© Borgis - Postępy Nauk Medycznych 10/2012, s. 800-805
*Ligia Brzezińska-Wcisło1, Dominika Wcisło-Dziadecka2, Elżbieta Meszyńska3, Małgorzata Latusek3, Anna Lis-Święty1
Nowe horyzonty patogenezy i terapii chorób włosów
New perspectives on the pathogenesis and treatment of hair disorders
1Dermatology Department, Medical University of Silesia, Katowice
Head of Department: prof. Ligia Brzezińska-Wcisło, MD, PhD
2Cosmetology Department, Institute of Structural Research of Skin of Medical University of Silesia, Katowice
Head: Krzysztof Jasik, MD, PhD
3Dermatology Department, Independent Public Clinical Hospital of Medical University of Silesia, Katowice
Head of Department: prof. Ligia Brzezińska-Wcisło, MD, PhD
W pracy przedstawiono nowe horyzonty patogenezy i terapii chorób włosów. W ostatnich latach równolegle z postępem cywilizacji narasta problem łysienia zarówno w aspekcie częstości występowania, jak i ciągle mało skutecznego leczenia. Najczęstsze przyczyny łysienia rozlanego to: niezbilansowana dieta, niedokrwistość, niedobór cynku, miedzi, żelaza, zatrucia metalami ciężkimi, palenie papierosów, stresy, nerwica. Do najczęstszych chorób powodujących łysienie rozlane należą: toczeń rumieniowaty układowy, choroby zakaźne, cukrzyca, zaburzenia hormonalne, niektóre choroby nowotworowe. We współczesnym świecie, gdzie postęp medycyny jest ogromny a przemysł farmaceutyczny wprowadza liczne środki lecznicze posiadające wiele działań niepożądanych pojawia się problem łysienia polekowego. Częstość występowania łysienia polekowego u ludzi w skali ogólnej nie jest znana, ale została określona w stosunku do niektórych leków.
In recent years, along with the progress of balding has been on the rise, which is reflected both in the prevalence of the problem and in the persistently low treatment efficacy. The leading causes of diffuse hair loss and a badly balanced diet, anaemia, zinc, copper or iron deficiency, same types of medication, heavy metal poisoning, smoking, chronic stress and neurosis. Diseases responsible most frequently for hair loss are systemic lupus erythematosis contagious diseases, diabetes, hormonal imbalances and some types of cancer. In today`s world, where the advancement of medicine is enormously fast and the pharmaceutical industry has been introducing numerous treatment agents with multiple side effects a problem of medication – induced balding has occurred. The overall prevalence of the problem in humans is not known, but has been established for some types of medication.
Hair on the head is primarily a subtle sensory organ. The scalp may protect against sunburn and constitute some form of insulation. Hair has a powerful ornamental function (1) and acting as a sensory organ it also transfers and receives sexual stimuli (2). Apart from having the above functions, hair is also important in areas of medicine such as physiology and forensic medicine, as well as other fields of science such as archeology. Examination of the hair of Egyptian mummies, which provided data important to archeologists and historians, could be noted here as an example. A change in hair density, colour, thickness and lustre may be indicative of an abnormal process in the body. Sudden hair loss disturbs the psychological balance of an individual and their social functioning as well as reducing their self-esteem (being a source of frustration) (3).
In recent years, along with the progress of civilization, the problem of balding has been on the rise, which is reflected both in the prevalence of the problem and in the persistently low treatment efficacy (3). The scalp may frequently be affected by metastases, especially from breast cancer. Cancer cells infiltrating the area can damage hair follicles, leading to hair loss (1).
Balding as a reaction of anagen hair follicles to harmful agents manifests itself in three different forms.
Firstly, the hair matrices may react with a sudden significant reduction in the number of mitoses in the cells or their complete suppression, which causes atrophy of the hair bulbs and the reduction, to varying degrees, of hair thickness, leading to hair breaking in the narrowest portion and to the loss of the so-called dystrophic hair. This type of hair loss is called anagen or dystrophic effluvium. Hair loss is usually observed within a few days up to less than 20 days after the harmful agent occurred.
Secondly, hair matrices may react to a harmful agent with a premature onset of hair follicle involution, which means an early entry of hair into the resting stage. This type of hair loss is called telogen effluvium. Hair shedding ensues after a long period of latency, which in humans is usually 2-4 months after the (onset of) exposure to the cause.
Thirdly, the anagen hair follicles may be affected by both types of hair loss mentioned above – anagen and telogen (2, 3).
Excessive hair loss may be determined by counting all individual hairs shed, both by themselves and during combing, per 24 hours over a period of a few days. This problem is present when one loses over a hundred hair per 24 hours over a period of a few weeks with cutting and shaving causing no improvement (4).
