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Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

Background

In pregnancy, increased numbers of hair follicles remain in the anagen phase for longer periods due to hormonal changes and return to the telogen phase within 3–6 months of delivery with a sudden drop in hormone levels. This results in excessive shedding of hair known as post-partum telogen effluvium.

Objective

To determine the changes in the hair cycle during gestation and the post-partum period.

Methods

We included 116 women in this study; 28 women at the 24th week of pregnancy, 30 pregnant women at term gestation, 29 women in the 4th post-partum month, and 29 in the first post-partum year. The number of breastfeeding mothers in the post-partum period and the month in which they were examined were also recorded. The ratios of anagen and telogen were measured using Trichoscan.

Results

A statistically significant difference was observed between the groups in terms of the anagen and telogen ratios (P = 0.042, P = 0.042). In the inter-group comparisons, the mean anagen rate in the 4th post-partum month was significantly lower than that in the 6th and 9th month of pregnancy (P = 0.045, P = 0.038), while the average telogen rate was significantly higher (P = 0.045, P = 0.038). The mean anagen rate in the 4th post-partum month in the breastfeeding group was significantly higher than that in the non- breastfeeding group (P = 0.014), while the mean telogen rate was significantly lower (P = 0.014). There was no statistically significant difference between the two groups (the breastfeeding and non-breastfeeding groups) in terms of the mean anagen and mean telogen ratios in the first post-partum year (P = 0.385).

Conclusion

The anagen rate increases during pregnancy and the telogen rate rises after delivery, however, there is no exaggeration in these changes in most women.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

During the entire life span, the human hair follicle shows patterns of cyclic activity with periods of massive growth (anagen), apoptosis-driven involution (catagen), a resting phase (telogen) and these phases last approximately 1000, 10 and 100 days respectively.[1, 2] Hair growth is usually randomized and non-synchronized.[3] In the scalp, 10% of terminal follicles are at the telogen phase at any given time and these follicles are scattered randomly in the scalp.[4]

A variety of hormones rise significantly throughout pregnancy, including thyroid hormone, secondary androgen and oestrogens hormones, which are known to affect hair. During pregnancy, there is an approximate ninefold increase in progesterone, fourfold increase in estrone (E1), eightfold increase in estradiol (E2) and a ninefold increase in estriol (E3) levels.[5]

Following removal of the placenta at birth, the levels of progesterone and oestrogens return to normal within 2–4 days.[5, 6] Prolactin synthesis rises with the increased effect of oestrogen during pregnancy; the mean plasma concentration elevates approximately 20-fold at term as compared to premenopausal non-pregnant women. Prolactin is nearly sevenfold higher in breastfeeding women on the 10th to 90th post-partum day as compared with pre-menopausal non-pregnant women, and is fivefold higher on the 90th to 180th post-partum day and is threefold higher than on the 180th post-partum day.[7] However, following stimulation of the nipple, this rate amounts to 80–150% of basal level.[8] Prolactin levels return to normal within seven post-partum days when lactation does not occur.[7]

Headington divided telogen effluvium (TE), seen most commonly in women, into five functional types based on changes during the different phases of the hair cycle. Of these, the best example of delayed anagen release is post-partum hair loss. In delayed anagen release, some follicles remain in the anagen phase longer than normal before entering the telogen phase.[4] Effective signal is the delayed beginning of the telogen phase. Release begins in the anagen phase when a sufficient number of follicles are involved, and increased hair loss would occur.[9]

Trichoscan is a non-invasive method, which combines epiluminescence microscopy with digital image analysis. It is called as ‘Trichoscan’, because it is a computerized and modified form of trichogram.[10] It was first developed for the diagnostic and therapeutic follow-up of androgenetic alopecia (AGA), however, in recent years it has also been utilized in the treatment and follow-up of hirsutism.[10-12] This method allows examination of all the biological parameters of hair growth (hair density (n/cm2), hair diameter, hair growth rate (mm/day) and the anagen-to-telogen ratio).[13] The Trichoscan method has many advantages. These include analysis independent of researchers, more readily accepted by patients due to its non-invasiveness, and it is quick and easy to perform.[10, 13]

The use of hair dye during pregnancy was shown not to have feto-toxic effects or be associated with childhood brain tumours.[14]

To our knowledge, post-partum TE, although a well-known entity, has not been studied since the study conducted by Lynfield in 1960 using trichogram.[15] We sought to determine changes in the hair cycle during gestation and the post-partum period.

Materials and methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

A total of 116 women were enrolled in this study. Of these women, 28 were in the 24th week of pregnancy, 30 were attending a gynaecology outpatient department following term gestation, 29 mothers were in the 29th post-partum month and 29 were in the first post-partum year and attending the paediatric outpatient department of our hospital. The 3rd Istanbul Clinical Research Ethics Committee gave approval to conduct the study. The scalp of each woman was examined and those with AGA, alopecia areata, trichotillomania, signs of hyperandrogenism and those who previously visited a doctor with the complaint of hair loss were excluded from the study.

