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Figure 1.
Flowchart of Participant Enrollment
Flowchart of Participant Enrollment

AGA indicates androgenetic alopecia.

Figure 2.
Comparison of Hormonal Parameters in Participants With AGA and Controls
Comparison of Hormonal Parameters in Participants With AGA and Controls

Illustrated are significantly increased free androgen index (FAI) as well as levels of dehydroepiandrosterone sulfate (DHEAS), luteinizing hormone (LH), and testosterone in men with early androgenetic alopecia (AGA) compared with controls. FSH indicates follicle-stimulating hormone; SHBG, sex hormone–binding globulin.

aAll values are reported as serum concentrations except LH/FSH ratio and FAI.

Table 1.  
Baseline Characteristics of Participants With AGA
Baseline Characteristics of Participants With AGA
Table 2.  
Hormonal Parameters in Participants With AGA and Controls
Hormonal Parameters in Participants With AGA and Controls
1.
Orentreich  N.  Pathogenesis of alopecia. J Soc Cosmet Chem. 1960;11:479-499.
2.
Yi  SM, Son  SW, Lee  KG,  et al.  Gender-specific association of androgenetic alopecia with metabolic syndrome in a middle-aged Korean population. Br J Dermatol. 2012;167(2):306-313.
PubMedArticle
3.
Trüeb  RM.  Molecular mechanisms of androgenetic alopecia. Exp Gerontol. 2002;37(8-9):981-990.
PubMedArticle
4.
Dusková  M, Cermáková  I, Hill  M, Vanková  M, Sámalíková  P, Stárka  L.  What may be the markers of the male equivalent of polycystic ovary syndrome? Physiol Res. 2004;53(3):287-294.
PubMed
5.
Yip  L, Rufaut  N, Sinclair  R.  Role of genetics and sex steroid hormones in male androgenetic alopecia and female pattern hair loss: an update of what we now know. Australas J Dermatol. 2011;52(2):81-88.
PubMedArticle
6.
Dusková  M, Stárka  L.  The existence of a male equivalent of the polycystic ovary syndrome: the present state of the issue. Prague Med Rep. 2006;107(1):17-25.
PubMed
7.
Stárka  L, Cermáková  I, Dusková  M, Hill  M, Dolezal  M, Polácek  V.  Hormonal profile of men with premature balding. Exp Clin Endocrinol Diabetes. 2004;112(1):24-28.
PubMedArticle
8.
Moura  HH, Costa  DL, Bagatin  E, Sodré  CT, Manela-Azulay  M.  Polycystic ovary syndrome: a dermatologic approach. An Bras Dermatol. 2011;86(1):111-119.
PubMedArticle
9.
Hamilton  JB.  Patterned loss of hair in man; types and incidence. Ann N Y Acad Sci. 1951;53(3):708-728.
PubMedArticle
10.
Norwood  OT.  Male pattern baldness: classification and incidence. South Med J. 1975;68(11):1359-1365.
PubMedArticle
11.
Trüeb  RM, Lee  W-S. Male Alopecia: Guide to Successful Management. Cham, Switzerland: Springer International Publishing; 2014.
12.
Sinclair  RD, Dawber  RP.  Androgenetic alopecia in men and women. Clin Dermatol. 2001;19(2):167-178.
PubMedArticle
13.
Gopinath  H, Upadya  GM.  Metabolic syndrome in androgenic alopecia  [Epub ahead of print]. Indian J Dermatol Venereol Leprol. 2016.
PubMed
14.
Matilainen  V, Koskela  P, Keinänen-Kiukaanniemi  S.  Early androgenetic alopecia as a marker of insulin resistance. Lancet. 2000;356(9236):1165-1166.
PubMedArticle
15.
McDonough  PH, Schwartz  RA.  Adolescent androgenic alopecia. Cutis. 2011;88(4):165-168.
PubMed
16.
Narad  S, Pande  S, Gupta  M, Chari  S.  Hormonal profile in Indian men with premature androgenetic alopecia. Int J Trichology. 2013;5(2):69-72.
PubMedArticle
17.
Stárka  L, Dusková  M, Cermakova  I, Vrbiková  J, Hill  M.  Premature androgenic alopecia and insulin resistance: male equivalent of polycystic ovary syndrome? Endocr Regul. 2005;39(4):127-131.
PubMed
18.
Mohamed  NE, Elkhazragy  YA, Tawfeek  NAE, Hammad  WA.  Early androgenetic alopecia as a predictor of ischemic heart disease. Am J Dermatol Venereol. 2015;4(2):18-25.
19.
Chakrabarty  S, Hariharan  R, Gowda  D, Suresh  H.  Association of premature androgenetic alopecia and metabolic syndrome in a young Indian population. Int J Trichology. 2014;6(2):50-53.
PubMedArticle
20.
Mumcuoglu  C, Ekmekci  TR, Ucak  S.  The investigation of insulin resistance and metabolic syndrome in male patients with early-onset androgenetic alopecia. Eur J Dermatol. 2011;21(1):79-82.
PubMed
21.
Matthews  DR, Hosker  JP, Rudenski  AS, Naylor  BA, Treacher  DF, Turner  RC.  Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412-419.
PubMedArticle
22.
Al Kindi  MK, Al Essry  FS, Al Essry  FS, Mula-Abed  WA.  Validity of serum testosterone, free androgen index, and calculated free testosterone in women with suspected hyperandrogenism. Oman Med J. 2012;27(6):471-474.
PubMedArticle
23.
Schmidt  JB.  Hormonal basis of male and female androgenic alopecia: clinical relevance. Skin Pharmacol. 1994;7(1-2):61-66.
PubMedArticle
24.
Yildiz  BO, Yarali  H, Oguz  H, Bayraktar  M.  Glucose intolerance, insulin resistance, and hyperandrogenemia in first degree relatives of women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2003;88(5):2031-2036.
PubMedArticle
25.
Legro  RS, Kunselman  AR, Demers  L, Wang  SC, Bentley-Lewis  R, Dunaif  A.  Elevated dehydroepiandrosterone sulfate levels as the reproductive phenotype in the brothers of women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2002;87(5):2134-2138.
PubMedArticle
26.
Cohen  PN, Givens  JR, Wiser  WL,  et al.  Polycystic ovarian disease, maturation arrest of spermiogenesis, and Klinefelter’s syndrome in siblings of a family with familial hirsutism. Fertil Steril. 1975;26(12):1228-1238.
PubMedArticle
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Original Investigation
September 2016

