Alopecia is the unwanted loss of hair from the scalp or body, affecting both men and women.1 Although it causes no direct physical harm, its psychological impact can be profound, often resulting in emotional distress and psychiatric symptoms.2Many affected individuals seek to halt hair loss and promote regrowth, driving research and the development of new therapies.3

Androgenetic Alopecia (AGA) — referred to as male-pattern hair loss (MPHL) in men — is the most prevalent form of alopecia, characterized by the gradual miniaturization of scalp hair follicles.4,5 In men, AGA is primarily due to increased sensitivity of hair follicles to androgens, particularly dihydrotestosterone (DHT), while in women the role of androgens is less clear. 4,5AGA affects nearly 80% of aging men with Hamilton reporting that 30%–50% of men develop AGA by age 50.6,7

Epidemiological studies have highlighted racial and age-related differences in AGA prevalence, with the highest rates observed among Caucasians.8An Indian study involving 1,005 subjects showed a 58% prevalence of AGA in men aged 30–50 years.9Regarding severity, Norwood type II or III patterns are the most common presentations among Indian males.10, 11

Hair loss significantly affects personal and social identity, often leading to negative psychological consequences.12Studies show that feelings of low self-esteem related to balding are consistent across Western and Asian populations.13,14 The psychological burden is often underestimated by others, further compounding patient distress.15It is vital for clinicians to address patients’ emotional responses and educate them about AGA, its natural progression, and available treatment options.16

The androgen DHT, produced from testosterone by the action of 5-alpha-reductase, plays a critical role in AGA.17Testosterone is converted to DHT by 5-α-reductase, prompting development of 5-α-reductase inhibitors as AGA treatments. International guidelines recommend topical Minoxidil (5%) and oral Finasteride (a type II 5-α- reductase inhibitor) for treatment of male AGA. Although finasteride significantly improves hair growth and slows hair loss, up to 30–50% of patients may not show satisfactory clinical improvement.19, 20Patients often seek not just stabilization but actual regrowth of hair.21, 22

Dutasteride, a dual inhibitor of type I and type II 5-alpha-reductase, offers more extensive DHT suppression than finasteride, reducing serum DHT levels by over 90% compared to 70% with finasteride.23,24,25,26 Clinical studies have demonstrated greater and faster hair growth with dutasteride compared to finasteride.27-33Dutasteride was approved in Korea for the treatment of AGA in 2009 following positive phase III trial results.31

Considering its broader mechanism of action and higher efficacy, this study aims to directly compare oral dutasteride and finasteride in terms of effectiveness and safety in male AGA.

AIMS AND OBJECTIVE

To compare efficacy of 0.5mg oral Dutasteride and 1mg Finasteride in male androgenetic alopecia.

To compare adverse effect profileof 0.5mg oral Dutasteride and 1mg Finasteride in male androgenetic alopecia.

Source of data: All the male patients with AGA between 18 to 50 years of age attending the outpatient department of Dermatology, Venereology and Leprology at MVJ Medical College and Research Hospital, Bangalore were included in the study.

Method of Collection of Data:

Study design: Hospital based, time bound, prospective Interventional study.

Study period: July2022- March2024

Place of study: MVJ Medical College and Research Hospital

Inclusion Criteria:

• Eligible men aged 18–50 years with Grade I –IV androgenetic alopecia. (Hamilton Norwood classification.)
• Exclusion Criteria:
• Patients who were using/ had used topical minoxidil and anti-androgenic medications within the past 3 months.
• Intake of drugs causing hypertrichosis (phenytoin, acetazolamide, cyclosporine, diazoxide, psoralens, penicillamine, streptomycin and cortisone) or hypotrichosis (anti-coagulants, retinoids, lithium and beta blockers) within past 6 months.
• Patients who developed severe side effects during study period treated and replaced with new subjects.

Sample size of estimation: Sample size was calculated using the formula (Zα + Zβ) X ([σ1+ σ2)/(μ1− μ2]), where Zα =1.96, Zβ = 0.84, σ1 = standard deviation of one group (49.86), σ2 = standard deviation of second group(51.0), μ1 = mean of one group (245.97) and μ2 = mean of second group (231.08). Mean and standard deviation of the two groups were used from an Indian study.[4] The size was calculated as 18.96 for each group. To account for dropouts during the study, we selected a sample size of 25 in each group.

