What is Medicine – Alopecia
Alopecia is the absence of hair from areas where it normally grows. It can be classified as scarring (cicatricial), nonscarring (noncicatricial), or structural. Hair that is brittle or fragile due to aberrant hair growth or external trauma is referred to as structural hair problems. EPIDEMIOLOGY Prevalence Androgenic alopecia: - In men, 30% Caucasian by age 30, 50% by age 50, and 80% by age 70 - In women, 70% of women over 65 - AA: 1/1,000 with lifetime risk of 1-2%, men and women affected equally - Scarring alopecia: rare, 3-7% of all hair disorder patients. Scarring (cicatricial) alopecia is an inflammatory condition that results in the follicle's permanent destruction. Lymphocytic, neutrophilic, and mixed inflammation are the three main kinds. Primary scarring includes discoid lupus, lichen planopilaris, dissecting cellulitis of the scalp, primary fibrosing, among other conditions. - Secondary scarring brought on by physical damage, such as tinea capitis, surgery, radiation, and neoplasm - The most prevalent type of scarring hair loss in African American women is central centrifugal cicatricial alopecia; its cause is unknown but is probably related to hair care habits. Noncicatricial (nonscarring) alopecia, Focal alopecia, and AA Patchy hair loss, typically due to an inflammatory condition, T cell-mediated inflammation, and an early transition into the catagen and telogen phases. Alopecia universalis, which causes a rapid loss of all body hair, and alopecia totalis, which affects only the scalp, are possible co-occurring conditions. High psychiatric comorbidity (1) - Frequent nail illness - Alopecia syphilitica: "moth-eaten" appearance, secondary syphilis - Postoperative, pressure-induced alopecia: caused by sustained pressure on a single scalp region Traction alopecia: patchy hair loss brought on by physical tension from braids, ponytails, and hair weaves. Temporal triangular alopecia: congenital patch of hair loss in the temporal area, unilateral or bilateral Hair changes from terminal to vellus hairs in those with androgenic alopecia, a kind of pattern hair loss. - Male pattern hair loss: androgen-mediated hair loss in a specific pattern; bitemporal and vertex hairs on the scalp are androgen sensitive. This disorder is primarily inherited. Increased 5-reductase and androgen receptors increase the rate at which testosterone is converted to dihydrotestosterone (DHT) in the follicle. As a result, follicle size is reduced and vellus hair is produced (2). Types I to VII of the Norwood Hamilton categorization Female pattern hair loss is characterised by vertex and frontal thinning (Ludwig classification, grades I to III). More testosterone is available for the conversion of to DHT in females with low levels of aromatase (3). This has an illegible pattern of inheritance (2). Adrenal hyperplasia, pituitary hyperplasia, and polycystic ovarian disease all cause androgen alterations that can cause alopecia. - Drugs (testosterone, progesterone, danazol, adrenocorticosteroids, anabolic steroids), medications (hormone replacement therapy, oral contraceptive pills), and oral contraceptive pills. Trichotillomania is the deliberate pulling out of hair from the scalp, and it can take many different forms. The abrupt transition of many follicles from the anagen to the telogen phase, which results in reduced hair density but no bald spots, is known as diffuse alopecia-telogen effluvium. Can be chronic with continuous illness, such as SLE, renal failure, IBS, HIV, thyroid disease, pituitary dysfunction, and occur 2 to 3 months after event. May occur after substantial stressors, such as delivery, accident, or illness; occurs 2 to 3 months after event Malnutrition from malabsorption, eating disorders, and a poor diet can all contribute. Adding or altering drugs (oral contraceptives, anticoagulants, anticonvulsants, SSRIs, retinoids, -blockers, ACE inhibitors, colchicine, cholesterol-lowering meds, etc.) is another factor. - A. effluvium Days to weeks following the triggering event; interruption of the anagen phase without a transition to the telogen phase The most frequent trigger is chemotherapy, although additional