dietary supplement increases anagen hair rate in women ... · deficiency of sulfur-containing amino...

RESEARCH ARTICLE

Dietary supplement increases anagen hair rate in women with telogen effluvium: results of a double-blind, placebo-controlled trial
Nadine Lengg1, Barbara Heidecker1, Burkhardt Seifert2 & Ralph M Trüeb1†
†Author for correspondence1Department of Dermatology, University Hospital of Zurich, Gloriastr. 31, 8091 Zurich, SwitzerlandE-mail: [email protected] of Biostatistics, Institute for Social and Preventive Medicine, University of Zürich, Zürich, Switzerland

part of

Keywords: anagen hair rate, CYP complex, dietary supplement, Pantogar®, telogen effluvium, TrichoScan, women

10.2217/14750708.4.1.59 © 20

Background: Dietary supplements are traditionally used over-the-counter products for the treatment of hair loss. Objectives: We aim to examine the effect of a specific L-cystine, medicinal yeast, pantothenic acid complex-based dietary supplement (Pantogar®) on telogen effluvium in healthy women. Methods: A randomized, double-blind, placebo-controlled study was conducted over 6 months in 30 healthy women suffering from telogen effluvium. The efficacy of the supplement was evaluated by means of digitalized epiluminescent microscopy (TrichoScan) performed before treatment and after 3 and 6 months. Additionally, global photographs were taken and evaluated by independent investigators. Results: Active compound led to a statistically significant improvement and normalization of the mean anagen hair rate within 6 months of treatment (p = 0.003), while there was no significant change in the placebo group (p = 0.85). These changes of the anagen hair rates were significantly different (p = 0.008). The appearance of hair growth in the global photographic assessment was judged better in the active compound than in the placebo group. Conclusions: This is the first study performed combining epiluminiscence microscopy with digital image analysis to demonstrate that a dietary supplement influences hair growth. The mode of action is not known, although it seems to result from an induction of anagen.

Dietary supplements are traditionally used over-the-counter (OTC) products for the treatmentor prevention of hair loss. Typically, they arebased on a combination of L-cystine and vita-mins, usually of the B-complex group, includ-ing pantothenic acid and p-aminobenzoic acid(PABA). The rationale for the use of L-cystinefor the treatment of hair loss is based on thebiochemistry of cystine metabolism, clinicalobservations in disorders of cystine metabolismand cystine deficiency and results of animal andhuman studies. L-cystine, a natural, aliphaticamino acid, is a constituent of keratin. Accord-ingly, hair contains a high proportion of L-cys-tine (15.9%). In trichothiodystrophy, there is adeficiency of sulfur-containing amino acids inthe hair, resulting in increased brittleness. Inhomocystinuria, the hair is thin and hypopig-mented. In HIV trichopathy, disorders of thecystine-dependent amino acid metabolism andglutathione-dependent detoxification mecha-nisms lead to dry, fragile hairs, hair loss and pre-mature graying. In the 1960s, the role ofL-cystine in the production of wool was investi-gated and it was found that enrichment of evenwhat appeared to be a normal diet with sulfur-containing amino acids increased wool produc-tion in sheep [1–3]. When considering which

dietary supplements could be used for improv-ing hair growth in humans, L-cystine was there-fore a candidate. In the early 1990s, studies onthe effect of dietary supplements containingL-cystine, in combination with B-complex vita-mins and medicinal yeast, a rich natural sourceof B-complex vitamins, were published, dem-onstrating improvements in the trichogram(hair pluck test), in hair swelling as a criterionfor hair quality and in the tensile strength of thehair fiber [4–6].

The aim of this study was to investigate theeffects of a L-cystine, medicinal yeast and pan-tothenic acid (CYP) complex-based dietarysupplement (Pantogar®) on hair growth inhealthy women with telogen effluvium usingthe TrichoScan.

Patients & methodsPatients & treatmentThe trial was carried out as a single-center,randomized, double-blind, controlled, para-llel-group study to compare the efficacy ofactive compound (Pantogar) with placebo intreating telogen effluvium in otherwise healthywomen over a treatment duration of 6 months.Women aged 25–65 years were recruitedthrough advertisement in the lay press.

