Radiation induced alopecia May be reversible or permanent Permanent alopecia occurs with >30gy of deep x rays or>50gy of soft x rays. 17. Toxic alopecia Occurs from occupational exposure to hazardouschemicals Many heavy metals are capable of disrupting the formationof the hair shaft through covalent binding with the sulfhydryl groups in keratin : thallium ,mercury, arsenic ,copper , cadmium and bismuth. 18. TELOGEN EFFLUVIUM TE is characterized by an abrupt onset, and rapid, diffuse, self-limited, excessive shedding of normal club hairs, usually seen 2-3 months after a triggering event. In one-third of cases, no trigger can be identified. Premature termination of anagen into catagen and telogen hair follicle is the main mechanism behind TE. Acute TE or classical TE is a self-limiting condition lasting for about 3-6 months if the stimulus/event that causes diffuse shedding persists beyond six months, then the condition becomes chronic. 19. Diagnostic features of telogen effluviumAbrupt onset, rapid diffuse generalized shedding of hairs, usually seen 2-3 months after a triggering event. Nearly 100-1000 hairs/day may be lost. 2. HAIR PULL TEST- Strongly positive Usually more than 10% of the total hairs pulled are easily extracted from any part of the scalp in the acute phase of TE, if the patient has not shampooed the hairs for more than 24 hours. Approximately, 60 hairs are grasped between the thumb and the index and middle fingers and gently pulled. A negative test (6 hairs obtained) indicates normal shedding, whereas a positive test (>6 hairs obtained) indicates active hair shedding. 1. 20. 3. A trichogram (forcible complete hair pluck of 40-60 hairs) showing significant reduction in anagen:telogen ratio. Usually, >25% of the plucked hairs are telogen hairs in acute phase. 4. Videodermoscopy will show large number of short-tip pointed regrowing hairs in the absence of hair diameter variability. 5. Biopsy shows normal histology except for an increase in the telogen follicles. The proportion of normal telogen follicles in excess of 15% is considered suggestive of TE. while a level of 25% or more is considered definitive. Normal telogen counts are typically in the range of 613%. 21. Chronic Telogen Effluvium CTE is an idiopathic distinct entity characterized by anexcessive alarming diffuse shedding of hairs in females aged 30-60 years, with a prolong fluctuating course and near-normal histology. The exact pathogenesis of CTE is not known, but it is theorized that it is due to reduction in the duration of anagen growth phase without miniaturization of hair follicles. Also, the etiology of CTE is unclear and it is diagnosed after excluding other causes of chronic diffuse hair loss. 22. Primary CTE represents a primary disorder and is a diagnosisof exclusion. Secondary CTE- secondary to variety of systemic disorders. 1. Iron deficiency 2. Other deficiency protein calorie malnutrition ,zinc deficiency 3. Thyroid diseases 4. Metabolic diseases-chronic liver or renal failure, advanced malignancy, pancreatic disease and upper GI disorder with malabsorption 5. SLE and other connective tissue disorders. 6. HIV infection 7. Drug induced 23. History and examination will generally suggest the cause ofTE if not, then a minimum battery of laboratory tests, which includes complete blood count (CBC), routine urine, serum ferritin, and T3, T4, and TSH should be performed. Iron deficiency anemia and thyroid hormone disorders are the two common conditions associated with TE . 24. Diagnostic features of chronic telogen effluvium History of abrupt, excessive, alarming, diffuse, generalizedshedding of hair from a normal looking head is the main feature of CTE. Chunks of hair are seen in the bathroom (may block the drain), pillow, brush and comb. Obvious diffuse thinning is not a feature of CTE, though many of these women do notice 50% reduction in the volume of their ponytail thickness. Moderate to severe bitemporal recession may also be seen. A positive pull test at all sites of scalp (vertex, occipit, and sides) is seen in active phase. 25. Absence of widening of central parting andminiaturization of hairs Absence of any underlying cause for chronic diffuse hair loss. Counting of total number of telogen hairs and vellus hairsshed during standardized shampooing (wash test) has been reported as a good tool to differentiate between CTE and FPHL. Ten percent or more of vellus hairs is considered enough to diagnose FPHL. Normal histological picture except for a slight increase in the telogen hair follicles. 26. Female Pattern Hair Loss FPHL is a gradual onset, slowly progressive nonscarringalopecia, which can be seen any time after menarche, but is most common in females aged 20-40 years. It results from a progressive reduction of successive hair cycle time leading to miniaturization of hair follicles. These changes are mediated through interaction between androgens, their respective receptors and enzymes like 5a reductase and p450 aromatase. 27. Three types of FPHL patterns have been described.1.Diffuse central thinning (Ludwig type): The diffuse hair loss is concentrated over frontoparietal region leading to thinning/rarefaction over central scalp with intact frontal hair line .Ludwig graded it into three stages depending upon whether the central thinning is mild (stage I), moderate (stage II), or severe, that is, near-complete baldness of the crown (stage III). 28. 2. Frontal accentuation (Olsen type): It leads to widening of central parting line and thereafter to chrismas-tree pattern. 3. Frontotemporal recession/vertex loss (male pattern/Hamilton type): It leads to recession of frontotemporal hairline or bitemporal recession and/or thinning at vertex. 29. Causes i. ii.Genetic Predisposition, Androgen excess, Ovarian cause- Polycystic ovarian syndrome, - Other ovarian tumor,. Unilateral benign microadenoma. . Leydig cell tumor . Hilar cell tumor. 30. Adrenal cause- Congenital adrenal hyperplasia (androgenital syndrome) due to deficiency of 21 hydroxylase (most common) 11- hygroxylase. 3- hydroxysteroid dehydrogenase. - Tumor Adrenal adenoma Carcinoma. 31. Hyperandrogenism is seen in