Produits Quantités ACETYLCYSTEINE, oral, 100mg/5ml, poudre, flacon 120ml ACETYLCYSTEINE, oral, 100mg/5ml, poudre, flacon 120ml ACETYLCYSTEINE, oral, 200mg, poudre, sachet, boite 20 ACETYLCYSTEINE, oral, 200mg, poudre, sachet, boite 20 ALBENDAZOLE, oral, 400mg, comprime, boite 100 AMOXICILLIN + CLAVULANIC ACID, oral, 500+62.5mg, comprime, boite 24 AMOXICILLIN, oral, 125mg/5ml, poudre,
Adnexa.itHair loss in women
A. TOSTI 1, B. M. PIRACCINI 1, A. SISTI 1, B. DUQUE-ESTRADA 2 Hair loss in women is a very common clinical
complaint, and is usually associated with severe
University of Bologna, Bologna, Italy emotional distress. In this article, the authors
review the most common clinical causes of hair
Prof. Rubem David Azulay, Rio de Janeiro, Brazil loss in women, and emphasize the role of hor-
monal changes in the regulation of hair loss and
Key words: Alopecia - Trichotillomania - Contra-
ceptive agents - Postpartum period - Biotin.
Telogen hair loss is due to mild/moderate insults that induce premature entering of sev-eral follicles in telogen, with shedding of tel- Hair loss in women is a very common clin- ogen hair after three months. ical complaint, that is usually associated The first step for the correct diagnosis of a Hair cycle
patient with hair loss is to establish if the hair density is normal or decreased. It is then nec- Hair follicles have a cyclic activity charac- essary to evaluate the severity of hair shed- terized by alternance of hair shaft produc- ding (pull test, Table I) and to examine the tion and resting (anagen, catagen, and telo- lost hair at the microscope 2, 3 (Table II), to establish if the hair loss involves the anagen or the telogen phase of the hair cycle.
Anagen hair loss is always dramatic, since it is due to diseases that acutely interrupt Grasp a tuft of hairs 2 cm from the scalp emergency and mitotic activity of anagen follicles (drugs, gently pull with the thumb and index fingers along thehair shafts toward the distal tip.
alopecia areata). Severe damage to the grow- ing hair results in hair breaking after scalp • Diffuse hair loss: the pull should be done in at least • Patterned hair loss: the pull should be done both in the androgen- and non androgen-dependent scalp Accepted for publication on March 25, 2009. • Patchy hair loss: the pull should be done at the patch margins and in the apparently unaffected scalp Corresponding author: A. Tosti, MD, Department of A pull test producing more than 10 hairs the same day or Dermatology, University of Bologna, via Massarenti 1, 40138 Bologna, Italy. E-mail: firstname.lastname@example.org one day after shampooing indicates increased shedding.
TABLE II.—Examination of lost hair at the microscope. Androgenetic Slowly progressive hair TE: telogen effluvium; PCOS: polycystic ovarian syndrome; DLE: discoid Lupus erythematosus; FD: folliculitis decalvans.
gen). During the anagen phase the follicles 85-90% of follicles are in the anagen phase produce the hair shaft. Duration of anagen, which in the scalp ranges from two to seven During pregnancy, there is an increase in years, determines hair shaftlength. Catagen is the number of hair follicles in anagen phase, a transitional phase, lasting two-three weeks, which precedes the resting telogen phase.
phase during the second and third trimesters During telogen, hair production is absent of pregnancy and for about a week after birth.
even if the shaft remains within the follicle to Six weeks after delivery, the anagen rate falls be shed only when, after three months, the to about 75%, as many follicles shift to the tel- follicle re-enters the anagen phase.
ogen phase simultaneously. The level of hair The hair cycle of adjacent scalp follicles is follicles in telogen rises sharply to 35%. As the not synchronized: in normal conditions, about telogen phase takes about three months, an be very severe and induce visible thinning.