A Comparison of the Hormonal Profile of Early Androgenetic Alopecia in Men With the Phenotypic Equivalent of Polycystic Ovarian Syndrome in Women

Author Affiliations
  • 1Department of Dermatology and Sexually Transmitted Diseases, Lady Hardinge Medical College and Associated Hospitals, New Delhi, India
  • 2Department of Biochemistry, Lady Hardinge Medical College and Associated Hospitals, New Delhi, India
JAMA Dermatol. 2016;152(9):986-991. doi:10.1001/jamadermatol.2016.1776
Abstract

Importance  Early androgenetic alopecia (AGA) is patterned hair loss occurring before age 30 years. Early AGA in men is frequently reported as the phenotypic equivalent of polycystic ovarian syndrome (PCOS) in women, which carries the risk of developing obesity, metabolic syndrome, and cardiovascular diseases. Very few studies have been conducted to evaluate this.

Objective  To study the hormonal profile of men with early AGA and to evaluate if early AGA in men can be considered as the phenotypic equivalent of PCOS, the associated risks of which are well known.

Design, Setting, and Participants  This case-control study was conducted from January 1, 2014, to March 31, 2015, in a tertiary care government hospital. Fifty-seven men aged 19 to 30 years presenting with patterned hair loss were recruited as study participants. Thirty-two age-matched men with no evidence of hair loss were recruited as controls. Men who had any established endocrine disorder, diabetes mellitus, or cardiovascular disease and those who took any oral medication or hormonal treatment for hair loss were excluded from the study. The serum concentrations of total testosterone, sex hormone–binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, fasting plasma glucose, and insulin levels were measured. Insulin resistance (IR) and free androgen index (FAI) were calculated and compared with age- and sex-matched controls.