Methodology:

1. Patients who fulfilled the inclusion criteria were recruited after taking an informed consent and were randomized into two groups of 25 sample size each receiving either 0.5 mg Dutasteride tablet or 1 mg Finasteride tablet daily for a period of 24 weeks.
2. Patients were counseled regarding the side effects of the medications prior to enrollment in the study. A detailed general examination, systemic examination, 34 complete dermatological examinations were done and relevant details were documented. Dermoscopic assessment was performed by using a hand held dermoscope (DERMALITE DL4 3RD GEN) with charge coupled device, imaging sensor of 310 kilo pixels, offering a pixel resolution of 640x480 pixels of 20 to 75 factors with automatic gain and exposure control. Standardized digital dermoscopic images of scalp were obtained at baseline and at 24 weeks to asses total hair count, thin hair count, thick hair count in 1cm2 area.
3. Subjective evaluationThe study subjects were asked to rate changes in the size of the vertex spot, hair loss on top of the scalp, hairline recession, the amount of hair shedding, hair quality and overall satisfaction with hair growth on a 3-point rating scale. (Increased no change or decreased)
4. Safety assessment Safety assessment was performed through enquiry, physical examination and laboratory evaluation. The sexual function evaluated by specifically asking about the occurrence of decreased libido, erectile dysfunction and ejaculatory dysfunction like decrease in volume of ejaculate and gynaecomastia.
5. Due permission and approval was taken from the Institutional Ethics Committee.
6. Written informed consent was taken before their participation in study.

STATISTICAL ANALYSIS: The data collected was analyzed using SPSS. Chi- square test was performed for association and T test to the compare efficacy and adverse events leading to withdrawal from study between treatment groups.

o Data Collection & statistical analysis plan: The data collected was entered into Microsoft excel sheet and was summarised using following procedure like distribution of Demographic data which was expressed as frequency and percentages, continuous data was expressed as mean with standard deviation.

oBy Inferential Statistics: To find the association between the pre treatment grading of AGA among both groups Chi-square test was used. Fischer’s exact test of significance was used when more than 20% cells showed expected frequencies < 5. Independent t-test was used to compare dermoscopic findings like mean total hair count, thick hair count and thin hair count The Kolmogorov–Smirnov test and the Shapiro–Wilk test was used to analyze if variables were normally distributed. The Skewness and Kurtosis values of study variables showed that the distribution of variables were normal. All the statistical analysis was carried out at 5% level of significance and a p-value of < 0.05 was considered as significant.

DEMOGRAPHIC COMPARISONS BETWEEN GROUPS

The age distribution was similar between the two groups, with most participants falling in the 21–30 and 31–40-year age brackets. Specifically, 44% of Dutasteride users and 48% of Finasteride users were aged 21–30 years, while 48% of Dutasteride users and 36% of Finasteride users were aged 31–40 years. Only a small proportion belonged to the 41–50-year age group. The difference in age distribution was not statistically significant (Chi-square = 1.13, df = 2, p = 0.56).

Occupational profiles were diverse. Both groups had an equal proportion (32%) of individuals engaged in business, and software engineers constituted 28% and 24% of Dutasteride and Finasteride users, respectively. However, certain occupations such as civil engineers and postgraduates were only reported in the Finasteride group, while teachers were only found among Dutasteride users. Although this variable did not reach statistical significance (Chi-square = 12.41, df = 7, p = 0.08), it indicated a trend toward different occupational backgrounds.

Smoking status showed a significant difference between the groups. A higher proportion of Dutasteride users (40%) were smokers compared to only 16% in the Finasteride group, a difference that reached statistical significance (Chi-square = 3.57, df = 1, p = 0.05). Alcohol intake was more common among Finasteride users (28%) than those on Dutasteride (8%), but this difference was not statistically significant (Chi-square = 3.38, df = 1, p = 0.06), though it approached significance.