Complete blood count, free T4 and TSH were measured in each woman. Women diagnosed with thyroid disease or anaemia and those taking drugs known to cause telogen effluvium,[16] were excluded from the study.

The number of breastfeeding mothers during the post-partum period was also recorded. The month the examination was performed was noted to identify seasonal hair loss.

All women were asked to wash and comb their hair on the day before examination. The occipital protuberance was chosen as the region of interest. We selected a site without haemangioma, birthmarkand scaling. After passing through the hole in the middle of the plastic card, all hair in the area was shaved using Hairliner, Wella, Germany (the shaved area was 1.8 cm2). Approximately 1 cm of hair dye was placed on a wooden spatula (Goldwell 2N Schwarz, Darmstadt, Germany), three drops of the cream (Rondo Coiffeur magic colour 6% creme-oxyde, Coiffeur, Cologne, Germany) were then poured onto the spatula and mixed with the hair dye. The dye was carefully applied to the shaved area, and was cleaned 12 min later using alcohol solution (Kodan Spray, Schülke & Mayr, Vienna, Austria). While the area was still wet, digital images were taken (×30 magnification, Molemax I Plus LulP Vienna, Austria). Three days later, images of the same area were again acquired. The anagen and telogen ratios from the second set of images were calculated using Trichoscan software (Tricholog GmbH, Freiburg, Germany).

Statistical analysis was performed with Number Cruncher Statistical System (NCSS) 2007 & Power Analysis and Sample Size (PASS) 2008 Statistical Software (Kaysville, UT, USA). The one-way anova test was used for inter-group comparisons (four groups) of the parameters showing normal distribution as well as of the descriptive statistical data (mean, standard deviation, median, frequency and rate). The groups showing differences were noted; the Student's t test was used for paired comparisons of the groups. The Kruskal–Wallis test was used for inter-group comparisons of the number of pregnancies not showing normal distribution, and the Mann–Whitney U test was used for paired comparisons. Qualitative data were compared using the chi-square test. The results were expressed with 95% confidence intervals. A < 0.05 was considered significant.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

The mean age of the 116 women was 27.78 ± 4.27 years (range 18–39 years). There was no statistically significant difference between the groups with respect to the ages of the women (P = 0.325) (Table 1).

Table 1. Mean age, anagen and telogen ratios in the four groups
 In the 6th month of pregnancy (n = 28)In the 9th month of pregnancy (n = 30)In the 4th post-partum month (n = 29)In the first post-partum year (n = 29) P
Mean ± SDMean ± SDMean ± SDMean ± SD
Age (years)29.07 ± 4.1927.43 ± 5.2427.48 ± 3.1827.17 ± 4.130.325
Anagen rate81.24 ± 4.6381.43 ± 4.5578.47 ± 4.5181.05 ± 4.140.042
Telogen rate18.76 ± 4.6318.57 ± 4.5521.53 ± 4.5118.94 ± 4.140.042

A statistically significant difference was observed between the groups for the mean anagen and mean telogen ratios (P = 0.042, P = 0.042) (Table 1). In the paired comparisons of the groups, the mean anagen rate in women in the 4th post-partum month was significantly lower compared with those in the 6th and the 9th month of pregnancy (P = 0.045, P = 0.038), while the average telogen rate was significantly higher (P = 0.045, P = 0.038).

There were no statistically significant differences in the other paired comparisons (Table 2).

Table 2. Paired comparisons of the anagen and telogen ratios in the groups
 Anagen RatioTelogen Ratio

In the 6th month of pregnancy *

In the 9th month of pregnancy

0.9980.998

In the 6th month of pregnancy *

In the 4th post-partum month

0.0450.045

In the 6th month of pregnancy *

In the first post-partum year

0.9990.999

In the 9th month of pregnancy *

In the 4th post-partum month

0.0380.038

In the 9th month of pregnancy *

In the first post-partum year

0.9890.989

In the 4th month of pregnancy *

In the first post-partum year

0.1280.128

The average anagen rate was significantly higher in breastfeeding mothers in the 4th post-partum month as compared with the non-breastfeeding group, while the average telogen rate was significantly lower (P = 0.014, P = 0.014 respectively).

No statistically significant difference was found between the breastfeeding and non-breastfeeding groups in terms of the mean anagen and mean telogen ratios in the first post-partum year (P = 0.385, P = 0.385 respectively) (Table 3).

Table 3. Anagen and telogen ratios depending on lactation in the 4th month and in the first post-partum year
 In the 4th Post-partum MonthIn the First Post-partum Year
No Lactation (n = 4)Lactation present (n = 25) P No Lactation (n = 15)Lactation present (n = 14) P
Mean ± SD (Median)Mean ± SD (Median)
Anagen Ratio73.37 ± 2.63 (73.05)79.28 ± 4.22 (78.30)0.01481.71 ± 4.30 (83.50)80.35 ± 3.99 (80.20)0.385
Telogen Ratio26.62 ± 2.63 (26.95)20.72 ± 4.22 (21.70)0.01418.29 ± 4.30 (16.50)19.65 ± 3.99 (19.80)0.385

A statistically significant difference was observed between the groups during the three seasons when the seasonal distribution of cases was analysed in the groups, (P = 0.001, P = 0.001, P = 0.042 respectively). No women were included in the study during the summer months. The number of cases was higher in the 6th month and 9th month of pregnancy in winter, in the 4th post-partum month and in the first post-partum year in the spring and in the first post-partum year in autumn.