Main Outcomes and Measures  The primary outcome was to measure the clinico-endocrinological profiles (LH, FSH, SHBG, DHEAS, and testosterone levels) of men with early AGA and to compare it with the PCOS profile; the secondary outcome was to establish a relationship between this endocrinological profile and IR.

Results  Compared with the 32 controls, the 57 participants with AGA showed significantly increased mean (SD) levels of testosterone (24.61 [7.97] vs 20.57 [4.9] nmol/L; P = .04), DHEAS (3.63 [2.19] vs 2.64 [1.49] µg/mL; P = .02), LH (7.78 [3.19] vs 4.56 [2.01] mIU/mL; P < .001), and prolactin (14.14 [9.48] vs 9.97 [3.12] ng/mL; P = .01) and decreased mean levels of FSH (4.02 [2.69] vs 5.66 [1.93] mIU/mL; P < .001) and SHBG (35.07 [11.11] vs 46.41 [14.03] nmol/L; P < .001). The mean FAI and LH/FSH ratio were was also increased in the AGA group. These hormonal parameters resemble the well-known profile of women with PCOS. The mean (SD) insulin levels did not show any significant difference between the cases and controls (6.34 [3.92] vs 5.09 [3.38] μIU/mL; P = .07). There was no statistically significant association between hormone levels and AGA or IR grade severity.

Conclusions and Relevance  Men with early AGA could be considered as male phenotypic equivalents of women with PCOS. They can be at risk of developing the same complications associated with PCOS, including obesity, metabolic syndrome, IR, cardiovascular diseases, and infertility.

Introduction

Androgenetic alopecia (AGA) is one of the oldest “disease” phenomena in human history. The term androgenetic alopecia was coined by Orentreich in 1960.1 It is a hereditary, androgen-dependent disorder characterized by a gradual conversion of terminal hair into miniaturized hair2 with typical bitemporal recession and balding vertex.3

Polycystic ovarian syndrome (PCOS) is the most common endocrinopathy in women and involves a genetic hormonal and metabolic imbalance.46 It is characterized by hyperandrogenemia, hyperinsulinemia, central obesity, polycystic ovaries, and anovulation.7 The hormonal profile of women with PCOS includes elevated levels of testosterone, dehydroepiandrosterone sulfate (DHEAS), and luteinizing hormone (LH) with altered LH/follicle-stimulating hormone (FSH) ratio, hyperinsulinemia due to increased insulin resistance (IR), and decreased sex hormone–binding globulin (SHBG).8

Abnormalities in hair in the form of increased hair or early-onset AGA have been suggested as the symptoms of the male phenotype of PCOS.5,6,9,10

Early AGA is a term repeatedly used in literature. There is a constant debate regarding the age limit to be used to label a patient as having early AGA. Some authors believe that alopecia manifesting between ages 10 and 20 years is premature alopecia or alopecia preacox.11 Some consider age 35 years as the cutoff for labeling premature or early-onset alopecia.1214 According to McDonough and Schwartz,15 pattern hair loss occurring in boys and girls younger than 18 years is adolescent AGA, whereas early-onset AGA refers to pattern hair loss before age 35 years.15 However, most authors have defined premature or early-onset alopecia as starting before age 30 years.12,1620 According to most studies, patterned hair loss in men occurring before age 30 years is considered the phenotypic equivalent of PCOS.5,6,9,10 Hence, the age group of 19 to 30 years was used in our study to define early AGA.

A remarkable proportion of men with early AGA show a similar pattern of steroid hormone levels as women with PCOS.6 Recently, the main interest in PCOS research has been oriented toward the genetics of the syndrome.4 There is a high frequency of occurrence in first-generation relatives of women with PCOS.7 These findings assume an oligogenic or polygenic autosomal type of inheritance.5 The autosomal genetic transfer of PCOS forms the basis for the hypothesis that there can exist a male equivalent of PCOS.4 Hence, it follows that a proportion of men with early AGA may represent the male equivalent of PCOS.

