Seo Wan Kim

Facial Skin Barrier Function Recovery After Microneedle Transdermal Delivery Treatment

BACKGROUND Microneedle treatment is currently used in the cosmetic industry for several skin conditions. Despite their extensive use, there is lack of sufficient data on the safety of microneedles. OBJECTIVE To investigate the degree of acute skin damage and the time required for facial skin barrier function to recover using different microneedle lengths and numbers of applications. MATERIALS AND METHODS Each side of a volunteers face was randomly treated with one of the following treatments: five applications of 0.15‐mm microneedles, five applications of 0.25‐mm microneedles, 10 applications of 0.15‐mm microneedles, or 10 applications of 0.25‐mm microneedles. Transepidermal water loss, stratum corneum hydration, and skin erythema were measured at baseline, immediately after treatment, 4 hours after treatment, and 8 hours after treatment and at 24‐hour intervals for 3 days. RESULTS Prompt recovery of barrier function (within 72 hours) was observed after microneedle treatment. CONCLUSION Microneedle treatment is simple and inexpensive, and the skin barrier disruption it causes resolves quickly. Therefore, it can serve as an effective physical method of enhancing transdermal delivery of medications for the treatment of many cosmetic and dermatological conditions.

A clinicopathologic study of thirty cases of acquired perforating dermatosis in Korea.

Background Acquired perforating dermatosis (APD) is histopathologically characterized by transepidermal elimination of materials from the upper dermis. APD can be divided into four diseases: Kyrles disease, perforating folliculitis, elastosis perforans serpiginosa, and reactive perforating collagenosis. APD is usually associated with systemic diseases, especially diabetes mellitus or chronic renal failure. So far, there have only been a few Korean studies of APD, which have a limited number of patients. Objective The aim of this study is to evaluate the clinical and histopathologic characteristics of 30 cases of APD and to examine the association with systemic diseases. Methods We retrospectively reviewed the medical records and biopsy specimens of 30 patients who were diagnosed with APD. Results The mean age was 55.5 years, and the average duration of the lesion was 7.8 months. The lower extremities (73.3%) were the most frequently occurring sites of the lesion. Twenty-five patients (83.3%) had pruritus, and Koebners phenomenon was present in 11 patients. Patients of 63.3% had at least one systemic disease. Diabetes mellitus (n=17, 56.7%) and chronic renal failure (n=10, 33.3%) were the most commonly associated conditions. Most patients received topical steroids (93.3%) and antihistamines (80.0%). The most common histopathologic type was reactive perforating collagenosis (n=23, 73.3%). Conclusion In this study, most patients had a systemic association to the diseases. Therefore, we suggest that further evaluation is necessary for patients who present with APD. This includes reviewing patients comprehensive past medical history, clinical exam, and additional diagnostic testing to check for the possibility of associated systemic diseases.

Ziprasidone-induced hypersensitivity syndrome confirmed by reintroduction

cient for professionals to feel confident in prescribing psychotropic medications. In this study, 88% of respondents reported that they did not feel comfortable in prescribing antidepressants, and 88% did not feel comfortable in prescribing antipsychotics. The present report marks the first study of its kind in Chile. It is limited by the low response rate to the survey and by the fact that Chilean dermatologists who have a special interest in psychodermatology would have been more likely to respond. Subsequent to appropriate educational changes, it will be interesting to measure these data in future generations of dermatologists.