causes include radiation, toxicity, and medicines. Structural hair diseases include Menkes disease, monilethrix, and other inherited hair conditions. These cause the development of weaker, aberrant hairs. may also be caused by heat or chemical damage from hair-processing procedures. Genetics Androgenic alopecia, like AA, is frequently accompanied with a family history of early patterned hair loss. RISK FACTORS include: genetic susceptibility; chronic illnesses such as autoimmune disorders, infections, and cancer; physiological stress such as childbirth; inadequate nutrition; medication, chemotherapy, and radiation; and hair chemical treatments, braids, and weaves/extensions. GENERAL PREVENTION Reduce risk factors as much as you can. COMMONLY ASSOCIATED CONDITIONS Vitiligo—a condition that affects 4.1% of people with AA and may be caused by the same autoimmune mechanisms DIAGNOSIS The history and examination are used to make a clinical diagnosis. HISTORY Description of the hair loss issue, including the amount of hair lost, where it is occurring, how much hair has been lost, and accompanying symptoms like itching and infection. Hair styling practises such as using prolonged heat, colouring, bleaching, chemical relaxers, and hair styling (braids and ponytails) are associated with pruritus, pain, or burning. Medications are also used to treat medical conditions such as chronic illness, recent illness, surgeries, pregnancy, thyroid disorder, iron deficiency, poisonings, and exposures Stress on the mind, dietary history, and changes in weight family history of autoimmune diseases or hair loss Physical examination: Generalised, patterned, and focused hair loss - Examine broken hair, vellus versus terminal hairs, and hair density. scaling, inflammation, papules, and pustules on the scalp Follicular ostia are used to categorise different types of alopecia. Test for hair pulling involves pinching 25–50 hairs between the thumb and forefinger and pulling slowly and gently while sliding the fingers up. Normal: 1 to 2 displacement Unusual: six dislodged hairs Hair that is broken (structural abnormality) Border patch with easily removeable broken-off hairs (in AA) Other-site hair loss, nail problems, and skin changes Clinical indicators of virilization include acne, hirsutism, acanthosis nigricans, and truncal obesity. Clinical signs of thyroid illness, lupus, or other conditions DETECTION & INTERPRETATION OF DIAGNOSIS Initial examinations (lab, imaging) Depending on the clinical presentation, testing might not be necessary. Nonandrogenic alopecia - TSH, CBC, ferritin - Take into account LFT, BMP, zinc, VDRL, ANA, and prolactin depending on the clinical history and exam Androgenic alopecia: Free testosterone and dehydroepiandrosterone sulphate should be taken into consideration, especially in females. Other/Diagnostic Procedures Light hair-pull test: Pull on 25 to 50 hairs; 6 or more hairs coming loose is indicative of shedding (effluvium, AA). Direct microscopic examination of the hair shaft - Exclamation point hairs: club-shaped root with thinner proximal shaft (AA) - Broken and distorted hairs may be related to various hair dystrophies. Anagen hairs have elongated, distorted bulbs with attached root sheaths. Telogen hairs have rounded bulbs without root sheaths. Biopsy: scarring (cicatricial) alopecia or, if the cause is still uncertain, two 4-mm punch biopsies are advised. Take the biopsy at the margin of inflammation in scarring alopecia. Take the biopsy in a region with thinning hair but not full hair loss if you have non-scarring alopecia. Lymphocytic inflammation with perifollicular fibrosis. Androgenic alopecia: fluctuating hair shaft size, follicular miniaturisation, and a 2:1 terminal: vellus hair follicle ratio Telogen effluvium: increased catagen:telogen ratio, unchanged number of hair follicles, and no follicle miniaturisation Increased catagen:telogen ratio, no change in the number of hair follicles, and follicular miniaturisation are all signs of AA. To rule out tinea capitis, potassium hydroxide preparation and ultraviolet light fluorescence GENERAL TREATMENT MEASURES Prior to starting treatment, weigh the advantages