Box Section Ref ID

Key Points

  • Question Does the hormonal profile of men with early androgenetic alopecia (AGA) resemble the profile of women with polycystic ovarian syndrome (PCOS)?

  • Findings In this case-control study of 57 men with early AGA and 32 men without AGA (controls), mean testosterone, dehydroepiandrosterone sulfate, luteinizing hormone, and prolactin levels as well as free androgen index and luteinizing hormone/follicle-stimulating hormone ratio were found to be increased in the study group compared with the control group. The hormonal parameters of the men with AGA resembled the profile of women with PCOS.

  • Meaning Men with early AGA could be considered the phenotypic equivalent of women with PCOS and may be at risk of developing obesity, metabolic syndrome, and cardiovascular diseases.

Methods

This case-control hospital-based study was conducted in a dermatology department of a tertiary care government hospital in New Delhi, India. Prior government institutional ethics committee board approval was obtained, and all participants provided their written informed consent. Fifty-seven men aged 19 to 30 years presenting with patterned hair loss (defined as grade 3 or higher on the alopecia classification scale of Hamilton9 with Norwood modification10) were enrolled as study participants. Thirty-two age-matched men with no evidence of hair loss were enrolled as controls. Men who had any established endocrine disorder, diabetes mellitus, or cardiovascular disease and those who took any oral medication or hormonal treatment for hair loss were excluded from the study.

Detailed anamneses were recorded for each individual. All participants were assessed by the same physician. Body mass index (BMI) was calculated. Total testosterone, SHBG, DHEAS, LH, FSH, prolactin, fasting plasma glucose, and insulin levels of the patients were obtained from blood samples drawn after an 8-hour fast in the morning from 8 am to 9 am and analyzed.

DHEAS and SHBG were estimated by enzyme-linked immunosorbent assay; testosterone, LH, FSH, prolactin, and insulin levels were assayed by electro-chemiluminescent immunoassay. Fasting glucose levels were analyzed by the glucose oxidase method. IR was calculated using the formula fasting insulin level (μIU/mL) × fasting glucose level (mmol/L)/22.5, and a value above 2.0 was considered to indicate IR.21 Free androgen index (FAI) was calculated using the formula testosterone (nmol/L) × 100/SHBG (nmol/L).22

Statistical Analysis

The results were analyzed using SPSS software, version 20 (IBM). Means and standard deviations were calculated for continuous parameters. Unpaired t tests and analysis of variance were used to compare quantitative variables, and the χ2 test was used to compare qualitative variables. P < .05 was considered to be statistically significant.

Results

Patient enrollment in the study is illustrated in Figure 1. The baseline characteristics of participants with AGA are summarized in Table 1. There was no difference in the baseline parameters of those in the AGA and control groups. The mean (SD) age in the AGA group was 24.7 (2.8) years; in the control group, it was 24.2 (2.6) years. The hormone profiles of both groups are detailed in Table 2 and Figure 2.

The mean (SD) BMI was high in cases compared with controls (22.9 [3.6] vs 21.1 [2.4]; P = .01). As detailed in Table 2, the mean levels of total testosterone (P = .04), DHEAS (P = .02), LH (P < .001), and prolactin (P = .01) were significantly higher in the AGA group, while mean values of FSH (P < .001) and SHBG (P < .001) were significantly decreased in the AGA group. The mean LH/FSH ratio was significantly higher in those with AGA compared with controls (P < .001). The mean FAI was significantly higher in those with AGA than in controls (P < .001). The mean (SD) value of insulin was higher in the AGA group (6.34 [3.92] µIU/mL) than among controls (5.09 [3.38] µIU/mL), but the difference was not statistically significant (P = .07). Twelve men with AGA (21%) had IR compared with 3 men (9%) in the control group. There was no statistically significant association between severity of grades of AGA (grades 3-7) with the various hormone levels or with IR. There was no significant association between positive family history of AGA with grades of AGA or hormone levels.