Marital status was comparable between the groups, with nearly equal distributions of married and unmarried participants. Notably, 8% of Finasteride users were separated, a category not present in the Dutasteride group. This difference, however, was not statistically significant (Chi-square = 2.43, df = 2, p = 0.29). Lastly, a family history of androgenetic alopecia (AGA) was more frequently reported among Dutasteride users (72%) compared to Finasteride users (48%). Although this finding did not reach statistical significance (Chi-square = 3.00, df = 1, p = 0.08), it suggested a possible trend toward a higher familial predisposition in the Dutasteride group.

TABLE 2

DISTRIBUTION OF PRE TREATMENT GRADE OF AGA BETWEEN TWO GROUPS

In the Dutasteride group, Grade 3 AGA was the most common, observed in 12 patients (48%), followed by Grade 4 in 9 patients (36%), and Grade 2 in 4 patients (16%). Similarly, in the Finasteride group, Grade 3 AGA was also the most frequent, seen in 13 patients (52%), with Grade 4 in 9 patients (36%) and Grade 2 in 3 patients (12%).

Both groups exhibited a similar distribution of AGA severity, with the majority of patients falling under Grade 3, followed by Grade 4. Grade 2 was the least common in both groups. The overall pattern suggests that the baseline severity of AGA was comparable between the Dutasteride and Finasteride groups, supporting a fair comparison of treatment outcomes.

The Chi-square test yielded a p-value of 0.613, indicating no statistically significant difference in the distribution of AGA grades between the two groups after 6 months of therapy. This suggests that, despite variations in individual grade shifts, the overall grade distribution post-treatment was comparable between the Dutasteride and Finasteride groups.

TABLE 3

COMPARISON OF MEAN TOTAL HAIR COUNT AMONG THE GROUPS

At baseline, the mean total hair count was slightly lower in the Dutasteride group (223.08 ± 5.34) compared to the Finasteride group (227.16 ± 2.60). This difference of 4.08 hairs was statistically significant (p = 0.001), suggesting a modest initial difference in hair density between the two groups.

After 24 weeks of treatment, the Dutasteride group showed a marked increase in hair count to 245.12 ± 3.66, while the Finasteride group had a more modest increase to 233.04 ± 3.50. The mean difference at this time point was 12.08 hairs, which was highly statistically significant (p = 0.000), indicating superior efficacy of Dutasteride in promoting hair regrowth over the study period.

When examining the change in hair count from baseline to 24 weeks, Dutasteride resulted in an average increase of 22.04 hairs, whereas Finasteride showed a smaller increase of 5.88 hairs. Although a p-value is not reported for this direct change, the results clearly demonstrate that Dutasteride leads to significantly greater improvement in hair count compared to Finasteride over a 24-week period.

TABLE 4

COMPARISON OF MEAN THICK HAIR COUNT AMONG THE GROUPS

The table presents a comparison of thick hair count between the Dutasteride and Finasteride groups at baseline and after 24 weeks of treatment, along with the mean differences and p-values indicating statistical significance.

At baseline, the mean thick hair count was slightly lower in the Dutasteride group (157.60 ± 2.10) compared to the Finasteride group (162.84 ± 2.34). This difference of 5.24 hairs was statistically significant (p = 0.000), indicating a modest but meaningful initial disparity in thick hair density.

After 24 weeks of treatment, the Dutasteride group showed a substantial increase in thick hair count to 189.12 ± 5.08, while the Finasteride group had a marginal increase to 166.96 ± 1.74. The mean difference between the two groups at this point was 22.16 hairs, which was also highly statistically significant (p = 0.000), favoring Dutasteride.

The change in thick hair count from baseline to 24 weeks was 31.52 hairs in the Dutasteride group, compared to just 4.12 hairs in the Finasteride group. Although no p-value is listed specifically for this change, the marked difference in improvement clearly indicates that Dutasteride was significantly more effective in promoting the growth of thick hairs over the 24-week treatment period.

TABLE 5

COMPARISON OF MEAN THIN HAIR COUNT AMONG THE GROUPS

The table compares thin hair count between the Dutasteride and Finasteride groups at baseline and after 24 weeks of treatment, along with the calculated mean differences and corresponding p-values.

At baseline, the Dutasteride group had a slightly lower mean thin hair count (64.68 ± 1.95) compared to the Finasteride group (67.04 ± 1.92), with a mean difference of –2.36 hairs, which was statistically significant (p = 0.038). This indicates that both groups started with a comparable thin hair count, although slightly higher in the Finasteride group.

