Iron Plays a Certain Role in Patterned Hair Loss

Iron Plays a Certain Role in Patterned Hair Loss

Dr Sanjay Agrawal, Leading Pharmaceutical Consultant and Editor-in Chief of IJMToday.

Loss of scalp hair is not a serious life threatening disorder, but it can cause psychological distress and affect quality of life adversely. Hairs are rapidly proliferating organ with much requirement of blood supply. Therefore, the relationship between micronutrients and hair loss has been evaluated in several studies since the 1960s. The most widely cited nutritional causes of hair loss include iron, one of the key micronutrients in metabolism of our body. From its diverse functions, it is well known that iron deficiency (ID) is associated with a lot of pathological conditions. However, its role in hair loss is not well established yet. When reviewing articles which have documented the relationship between ID and hair loss including female pattern hair loss (FPHL), telogen effluvium, alopecia areata, alopecia universalis or totalis, some advocated the association between ID and hair loss and others were against it. This controversy might be caused by study designs, methodology and clinical condition defining hair loss. For detection of ID, serum ferritin level can be used as a very early marker. It is a main iron-binding protein in nonerythroid cells reflecting total body iron stores. It decreases from very early stage of ID as iron reserves go down. Because only ID can cause very low serum ferritin concentration (FC), a FC is very specific for ID. However, it can play a role in inflammation as a reactive protein, patients with active infection and/or inflammation should not be included in the analysis when we consider FC is used for detecting ID. Hormonal status can affect hair loss and it should be considered when interpreting the clinical condition, too.

The association between ID and hair loss is still a debating issue. Kantor et al. reported that alopecia areata, FPHL and telogen effluvium patients under 40 yr old showed lower serum ferritin concentration than controls without hair loss. Rushton et al. also demonstrated that there was significant decrease of hair loss and increase of FC in patients with telogen effluvium who received oral iron therapy. These results are supported by Moeinvaziri et al. who suggested that serum FC and transferrin saturation is lower in patients with telogen effluvium based on the case control study design. In contrast, Sinclair reported that response rates to iron supplementation were not different between low ferritin (< 20 ng/mL) and normal group (≥ 20 ng/mL) in FPHL patients. Olsen et al. also showed no differences in prevalence of ID between female patients with (285 FPHL patients and 96 telogen effluvium patients) or without hair loss (a total of 76 Caucasian women older than 18 yr old). Rushton et al. criticized study of Olsen et al. in that it appears to have some confounding issues and contradictions such as no-standardized evaluation in blood sampling and no quantitative hair evaluation in control group. Reviewing previous studies, the role of iron in hair loss appears untangled until now. Therefore, we conducted this study in order to find out the relationship between body iron status and various conditions with hair loss. In order to overcome the limitation of retrospective study, we carefully selected patients diagnosed with FPHL and MPHL who had visited our clinic between January 2010 and February 2011 and underwent the screening test at their first visit. We excluded patients with abnormal thyroid function or any medical history which can affect body iron status. For the better comparison, age-sex matched healthy controls without complaint of hair loss were selected who had visited the hospital for a check-up which includes all blood tests of initial screening test. ID is a continuum of various status of iron deposition in the body. Iron depletion is the mildest form of ID followed by iron deficient erythropoiesis and iron deficient anemia being the most severe form. Body iron stores can be assessed by serum FC but there is no consensus which ferritin level is the right one to define ID in practice. Although many laboratories use FC of 10 to 15 µg/L as the lower limits of normal based on reference sample groups, this only gives a sensitivity of 59% and a specificity of 99% for diagnosing iron deficiency. In women of childbearing age, using a cutoff of 10 to 15 µg/L yields a sensitivity of 75% and specificity of 98% in diagnosis of ID. A cutoff of 30 µg/L yields a sensitivity of 92% and a specificity of 98%, while a cutoff of 41 µg/L yields a sensitivity of 98% and a specificity of 98%. It might have contributed to the controversy that there is no guideline to define ID. From this study, over 80% of FPHL showed serum FC lower than 70 µg/L, while only less than 20% of age matched healthy female controls showed it. No female healthy controls showed serum FC lower than 30 µg/L in this study. Therefore, serum FC lower than 30 µg/L might be a clinically significant indicator for ID especially in female hair loss patients considering their menstrual status. In this study, patients with MPHL show relatively early onset age, which means they appear to visit the clinic earlier than those with FPHL. Patients with FPHL show definitely lower serum FC compared with age/sex-matched normal controls. Female patients with FPHL were divided into two groups based on their menstrual status. Premenopausal patients with FPHL demonstrate much lower serum FC than postmenopausal FPHL patients. When compared with normal age/sex matched controls, statistically significant low serum FC is observed in FPHL premenopausal patients, while it is not significantly different between FPHL patients and normal controls after menopause. This result implicates that ID plays a certain role in premenopausal female patients with FPHL. However, weak association of ID with FPHL in postmenopausal patients could be addressed from this study. Patients with MPHL show considerably lower serum FC on the average than age-sex matched healthy controls, although the serum level of FC is within normal range. We failed to prove the correlation between onset age and serum FC in MPHL patient, either (r = 0.12). However, approximately 20% of MPHL show serum FC lower than 70 µg/L and their age matched controls do not show that low serum FC. This result implicates that screening of iron status in even male patients with hair loss might provide clinical benefits. Clinical manifestations of F type of MPHL looks like those of FPHL in female patients. Therefore, we looked into patients with MPHL according to types (M type, F type and others based on BASP classification), which turns out there was no strong relationship between subtype of MPHL and ID. Patients showing low FC level < 70 µg/L had been on oral ferrous sulfate (130 mg of elemental iron/day) and serum level of FC doubled after 6 months of supplementation. Clinical response to iron supplementation proves not to be much higher than expected. Especially patients with MPHL patients rated lower PGA and PS when they were on oral iron supplementation. Oral 5 alpha reductase inhibitor is the first line treatment to MPHL patients and if MPHL patients showed lower FC, iron supplementation was first given to patients during almost 6 months until FC became higher than 70 μg/L. Therefore, iron supplementation group did not receive any kind of oral 5 alpha reductase inhibitor, which might cause significantly lower PGA and PS. This study owns its value because it demonstrates the first direct comparison between hair loss patients and same number of healthy controls matched by age and sex. It strongly supports the previous studies that ID can be a certain factor of developing or worsening FPHL especially in premenopausal female patients. Its role in MPHL is hard to conclude from this study. However, screening for ID as the first evaluation of hair loss in even male patients might be worthwhile in the clinical field.

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