Discussion

Androgenetic alopecia involves an interplay between androgens and genetics. Evaluating hormones derived from the testes as well as the adrenal and pituitary glands in these men is essential to evaluate the etiopathogenesis of early AGA and to manage the condition. Various studies have linked the hormonal profiles of these men with those of women with PCOS and considered early AGA in men to be the phenotypic equivalent of PCOS.

In the present study, the mean value of testosterone in the AGA group was significantly higher than that in the control group, in agreement with studies by Narad et al,16 Schmidt,23 and Yildiz et al.24 However, Dusková et al4 and Stárka et al7 found subnormal levels of testosterone among their men with AGA. Increased levels of testosterone leads to increased dihydrotestosterone levels by 5α reductase and thus increased action of these androgens on the dermal papillae cells of hair follicles in these patients. AGA in patients with normal testosterone levels could be attributed to increased androgen receptors or increased androgen sensitivity.

The mean DHEAS levels in the present study were significantly increased in the AGA group, similar to the findings of Dusková et al4 and Legro et al.25 However, Narad et al16 and Schmidt23 found normal values of DHEAS among men with AGA in their studies. Increased levels of DHEAS indirectly point toward increased androgen levels, which result in premature balding by acting on the dermal papillae cells. Interestingly, substantially elevated levels of DHEAS were reported by Legro et al25 in their study of acne in men, supporting it as a marker of male hyperandrogenism. Furthermore, DHEAS has special properties such as long half-life and lack of pulsatility, which make it useful as a marker of hyperandrogenism in men.

The mean value of SHBG in the AGA group in the present study was significantly lower than among controls. Similar findings were noted by Dusková et al4 and Narad et al.16 The lower the levels of SHBG, the higher the free testosterone levels, and thus hyperandrogenism aggravates AGA.

In the present study, the mean FAI was significantly higher in the AGA than in the control group. FAI is homologous to free testosterone, which is not bound to albumin or to SHBG and is freely available for action at the tissue level. Free testosterone accelerates gradual transformation of large terminal scalp follicles to tiny villous ones causing premature AGA in genetically predisposed persons. This finding shows that FAI is the best marker of a person’s androgen status because it can bind to tissue receptors.

The mean level of LH was significantly higher in men with AGA than in controls in the present study. Cohen et al26 noted increased levels of LH in male members of PCOS kindreds. However, Narad et al16 did not show significant difference in LH levels between cases and controls. Increased LH leads to increased testosterone levels and thus contributes to increased male pattern baldness. In addition, LH also stimulates the adrenal gland to produce androstenedione, a weaker androgen. Increased levels of LH thus suggest that the hypophyseal-adrenal axis contributes to the pathogenesis of premature AGA.

We found that the mean level of FSH was significantly lower in the AGA group than among controls. Significantly low FSH levels were also demonstrated by Stárka et al7 in men with AGA. In men, FSH stimulates the Sertoli cells in the testes to produce testosterone and inhibin. Inhibin decreases the output of FSH by a negative feedback loop. Increased testosterone level also creates a negative feedback loop that decreases FSH.

The mean LH/FSH ratio in the present study was significantly higher in men with AGA than among controls. This has been supported by Narad et al16 and Dusková et al.4 Altered LH/FSH ratio is also an important characteristic of women with PCOS, and so this finding supports our thesis that men with early AGA are phenotypically equivalent to women with PCOS.

We found increased levels of prolactin, which plays a role in pathogenesis of premature balding by stimulating suprarenal androgen release at the central level and modulating the activities of 5α reductase at the tissue level.

The mean insulin levels did not show any significant difference between the AGA and control groups (P = .07) in the present study, similar to the findings of Narad et al.16 However Dusková et al4 and Stárka et al7 showed significantly raised insulin levels in their cases. Twelve (21%) of our participants with AGA showed IR compared with only 3 (9%) of the controls. Though this difference in IR was not statistically insignificant (P = .06), it is clear that a larger proportion of those with AGA than controls showed IR. This can be attributed to our exclusion criteria of raised blood glucose levels, which might have eliminated a few cases of IR. Also, our participants with AGA were young (<30 years), and IR may be subclinical and not become overt until older age.16

Insulin resistance is a common finding in women with PCOS and is an important, but not essential, criterion to diagnose PCOS. It leads to metabolic and cardiovascular risks in later life. In the present study, IR was found to be associated with premature AGA in 21% of cases. Subclinical IR might be present in other men with AGA, and it might become clinically evident with advancing age. There was no statistically significant association between severity of AGA grade and IR or hormone levels, which might be owing to small sample size. There was no significant association between positive family history of AGA and grade of AGA or hormone levels.

