Sir,
Diffuse hair loss is a common and multifactorial problem in women which is quite challenging to treat. Telogen effluvium (TE) is the most common cause followed by female pattern hair loss (FPHL) and chronic telogen effluvium (CTE).[1] Overlapping clinical features of different entities pose difficulties in clinical diagnosis. So, we decided to assess the clinical and etiological profile of women presenting with diffuse hair loss.
We noted down the detailed history, examination, and investigation findings [serum hemoglobin, total iron-binding capacity (TIBC), serum ferritin, thyroid stimulating hormone (TSH), leutinizing hormone (LH), follicle stimulating hormone (FSH), and free testosterone levels] of 100 females presenting with diffuse hair loss to our outpatient department. The diagnosis of FPHL, TE, and CTE was made based on the history and clinical presentation at the time of first visit of the patient. Patients giving preceding history of stress in the past 2–3 months and positive hair pull test were diagnosed as TE. Patients presenting with hair thinning over central/bitemporal areas and negative hair pull test were diagnosed as FPHL. Patients with hair fall for >6 months without any widening of central parting and positive hair pull test were diagnosed as CTE. In patients having overlapping features, a diagnosis was made on the basis of most prominent clinical signs. We did not include minors (<18 years) and pregnant females.
The mean age was 31.06 ± 9.84 years. Maximum number of patients (23) belonged to the age group of 18–22 years followed by 28–32 years. The most common presentation was FPHL (61%), followed by TE (25%), and CTE (14%). The duration of hair loss ranged from 15 days to 2 years, and the mean duration was 18.84 ± 25.5 months. About 28% of the patients suffered from chronic infection or disease, including hypothyroidism in 14%, pulmonary tuberculosis in 5%, diabetes mellitus and infertility in 2% each, hypertension, dysfunctional uterine bleeding, asthma, gout, and fibroid in 1% each. History of preceding emotional stress in the past 3 months of onset of hair fall was present in 22% of patients. History of preceding drug intake was present in 28%, the most common ones being thyroxine, oral hypoglycemic agents, antihypertensives, oral contraceptives, and non-steroidal anti-inflammatory drugs. Four patients had a history of undergoing major surgery in the past 3 months. Menstrual history revealed hypomenorrhea/oligomenorrhea in 18 patients, hypermenorrhea/menorrhagia in 7 patients, and 13 of them were postmenopausal. About 35% had a history of weight gain in the past 6 months. Family history in first degree relative could be elicited in 38% of the patients. On examination, hair thinning was present in 61% (around central parting – 40%, bitemporal – 11%, and Christmas tree pattern– 24%), hair pull test was positive in 39%, and clinical signs of hyperandrogenism, such as seborrhea were present in 47%, concomitant acne vulgaris in 26%, 10% had hirsutism, and 7% of them suffered from polycystic ovarian syndrome (PCOS). Among the patients having PCOS, 71.4% presented with FPHL, and the remaining 28.6% presented with TE.
Around 32% of the patients were mildly anemic (Hb11–11.9 g%), 18% moderately anemic (Hb8–10.9 g%), and the rest 2% suffered from severe anemia (Hb < 8 g%) [Table 1]. The mean hemoglobin levels in patients with CTE (10.36 ± 1.72) were significantly lower (P value < 0.05) as compared to those with TE (11.34 ± 1.54) and FPHL (12.36 ± 1.30). High serum TIBC levels (>400 μg/dl) were detected in 18% of the patients. The mean serum TIBC levels were higher in CTE group (362.26 ± 84.96), as compared to TE group (344.69 ± 64.70) and FPHL group (308.54 ± 60.15). Low serum ferritin levels were found in 16% of patients and the mean serum ferritin levels were lower in patients with CTE (21.21 ± 15.86) as compared to those with TE (29.44 ± 21.64) and FPHL (30.38 ± 18.78).
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Table 1: Biochemical test results in diffuse hair loss
Serum TSH levels were increased in 4 (6.6%) patients with FPHLand one (7.1%) patient with CTE, and was decreased in 2 (3.3%) patients with FPHL.
Serum LH levels (1.68–15IU/L) were increased in 1 (4%) patient with TE and 3 (4.9%) patients with FPHL. Serum FSH levels (1–10IU/L) were decreased in 1 (1.6%) patient with FPHL, and increased in 4 (6.6%) patients with FPHL and 3 (21.4%) patients with CTE. Serum free testosterone levels (0.3–1.9ng/dl) were increased in 4 (6.6%) patients with FPHL and 2 (8%) patients with TE, and decreased in only 1 (4%) patient with TE.
We found that stress was an important predisposing factor for all the types of diffuse hair loss. Patients with hypothyroidism presented mainly with FPHL. Drug intake was associated with all the three presentations. Patients with hypermenorrhea/menorrhagia presented only with FPHL, while those with hypomenorrhea/oligomenorrhea presented with all the three types. Weight gain and hirsutism were associated with all the three groups, but PCOS was found only in TE and FPHL patients.
Anemia was a common factor in all the three groups, while severe anemia was detected only in TE and CTE patients. Patients with CTE and TE had significantly low hemoglobin, ferritin, and higher TIBC levels, as opposed to those with FPHL. Thus, CTE and TE can be a manifestation of low iron stores. Some studies have reported significant improvement in hair shedding in patients with CTE following iron and L-lysine supplementation.[2] So, iron studies may be recommended in females presenting with CTE and TE.
FPHL may also be a manifestation of hypo- or hyperthyroidism. Screening for T3, T4, and TSH has been recommended when no apparent cause of diffuse hair loss is found.[3]
Elevated levels of testosterone were found in 6.6% of patients with FPHL. The role of androgens in FPHL is a matter of debate. In a study comprising 109 women with FPHL, 38.5% were found to have a clinical or biochemical evidence of hyperandrogenism.[4] On the contrary, other authors have failed to find the evidence of raised androgens in FPHL.[5] Therefore, estimation of androgen levels in patients with FPHL could be considered.
Our present study should stimulate further detailed research on this challenging problem to give insights into the exact etiopathogenesis of diffuse hair fall in females for a holistic management.
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Nil.
Conflicts of interest
There are no conflicts of interest.
REFERENCES
1. Shrivastava SB. Diffuse hair loss in an adult female: Approach to diagnosis and management Indian J Dermatol Venereol Leprol. 2009;75:22–7
2. Rushton DH. Nutritional factors and hair loss Clin Exp Dermatol. 2002;27:396–404
3. Chartier MB, Hoss DM, Grant-Kels JM. Approach to the adult female patient with diffuse non scaring alopecia J Am Acad Dermatol. 2002;47:809–19
4. Futterweit W, Dunaif A, Yeh HC, Kingsley P. The prevalence of hyperandrogenism in 109 consecutive female patients with diffuse alopecia J Am Acad Dermatol. 1988;19:831–6
5. Rushton DH, Ramsay ID, James KC, Norris MJ, Gilkes JJ. Biochemical and trichological characterization of diffuse alopecia in women Br J Dermatol. 1990;123:187–97