07 Future Medicine Ltd ISSN 1475-0708 Therapy (2007) 4(1), 59–65 59

RESEARCH ARTICLE – Lengg, Heidecker, Seifert & Trüeb

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Inclusion criteria were a history of increasedhair loss, with or without clinical findings offemale pattern hair loss (FPHL) Ludwig type Ior II and a centroparietal telogen hair rategreater than 20%, determined by TrichoScan.

Exclusion criteria included: symptomatic dif-fuse alopecia (e.g., resulting from iron deficiencyor thyroid gland disorder); FPHL Ludwigtype III; androgenic alopecia with or withoutsigns of virilization as result of polycystic ovaries,late onset adrenogenital syndrome or tumors ofthe ovaries, adrenals or pituitary gland; systemicautoimmune diseases; wasting diseases(e.g., AIDS or malignant disease); alopeciaareata; inflammatory scarring or other scarringalopecias; other inflammatory conditions affect-ing the scalp (e.g., seborrhoeic dermatitis, pso-riasis or contact dermatitis); any treatment forhair loss or participation in another clinical trialwithin 3 months prior to entering the study; useof drugs that may cause hair loss (e.g., anticoag-ulants, lipid-lowering drugs, retinoids, antiepi-leptics, β-blocking agents, angiotensin-converting enzyme (ACE) inhibitors, antithy-roid drugs, androgens, progestagens with partialandrogenic effect, aromatase inhibitors,cytokines or cytotoxic drugs) within 3 monthsprior to entering the study; use of sulfonamide-containing drugs (interaction with PABA); initi-ation or termination of hormone-replacementtherapy or hormonal contraception within6 months prior to entering the study; any typeof hormone-replacement therapy or oral contra-ception containing a progestagen with andro-genic effect (e.g., norethisterone, norgestrel,levonorgestrel, lynestrenol or tibolone); preg-nancy or lactation; or known hypersensitivity toany component of Pantogar.

The study was approved by the local EthicsCommittee. If the patient was suitable for thestudy and had given written informed con-sent, she was randomized into one of the twotreatment arms and supplied with the activecompound or placebo.

The composition of the active compound was:

• One active compound capsule: L-cystine20 mg, keratin 20 mg, medicinal yeast100 mg, calcium pantothenate 60 mg, thia-mine nitrate 60 mg and PABA 20 mg.

• One placebo capsule: no active ingredient, lac-tose, microcrystalline cellulose and magne-sium stearate.

The dosage was one capsule three-times dailywith meals for the 6-month study duration.

MethodsThe diagnosis of telogen effluvium was basedon an increase of the telogen hair rate greaterthan 20% in the centroparietal scalp area,determined by the TrichoScan, and carefulexclusion of other causes of hair loss. Thisincluded an in-depth history and clinicalexamination related to the start and durationof hair loss and its pattern. A careful personalhistory of diet, illness, operations and medica-tions, including hormones, was taken. The fol-lowing laboratory screening tests wereperformed (normal ranges): C-reactive protein(CRP; <5 mg/l), ferritin (>10 µg/l) and basalTSH (0.27–4.20 mU/l).

To determine the telogen hair rate for inclu-sion, the anagen hair rate, hair count, hair den-sity and cumulative hair shaft diameterthroughout the study, an area of 1.8 cm2 wasdefined in the centroparietal scalp using a sten-cil template (diameter 16 mm). In this testzone, the hair was clipped (Hairliner, WellaGermany). All clipped areas were marked with acentral, single red tattoo. The tattoo was visiblethroughout the study. Gray or fair hairs haveonly limited contrast compared with the scalp,therefore, the clipped hairs within the targetarea were dyed with a commercially availablesolution (RefectoCil®, Gschwentner, Vienna,Austria). Thereafter, the colored area wascleansed with an alcoholic solution (Kodan®

Spray, Schülke & Mayr, Vienna, Austria) anddigital images were obtained at 20-fold (ana-lyzed area: 0.62 cm2) magnification by meansof a digital epiluminiscence microscopy (ELM)system (Fotofinder DERMA, Teachscreen Soft-ware, Bad Birnbach, Germany) while the areawas still wet. This digital camera is equippedwith a rigid contact lens that ensures that theimages are always taken at the same distancefrom the scalp. Images were taken at day 0immediately after clipping, 3 days after clip-ping and 3 and 6 months after the initial visit,respectively. For measurement of anagen hairrate, hair count, hair density and cumulativehair diameter, a commercially available soft-ware (TrichoScan) developed specially for thispurpose was used (DatInf, Tübingen) [7].