There were few shortcomings in our study, including small sample size. In addition, the parameters of assessing alopecia grade are subjective, and the clinical data were based on patients’ memory. The men in the AGA group in our study were not related to women with PCOS.

We suggest that all patients with premature AGA should be assessed for baseline risk factors such as positive family history of AGA or PCOS, obesity, and abnormal blood glucose levels. Large, multicenter case-control studies should be undertaken to study the endocrinological profile in men with early AGA and these risk factors. We also suggest the same for cases of adolescent alopecia (patterned hair loss occurring before age 18 years), which are increasing in number.

Sequential follow-up for these men should be undertaken into their 40s and 50s to learn about the changes in endocrinological hormones with increasing age. These men should also be followed up for development of PCOS-associated risk factors like obesity, metabolic syndrome, IR, cardiovascular diseases, and infertility in later life, and they should be counseled regarding the appropriate steps to manage these risks, including lifestyle modification, exercise, dietary changes, and regular checkups. The study can also be conducted in siblings of women with PCOS to establish a stronger genetic association of early AGA in men with PCOS.

Conclusions

We found significantly increased LH, DHEAS, total testosterone, and prolactin levels along with significantly decreased FSH and SHBG levels in our AGA group. The LH/FSH ratio was higher in men with AGA. These hormonal parameters more or less resemble the profile of women with PCOS, and we propose that these men can be considered phenotypic equivalents to women with PCOS. These men could be exposed to the same risks as women with PCOS, including metabolic syndrome, IR, cardiovascular disease, and infertility, which needs to confirmed by large, multicenter studies. Men with early AGA may be exposed to these risks regardless of AGA grade or severity.

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Article Information

Accepted for Publication: April 24, 2016.

Corresponding Author: Sarita Sanke, MD, Department of Dermatology and Sexually Transmitted Diseases, Lady Hardinge Medical College and Associated Hospitals, Shaheed Bhagat Singh Marg, New Delhi 110001, India (sankesarita@gmail.com).

Published Online: June 15, 2016. doi:10.1001/jamadermatol.2016.1776.

Author Contributions: Dr Sanke had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Sanke, Chander, Garg, Yadav.

Acquisition, analysis, or interpretation of data: Chander, Jain, Garg, Yadav.

Drafting of the manuscript: Sanke, Chander, Garg.

Critical revision of the manuscript for important intellectual content: Sanke, Chander, Jain, Garg, Yadav.

Statistical analysis: Garg, Yadav.

Administrative, technical, or material support: Sanke, Chander, Jain, Garg.

Study supervision: Sanke, Chander, Jain, Garg, Yadav.

Conflict of Interest Disclosures: None reported.