In order to establish the cause of hair loss, the following laboratory tests need to be carried out: full blood count, glycemia, the level of protein, iron, ferritin, alkaline posphatase as well as tests of such hormones as FT3, FT4, TSH, prolactin, progesterone and testosterone. It is always necessary to administer a trichogram (hair root condition test), conduct a histopathologic examination of a scalp sample (not routinely conducted, indicated in alopecia areata and its varieties), as well as the gentle pull test.
Scalp biopsy should always be conducted in the direction of hair growth and in alopecia areata the sample is to be taken from the lesion’s rim. In the case of massive hair loss, biopsy should be taken from the parietal and occipital areas (1).
One of the modern diagnostic techniques for hair disorders is trichoscopy. In order to diagnose and monitor hair conditions, a dermatoscope with suitable computer software and a digital camera (videodermatoscope) is used. The application of an optical system allows lesion examination in magnification of up to 70x. This technique is non-invasive, painless, easy to handle and it allows objective assessment of the disease intensity. It does not require the hair to be shaved off or dyed. The only requirement for the use of this technique is abundant experience of the examiner. Non-invasiveness and the possibility of image preservation constitute major advantages of this technique. The use of trichoscans and phototrichograms, in contrast, requires special software as well as shaving and dying of the hair. These techniques are not very precise, have little clinical value and are labour-intensive (5-7).
Balding may be congenital or acquired, reversible or irreversible, and- depending on its scale and development – limited, diffuse or complete.
The leading causes of diffuse hair loss are a badly balanced diet (slimming, low in calories and protein, leading to deficient levels of essential unsaturated fatty acids, vitamins B, biotin and minerals), anaemia, zinc, copper or iron deficiency, some types of medication, heavy metal poisoning (involving lead, thallium and mercury), smoking, chronic stress and neurosis.
Diseases responsible most frequently for hair loss are systemic lupus erythematosus, contagious diseases (e.g. typhoid fever, meningitis, tuberculosis or syphilis), diabetes, hormonal imbalances (hypo- and hyperthyroidism) and some types of cancer (e.g. gastric and liver cancer).
The extent of chemotherapy-induced alopecia depends on the dose of the agent and the length of treatment. Hair loss in this case affects mainly the top of the head, while the peripheral parts are spared (8).
Systemic lupus erythematosus involves mainly diffuse reversible hair loss, whose intensity depends on the course of the underlying condition.
In contagious diseases, the intensity and length of fever are the predominant factors causing hair loss.
Diabetic patients are affected by hair loss or thinning at the top of the head. Insulin, as opposed to oral anti-diabetic medication, increases the proportion of hair in the stage of growth. Hair loss takes place between 30 and 40 years of age (usually accompanied by seborrhea), mainly in patients with badly managed diabetes.
Hypothyroidism causes hair thinning, dryness, roughness and brittleness. Hertoghe sign may occur, which involves the loss of the outer 1/3 (one third) of eyebrows. Hyperthyroidism, on the other hand, causes hair to be thinner, silky, with increased shine, while hair loss is of diffuse character or can be limited to the forehead.
In some types of cancer, especially gastric cancer and in heavy liver damage, the so-called Schridde hair may occur at the temples, eyebrow arches and the chin area. Such hair is dark, thick and lustreless. Male pattern pubic hair may adopt the female pattern. This phenomenon is called Chvostek sign. Apart from that thinning or lack of armpit or chest hair may be found in both sexes (9).
In today’s world, where the advancement of medicine is enormously fast and the pharmaceutical industry has been introducing numerous treatment agents with multiple side effects, a problem of medication-induced balding has occurred. The overall prevalence of this problem in humans is not known, but has been established for some types of medication.
Chemotherapeutic agents cause hair loss in the majority of patients and the extent of balding depends on the type, dosage and length of exposure to the agent used (10). The treatment affects exclusively hair in the stage of growth, while eyebrow, pubic, armpit and terminal hair is spared due to a shorter hair cycle in those areas.
Anticoagulants cause balding in 50% of the patients, which occurs 1-12 weeks after the last dose is administered. Originally unfractioned heparin was mainly blamed for this condition, however it has recently been demonstrated that low molecular weight heparins and warfarin have the same side effect.
Anticoagulants belonging to the vitamin K antagonist group involve hair thinning usually between 3 and 20 weeks after the onset of the therapy. Most cases of hair loss are of benign nature and only 20% of patients display pronounced clinical symptoms, initially present on the scalp and later occurring in the eyebrow, armpit and pubic areas (10, 11).
Retinoids also are reported to damage the hair follicle as hair loss occurs in up to 20-30% of patients admitted to the therapeutic regimen.