and disadvantages for the patient. A better quality of life will benefit many people. If you can, stop taking any medications that might be the source of your telogen effluvium. Address underlying medical issues (such as syphilis or a thyroid condition). Traction alopecia: Alter hair-care routines and provide instruction Trichotillomania: psychological treatment is frequently needed to change behaviour NON-SCARING MEDICATION Androgenic alopecia: Treatment must be continued continuously; it may be used in conjunction with Minoxidil (Rogaine), which is effective in 60% of cases and comes as 2% and 5% topical solutions (1 mL BID) for women and foam (daily) for men. Skin irritation, hypertrichosis of the hands/face, and tachycardia are side effects that are Category C in pregnancy; the drug's mechanism of action is unclear and it seems to prolong the anagen phase. Finasteride (Propecia): 1 mg/day for men and women (off-label); 30-50% improvement in men; poor data in women; 5-reductase inhibitor; reduces DHT in system; increases total and anagen hairs; slows transition of terminal to vellus hairs; adverse effects: loss of libido, gynecomastia, depression. Category X, dependable contraception is required for female usage, with caution in the presence of liver disease, and absolutely no use or contact during pregnancy.- 100 to 200 mg/day (off-label) of spirolactone (Aldactone)Ketoconazole reduces DHT levels at follicles and works best when combined with minoxidil to treat female androgenic alopecia. It is an aldosterone antagonist and antiandrogen that blocks the effect of androgens, reducing testosterone production. - Combination: Compared to monotherapy, finasteride with minoxidil is more effective. AA: high rate of spontaneous remission in patchy AA; no FDA-approved treatment Intralesional steroids (triamcinolone: 2.5 to 5.0 mg/mL) are injected every 4 to 6 weeks into the deep dermal layer at intervals of 0.5 to 1.0 cm using a 1/2 inch 30-gauge needle. Adverse effects include local burning, itching, and skin atrophy. - Systemic glucocorticoids: Used in severe, multifocal AA; may stimulate regrowth; long-term monthly treatment is necessary to sustain growth Negative effects include obesity, cataracts, osteoporosis, hyperglycemia, and adrenal insufficiency. - Prednisone and PUVA light therapy: modest effectiveness in diffuse AA Tinea (Capitis, Corporis, Cruris): See "Tinea (Capitis, Corporis, Cruris)." SURGICAL/OTHER PROCEDURES Extensions, hairpieces, and wigs Surgery is sometimes performed to treat scarring alopecia and involves graft transplantation, flap transplantation, or removal of the scarred area. Platelet-rich plasma has been demonstrated to revive dormant hair follicles and promote new hair development. ALTERNATIVE & COMPLEMENTARY MEDICINE Volumizing shampoos can make the remaining hair appear fuller; there are many herbal treatments available. CONTINUING CARE Supplementation may be required if a nutritional shortfall is found. EDUCATION OF PATIENTS Website of the National Alopecia Areata Foundation Androgenic alopecia prognosis is based on how well the patient responds to treatment. AA: Even without therapy, it frequently grows back within a year. Recurrence is frequent. 10% of cases are severe and chronic, and the likelihood of a poor prognosis increases with time, substantial hair loss, autoimmune disease, nail involvement, and young age. Telogen effluvium: maximal shedding occurs three months after the trigger event, and recovery occurs after the cause is addressed. usually goes away in 3 to 6 months, but it takes 12 to 18 months for cosmetically significant hair growth to resume; rare cases of permanent hair loss, which are typically associated with long-term sickness. Anagen effluvium: Shedding starts days to a few weeks after the triggering event, recovering if the cause is corrected; in rare cases, permanent hair loss occurs. Excellent prognosis for traction alopecia with behaviour adjustment Cicatricial alopecia: irreversible damage to hair follicles; prognosis depends on alopecia type and available therapies. Excellent prognosis for tinea capitis with therapy
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