Idiopathic Acquired True Leukonychia Totalis and Partialis

Dear Editor: A 19-year-old male patient presented with one-month history of progressive whitening of his toenails. The nail change began with central white spots on the toenails that progressed over one month to almost total nail whitening. The growth of the nails was otherwise normal. He was healthy and without a previous medical history. He had not experienced any exposure to medications, chemicals, or mechanical trauma to the nails. There was no family history of leukonychia or other dermatologic diseases. On physical examination, partial to total leukonychia of all toenails was observed. The right great toenail exhibited a totally chalky white discoloration. However, the distal portion of the other toenails had a pink transverse band about 2 or 3 mm wide at the free edge (Fig. 1). The surface of the nail did not demonstrable further change, such as pitting, ridging, or subungual hyperkeratosis. Otherwise, all fingernails were normal and the patient had no other organ abnormalities. Fig. 1 All toenails showed chalky white and opaque nail plates characteristic of leukonychia. The results of the laboratory studies, including complete blood count, blood chemistry profile, and urinalysis, were all within normal limits. Repeated potassium hydroxide preparations and fungal cultures of the toenails were negative. Punch biopsy was performed at the proximal nail fold of his left great toenail. Histopathologic examination of the nail plate revealed sparse parakeratosis with globular collection of keratohyaline granules (Fig. 2). A biopsy specimen from the nail bed and nail matrix were unremarkable. During the 6-month follow-up period, the discoloration of the toenails did not significantly change. Fig. 2 Histopathology of the nail plate showed sparse parakeratosis with globular collection of keratohyaline granules keratohyaline granules (HE A: ×40, B: ×200). Leukonychia is the most common chromatic abnormality of the nail. True leukonychia is an abnormality of the nail plate that originates in the matrix1. The mechanism of leukonychia is not clear. The nail plate normally consists of cornified cells that contain keratin. However in leukonychia, as a result of abnormal matrix keratinization, persistent parakeratosis, keratohyaline granules, and dissociation of keratin bundles are present. Disorganization of the keratin fibrils leads to the diffraction of visible light in the parakeratotic cells, resulting in a white nail, which prevents visualization of the underlying pink vascular bed2,3,4,5. True leukonychia may be inherited or acquired. Inherited leukonychia can be an isolated condition or one of several inherited leukonychia syndromes2. If true leukonychia is acquired, it may be associated with trauma, chemotherapeutic agents, hypocalcemia, zinc deficiency, heavy metal poisoning, local infection, and systemic diseases1,2,4,5. Idiopathic acquired true leukonychia is a rare condition, with only six reported cases in the literature1,2,3,4,5. All of those cases as well as our case showed progression from leukonychia partialis to combined leukonychia totalis and partialis. All of previous reported cases involved the fingernails, and among these, four cases appeared at the fingernails and toenails. Our case is different from those reported cases; because of our case involved only the toenails without involvement of the fingernails. In conclusion, true leukonychia can occur associated with trauma, drugs, infection, or systemic diseases. We thought that one of these must be the cause of development of true leukonychia, but we could not find any trauma history, systemic problem, or onychomycosis in our cases. Based on previous reports, we suggest that leukonychia might develop without underlying causes in some patients. This was a rare case with asymptomatic progressive idiopathic acquired true leukonychia totalis and partialis of the toenails without a hereditary cause.

The efficacy and safety of gamma-linolenic acid for the treatment of acne vulgaris.

References 1 Kuske H. Epidermolysis traumatica, regionar uber beiden Tibiae zur Atrophie fuhrend, mit dominanter Vererbung. Dermatologica 1946; 92: 304–305. 2 Naeyaert JM, Nuytinck L, De Bie S, et al. Genetic linkage between the collagen type VII gene COL7A1 and pretibial epidermolysis bullosa with lichenoid features. J Invest Dermatol 1995; 104: 803–805. 3 Lee YY-J, Chen H-C, Lin S-J. Pretibial epidermolysis bullosa: a clinicopathologic study. J Am Acad Dermatol 1993; 29: 974–981. 4 Hamada T, Fukuda S, Ishii N, et al. A Japanese family with dominant pretibial dystrophic epidermolysis bullosa: identification of a new glycine substitution in the triple-helical collagenous domain of type VII collagen. J Dermatol Sci 2009; 54: 212–214. 5 Betts CM, Posteraro P, Costa AM, et al. Pretibial dystrophic epidermolysis bullosa: a recessively inherited COL7A1 splice site mutation affecting procollagen VII processing. Br J Dermatol 1999; 141: 833–839. 6 Lee HS, Park K, Son SJ, et al. Pretibial epidermolysis bullosa: is this case a new subtype with loss of types IV and VII collagen? Int J Dermatol 2009; 48: 879–881. 7 Tang WY, Lee KC, Chow TC, et al. Three Hong Kong Chinese cases of pretibial epidermolysis bullosa: a genodermatosis that can masquerade as an acquired inflammatory disease. Clin Exp Dermatol 1999; 24: 149–153.