The measures of outcome were the anagenhair rate at baseline, and after 3 and 6 monthsof treatment, and the hair count, hair densityand cumulative hair shaft diameter at baselineand close-out (6 months). Standardized Polar-oid photographs were taken for documentationof clinical outcome at baseline and close-out.

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Dietary supplement in women with telogen effluvium – RESEARCH ARTICLE

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Table 1. Results of a

n M

T = 0 months 15 7

T = 3 months 14 7

T = 6 months 15 8

SD: Standard deviation.

For this purpose, the patients’ head was placedin a stereotactic device and Polaroid photo-graphs were taken of the vertex and frontalareas, as described previously [8]. Assessment ofthe serial photographs was made independ-ently and in a blinded manner by each of thethree investigators.

Randomization of patients was performedwith RANCODE version 3.6, including 50patients in blocks of ten. Treatment 1 was verumand treatment 2 was placebo at a ratio of 1:1,with no stratification.

StatisticsPatients receiving active compound were com-pared with placebo at baseline (T = 0),3 months (T = 3) and 6 months (T = 6), usingthe Mann-Whitney test. The statistical evalua-tion within one group (i.e., active compound orplacebo patients) was performed with the Wil-coxon signed rank test. These procedures pro-vide parameter-free methods with norequirements for a normal distribution of thepatient population. Regression analysis was car-ried out to determine the influence of age,serum ferritin levels (within nomal range) andpresence or not of FPHL Ludwig types I and IIon the change in anagen hair rate from baseline(T = 0) to close-out (T = 6).

ResultsA total of 47 patients were enrolled and 30 com-pleted the study: 15 in the active compoundgroup and 15 in the placebo group. In total,17 patients withdrew from the trial due to: ini-tiation of other treatment for hair loss (topicalestradiol; one on placebo) or use of drugs thatmay cause hair loss (desogestrel, antiepileptic,vitamin A and β-blocker; four, all on verum),patient individually unblinding capsules (three,all on placebo), other forms of noncompliance(three on verum), intercurrent febrile illness(two, one on placebo and one on verum), inter-current pregnancy (one on placebo), intercurrent

autoimmune disease (one on verum), gastroin-testinal upset (one on verum) and elevation ofpancreatic enzymes (one on verum).

The age range of those who completed the studywas between 38 and 61 years (mean: 51 years) inthe active compound group and 25 and 61 years(mean: 46 years) in the placebo group.

In 12 patients, no thinning of hair was discerni-ble (seven in the active compound group and fivein the placebo group), 15 women showed Ludwigtype I FPHL (seven in the active compound groupand eight in the placebo group) and three patientshad Ludwig type II FPHL (one in the activecompound group and two in the placebo group).

The serum ferritin levels (inclusion criterion>10 µg/l) in the total patient population was11–241 µg/l (mean: 62 µg/l). These levels were11–142 µg/l (mean: 51 µg/l) in the active com-pound group and 13–241 µg/l (mean: 73 µg/l)in the placebo group.

The results of the anagen hair rates (as per-centages) at baseline, 3 and 6 months are pre-sented in terms of descriptive statistics inTable 1. Baseline mean anagen hair rate was sim-ilar between the active compound (73%) andplacebo groups (75%). At the 3-month follow-up, both groups demonstrated improved ana-gen hair rates (78% in both groups) that wassatistically not significant. At 6 months, thebenefit from active treatment showed an addi-tional increment of the mean anagen hair rateto 81%, in contrast with placebo, which practi-cally fell back to baseline. The most remarkablefinding was that the active compound groupreached a physiological range of anagen hairrate greater than 80%, while the placebo groupdid not (Figure 1). Statistical analysis of thechange in the mean anagen hair rate in theactive compound group within the 6 monthsof treatment showed a statistically significantimprovement (p = 0.003), while there was nosignificant change in the placebo group(p = 0.85). Analysis of the change of the meananagen hair rate within the active compound

nagen hair count (%).