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References

A possible reason for delayed anagen release is metabolic and/or endocrine-related changes. Prolonged anagen shows that the anagen period is not varied. Time to hair loss after giving birth is to some extent variable and often reaches a peak in the 2nd or 3rd post-partum month. However, this period may extend up to 6 months in some patients. This long period depends on the length of the individual catagen-telogen phase or persistent partial cyclic synchrony.

The answers to the questions on whether normal random asynchrony could be regained after post-partum TE or whether a general or a regional loss will continue indefinitely in some patients are controversial.[4]

Women at risk of AGA tend to develop post-partum alopecia.[17] The anagen period is shortened in AGA.[18] Thus, because the number of follicles exposed to prolonged anagen is greater in women with AGA, the number of follicles entering the telogen phase is greater in the post-partum period.

Although post-partum TE is a well-known entity and is presumed by physicians to be common, our findings of a 3% change in telogen rates, suggest that post-partum TE is an infrequent cause of hair shedding. While this speculation may be influenced by the inclusion of women without complaints of hair shedding and by the lack of screening in a dermatology clinic, our long-term clinical experience enables us to speculate that there are not many patients presenting with the complaint of post-partum hair shedding and, of those who seek medical attention for this complaint, a significant proportion may well have AGA as the underlying problem.

Hormones, growth factors, cytokines and neuropeptides affect the hair follicle cycle.[19] In addition, female hormones (oestrogens, prolactin, or progesterone) affect the hair growth cycle.[9] Given the multiple and complex endocrine changes (dramatic fluctuations in progestagens, and prolactin levels) during and after pregnancy and during lactation, it is difficult to distinguish the effects of hair growth due to E2 on scalp hair from that of other hormones.[20]

Recent studies have shown that oestrogen has an important role in hair growth in all mammals, including humans. This effect varies according to species, gender and body site.[20] Oestrogens (17-β estradiol, E2) modulate hair growth, affect hair growth inhibitors and due to these characteristics they are often used in the treatment of AGA and TE.[20, 21] Topical application of E2 to the human scalp reduces the rate of telogen, and prolongs the anagen phase. In addition, E2 slightly elongates the anagen phase both in male and female frontotemporal hair follicles.[20] Yet, there is a significant increase in the hair length in pregnant women and in the anagen phase.[2, 14, 20] The hair diameter in pregnant women is also increased compared with non-pregnant women.[3]

AGA-like hair loss, amenorrhoea, infertility, hirsutism and acne vulgaris are seen in hyperprolactinemia. This may be associated with the incremental effect of prolactin on adrenal androgen production, although prolactin has an inhibitory effect on 5 alpha reductase. Prolactin and its receptors have been demonstrated in the human skin and hair follicles. High-level prolactin (400 ng/dL) in tissue cultures of human hair follicles has been shown to inhibit hair shaft elongation, induce the development of early catagen, reduce proliferation in hair bulbus keratinocytes and to induce apoptosis. Thus, the expression of prolactin receptors in hair follicles is functional. Prolactin acts like an autocrine modulator of hair follicles and its inhibitory effect on hair follicles may be an underlying cause of TE seen in women with hyperprolactinemia, which is not fully understood.[22] These findings suggest that prolactin also has an effect on post-partum TE. Prolactin levels decrease in breastfeeding mothers in the post-partum period as compared to gestation; however, the level is still high compared to the pre-pregnant period. These levels quickly return to pre-pregnancy levels in non-breastfeeding women. Given these data, post-partum TE is expected to begin earlier and to be felt more prominently in breastfeeding mothers. In this study, in contrast to this effect, the rate of anagen was significantly higher in breastfeeding women in the 4th post-partum month as compared to non-breastfeeding mothers. These results may have been confounded by the low number of non-breastfeeding cases, not following up the same women in the course of the study period, and may be inconclusive due to the fact that the structures in the complex mechanisms controlling the hair cycle are not fully known due to little available information.

No differences between the breastfeeding and non-breastfeeding groups in the first post-partum year can be explained by the fact that the hair cycle returns to asynchrony at the end of a 1-year period independent of prolactin.

Hair growth increases during the warm months, reaching peak levels in September, then decreases to the lowest level in December-January. The anagen rate was 90% in August and September. When delivery takes place in the fall, together with concurrent seasonal hair shedding occurring in December–January, post-partum TE results in a more prominent effluvium.[23] We observed a difference between the groups with respect to the seasonal distribution of TE. The number of women in the 4th post-partum month was low in the winter months. Therefore, we can say that seasonal hair shedding does not have an incremental effect on statistical significance, but has a mitigating effect.

In conclusion, this study shows that the anagen rate increases during pregnancy in women without disease that affects the hair cycle and that the telogen rate rises after delivery, but it is not exaggerated in most women.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. References