three months after delivery.4 Available infor- Patients with postpartum TE are often very mation indicates that 17-β estradiol may pos- sibly cause prolongation of the anagen phase assume that it will lead to baldness. The during pregnancy and prolactin is involved in patient should be explained that TE repre- sents excessive hair shedding rather than actual hair loss, but that the condition needs pregnancy that contributes to the large vol- strict monitoring as it may precipitate the umes of hair observed during this period is development of androgenetic alopecia in pre- the increase of the hair shaft diameter that is plete in the majority of patients, however, in some cases, hair regrowth is incomplete and Clinical evaluation
patients concern about reduction of scalp hair and deterioration of the hair quality with A normal hair density suggests a diagnosis increased loss of telogen hair. It may be acute decreased postnatal levels of estradiol and thyroxine. According to this theory, restora- estradiol, rather than hormone replacement therapy, should improve clinical symptoms.
temic diseases, drugs, fever, stress, weight loss, delivery, iron deficiency and inflamma- tory scalp disorders. In cases where no appar- Interruption of oral contraceptives is also ent cause is found, screening for thyroid dis- frequently followed by TE. This is due to the ease with T4 and TSH must be done, as both, fact that the estrogens contained in the con- hypo- and hyper-thyroidism may cause TE.
traceptives prolong anagen duration and syn- Syphilis serology and antinuclear antibody chronize the hair cycle, similarly to what hap- pens in pregnancy. This is followed by con- A patient suffering from TE claims that hair temporary entry into telogen of a large num- is falling out. In TE, daily shedding increas- ber of follicles after estrogen interruption. In es and hair loss is severe with a daily shed- some cases, however, transitory hair loss is ding of 100 to 200 telogen hair and patients seen 3-5 months after beginning of treatment remember quite precisely when the increased hair shedding had started. Acute TE does not usually produce visible alopecia, as about 50% of hair should be lost before noticing Epidemiology studies show that iron defi- an evident reduction of the hair density. ciency is very common in adult females and At the pull test six or more telogen hairs are that iron intake with the diet is today scarce in many developed countries. Screening for iron deficiency can be done using hemoglo- bin and serum ferritin. Although most labo- A typical example of acute TE is postpar- ratories consider as normal a value of fer- tum effluvium. Postpartum TE does not occur ritin of 10-15 ng/ml, this cut off is definitely not sensitive in detecting iron deficiency in might not develop TE after each pregnancy.
It usually starts two to four months after deliv- and UK experts in the hair field believe that ery and may last as long as one year, even if it usually resolves after six months. It may patients maintain a serum ferritin concentra- tion greater than 70 ng/mL.9 We personally reduction in the diameter, length and pig- mentation of the hair. Hair thinning is limit- ed to androgen dependent scalp regions and results from the effects of the testosterone androgen-sensitive hair follicles. Androgen aggravate TE. A “brain-hair follicle axis” has sensitivity is genetically determined and been recently proposed, based on anatomi- cal and biochemical evidence and on exper- imental studies in mice.10 According with this AGA is well known, but the causative genes hypothesis, stress may increase substance P, are still undiscovered: variability in the andro- both systemically and locally. This may lead by several groups.13 A genetic test that eval- to mast cell and macrophage activation with release of inflammatory antiproliferative cytokines that induce hair follicle apoptosis introduced to predict risk for androgenetic with premature termination of hair growth.11 The occurrence of acute reversible TE 2-4 months after a severe emotional stress is well- sign of hyperandrogenism, together with hir- known and represents an in vivo evidence of sutism and acne. Female androgenetic alope- absence of biochemical and/or clinical evi- dence of androgen excess; this has been tra- This condition is characterized by increased ditionally explained as the result of an exces- sive follicular sensitivity to androgens. The months. It mostly affects middle aged women possibility that non-androgen dependent fac- tors can be important in female hair loss is suggested by the moderate efficacy of antian- than 100 hairs), but patients are very dis- drogens in the treatment of women with AGA tressed and complain of progressive tempo- and by the occurrence of this condition in ral thinning and decreased hair mass. Scalp women with genetic disorders characterized pain (trichodynia) is frequently reported.
Female AGA presents with diffuse hair thin- patient’s complaint and clinical evidence, ning of the crown region with maintenance since these patients usually have a high hair of the frontal hairline (Ludwig pattern). This density and feel not considered by the doc- can easily be appreciated by making a cen- tor who does not see any clinical abnormal- tral parting and comparing the hair density at ity. They may even bring in envelops of shed the top with hair density at the occipital hairs to prove the amount of hair loss.