Active compound Placebo

ean (± SD) 1stquartile

Median 3rdquartile

n Mean (± SD) 1stquartile

Median 3rdquartile

2.5 (± 6.5) 67 76 77 15 75.3 (± 3.5) 74 76 77

8.5 (± 5.4) 75 79 83 15 78.2 (± 7.2) 71 81 84

0.5 (± 5.3) 76 83 85 15 75.6 (± 6.7) 69 77 69

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group compared with that of the placebo group inthe 6 months of treatment was also statisticallysignificant (p = 0.008).

The hair count, hair density and cumulative hairshaved diameter were not significantly differentfrom the baseline values in either group (Table 2).

The appearance of hair growth in the globalphotographic assessment was judged better inthe active compound than in the placebogroup (Table 3).

Finally, regression analysis did not show anyeffect of age, presence of visible hair thinning inthe vertex areas (FPHL) and serum ferritin lev-els above the lower limit of normal (10 µg/l) onchanges in anagen hair rate.

The active compound was generally well tol-erated. Four patients reported gastrointestinalsymptoms, four complained of weight gain andone had transient elevation of serum pancreaticenzymes, which was probably not related to theintake of active compound.

DiscussionTelogen effluvium in apparently healthy womenwas originally considered a distinct entity [9].Since the recognition of FPHL in women byLudwig [10], it seems that a majority of cases havebeen attributed to this diagnosis. The differentialdiagnosis includes symptomatic hair loss result-ing from hormonal disorders, malnutrition, pre-ceding or concomitant internal disease or adversedrug reactions [11]. In an estimated third of

women with persistent telogen effluvium, noprecipitating cause can be found. On the onehand, it is believed that complex etiologiesunderlie this type of hair loss, in which there isnot only one, but several factors interacting tocause the hair loss. On the other hand, ‘diffuseandrogen-dependent alopecia’ was proposed asan alternative explanation, on the assumptionthat it is also androgen-induced and thereforeFPHL [12]. However, controversy has arisen withrespect to the role of androgens in FPHL (sinceFPHL may occur before the onset of puberty),has been described in individuals with hypo-gonadism and does not respond to treatmentwith cyproterone acetate or finasteride in theabsence of pathologically elevated androgen lev-els [13–17]. Finally, diffuse cyclic hair loss inwomen, first described by Guy and Edmundson[18], has recently been redefined as a distinctentity on the basis of histological studies and re-named ‘chronic telogen effluvium’ (CTE) [19].This type of hair loss affects otherwise healthywomen complaining of persistent diffuse hairloss [20]. The authors attribute the disorder tosynchronization phenomena of hair cycling. Itactually represents exaggerated hair shedding orteloptosis, rather than regressive alopecia that ischaracteristic of FPHL or senescent alopecia.Accordingly, FPHL eventually presents with visi-ble thinning of the hair over the vertex area, andsenescent alopecia as age-dependent diffuse thin-ning of hair, as a result of progressive shortening

Figure 1. Improvement of anagen hair rate after treatment.

Mean ± standard deviation.

0 3 665

70

75

80

85

Months

An

agen

hai

r ra

te (

%) Normal range

Active

Placebo




Table 3. Assessment

A

Investigator 1 0

Investigator 2 0

Investigator 3 0

A: Active compound; P: Pla

of the anagen phase of the hair cycle. By con-trast, CTE essentially does not cause thinning ofthe vertex area. Although FPHL is not primarilydue to synchronization of hair cycling, partialsynchronization phenomena tend to complicateits course, particularly on a seasonal basis inautumn [21]. It has correctly been noted that thecombination of FPHL with CTE represents apotential complication for clinical trials, withdrugs such as minoxidil developed specificallyfor FPHL [22].