After 24 weeks of treatment, the Dutasteride group showed a more substantial reduction in thin hair count to 60.16 ± 2.07, while the Finasteride group had a smaller reduction to 65.72 ± 1.45. The mean difference at this stage was –5.56 hairs, which was highly statistically significant (p = 0.000).

The change in thin hair count from baseline to 24 weeks was a reduction of 4.52 hairs in the Dutasteride group, compared to a smaller reduction of 1.32 hairs in the Finasteride group. Although the p-value for this specific change is not listed, the data clearly indicate that Dutasteride was more effective in reducing thin hairs, supporting its superior efficacy in improving hair quality and density over the treatment period.

Table 6

Comparison of Adverse effects among both groups after treatment

The overall incidence of adverse events was similar in the two treatment groups. There was no statistical difference between dutasteride and finasteride in the incidence of adverse events. Erectile dysfunction and loss of libido was seen in 2 and 3 patients in the dutasteride group as compared to 1 and 2 patients in finasteride group, respectively but this was not statistically significant. Conjuctival congestion was seen among 2 patients of finasteride group.

This study evaluated 50 male patients with androgenetic alopecia (AGA), randomized equally into Dutasteride (0.5 mg) and Finasteride (1 mg) treatment groups over 24 weeks. The majority were aged 21–30 years (46%), with a mean age of 32.52 ± 6.66 years, comparable to Shah KB et al.34 (30.6 years) but lower than De Villez et al.35 (36.9 years) and higher than Hajheydari et al.36 (22.8 years).

A family history of AGA was positive in 72% of the Dutasteride group and 48% of the Finasteride group, aligning with findings by Paik et al.37 (48.5%) and Shah KB et al. 34 (54%), but lower than Hajheydari et al. (81.6%). Baseline AGA grading revealed Grade 3 as most common (50%), which is comparable to Shah KB et al. 34, where Stage 3 was also predominant (50%).

After 24 weeks, Dutasteride showed superior efficacy with a mean increase in total hair count of 22.04/cm² vs. 5.88/cm² in the Finasteride group. Similarly, thick hair count increased significantly in the Dutasteride group (31.52/cm²) compared to Finasteride (4.12/cm²). These results are consistent with Shanshanwal et al.30, who reported greater gains in total and thick hair count with Dutasteride. Olsen et al.38 and Harcha et al.39 also found dose-dependent improvements with Dutasteride, with Dutasteride 0.5 mg and 2.5 mg outperforming Finasteride in hair regrowth.

The reduction in thin hair count was greater in the Dutasteride group (4.52/cm²) than in Finasteride (1.32/cm²), supporting previous findings by Shanshanwal et al.30 Genetic factors such as the V89L polymorphism in the 5-alpha reductase gene, which is common in the Indian population, may explain the relatively reduced response to Finasteride.

Subjective satisfaction scores were higher in the Dutasteride group, though not statistically significant. Dutasteride was well tolerated, with sexual side effects reported in 15.6%—comparable to Jung et al.40(17.1%). These adverse effects were mild and reversible, consistent with Olsen et al.38, Harcha et al.39, and large placebo-controlled trials, which reported no clear long-term impact on sexual function. Finasteride-related sexual dysfunction has also been attributed in part to the nocebo effect.

Dutasteride demonstrated superior clinical efficacy in improving both hair density and thickness compared to Finasteride, with a comparable safety profile, consistent with findings from earlier randomized controlled trials.

In our study oral dutasteride showed more efficacy than finasteride in terms of total hair count and reversal of miniaturisation. The overall incidence of adverse effects with both the drugs was similar. The limitation of this study was, a small sample size, short duration of treatment and follow up and absence of blinding.