References
1.
Orentreich  N.  Pathogenesis of alopecia. J Soc Cosmet Chem. 1960;11:479-499.
2.
Yi  SM, Son  SW, Lee  KG,  et al.  Gender-specific association of androgenetic alopecia with metabolic syndrome in a middle-aged Korean population. Br J Dermatol. 2012;167(2):306-313.
PubMedArticle
3.
Trüeb  RM.  Molecular mechanisms of androgenetic alopecia. Exp Gerontol. 2002;37(8-9):981-990.
PubMedArticle
4.
Dusková  M, Cermáková  I, Hill  M, Vanková  M, Sámalíková  P, Stárka  L.  What may be the markers of the male equivalent of polycystic ovary syndrome? Physiol Res. 2004;53(3):287-294.
PubMed
5.
Yip  L, Rufaut  N, Sinclair  R.  Role of genetics and sex steroid hormones in male androgenetic alopecia and female pattern hair loss: an update of what we now know. Australas J Dermatol. 2011;52(2):81-88.
PubMedArticle
6.
Dusková  M, Stárka  L.  The existence of a male equivalent of the polycystic ovary syndrome: the present state of the issue. Prague Med Rep. 2006;107(1):17-25.
PubMed
7.
Stárka  L, Cermáková  I, Dusková  M, Hill  M, Dolezal  M, Polácek  V.  Hormonal profile of men with premature balding. Exp Clin Endocrinol Diabetes. 2004;112(1):24-28.
PubMedArticle
8.
Moura  HH, Costa  DL, Bagatin  E, Sodré  CT, Manela-Azulay  M.  Polycystic ovary syndrome: a dermatologic approach. An Bras Dermatol. 2011;86(1):111-119.
PubMedArticle
9.
Hamilton  JB.  Patterned loss of hair in man; types and incidence. Ann N Y Acad Sci. 1951;53(3):708-728.
PubMedArticle
10.
Norwood  OT.  Male pattern baldness: classification and incidence. South Med J. 1975;68(11):1359-1365.
PubMedArticle
11.
Trüeb  RM, Lee  W-S. Male Alopecia: Guide to Successful Management. Cham, Switzerland: Springer International Publishing; 2014.
12.
Sinclair  RD, Dawber  RP.  Androgenetic alopecia in men and women. Clin Dermatol. 2001;19(2):167-178.
PubMedArticle
13.
Gopinath  H, Upadya  GM.  Metabolic syndrome in androgenic alopecia  [Epub ahead of print]. Indian J Dermatol Venereol Leprol. 2016.
PubMed
14.
Matilainen  V, Koskela  P, Keinänen-Kiukaanniemi  S.  Early androgenetic alopecia as a marker of insulin resistance. Lancet. 2000;356(9236):1165-1166.
PubMedArticle
15.
McDonough  PH, Schwartz  RA.  Adolescent androgenic alopecia. Cutis. 2011;88(4):165-168.
PubMed
16.
Narad  S, Pande  S, Gupta  M, Chari  S.  Hormonal profile in Indian men with premature androgenetic alopecia. Int J Trichology. 2013;5(2):69-72.
PubMedArticle
17.
Stárka  L, Dusková  M, Cermakova  I, Vrbiková  J, Hill  M.  Premature androgenic alopecia and insulin resistance: male equivalent of polycystic ovary syndrome? Endocr Regul. 2005;39(4):127-131.
PubMed
18.
Mohamed  NE, Elkhazragy  YA, Tawfeek  NAE, Hammad  WA.  Early androgenetic alopecia as a predictor of ischemic heart disease. Am J Dermatol Venereol. 2015;4(2):18-25.
19.
Chakrabarty  S, Hariharan  R, Gowda  D, Suresh  H.  Association of premature androgenetic alopecia and metabolic syndrome in a young Indian population. Int J Trichology. 2014;6(2):50-53.
PubMedArticle
20.
Mumcuoglu  C, Ekmekci  TR, Ucak  S.  The investigation of insulin resistance and metabolic syndrome in male patients with early-onset androgenetic alopecia. Eur J Dermatol. 2011;21(1):79-82.
PubMed
21.
Matthews  DR, Hosker  JP, Rudenski  AS, Naylor  BA, Treacher  DF, Turner  RC.  Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412-419.
PubMedArticle
22.
Al Kindi  MK, Al Essry  FS, Al Essry  FS, Mula-Abed  WA.  Validity of serum testosterone, free androgen index, and calculated free testosterone in women with suspected hyperandrogenism. Oman Med J. 2012;27(6):471-474.
PubMedArticle
23.
Schmidt  JB.  Hormonal basis of male and female androgenic alopecia: clinical relevance. Skin Pharmacol. 1994;7(1-2):61-66.
PubMedArticle
24.
Yildiz  BO, Yarali  H, Oguz  H, Bayraktar  M.  Glucose intolerance, insulin resistance, and hyperandrogenemia in first degree relatives of women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2003;88(5):2031-2036.
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