LETTER TO EDITOR
Year : 2012 | Volume
: 4 | Issue : 1 | Page : 47--48
Tackling chemotherapy-induced alopecia
Department of Internal Medicine, AMC, Medwin Hospital, Chirag Ali Lane, Nampally, Hyderabad, Andhra Pradesh, India
Registrar, Internal Medicine, AMC, 3rd Floor, Medwin Hospital, Chirag Ali Lane, Nampally, Hyderabad - 500 001, Andhra Pradesh
|How to cite this article:|
Gude D. Tackling chemotherapy-induced alopecia.Int J Trichol 2012;4:47-48
|How to cite this URL:|
Gude D. Tackling chemotherapy-induced alopecia. Int J Trichol [serial online] 2012 [cited 2020 Jul 14 ];4:47-48
Available from: http://www.ijtrichology.com/text.asp?2012/4/1/47/96098
Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia. Forty-seven percent of female patients feel that hair loss is the most traumatic aspect of chemotherapy, and 8% would decline chemotherapy because of fear of hair loss. 
Chemotherapy-induced alopecia (CIA) is acute diffuse hair loss caused by dystrophic anagen effluvium, although different clinical patterns of hair loss are seen. Anagen effluvium due to chemotherapy is usually reversible, but certain chemotherapy regimens can cause dose-dependent permanent alopecia. In cases of permanent alopecia after chemotherapy (taxanes, busulfan, cisplatin, and etoposide), moderate to very severe hair thinning (may be more accentuated on androgen-dependent scalp regions) and altered texture may be seen. Histologically, a nonscarring pattern similar to androgenetic alopecia may be seen with a preserved number of follicular units and lack of fibrosis. Decreased number of terminal hairs, increased telogen hairs, and increased miniaturized vellus-like hairs with increased fibrous streamers (stellae) and Arao-Perkins bodies may be seen. 
Laminin-332 and its receptor α6β4 integrin are upregu-lated (both quantitatively and spatially) after mid to late dystrophic catagen in the lower third of hair follicles in CIA. In contrast, laminin-511 is downregulated after mid dystrophic catagen at the protein level. In experimental models, injection of a laminin-511-rich protein extract delayed hair loss in cyclophosphamide-induced alopecia. 
Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, arrests the cell cycle and reduces the sensitivity of the epithelium to many cell cycle-active antitumor agents. In animal models, topical application of potent small-molecule inhibitors of CDK2 is known to reduce hair loss at the site of application in 33 to 50%.
Treatment of cancer cells with the ligand ectodysplasin -A2, which is known to specifically activate EDA2-receptor (EDA2R which is transactivated by p53 during CIA), results in p53-dependent cell death.
Scalp cooling (penguin caps, etc.) is used as a method of preventing hair loss during chemotherapy. Although well-tolerated side-effects like headache, coldness, dizziness, and sometimes claustrophobia may be seen. Two percent topical minoxidil as a therapy for accelerating regrowth after chemotherapy is effective.
Alpha lipoic acid derivative sodium zinc dihydrolipoy-lhistidinate attenuates the inflammatory cell infiltration of hair follicles which is central in CIA.
PTH-CBD (an agonist fusion protein of Parathyroid hormone-collagen binding domain of Clostridium histolyticum collagenase) in CIA showed rapid regrowth and repigmentation of hair and histologically normal number of hair follicles. 
Tellurium immunomodulator - AS101 has reduced the severity and shortened the duration of CIA. Selected immunophilin ligands such as cyclosporine A and FK 506 inhibit cyclophosphamide-induced hair loss and have shown promise in inducing hair growth. They are known to modulate hair growth possibly through the expression of p-glycoprotein. Cyclosporine may also prevent alopecia by increasing IL-1 receptor expression. 
Imuvert (a biological response modifier produced by the bacterium Serratia marcescens), pretreatment with topical calcitriol [1,25(OH)2-D3], administration of IL-1, high doses of alpha tocopherol, subcutaneous/intradermal injection of geldanamycin or 17-(allylamino)-17-demethoxygeldanamycin  have shown promise in fighting CIA.
|1||Trüeb RM. Chemotherapy-induced hair loss. Skin Therapy Lett 2010;15:5-7.|
|2||Miteva M, Misciali C, Fanti PA, Vincenzi C, Romanelli P, Tosti A. Permanent alopecia after systemic chemotherapy: A clinicopathological study of 10 cases. Am J Dermatopathol 2011;33:345-50.|
|3||Imanishi H, Tsuruta D, Tateishi C, Sugawara K, Paus R, Tsuji T, et al. Laminin-511, inducer of hair growth, is down-regulated and its suppressor in hair growth, laminin-332 up-regulated in chemotherapy-induced alopecia. J Dermatol Sci 2010;58:43-54.|
|4||Katikaneni R, Ponnapakkam T, Suda H, Miyata S, Sakon J, Matsushita O, et al. Treatment for chemotherapy-induced alopecia in mice using parathyroid hormone agonists and antagonists linked to a collagen binding domain. Int J Cancer 2011 Nov 30. [Epub ahead of print]|
|5||Maurer M, Handjiski B, Paus R. Hair growth modulation by topical immunophilin ligands: Induction of anagen, inhibition of massive catagen development, and relative protection from chemotherapy-induced alopecia. Am J Pathol 1997;150:1433.|
|6||Jimenez JJ, Roberts SM, Mejia J, Mauro LM, Munson JW, Elgart GW, et al. Prevention of chemotherapy-induced alopecia in rodent models. Cell Stress Chaperones 2008;13:31-8.|