1. Olsen EA, Messenger AG, Shapiro J, Bergfeld WF, Hordinsky MK, Roberts JL, Stough D, Washenik K and Whiting DA. Evaluation and treatment of male and female pattern hair loss. J Am AcadDermatol. 2005; 52(2):301- 311.
2. Passchier J, Erdman J, Hammiche F and Erdman RA. Androgenetic alopecia: stress of discovery. Psychol Rep. 2006; 98(1):226-228.
3. Seidel P, Remus M, Delacher M, Grigaravicius P, Reuss DE, Frappart L, Von Deimling A, Feuerer M, Abdollahi A and Frappart PO. Epidermal Nbn deletion causes premature hair loss and a phenotype resembling psoriasiform dermatitis. Oncotarget. 2016; 7:23006-23018. doi: 10.18632/oncotarget.8470.
4. English RS. A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors. Med Hypotheses. 2018;111:73–81. doi:10.1016/j.mehy.2017.12.027
5. Lolli F, Pallotti F, Rossi A, et al. Androgenetic alopecia: a review. Endocrine. 2017;57:9–17. doi:10.1007/s12020-017-1280-y
6. York K, Meah N, Bhoyrul B, Sinclair R. A review of the treatment of male pattern hair loss. Expert OpinPharmacother. 2020;21(5):603–612. doi:10.1080/14656566.2020.1721463
7. Hamilton JB. Patterned loss of hair in man; types and incidence. Ann. N. Y. Acad. Sci. 1951;53(3):708–728. [PubMed]
8. Olsen- EA. Disorders of hair growth: diagnosis and treatment. New York: McGraw Hill; 2003; 48-52
9. Shankar DK, Chakravarthi M, Shilpakar R. Male androgenetic alopecia: Population- based study in 1,005 subjects. Int J Trichol 2009;1:131-3.
10. Grover S. A study of patterns of androgenetic alopecia in men: An Indian 72 perspective. Br J Dermatol 2005;152:572-4.
11. Sehgal VN, Kak R, Aggarwal A, Srivastava G, Rajput P. Male pattern androgenetic alopecia in an Indian context: A perspective study. J EurAcadDermatolVenereol 2007;21:473-9.
12. Cash TF. The psychological effects of androgenetic alopecia in men. J. Am. Acad. Dermatol. 1992;26(6):926–931.
13. Budd D, Himmelberger D, Rhodes T, Cash TE, Girman CJ. The effects of hair loss in European men: a survey in four countries. Eur. J. Dermatol. 2000;10(2):122– 127.
14. Lee H-J, Ha S-J, Kim D, Kim H-O, Kim J-W. Perception of men with androgenetic alopecia by women and nonbalding men in Korea: how the nonbald regard the bald. Int. J. Dermatol. 2002;41(12):867–869.
15. Passchier J. Quality of life issues in male pattern hair loss. Dermatology. 1998;197(3):217–218.
16. Tabolli S, Sampogna F, di Pietro C, Mannooranparampil TJ, Ribuffo M, Abeni D. Health status, coping strategies, and alexithymia in subjects with androgenetic alopecia: a questionnaire study. Am J ClinDermatol. 2013 Apr;14(2):139-45. doi: 10.1007/s40257-013-0010-3. PMID: 23413102.. 2013;14(2):139–145.
17. Kaufman KD. Androgens and alopecia. Mol Cell Endocrinol 2002; 198:89-95.
18. Kanti V, Messenger A, Dobos G, Reygagne P, Finner A, Blumeyer A, et al. Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men - short version. J EurAcadDermatolVenereol 2018;32:11-22.
19. Kaufman KD, Olsen EA, Whiting D, Savin R, DeVillez R, Bergfeld W, et al. Finasteride in the treatment of men with androgenetic alopecia. Finasteride male pattern hair loss study group. J Am AcadDermatol 1998;39(4 Pt 1):578-89.
20. McClellan KJ, Markham A. Finasteride: A review of its use in male pattern hair loss. Drugs 1999;57:111-26.
21. Van Neste D, Fuh V, Sanchez-Pedreno P, Lopez-Bran E, Wolff H, Whiting D, et al. Finasteride increases anagen hair in men with androgenetic alopecia. Br J Dermatol 2000;143:804-10
22. Price VH, Menefee E, Sanchez M, Kaufman KD. Changes in hair weight in men with androgenetic alopecia after treatment with finasteride (1 mg daily): Three- and 4- year results. J Am AcadDermatol 2006;55:71-4.