Alopecia, due to Vitamin A intake in a daily dose of 500.000 IU, occurs after several months of treatment. In contrast, hair loss starts after 3-8 weeks of administration of II generation monoaromatic retinoids. The hair loss is usually severe and affects not only the scalp but also the eyelashes, eyebrows and genital hair. The condition usually is reversible and hair regrows after discontinuation of the drug, within 2-3 months (12).
The relation between DMARD (disease-modifying antirheumatic drugs) intake and hair loss have also been proven. Drugs that belong to this group are: gold salts, methotrexate, leflunamide, sulfasalazine, takrolimus, mofetile mycophenolan. The hair loss varies and may be due to the toxic effect of the drug on the hair follicle matrix (methotrexate) or skin damage (gold salts) (13).
Drugs used in psychiatry, neurology and cardiology are also responsible for drug induced alopecia.
Carbimazole and karbamazepine induce hair loss in up to 10.0% of individuals. Valproic acid in 2.6-12%, lithium salts in 12-17% and dopaminergic drugs in up to 30% of patients submitted to the therapeutic regimen (13,14).
In addition, cardiology patients may report hair loss due to: lipid lowering agents, angiotensin converting enzyme inhibitors, β-blockers and calcium channel blockers (15).
Lipid lowering agents such as statins and fibrates are responsible for alopecia in 1-5% of the patients admitted to the therapeutic regimen. The hair loss is usually transient, and affects not only the scalp but also other body regions (16, 17).
Other toxic effects of drugs used in a therapy of hypertension, ischemic disease and cardiovascular insufficiency vary, however they are usually transient.
Alopecia, due to angiontensin converting enzyme inhibitors, occurs in up to 5% of the treated patients, and depends on the type of drug. Hair loss affects usually the scalp, is reversible after discontinuation of the treatment and occurs both in adults and children (18).
Azole antifungal drugs are also reported to produce transient hair loss that affects the scalp. It depends on the type of drug and time of exposure.
Sometimes hair loss is very severe, affects other body hair and leads to malignant alopecia. The loss of hair is probably due to hormonal changes during the antifungal therapy.
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1. Burgdorf WHC, Plewig G, Wolff HH et al.: Braun-Falco. Dermatologia. Tom II. Lublin: Wyd. Czelej 2010.
2. Brzezińska-Wcisło L, Lis A, Kamińska G et al.: Fizjologia i patologia wzrostu i utraty włosów na głowie człowieka. Post Dermatol Alergol 2003; 20: 260-266.
3. Brzezińska-Wcisło L: Badania wpływu wybranych leków na dynamikę wzrostu włosów przeprowadzone na podstawie wariantu doświadczalnego na modelu szczurów rasy Wistar oraz ocena skuteczności tych leków w aspekcie klinicznym i trichologicznym w łysieniu rozlanym kobiet. Rozprawa habilitacyjna. Śląska Akademia Medyczna w Katowicach. Katowice 1996.
4. Kozłowska U, Kozłowska A: Patofizjologia wzrostu i utraty włosów. Przegl Dermatol 2001; 1: 19-25.
5. Olszewska M, Rudnicka L: Videodermoscopy as tool for differentia diagnosis and monitoring of hair loss. Exp Dermatol 2006; 15: 5.
6. Olszewska M, Rudnicka L, Rakowska A et al.: Postępy w diagnostyce łysienia. Przegl Dermatol 2009; 96: 247-253.
7. Ross EK, Vincenzi C, Tosti A: Videodermatoscopy in the evaluation of hair and scalp disorders. J Am Acad Dermatol 2006; 55: 799-806.
8. Kostanecki W: Choroby włosów. Warszawa: Wyd. PZWL 1979.
9. Brzezińska-Wcisło L: Łysienia związane z chorobami ustroju. Przew Lek 2000; 5: 97-98.
10. Aspner R, Horl WH, Sunder-Plassmann G: Dalteparin induced alopecia in hemodialysis patients: reversal by regional citrate anticoagulation. Blood 2001; 97: 2914-2915.
11. Wang YY, Po HL: Enoxaparin – induced alopecia in patients with cerebral venous thrombosis. J Clin Pharm Ther 2006; 31: 513-517.
12. Chave TA, Mortimer NJ, Hutchinson PE: Agranulocytosis and total scalp alopecia following acitretin. Br J Dermatol 2003; 148: 1063-1064.
13. Burrows NP, Grant JW, Crisp AJ et al.: Scarring alopecia following gold therapy. Acta Derm Venereol 1994; 74: 486.
14. Piraccini BM, Iorizzo M, Rech G et al.: Drug-induced hair disorders. Curr Drug Saf 2006; 3: 301-305.
15. Llau ME, Viraben R, Montastruc JL: Drug-induced alopecia: review of the literature. Therapie 1995; 2: 145-150.
16. Trüeb RM: Diffuse hair loss. [In:] Blume – Peytavi U, Tosti A, Whiting DA, Trüeb R, editors. Hair growth and disorders. Berlin Heidelberg: Springer-Verlag 2008; 269.
