I am 54 years old and experiencing alopecia areata since last year. I had a sudden period of extreme stress that may have prompted the loss, but had also tried a medicine for a nail fungus around the same time. I see one doctor (a rheumatologist ) for a possible lupus diagnosis ( lupus is difficult to diagnose) and my primary care doctor was also treating me for hypothyroidism since I was gaining weight, and had increased my dosage from a very low beginning strength to a slight increase. With all of that going on I am not sure what the exact cause of the hair loss was. I stopped all medications immediately. I jokingly told my doctor that I can handle being fat, I"m ok with getting old, but old, fat and bald wasn"t going to work for me. My other doctor did some blood work and suggested I take zinc supplements , and things improved. The nail fungus went away, my hair started re-growing, and I perked up a little despite being off the thyroid medicines. Just this week I noticed a quarter sized spot which is increasing in size, and I"m back online searching for answers. The only changes this time is that I had changed brands of zinc, maybe it"s time to go back to what was working.
Alopecia areata (AA) is a common inflammatory disease targeting the anagen-stage hair follicle. Different cytokines have been implicated in the disease profile, but their pathogenic role is not yet fully determined. We studied biopsies of pretreatment lesional and non-lesional (NL) scalp and post-treatment (intra-lesional steroid injection) lesional scalp of 6 patchy patients with AA using immunohistochemistry and gene expression analysis. Immunohistochemistry showed increases in CD3(+) , CD8(+) T cells, CD11c(+) dendritic cells and CD1a(+) Langerhans cells within and around hair follicles of pretreatment lesional scalp, which decreased upon treatment. qRT-PCR showed in pretreatment lesional scalp (compared to NL) significant increases (P < ) in expression of inflammatory markers (IL-2, IL-2RA, JAK3, IL-15), Th1 (CXCL10 and CXCL9), Th2 (IL-13, CCL17 and CCL18), IL-12/IL-23p40 and IL-32. Among these, we observed significant downregulation with treatment in IL-12/IL-23p40, CCL18 and IL-32. We also observed significant downregulation of several hair keratins in lesional scalp, with significant upregulation of KRT35, KRT75 and KRT86 in post-treatment lesional scalp. This study shows concurrent activation of Th1 and Th2 immune axes as well as IL-23 and IL-32 cytokine pathways in lesional AA scalp and defined a series of response biomarkers to corticosteroid injection. Clinical trials with selective antagonists coupled with cytokine-pathway biomarkers will be necessary to further dissect pathogenic immunity.
In cases of severe hair loss, limited success has been achieved by using the corticosteroids clobetasol or fluocinonide , corticosteroid injections, or cream. The cream is not as effective and it takes longer in order to see results. Steroid injections are commonly used in sites where the areas of hair loss on the head are small or especially where eyebrow hair has been lost. Whether they are effective is uncertain. Some other medications that have been used are minoxidil , Elocon (mometasone) ointment (steroid cream), irritants (anthralin or topical coal tar), and topical immunotherapy ciclosporin , sometimes in different combinations. Topical corticosteroids frequently fail to enter the skin deeply enough to affect the hair bulbs, which are the treatment target,  and small lesions typically also regrow spontaneously. Oral corticosteroids decrease the hair loss, but only for the period during which they are taken, and these drugs can cause serious side effects .