Metastatic gastric signet ring cell carcinoma clinically mimicking radiation recall dermatitis.

A 53-year-old woman presented to the dermatology clinic with a history of a bilateral circular orange discoloration around the upper and lower eyelids. On physical examination, the orange flat plaque lesions involved both the upper and lower eyelids, resembling a pair of circles. The lesions of the medial side of both of the upper eyelids were particularly large (Fig. 1a,b). There was orange discoloration of the palms (Fig. 1c) and soles. The sclerae and oral mucosa appeared normal. She had no organomegaly. We learned that the patient ate too much carrot and orange over the last two months, which underlined her anamnesis. In the light of the clinical exam and anamnesis, the patient was diagnosed xanthelasmas and carotenoderma. Laboratory tests were evaluated, and the total cholesterol, high-density lipoprotein cholesterol, and triglyceride levels were 258 mg/dl (range 50–200 mg/dl), 35.2 mg/dl (range 35– 55 mg/dl), and 137 mg/dl (0–150 mg/dl). Respectively, the total cholesterol level was in the higher than normal range. Xanthelasma is the most common type of cutaneous xanthoma. They may indicate hyperlipidemia, but 25– 70% of patients in most cases are normolipidemic. Histologically, foamy histiocytes occur in the perivascular area, mostly in the middle and superficial layers of the dermis. They contain membrane-bound lipid vacuoles, cholesterol crystals, lysosomes, and residual bodies. Carotenoderma is a phenomenon characterized by orange pigmentation of the skin, resulting from carotene deposition mainly in the stratum corneum, in sweat and in sebum, such as the nasolabial folds, palms, and soles. The sclerae are not affected, and this helps to distinguish carotenoderma from jaundice. Both diseases are distinct clinical manifestations. Carotene exclusively accumulates in the regions such as thick stratum corneum, where the proportion of sebum is high. In this case, the orange ring occurred due to the accumulation of carotene in xanthelasma lesions, where the amount of lipid is rather high. Mualla Polat, MD Department of Dermatology Medical Faculty Abant Izzet Baysal University Bolu Turkey E-mail: polatmualla@gmail.com

A case of vitiligo associated with paraffin injection.

Dear Editor: Vitiligo is an acquired depigmentation disorder characterized by a progressive loss of melanocytes. The exact pathologic mechanism has not been clarified yet; however, the autoimmune hypothesis is the most widely accepted explanation. In some case reports, vitiligo was induced by trauma such as tattooing, eyebrow plucking, and intense pulse light treatment1,2,3. A 51-year-old woman presented with a 5-month history of multiple depigmented patches on both hands and the right foot. Importantly, she had received a paraffin injection on the dorsum of both hands, which had been performed by an unlicensed person 2 years ago. This was complicated by foreign body reaction accompanied by painful swelling of the injection sites, 1 month after the procedure. She had undergone partial removal of the granulomatous lesions and had been treated with oral corticoste intermittently for episodes of recurrent painful swelling. Five months ago, she began to notice numerous depigmented patches on both hands, including the paraffin injection sites, which were followed by new depigmented patches on the dorsum of the right foot, a month later. There was no personal or family history of vitiligo. Physical examination revealed multiple well-demarcated depigmented patches on the dorsum of both hands and on the dorsum of the right foot (Fig. 1A, B). Histopathological examination of the lesion showed aggregations of multiple clear vacuoles and lipophages in deep dermis (Fig. 2A, B). Additionally, Fontana-Masson and Melan-A staining demonstrated the loss of melanin pigments and melanocytes (Fig. 2C, D). Given the patients history, clinical characteristics, and histopathologic findings, we diagnosed this case as vitiligo associated with paraffin injection. