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Guidelines of care for androgenetic alopecia
This report reflects the best data available at the time the report was prepared, but caution should be exercised in interpreting the data; the results of future studies may require alteration of the conclusions or recommendations set forth in this report.
Guidelines of care for androgenetic alopecia Guidelines~Outcomes Committee: Lynn A. Drake, MD, Chairman, Scott M. Dinehart, MD, Evan R. Farmer, MD, Robert W. Goltz, MD, Gloria F. Graham, MD, Maria K. Hordinsky, MD, Charles W. Lewis, MD, David M. Pariser, MD, Stephen B. Webster, MD, Duane C. Whitaker, MD, Barbara Butler, CPA-SDR Consultant, and Barbara J. Lowery, M P H Task Force: Vera H. Price, MD, Chairman, Howard Baden, MD, Richard L. DeVillez, MD, L y n n A. Drake, MD, Maria K. Hordinsky, MD, Elise Olsen, MD, and Jerome L. Shupack, MD Introduction The American Academy of Dermatology's Guidelines/Outcomes Committee is developing guidelines of care for our profession. The development of guidelines will promote the continued delivery of quality care and assist those outside our profession in understanding the complexities and scope of care provided by dermatologists. For the benefit of members of the American Academy of Dermatology who practice outside the jurisdication of the United States, the listed treatments may include agents that are not currently approved by the U.S. Food and Drug Administration. II. Definition Androgenetic alopecia, also known as common balding in men and hereditary thinning in women, is a common trait caused by androgens in genetically susceptible men and women. It begins in the teens, 20s, or 30s in both sexes and frequently is fully expressed by the 40s. In men, the patterns of androgenetic alopecia vary from accentuation of the bitemporal recession, to frontal and/or vertex thinning, to loss of all hair except hair along the occipital and temporal margins. A significant difference between the genders is that women do not become completely bald. Instead, women have diffuse thinning, often worse centrally, and the scalp may become visible; there may be accentuation of the M-shaped frontal/temporal hairline. AndrogeReprint requests: American Academy of Dermatology, P.O. Box 4014, Schaumburg, IL 60168-4014. (Provided free of charge) J Am Acad Dermatol 1996;35:465-9. Copyright © 1996 by the American Academy of Dermatology, Inc. 0190-9622/96 $5.00 + 0 16/1/74566
netic alopecia represents the gradual transformation of terminal follicles to velluslike follicles, which in turn produce shorter and finer hairs called miniaturized hairs. These miniaturized hairs show much variation in diameter and length and are a hallmark of androgenetic alopecia. Ill. Rationale A. Scope Androgenetic alopecia is the most common cause of hair thinning in both men and women. Hair thinning may begin any time after puberty when androgens are synthesized and manifest their presence by the reshaping of the frontal hairline from a straight hairline to an M-shaped hairline. Precise studies of prevalence of androgenetic alopecia in different population groups are not available. In the United States, about half of the men and women show some expression of this trait by the age of 40. In women, the presence of hair thinning is often unnoticed because of its milder presentation and the fact that women tend to mask the hair thinning with effective styling. B. Issue The precise mode of inheritance is not estabfished. In the genetically marked follicles, some data suggest there may be increased reduction of testosterone to dihydrotestosterone by the enzyme 5oL-reductase.This occurs in both men and women with androgenefic alopecia. However, women have a milder form of hair thinning probably because, compared with men, they have lower levels of circulating testosterone, lower levels of the 5oL-reductase enzyme in scalp follicles, and increased aromatase in 465
466
Drake et aL scalp follicles, an enzyme that aromatizes testosterone to estradiol. Androgenetic alopecia may have a marked psychosocial impact, and therapeutic intervention may be desired to assist the patient to function normally in society. Because of the psychosocial impact, patients may seek inappropriate and unproven therapies that are available in nonmedical settings, often at great expense to the consumer. The aim of treatment of androgenetic alopecia is to increase scalp coverage or to retard the progression of hair thinning, or both. Agents used to treat androgenetic alopecia may be nonspecific biologic response modifiers that enlarge suboptimal hair follicles regardless of the underlying pathophysiology, androgen blockers to interrupt the 5c~-reductase enzyme, or androgen receptor protein inhibitors to specifically block the binding and transport of androgens to the cell nucleus. Before treatment is recommended, patients should be carefully examined to establish the diagnosis and rule out other causes of hair loss by history and physical findings, as well as laboratory tests if needed. Less obvious causes of hair loss, particularly in women, include thyroid disease and other endocrine disorders, poor nutritional status, iron deficiency, drugs, severe infection, systemic disease, malignancy, as well as other causes of telogen effluvium. It is important to note that patients may not have active telogen effluvium at the time of the examination.
IV. Diagnostic criteria A. Clinical 1. History a. General medical history, as indicated b. Age at onset of hair thinning, bitemporal recession c. Health history d. Medications, including vitamins e. Use of anabolic steroids f. Diet including adequacy of protein and iron intake, and use of "health foods," "crash dieting" g. Family history of thinning hair and/or balding in parents, siblings, aunts, uncles, grandparents on both sides of family h. Hair-care procedures or use of products that may cause hair breakage i. Thyroid and other endocrine disorders j. Malignancy k. Systemic disease 1. Life-style/habits
Journal of the American Academy of Dermatology September 1996
m. Change of hair style or hair care to compensate for thinner and/or shorter hair n. Increased hair shedding (telogen effluvium) before unmasking diffuse thinning o. For women 1) Menstrual history 2) Pregnancy history 3) Use of oral contraceptives
4) Infertility 5) Galactorrhea 6) Hirsutism 7) Virilization 8) Severe cystic acne 9) Changes in hair style a) Cutting hair shorter to compensate for wispy and uneven distal ends b) Rearranging longer hair to enhance scalp coverage p. Other 2. Physical examination a. General physical examination as indicated b. Pattern and distribution The pattern and distribution of hair thinning are usually as described below. However, variations occasionally occur, with some men showing diffuse thinning and a few women having a more male-like pattern. 1) In men a) Bitemporal recession b) CenWal scalp thinning, especially of the frontal/parietal area c) Vertex thinning or balding d) Density greatest over occipital and temporal scalp 2) In women a) Diffuse thinning b) Central scalp thinning, especially of the frontal/parietal area c) Density often greater over occipital scalp d) Retention of hair along frontal hairline that may be straight or M-shaped e) Central part appears widened because of increased spacing between the hairs c. Miniaturized hairs; variation in diameter and length of hair shafts d. Pull or pluck test (or both) e. Normal follicular ostia
Journal of the American Academy of Dermatology Volume 35, Number 3, Part 1
f. Absence of hair breakage, patchy loss, or scarring g. Hair texture h. In women: distal thinness or tapering of scalp hair i. In men 1) Hair on top of head no longer needs to be trimmed 2) Whisker hairs on temporal scalp (coarse, kinky, whiskerlike hairs) j. Other 3. Other Photographs may be useful in documenting response to treatment. B. Diagnostic tests The diagnosis of androgenetic alopecia is usually made from the history and clinical findings alone. In women, extensive hormonal evaluation may not be needed if the patient has no menstrual irregularities, infertility, hirsutism, severe cystic acne, vifilization, or galactorrhea. 1. ff one or more of the above symptoms are present in a woman, it may be useful to evaluate the following: a. Total testosterone b. Free testosterone c. Dehydroepiandrosterone sulfate d. Prolactin e. When indicated, other androgen excess laboratory testing f. Other 2. In some instances the fonowing laboratory tests are ordered to exclude other treatable causes of hair thinning: a. Thyroid-stimulating hormone, thyroxine b. Serum iron, serum ferritin, and/or total iron-binding capacity c. Complete blood cell count d. Other 3. Microscopic evaluation of hair shaft/bulb 4. Measure of hair growth 5. Scalp biopsy may be indicated 6. Patients with abnormal or questionable test results may be referred to an appropriate specialist. 7. Other C. Inappropriate diagnostic tests Hair analysis for protein, trace elements, and minerals D. Exceptions Not applicable E. Evolving diagnostic tests Not applicable
Drake et aL 467 V. Recommendations A. Treatment 1. Medical The aim of treatment is to promote haft regrowth and to retard further thinning of the hair. Topical minoxidil (2%) has been shown to promote hair growth in large controlled clinical studies. Other agents may be used either in combination with minoxidil or separately. All therapies may need to be used indefinitely to maintain their effect. a. Topical minoxidil (2%) solution b. In certain selected cases, the following treatments may be helpful in women only: 1) Estrogen
a) Oral (1) ff menstruating, estrogen-dominant birth control pill (2) Postmenopausal, estrogen replacement therapy b) Topical 2) Spironolactone (oral) c. Other 2. Surgical a. Hair transplants b. Scalp reduction c. Scalp rotation d. Other 3. Aesthetic a. Hair dyeing b. Permanent waving c. Sprays d. Mousses e. Scalp camouflage 1) Crayons 2) Creams 3) Sprays 4) Other f. Integration pieces g. Hair swatches, hair weaving h. Full scalp prostheses i. Other 4. Evolving therapy a. Tretinoin (topical) as adjunct to topical minoxidil solution b. Cyproterone acetate (oral) c. The following agents are under investigation. 1) Topical minoxidil (5%) solution 2) Oral fmasteride (5c~-reductase type 2 inhibitor) d. Other
468
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B. Education and counseling Because of the psychosocial impact of hair loss, it is important to explain the evaluation to the patient and inform the patient, to the extent possible, of what they may expect in terms of continuing hair loss, and that response to any therapy may be slow and may include hair regrowth and/or retardation of further thinning. No medical treatment may be an appropriate option for certain patients. C. Miscellaneous Not applicable
gI. Supporting evidence See Bibliography (Appendix) VII. Disclaimer Adherence to these guidelines will not ensure successful treatment in every situation. Further, these guidelines should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed to obtaining the same results. The ultimate judgment regarding the propriety of any specific procedure must be made by the physician in light of all the circumstances presented by the individual patient. For the benefit of members of the American Academy of Dermatology who practice outside the jurisdiction of the United States, the listed treatments may include agents that are not currently approved by the U.S. Food and Drug Administration.
Appendix. Bibliography Bazzano GS, Terezakis N, Galen W. Topical tretinoin for hair growth promotion. J Am Acad Dermatol 1986;15:880-93. Bergfeld WF. Androgenetic alopecia: an autosomal dominant disorder. Am J Med 1995;98(suppl):95S-8S. Buhl AE. Minoxidil's action in hair follicles. J Invest Dermatol 1991 ;96(suppl):73S-4S. Dallob AL, Sadick NS, Unger W, et al. The effect of fmasteride, a 5-alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness. J Clin Endocrinol Metab 1994;79:703-6. DeVfllez RL, Jacobs JP, Szpunar CA, et al. Androgenetic alopecia in the female: treatment with 2% topical minoxidil solution. Arch Dermatol t994;130:303-7.
Diani All, Mulholland MJ, Shull KL, et al. Hair growth effects of oral administration of finasteride, a steroid 5alpha-reductase inhibitor, alone and in combination with topical minoxidil in the balding stmnptail macaque. J Clin Endocrinol Metab 1992;74:345-50. Fratianni CM, Imperato-McGinley J. The syndrome of 5alphareductase deficiency. Endocrinologist 1994;4:302-14. Frieden LI, Price VH. Androgenetic alopecia. In: Thiers BH, Dobson RL, editors. Pathogenesis of skin disease. New York: Churchill-Livingstone, 1986:41-55. Imperato-McGinley J, Guerrero L, Gautier T, et al. Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism. Science 1974;186:1213-5. Katz HI, Hien NT, Prawer SE, et al. Long-term efficacy of topical minoxidil in male pattern baldness. J Am Acad Dermatol 1987;16:711-8. Ktister W, Happle R. The inheritance of common baldness: Two B or not two B? [commentary] J Am Acad Dermatol 1984; 11:921-6. Olseu EA. Androgenetic alopecia. In: Olsen EA, editor. Disorders of hair growth. New York: McGraw-Hill, 1994:257-83. Olsen EA, Weiner MS, Amara IA, et al. Five-year follow-up of men with androgenetic alopecia treated with topical minoxidil. J Am Acad Dermatol 1990;22:643-6. Orfanos CE. Androgenetic alopecia: clinical aspects and treatment. In: Orfanos CE, Happle R, editors. Hair and hair diseases. New York: Springer-Verlag, 1990:485-527. Price VH, Menefee E. Quantitative estimation of hair growth. I. Androgenetic alopecia in women: effect of minoxidil. J Invest Dermatol 1990;95:683-7. Redmond GP, Bergfeld WF. Diagnostic approach to androgen disorders in women: ache, hirsutism, and alopecia. Cleve Clin J Med 1990;57:423-7. Redmond GP, Bergfeld WF. Treatment of androgen disorders in women: ache, hirsutism, and alopecia. Cleve Clin J Med 1990;57:428-32. Sawaya ME, Price VH, Harris KA. Human hair follicle aromatase activity in females with androgenetic alopecia [abstract]. J Invest Dermatol 1990;94:575. Schweikert HU, Wilson JD. Regulation of human hair growth by steroid hormones. I. Testosterone metabolism in isolated hairs. J Clin Endocrinol Metab 1974;38:811-9. Schweikert HU, Wilson JD. Regulation of human hair growth by steroid hormones. II. Androstenedione metabolism in isolated hairs. J Clin Endocrinol Metab 1974;39:1012-9. Walsh DS, Dunn CL, James WD. Improvement in androgenetic alopecia (stage V) using topical minoxidil in a retinoid vehicle and oral finasteride. Arch Dermatol 1995;131:1373-5. Whiting DA. Diagnostic and predictive value of horizontal sections of scalp biopsy specimens in male pattern androgenetic alopecia. J Am Acad Dermatol 1993;28:755-63.
CORRECTION In the "Guidelines o f Care for D e r m a t o m y o s i t i s " b y D r a k e et al., w h i c h appeared in the M a y , Part 1, 1996 issue o f the Journal (34:824-9), am error was m a d e in the alignment o f items in the fight-hand c o l u n m on p a g e 825. T h e corrected page is given opposite with the corrections s h o w n in boldface.
Guidelines of care for androgenetic alopecia Guidelines~Outcomes Committee: Lynn A. Drake, MD, Chairman, Scott M. Dinehart, MD, Evan R. Farmer, MD, Robert W. Goltz, MD, Gloria F. Graham, MD, Maria K. Hordinsky, MD, Charles W. Lewis, MD, David M. Pariser, MD, Stephen B. Webster, MD, Duane C. Whitaker, MD, Barbara Butler, CPA-SDR Consultant, and Barbara J. Lowery, M P H Task Force: Vera H. Price, MD, Chairman, Howard Baden, MD, Richard L. DeVillez, MD, L y n n A. Drake, MD, Maria K. Hordinsky, MD, Elise Olsen, MD, and Jerome L. Shupack, MD Introduction The American Academy of Dermatology's Guidelines/Outcomes Committee is developing guidelines of care for our profession. The development of guidelines will promote the continued delivery of quality care and assist those outside our profession in understanding the complexities and scope of care provided by dermatologists. For the benefit of members of the American Academy of Dermatology who practice outside the jurisdication of the United States, the listed treatments may include agents that are not currently approved by the U.S. Food and Drug Administration. II. Definition Androgenetic alopecia, also known as common balding in men and hereditary thinning in women, is a common trait caused by androgens in genetically susceptible men and women. It begins in the teens, 20s, or 30s in both sexes and frequently is fully expressed by the 40s. In men, the patterns of androgenetic alopecia vary from accentuation of the bitemporal recession, to frontal and/or vertex thinning, to loss of all hair except hair along the occipital and temporal margins. A significant difference between the genders is that women do not become completely bald. Instead, women have diffuse thinning, often worse centrally, and the scalp may become visible; there may be accentuation of the M-shaped frontal/temporal hairline. AndrogeReprint requests: American Academy of Dermatology, P.O. Box 4014, Schaumburg, IL 60168-4014. (Provided free of charge) J Am Acad Dermatol 1996;35:465-9. Copyright © 1996 by the American Academy of Dermatology, Inc. 0190-9622/96 $5.00 + 0 16/1/74566
netic alopecia represents the gradual transformation of terminal follicles to velluslike follicles, which in turn produce shorter and finer hairs called miniaturized hairs. These miniaturized hairs show much variation in diameter and length and are a hallmark of androgenetic alopecia. Ill. Rationale A. Scope Androgenetic alopecia is the most common cause of hair thinning in both men and women. Hair thinning may begin any time after puberty when androgens are synthesized and manifest their presence by the reshaping of the frontal hairline from a straight hairline to an M-shaped hairline. Precise studies of prevalence of androgenetic alopecia in different population groups are not available. In the United States, about half of the men and women show some expression of this trait by the age of 40. In women, the presence of hair thinning is often unnoticed because of its milder presentation and the fact that women tend to mask the hair thinning with effective styling. B. Issue The precise mode of inheritance is not estabfished. In the genetically marked follicles, some data suggest there may be increased reduction of testosterone to dihydrotestosterone by the enzyme 5oL-reductase.This occurs in both men and women with androgenefic alopecia. However, women have a milder form of hair thinning probably because, compared with men, they have lower levels of circulating testosterone, lower levels of the 5oL-reductase enzyme in scalp follicles, and increased aromatase in 465
466
Drake et aL scalp follicles, an enzyme that aromatizes testosterone to estradiol. Androgenetic alopecia may have a marked psychosocial impact, and therapeutic intervention may be desired to assist the patient to function normally in society. Because of the psychosocial impact, patients may seek inappropriate and unproven therapies that are available in nonmedical settings, often at great expense to the consumer. The aim of treatment of androgenetic alopecia is to increase scalp coverage or to retard the progression of hair thinning, or both. Agents used to treat androgenetic alopecia may be nonspecific biologic response modifiers that enlarge suboptimal hair follicles regardless of the underlying pathophysiology, androgen blockers to interrupt the 5c~-reductase enzyme, or androgen receptor protein inhibitors to specifically block the binding and transport of androgens to the cell nucleus. Before treatment is recommended, patients should be carefully examined to establish the diagnosis and rule out other causes of hair loss by history and physical findings, as well as laboratory tests if needed. Less obvious causes of hair loss, particularly in women, include thyroid disease and other endocrine disorders, poor nutritional status, iron deficiency, drugs, severe infection, systemic disease, malignancy, as well as other causes of telogen effluvium. It is important to note that patients may not have active telogen effluvium at the time of the examination.
IV. Diagnostic criteria A. Clinical 1. History a. General medical history, as indicated b. Age at onset of hair thinning, bitemporal recession c. Health history d. Medications, including vitamins e. Use of anabolic steroids f. Diet including adequacy of protein and iron intake, and use of "health foods," "crash dieting" g. Family history of thinning hair and/or balding in parents, siblings, aunts, uncles, grandparents on both sides of family h. Hair-care procedures or use of products that may cause hair breakage i. Thyroid and other endocrine disorders j. Malignancy k. Systemic disease 1. Life-style/habits
Journal of the American Academy of Dermatology September 1996
m. Change of hair style or hair care to compensate for thinner and/or shorter hair n. Increased hair shedding (telogen effluvium) before unmasking diffuse thinning o. For women 1) Menstrual history 2) Pregnancy history 3) Use of oral contraceptives
4) Infertility 5) Galactorrhea 6) Hirsutism 7) Virilization 8) Severe cystic acne 9) Changes in hair style a) Cutting hair shorter to compensate for wispy and uneven distal ends b) Rearranging longer hair to enhance scalp coverage p. Other 2. Physical examination a. General physical examination as indicated b. Pattern and distribution The pattern and distribution of hair thinning are usually as described below. However, variations occasionally occur, with some men showing diffuse thinning and a few women having a more male-like pattern. 1) In men a) Bitemporal recession b) CenWal scalp thinning, especially of the frontal/parietal area c) Vertex thinning or balding d) Density greatest over occipital and temporal scalp 2) In women a) Diffuse thinning b) Central scalp thinning, especially of the frontal/parietal area c) Density often greater over occipital scalp d) Retention of hair along frontal hairline that may be straight or M-shaped e) Central part appears widened because of increased spacing between the hairs c. Miniaturized hairs; variation in diameter and length of hair shafts d. Pull or pluck test (or both) e. Normal follicular ostia