Chronic TE has a chronic course with peri- Androgenetic alopecia is often precipitat- ed and worsened by conditions that induce specific scalp regions (patterned alopecia), increased hair loss is followed by regrowth of involve the whole scalp (diffuse thinning), or thinner hairs, or by drugs with androgenic present with bald patches (patchy alopecia).
effects. Contraceptives containing androgenic progestants (nortestosterone-derivatives lev- onorgestrel) may in fact induce or worsen androgenetic alopecia.15 Acne, androgenetic common form of hair loss, affecting up to effects of levonorgestrel releasing-implants, 50% of women in the course of their life. due to the androgenic effects of their prog- estants. These side effects are more common AA affects both sexes at any age and often in the initial months of use, when the prog- starts during childhood. Clinical examination estin levels are higher, than later on.16 reveals one or multiple well-circumscribed Androgenetic alopecia has also been report- smooth patches of non-scarring absence of ed in children treated with triptorelin for pre- hair that enlarge in a centrifugal way. The cocious puberty.17 Goserelin may cause hair margin of the patches often presents 3-mm loss and androgenetic alopecia in susceptible women.18 Tamoxifene and non-steroidal aro- (exclamation point hairs) that indicate dis- matase inhibitors utilized for the therapy of ease progression. AA may affect any hairy cause or worsen androgenetic alopecia.
whole scalp (AA totalis) or all body hair (AA common side effects of treatment with the non-steroidal aromatase inhibitors letrozole and vorozole.19 Up to 12% of women receiv- mune diseases, most commonly thyroid dis- ing oral esterified estrogens-methyltestos- eases. Other possible associations include menopause experience alopecia and/or oth- Trichotilomania is an intriguing psychoso- er androgen dependent skin signs, such as matic entity in which there is an irresistible desire to manipulate and pull out the hair.
AGA is a progressive disease that tends to The process results in an instant release of tension, a sense of relief and security. It usu- ally involves the scalp hair, but may occa- other parts of the body. On physical exami- nation, the scalp shows irregular patches of leading to diffuse alopecia is a typical side hair loss with typical bizarre borders. Inside effect of cancer chemotherapy and scalp radi- the plaques, short broken hair with variable Hair loss usually starts four-six weeks after crusts or scales due to follicle damage. The drug intake and is severe with up to 1 000 development of trichobezoar following inges- tion of the pulled hair is a rare complication. Hair regrowth is usually very fast after dis- continuation of therapy, but hair shape and Treatment
are completely devoid of hair (alopecia area- ta, cicatricial alopecia) or present short bro- ferritin levels should be at least 40 ng/mL despite the fact that normal serum ferritin levels range from 20-70 ng/mL.23, 24 Oral iron non-cicatricial alopecia, affecting up to 2% of the population, characterized by patchy given until a concentration of 70 ng/mL is hair loss in the absence of skin inflammato- genetically predisposed individuals, differ- ent triggering factors (stress, viral infections) cause an autoimmune T cell-mediated reac- Biotin is a water-soluble B-complex vita- tion against the hair follicles that result in min, present in a variety of foods and is also synthesized by intestinal bacteria. Biotin is found in egg yolks and it has very high affin- strength, making the scaling disappear, and ity to avidin, which is found in egg whites.25 accelerating the hair growth rate, hence the It was discovered as a vitamin when it was recognized that could prevent dermatitis, alopecia and neurological abnormalities in been reported that mild degrees of biotin animals given a diet containing large amounts deficiency is common in normal pregnancy.
of raw eggs.26 Biotin is required by carboxy- This finding was interestingly reversible with lases catalyzing the cellular metabolism of biotin supplementation 30 during pregnancy.
glucose, amino acids, and fatty acids. The Biotin supplementation after delivery can be important role of biotin in human physiolo- useful to prevent or reduce postpartum TE, gy has been highlighted by the recognition of even though controlled studies are needed.