17. Shapiro J: Hair loss in women. N Eng J Med 2007; 357: 1620-1630.
18. Keplar KE: Alopecia, Hirsutism and Hypertrichosis. [In:] Tisdale JE, Miller DA, editors. Drug-Induced Diseases. Prevention, detection and management. 2nd ed. Bethesda: American Society of Health-System Pharmacists 2010; 135-179.
19. Sugar AM, Alsip SG, Galgiani JN et al.: Pharmacology and toxicity of high-dose ketoconazole. Antimicrob Agents Chemother 1987; 31: 1874-1878.
20. Thiedke CC: Alopecia in women. Am Fam Physician 2003; 67: 1007-1014.
21. Broniarczyk-Dyła G, Tazbir M: Zastosowanie mezoterapii w lecznictwie dermatologicznym. Przegl Dermatol 2009; 96: 121-125.
22. Brzezińska-Wcisło L, Lis-Święty A, Wcisło-Dziadecka D et al.: Wrodzone i nabyte zmiany struktury włosów. Post Dermatol Alergol 2007; 6: 282-289.
23. Kruś S, Arct J, Pytkowska K et al.: Kosmetyczne metody regulacji wzrostu włosów – mity i rzeczywistość. Dermatol Estet 2007; 6: 367-378.
24. Shapio J, Wiseman M, Lui H: Practical management of hair loss. Canad Fam Phys 2000; 46: 1469-1477.
25. Joss-Wichman E, Broniarczyk-Dyla G: Współczesne poglądy na etiopatogenezę łysienia plackowatego. Post Dermatol Alergol 2005; 4: 189-198.
26. Brzezińska-Wcisło L, Lis-Święty A: Choroby włosów – co nowego? [W:] Szepietowski J, Reich A, red. Dermatologia co nowego? Wrocław: Cornetis 2009; tom I: 187-200.
27. Otberg N: Systemic treatment for alopecia areata. Dermatologic Therapy 2011; 24: 320-325.
28. Chartaux E, Joly P: Long-term follow-up of the efficacy of methotrexate alone or in combination with low doses of oral corticosteroids in the treatment of alopecia areata totalis or universalis. Ann Dermatol Venereol 2010; 137: 507-513.
29. Farshi S, Mansouri P, Safar F et al.: Could azathioprine be considered as a therapeutic alternative in the treatment of alopecia areata? A pilot study. Int J Dermatol 2010, 49: 1188-1193.
30. Cho HR, Lew BL, Lew H et al.: Treatment effects of intradermal botulinum toxin type A injection on alopecia areata. Dermatol Surg 2010; 4: 2175-2181.
31. Willemsen R, Haentjens P, Roseeuw D et al.: Hypnosis and alopecia areata: Long-term beneficial effects on psychological well-being. Acta Derm Venereol 2011; 91: 35-39.
32. Hordinsky MK: Treatment of alopecia areata: What is new on the horizon? Dermatologic Therapy 2011; 24: 364-368.
33. Brzezińska-Wcisło L, Bergler-Czop B, Lis-Święty A et al.: Choroby włosów – co nowego? Dermatol Prakt 2009; 5: 9-13.
34. Brzezińska-Wcisło L, Lis-Święty A, Wcisło-Dziadecka D et al.: Najczęstsze choroby owłosionej skóry głowy wieku dziecięcego. Post Dermatol Alergol 2009; 5: 257-269.
35. Franklin ME, Zagrabbe K, Benavides KL: Trichotillomania and its treatment: a review and recommendations. Expert Rev Neurother 2011; 11: 1165-1174.
36. Pham CM, Krejci-Manwaring J: Loose anagen hair syndrome: an underdiagnosed condition in males. Pediatr Dermatol 2010; 27: 408-409.
37. Dhurat RP, Deshpande DJ: Loose anagen hair syndrome. Int J Trichology 2010; 2: 96-100.
38. Mirmirani P, Uno H, Price VH: Abnormal inner root sheath of the hair follicle in the loose anagen hair syndrome: an ultrastructural study. J Am Acad Dermatol 2011; 64: 129-134.
39. Giacomini F, Starace M, Tosti A: Short anagen syndrome. Pediatr Dermatol 2011; 28: 133-134.
40. Avashia N, Woolery-Lloyd H, Tosti A et al.: Short anagen syndrome in an African American woman. J Am Acad Dermatol 2010; 63: 1092-1093.