Journal of the American Academy of Dermatology Volume 35, Number 3, Part 1
f. Absence of hair breakage, patchy loss, or scarring g. Hair texture h. In women: distal thinness or tapering of scalp hair i. In men 1) Hair on top of head no longer needs to be trimmed 2) Whisker hairs on temporal scalp (coarse, kinky, whiskerlike hairs) j. Other 3. Other Photographs may be useful in documenting response to treatment. B. Diagnostic tests The diagnosis of androgenetic alopecia is usually made from the history and clinical findings alone. In women, extensive hormonal evaluation may not be needed if the patient has no menstrual irregularities, infertility, hirsutism, severe cystic acne, vifilization, or galactorrhea. 1. ff one or more of the above symptoms are present in a woman, it may be useful to evaluate the following: a. Total testosterone b. Free testosterone c. Dehydroepiandrosterone sulfate d. Prolactin e. When indicated, other androgen excess laboratory testing f. Other 2. In some instances the fonowing laboratory tests are ordered to exclude other treatable causes of hair thinning: a. Thyroid-stimulating hormone, thyroxine b. Serum iron, serum ferritin, and/or total iron-binding capacity c. Complete blood cell count d. Other 3. Microscopic evaluation of hair shaft/bulb 4. Measure of hair growth 5. Scalp biopsy may be indicated 6. Patients with abnormal or questionable test results may be referred to an appropriate specialist. 7. Other C. Inappropriate diagnostic tests Hair analysis for protein, trace elements, and minerals D. Exceptions Not applicable E. Evolving diagnostic tests Not applicable
Drake et aL 467 V. Recommendations A. Treatment 1. Medical The aim of treatment is to promote haft regrowth and to retard further thinning of the hair. Topical minoxidil (2%) has been shown to promote hair growth in large controlled clinical studies. Other agents may be used either in combination with minoxidil or separately. All therapies may need to be used indefinitely to maintain their effect. a. Topical minoxidil (2%) solution b. In certain selected cases, the following treatments may be helpful in women only: 1) Estrogen
a) Oral (1) ff menstruating, estrogen-dominant birth control pill (2) Postmenopausal, estrogen replacement therapy b) Topical 2) Spironolactone (oral) c. Other 2. Surgical a. Hair transplants b. Scalp reduction c. Scalp rotation d. Other 3. Aesthetic a. Hair dyeing b. Permanent waving c. Sprays d. Mousses e. Scalp camouflage 1) Crayons 2) Creams 3) Sprays 4) Other f. Integration pieces g. Hair swatches, hair weaving h. Full scalp prostheses i. Other 4. Evolving therapy a. Tretinoin (topical) as adjunct to topical minoxidil solution b. Cyproterone acetate (oral) c. The following agents are under investigation. 1) Topical minoxidil (5%) solution 2) Oral fmasteride (5c~-reductase type 2 inhibitor) d. Other
468
Journal of the American Academy of Dermatology September 1996
Drake et aL
B. Education and counseling Because of the psychosocial impact of hair loss, it is important to explain the evaluation to the patient and inform the patient, to the extent possible, of what they may expect in terms of continuing hair loss, and that response to any therapy may be slow and may include hair regrowth and/or retardation of further thinning. No medical treatment may be an appropriate option for certain patients. C. Miscellaneous Not applicable
gI. Supporting evidence See Bibliography (Appendix) VII. Disclaimer Adherence to these guidelines will not ensure successful treatment in every situation. Further, these guidelines should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed to obtaining the same results. The ultimate judgment regarding the propriety of any specific procedure must be made by the physician in light of all the circumstances presented by the individual patient. For the benefit of members of the American Academy of Dermatology who practice outside the jurisdiction of the United States, the listed treatments may include agents that are not currently approved by the U.S. Food and Drug Administration.