two discovered human inborn errors of the metabolism of biotin. The molecular defect in the neonatal-onset disease is in the enzyme holocarboxylase synthetase and the defect in the later infantile-onset disease is in the loss with scalp cooling has been proposed by enzyme biotinidase. Both disorders present some authors. Despite the fact that there are with impressive clinical manifestations involv- only few case series and no patterned para- ing the skin and hair. In the neonatal dis- ease, alopecia totalis is associated with a chemotherapy-induced hair loss, especially bright red scaly total body eruption. In bio- when anthracyclines or taxanes are used.21 tinidase deficiency, alopecia presents as Minoxidil 2% has also proven to shorten the patches and the skin lesions resemble acro- period of baldness caused by chemotherapy.22 dermatitis entheropatica. Diagnosis is straight- forward, by biotinidase activity determina- tion in plasma or serum, and the condition should be considered in any cases of hair Medical treatments of AGA include 2% top- loss particularly associated with neurologi- ical minoxidil and the oral type II 5 alpha cal, dermatological, or respiratory illness.
reductase inhibitor finasteride at the dosage Both disorders are rapidly responsive to oral biotin (10 mg daily), and early diagnosis and women should be associated with oral con- traception.31 Treatment should be prolonged It is also reported that the antiepileptic drug valproic acid may lead to biotin defi- ciency and low serum and liver tissue bio- tinidase enzyme activity. In a recent study, The fist episode of AA frequently resolves biotin supplementation decreased the inci- spontaneously. Effective treatments include dence of alopecia in rats, from to 40% in the systemic steroids at high dosages, high poten- valproic acid group vs. 13% in the valproic cy topical steroids under occlusion and top- ical immunotherapy.37-39 Treatment is less effective in severe alopecia areata and relaps- to improve the hair quality in patients with es occur in a high percentage of patients, “umcombable hair” (pili trianguli et canali- culi) a hair shaft disorder characterized by dry, unruly, hair (spun-glass) due to abnor- mal hair shaft shape. Biotin supplementation at the dosage of 5 mg daily improves clinical appearance and combing problems,28 despite eral agents including selective serotonin reup- the hair shaft defect seen at scanning electron take inhibitors (SSRIs) at high dosage and microscopy remain. Shelley and Shelley sug- gested that biotin acts by increasing the root tive-behavior therapy are also useful.
16. Brache V, Faundes A, Alvarez F, Cochon L. Non-men- strual adverse events during use of implantable con- traceptives for women: data from clinical trials.
17. Kauschansky A, Lurie R, Ingber A. Hair loss in chil- La caduta dei capelli nelle donne è un segno cli- dren on long-acting gonadotropin-releasing hormone nico frequentemente riportato, ed è solitamente agonist triptorelin treatment. Acta Derm Venereol associato a gravi situazioni di stress emotivo. In que- sto articolo, gli autori presentano una revisione del- 18. Gateley CA, Bundred NJ. Alopecia and breast disease.
le cause cliniche più frequenti di caduta dei capel- 19. Simpson D, Curran MP, Perry CM. Letrozole: a review li nelle donne, ed enfatizzano il ruolo dei cambia- of its use in postmenopausal women with breast can- menti ormonali nella regolazione della caduta e cre- 20. Phillips E, Bauman C. Safety surveillance of esterified estrogens-methyltestosterone (Estratest and Estratest Parole chiave: Alopecia - Alopecia areata - Tricotillo- HS) replacement therapy in the United States. Clin 21. Grevelman EG, Breed WP. Prevention of chemother- apy-induced hair loss by scalp cooling. Ann Oncol 22. Duvic M, Lemak NA, Valero V, Hymes SR, Hymes SR, References
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WIE MAN(N) EINE PRINZESSIN WIRD © Copyright Cheryl Ann Costa 1994. All rights reserved. © Copyright der deutschen Übersetzung Thespis-Verlag, 1999Dieses Stück kann entweder als Monolog oder als Einakter umge-In der Version als Einakter gibt es Teile eines metaphorischenMärchens vor jeder Szene, welche in der Monolog-Version wegge-lassen oder eingangs als ganzes Märchen erzählt werde