Twenty-nail dystrophy (TND) is not rare in patients presenting with alopecia areata (AA); however, to date, no universally accepted treatment strategy has been established for TND1. We present a patient with TND treated with hydroxychloroquine. We received the patient's consent form about publishing all photographic materials.

A 49-year-old female patient presented with nail fragility and patchy hair loss, which both started a year ago. Prior to visiting Chonnam National University Hospital, the patient reported receiving systemic antifungal and topical corticosteroid drugs for the nails without improvement. Her scalp showed patches of hair loss (Fig. 1A). Her nails showed ridging, lack of luster and brownish discoloration (Fig. 1B, D). Potassium hydroxide preparation (KOH) and fungal cultures of the nail specimens showed negative results. Histopathological examination of the nail matrix revealed hyperkeratosis, acanthosis, mild spongiosis, epidermal lymphoid cells infiltrates and vacuolar degeneration of the basal keratinocytes (Fig. 2). On medical history, she has been treated with diabetes mellitus for 6 years. Routine blood tests were normal and no other cutaneous disorder was detected. The patient was treated with intralesional injections of trimacinolone acetonide for AA and hydroxychloroquine (200 mg/d) for TND. AA improved after 4 months whereas TND improved after a year (Fig. 1C, E). Notably, discontinuation of hydroxychloroquine administration led to the recurrence of TND after 6 months, which however showed resolution following re-treatment with hydroxychloroquine for 20 months without recurrence and drug-induced adverse events.

TND or trachyonychia is characterized by diffuse ridging, lack of luster, and a sandpaper-like roughening of the nail surface. TND could be an idiopathic condition or a manifestation of disorders including AA, psoriasis, and lichen planus2. Kasumagic-Halilovic and Prohic1 proposed that because of the similarity in structure and growth patterns between hair follicles and nails, these appendages are common targets for inflammatory cells in AA. The histopathological feature also suggests the possibility of coincident lichen planus in our case2. Treatment options for TND include systemic treatment with oral prednisone and griseofulvin, psoralen ultraviolet A, topical steroids and retinoids, and/or steroid injections.

In our case, hydroxychloroquine induced remission of TND, which was nonresponsive to topical steroid treatment. Systemic steroid was not priorly considered because of high blood sugar. The mechanism of antimalarials in dermatologic disorders includes interfering antigen presentation by major histocompatibility complex molecules3. They also reduce activity levels of inflammatory cytokines such as interleukin (IL)-1, IL-2, IL-5, and IL-6. Additionally, antimalarials modulate the innate immune system by inhibiting toll-like receptor (TLR)-9 signaling. Interestingly, AA is an autoimmune disease mediated by autoreactive CD8+ T-cells, which recognize hair follicles and nails as antigens1. Moreover, IL-2 is a well-known driver of CD8+ T-cells in AA, and the expression of TLR-9 in mononuclear cells in the peripheral blood is significantly up-regulated in patients with AA45. We speculate that the administration of hydroxychloroquine may have interfered with one or more of these pathways in our case. As far as we know, this is the first case of TND treated with hydroxychloroquine in Korean literature. We authors suggest that hydroxychloroquine can be a both effective and safe treatment option for TND.