For the treatment of FPHL, minoxidil hasproven efficacy, while the management of CTEand the role of dietary supplements for thisindication have remained controversial. Previ-ous accounts of a benefit from the active com-pound Pantogar on hair growth have beenbased on patient questionnaires and tricho-gram examinations [4–6]. Direct questioning ofusers is popular in the assessment of hair thera-peutics; however, everyday practice shows thatit is not easy to put subjective complaints ofhair loss into objective terms, or to evaluatetreatment efficacy, particularly in women [23].Office-based techniques for evaluating hairloss, such as the trichogram and global photo-graphic assessment, are of limited use owing topoor reproducibility and are useful only in a

minority of patients who show clinically dis-cernible improvement of hair growth, respec-tively. Thus, a simple to perform, noninvasive,reproducible method for objective measure-ment of hair growth parameters was required.For this purpose, the TrichoScan was devel-oped, which combines ELM with digital imag-ing [7]. Relevant hair growth parametersmeasured with this technique are: anagen hairrate, hair count, hair density and cumulativehair shaft diameter.

This is the first study performed with the Tri-choScan to demonstrate that a CYP complex-based dietary supplement (Pantogar) influenceshair growth. After 6 months of treatment, theactive compound group showed a statistical sig-nificant improvement in anagen hair rate, whilethe placebo group did not. Although there was alarge number of drop-outs from the study (over athird of those enrolled), a breakdown of with-drawal criteria in relation to placebo or activecompound groups, following unblinding aftertermination of the study, did not suggest thatexclusion of these subjects should have biasedthe results. Improvement of the anagen counthas previously also been shown for treatment ofhair loss in women with another combinationproduct with L-cystine using the phototricho-

Table 2. Results of hair count, hair density and cumulative hair shaft diameter.

Active compound Placebo

n Mean (± SD) n Mean (± SD)

Hair count (n)

T = 0 months 15 188 (± 45) 15 171 (± 46)

T = 6 months 15 175 (± 36) 15 167 (± 39)

Hair density (n/cm2)

T = 0 months 15 233 (± 52) 15 219 (± 52)

T = 6 months 15 218 (± 37) 15 217 (± 46)

Cumulative hair shaft diameter (µm)

T = 0 months 15 19.1 (± 5.4) 15 17.3 (± 5.7)

T = 6 months 15 18.5 (± 4.3) 15 16.9 (± 4.5)

of global photographs.

Worsening Unchanged Improvement NA

-2 -1 0 +1 +2

P A P A P A P A P

0 0 1 3 9 3 0 0 0 12

1 0 1 2 5 6 3 0 0 10

0 0 2 3 7 5 1 0 0 10

cebo; NA: Not applicable.



64

Figure 2. TrichoScan

Increase in the proportionat close-out with the sam

Figure 3. Global pho

Example of clinical impro(B) 6 months after treatm

A

A

gram [24]. The hair count, hair density andcumulative hair shaft diameter did not show sig-nificant changes from the baseline values. Never-theless, the increase in anagen hair rate wasreflected in clinical outcome, since the appear-ance of hair in the global photographic assess-ment was also judged better in the activecompound group (Figure 2 & 3) compared withplacebo (Table 3). A conceivable explanation forthis observation would be the proportionateincrease in the number of terminal hairs in ana-gen, that is, actively growing terminal hairs. Thisis not detected by the hair count, hair density,and cumulative hair shaft diameter, since thesemainly reflect a gain of hair mass through vellus-to-terminal hair transformation. It is imaginablethat these observations would also exclude newlyacquired hypertrichosis as undesired effect of the

CYP complex-based compound (in contrast tominoxidil) since, on the body, vellus hairs wouldonly be driven into anagen. The mechanism ofaction is not known, although these data suggestthat the CYP complex-based active compound(Pantogar) has a therapeutic effect owing to aninduction of anagen. A similar effect has beenshown for topical melatonin, which is known tohave physiological effects on the hair cycle [25].