23. Hirshburg JM, Kelsey PA, Therrien CA, Gavino AC, Reichenberg JS. Adverse effects and safety of 5-alpha reductase inhibitors (finasteride, dutasteride): a systematic review. J ClinAesthetDermatol 2016;9:56-62.
24. Clark RV, Hermann DJ, Cunningham GR, Wilson TH, Morrill BB, Hobbs S. Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by dutasteride, a dual 5alpha-reductase inhibitor. J ClinEndocrinolMetab 2004;89:2179-2184.
25. Dallob AL, Sadick NS, Unger W, Lipert S, Geissler LA, Gregoire SL, et al. The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations patients with male pattern baldness. J ClinEndocrinolMetab 1994;79:703-6.
26. Messenger AG, Sinclair RD, Farroukh P, Deberks DAB. Acquired disorders of hair. In: Griffith CE, editor. Rook’s textbook of dermatology. 9th ed. West Sussex: John Wiley & Sons Ltd; 2016. p. 89.1-89.2.
27. Chung HC, Lee S, Lee WS. Long-term efficacy and safety of the dual 5- alpha reductase blocker dutasteride on male androgenetic alopecia patients. J Dermatol 2017;44:1408-1409.
28. Eun HC, Kwon OS, Yeon JH, Shin HS, Kim BY, Ro BI, et al. Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male pattern hair loss: a randomized, double-blind, placebo-controlled, phase III study. J Am AcadDermatol 2010;63:252- 258.
29. GubelinHarcha W, BarbozaMartínez J, Tsai TF, Katsuoka K, Kawashima M, Tsuboi R, et al. A randomized, active- and placebo controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia. J Am AcadDermatol 2014;70:489- 498.e3.
30. Shanshanwal SJ, Dhurat RS. Superiority of dutasteride over finasteride in hair regrowth and reversal of miniaturization in men with androgenetic alopecia: a randomized controlled open-label, evaluator-blinded study. Indian J DermatolVenereolLeprol 2017;83:47-54.
31. Roberts JL, Fiedler V, Imperato-McGinley J, Whiting D, Olsen E, Shupack J, et al. Clinical dose ranging studies with finasteride, a type 2 5alpha-reductase inhibitor, in men with male pattern hair loss. J Am AcadDermatol 1999;41:555-63.
32. Whiting DA, Olsen EA, Savin R, Halper L, Rodgers A, Wang L, et al. Efficacy and tolerability of finasteride 1 mg in men aged 41 to 60 years with male pattern hair loss. Eur J Dermatol 2003;13:150-60.
33. Olsen EA, Hordinsky M, Whiting D, Stough D, Hobbs S, Ellis ML, et al. The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. J Am AcadDermatol 2006;55:1014-23.
34. Shah KB, Shah AN, Solanki RB, Raval RC. A comparative study of microneedling with platelet-rich plasma plus topical minoxidil (5%) and topical minoxidil (5%) alone in androgenetic alopecia. Int J Trichol 2017;9:14-8.
35. De Villez RL. Topical minoxidil therapy in hereditary androgenetic alopecia. Arch Dermatol 1985; 121:197-202.
36. Hajheydari Z, Akbari J, Saeedi M, Shokoohi L. Comparing the therapeutic effects of finasteride gel and tablet in treatment of the androgenetic alopecia. Indian J DermatolVenereolLeprol 2009;75:47-51.
37. Paik JH, Yoon JB, Sim WY, Kim BS, Kim NI.The prevalence and types of androgenetic alopecia in Korean men and women. Br J Dermatol 2001; 145:95-9.
38. Olsen EA, Hordinsky M, Whiting D, Stough D, Hobbs S, Ellis ML, et al. The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. J Am AcadDermatol 2006;55:1014-23.
39. GubelinHarcha W, BarbozaMartínez J, Tsai TF, Katsuoka K, Kawashima M, Tsuboi R, et al. A randomized, active- and placebo controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia. J Am AcadDermatol 2014;70:489- 498.e3.
40. Jung JY, Yeon JH, Choi JW, Kwon SH, Kim BJ, Youn SW, et al. Effect of dutasteride 0.5 mg/d in men with androgenetic alopecia recalcitrant to finasteride. Int J Dermatol 2014;53:1351-7.