Appendix. Bibliography Bazzano GS, Terezakis N, Galen W. Topical tretinoin for hair growth promotion. J Am Acad Dermatol 1986;15:880-93. Bergfeld WF. Androgenetic alopecia: an autosomal dominant disorder. Am J Med 1995;98(suppl):95S-8S. Buhl AE. Minoxidil's action in hair follicles. J Invest Dermatol 1991 ;96(suppl):73S-4S. Dallob AL, Sadick NS, Unger W, et al. The effect of fmasteride, a 5-alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness. J Clin Endocrinol Metab 1994;79:703-6. DeVfllez RL, Jacobs JP, Szpunar CA, et al. Androgenetic alopecia in the female: treatment with 2% topical minoxidil solution. Arch Dermatol t994;130:303-7.
Diani All, Mulholland MJ, Shull KL, et al. Hair growth effects of oral administration of finasteride, a steroid 5alpha-reductase inhibitor, alone and in combination with topical minoxidil in the balding stmnptail macaque. J Clin Endocrinol Metab 1992;74:345-50. Fratianni CM, Imperato-McGinley J. The syndrome of 5alphareductase deficiency. Endocrinologist 1994;4:302-14. Frieden LI, Price VH. Androgenetic alopecia. In: Thiers BH, Dobson RL, editors. Pathogenesis of skin disease. New York: Churchill-Livingstone, 1986:41-55. Imperato-McGinley J, Guerrero L, Gautier T, et al. Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism. Science 1974;186:1213-5. Katz HI, Hien NT, Prawer SE, et al. Long-term efficacy of topical minoxidil in male pattern baldness. J Am Acad Dermatol 1987;16:711-8. Ktister W, Happle R. The inheritance of common baldness: Two B or not two B? [commentary] J Am Acad Dermatol 1984; 11:921-6. Olseu EA. Androgenetic alopecia. In: Olsen EA, editor. Disorders of hair growth. New York: McGraw-Hill, 1994:257-83. Olsen EA, Weiner MS, Amara IA, et al. Five-year follow-up of men with androgenetic alopecia treated with topical minoxidil. J Am Acad Dermatol 1990;22:643-6. Orfanos CE. Androgenetic alopecia: clinical aspects and treatment. In: Orfanos CE, Happle R, editors. Hair and hair diseases. New York: Springer-Verlag, 1990:485-527. Price VH, Menefee E. Quantitative estimation of hair growth. I. Androgenetic alopecia in women: effect of minoxidil. J Invest Dermatol 1990;95:683-7. Redmond GP, Bergfeld WF. Diagnostic approach to androgen disorders in women: ache, hirsutism, and alopecia. Cleve Clin J Med 1990;57:423-7. Redmond GP, Bergfeld WF. Treatment of androgen disorders in women: ache, hirsutism, and alopecia. Cleve Clin J Med 1990;57:428-32. Sawaya ME, Price VH, Harris KA. Human hair follicle aromatase activity in females with androgenetic alopecia [abstract]. J Invest Dermatol 1990;94:575. Schweikert HU, Wilson JD. Regulation of human hair growth by steroid hormones. I. Testosterone metabolism in isolated hairs. J Clin Endocrinol Metab 1974;38:811-9. Schweikert HU, Wilson JD. Regulation of human hair growth by steroid hormones. II. Androstenedione metabolism in isolated hairs. J Clin Endocrinol Metab 1974;39:1012-9. Walsh DS, Dunn CL, James WD. Improvement in androgenetic alopecia (stage V) using topical minoxidil in a retinoid vehicle and oral finasteride. Arch Dermatol 1995;131:1373-5. Whiting DA. Diagnostic and predictive value of horizontal sections of scalp biopsy specimens in male pattern androgenetic alopecia. J Am Acad Dermatol 1993;28:755-63.
CORRECTION In the "Guidelines o f Care for D e r m a t o m y o s i t i s " b y D r a k e et al., w h i c h appeared in the M a y , Part 1, 1996 issue o f the Journal (34:824-9), am error was m a d e in the alignment o f items in the fight-hand c o l u n m on p a g e 825. T h e corrected page is given opposite with the corrections s h o w n in boldface.