Since regressive alopecias, such as FPHL andsenescent alopecia, are due to progressive shorten-ing of the anagen phase and miniaturization ofthe hair follicle, it is apparent that they benefitfrom treatment with an agent with impact onhair count, hair density and cumulative hair shaftdiameter, such as minoxidil. Nevertheless, syn-chronization phenomena tend to complicate thecourse of regressive alopecias since, with a short-ened anagen phase, synchronization will tend tobe more marked. In this case, it is imaginable thatadding a CYP complex-based dietary supplementto the treatment regimen may be beneficial.Moreover, it has been shown in whole-hair folli-cle cultures that minoxidil not only increases theincorporation of thymidine (as a marker of celldivision), but also leads to an increased uptake ofcysteine by the hair follicle [26]. Consistent withthis, regression analysis showed that age (in viewof senescent alopecia) and presence of hair thin-ning at the vertex (in view of FPHL) did notinfluence changes in anagen hair rate.

Finally, serum ferritin levels within the nor-mal range above 10 µg/l did not influencechanges in anagen hair rate.

ConclusionIn summary, this is the first randomized, dou-ble-blind, placebo-controlled study performedwith the TrichoScan to demonstrate that aCYP complex-based dietary supplement (Pan-togar) leads to an increase of anagen hair rateand an improvement of the overall photo-graphic appearance within 6 months in other-wise healthy women with telogen effluvium.Due to its action on synchronization phenom-ena of hair cycling, indications for CYP com-plex-based dietary supplementation (Pantogar)would thus include postpartum effluvium, sea-sonal effluvium and diffuse cyclic hair loss inwomen or CTE. The effects were observedirrespective of patient’s age, presence of FPHLand serum ferritin levels within the normalrange above 10 µg/l. Therefore, it is conceiva-ble that CYP complex-based dietary supple-mentation may be useful in addition to

images.

of anagen hairs from (A) 65% at close-in to (B) 82% e hair count in the active compound group.

tograph.

vement in the active compound group, (A) before and ent.

B

B




Highlights

• Dietary supplements, acid (CYP complex) arthe treatment of hair

• This is the first randomperformed combininganalysis (TrichoScan) tsupplement influence

• The mode of action reinduction of anagen.

• Active coumpound lenormalization of the min otherwise healthy w

minoxidil therapy in the treatment of FPHL,whenever there is partial synchronization intelogen. Iron supplementation therapy seems

to be of less relevance in the treatment of dif-fuse hair loss in healthy women with normalserum ferritin levels, as previously alsochallenged by other authors [27,28].

DisclaimerThis study represents the Inaugural Dissertation of NadineLengg, University of Zurich, Switzerland. The results werepresented by Ralph M Trüeb on the occasion of the 11th

Annual Meeting of the European Hair Research Society

in Zurich, 7th–9th July, 2005.

AcknowledgementThe authors acknowledge Rolf Hoffmann, Freiburg i.B.,Germany, for assistance in analyzing the TrichoScan images.This study was performed with financial support from MerzPharmaceuticals GmbH, Germany.

such as L-cystine, medicinal yeast and pantothenic e traditionally used over-the-counter products for loss.ized, double-blind, placebo-controlled study

epiluminiscence microscopy with digital image o demonstrate that a CYP complex-based dietary s hair growth.mains unknown, although it seems to result from

d to a statistically significant improvement and ean anagen hair rate within 6 months of treatment omen with telogen effluvium.

Bibliography1. Gillespie JM, Reis PJ: Dietary regulated

biosynthesis of high-sulfur wool proteins. Biochem. J. 98, 669–677 (1966).

2. Reis PJ, Tunks DA, Sharry LF: Plasma amino acid patterns in sheep receiving abomasal infusions of methionine and cystine. Aust. J. Biol. Sci. 26, 635–644 (1973).

3. Frenkel MJ, Gillepsie JM, Reis PJ: Factors influencing the biosynthesis of the tyrosine-rich proteins of wool. Aust. J. Biol. Sci. 27, 31–38 (1974).

4. Petri H, Perchalla P, Tronnier H: Die wirksamkeit einer medikamentösen therapie bei haarstrukturschäden und diffusen effluvien – vergleichende doppelblindstudie. Schweiz Rundsch Med Prax 79, 1457–1462 (1990).

5. Budde J, Tronnier H, Rahlfs VW, Frei-Kleiner S: Systemische therapie von diffusem effluvium und haarstrukturschäden. Hautarzt 44, 380–384 (1993).

6. Ahrens J: Systemische behandlung des diffusen haarausfalls. Therapiewoche Schweiz 10, 551–554 (1994).

7. Hoffmann R: TrichoScan: combining epiluminiscence microscopy with digital image analysis for the measurement of hair growth in vivo. Eur. J. Dermatol. 11, 362–368 (2001).

8. Trüeb RM, Itin P: Schweizerische arbeitsgruppe für trichologie: fotografische dokumentation der wirksamkeit von 1 mg oralem finasterid in der behandlung der androgenetischen alopezie des mannes im praxisalltag. Schweiz Rundsch Med Prax 90, 2087–2093 (2001).

9. Sulzberger MB, Witten VH, Kopf AW: Diffuse alopecia in women. Its unexplained apparent increase in incidence. Arch. Dermatol. 81, 556–560 (1960).

10. Ludwig E: Classification of the types of androgenetic alopecia (common baldness) occurring in the female sex. Br. J. Dermatol. 97, 247–254 (1977).

11. Trüeb RM: Diffuser haarausfall bei frauen. Therapeutische Umschau. 59, 217–222 (2002).

12. Rushton DH, Ramsay ID, James KC et al.: Biochemical and trichological characterization of diffuse alopecia in women. Br. J. Dermatol. 123, 187–197 (1990).

13. Birch MP, Messenger JF, Messenger AG: Hair density, hair diameter and the prevalence of female pattern hair loss. Br. J. Dermatol. 144, 297–304 (2001).

14. Norwood OT: Incidence of female androgenetic alopecia (female pattern alopecia). Dermatol. Surg. 27, 53–54 (2001).

15. Orme S, Cullen DR, Messenger AG: Diffuse female hair loss: are androgens necessary? Br. J. Dermatol. 141, 521–523 (1999).

16. Vexiau P, Chaspoux C, Boudou P et al.: Effects of minoxidil 2% vs. cyproterone acetate treatment on female androgenetic alopecia: a controlled, 12-month randomized trial. Br. J. Dermatol. 146, 992–999 (2002).

17. Price VH, Roberts JL, Hordinsky M et al.: Lack of efficacy of finasteride in postmenopausal women with androgenetic alopecia. J. Am. Acad. Dermatol. 43, 768–776 (2000).

18. Guy WB, Edmundson WF: Diffuse cyclic hair loss in women. Arch. Dermatol. 81, 205–27 (1960).

19. Whiting DA: Chronic telogen effluvium: increased scalp hair shedding in middle-aged women. J. Am. Acad. Dermatol. 35, 899–906 (1996).

20. Trüeb RM: Das idiopathische chronische telogen effluvium der frau. Hautarzt 51, 899–905 (2000).

21. Randall VA, Ebling FJG: Seasonal changes in human hair growth. Br. J. Dermatol. 124, 146–151 (1991).

22. Rand S: Chronic telogen effluvium: potential complication for clinical trials in female androgenetic alopecia? J. Am. Acad. Dermatol. 37, 1021 (1997).

23. Guarrera M, Semino MT, Rebora A: Quantitating hair loss in women: a critical approach. Dermatology 194, 12–16 (1997).

24. Gehring W, Gloor M: Das phototrichogramm als verfahren zur beurteilung haarwachstumsfördernder präparate am beispiel einer kombination von hirsefruchtextrakt, L-cystin und calciumpantothenat. Zeitschrift für Hautkrankheiten 75, 419–423 (2000).

25. Fisher TW, Burmeister G, Schmidt HW et al.: Melatonin increases anagen hair rate in women with androgenetic alopecia or diffuse alopecia: results of a pilot randomized controlled trial. Br. J. Dermatol. 150, 341–345 (2004).

26. Buhl AE, Waldon DJ, Kawabe TT et al.: Minoxidil stimulates mouse vibrissae follicles in organ culture. J. Invest. Dermatol. 92, 315–320 (1989).

27. Aydingoz IE, Ferhanoglu B, Guney O: Does tissue iron status have a role in female alopecia? J. Eur. Acad. Dermatol. Venereol. 13, 65–67 (1999).

28. Sinclair R: There is no clear association between low serum ferritin and chronic diffuse telogen hair loss. Br. J. Dermatol. 147, 982–984 (2002).


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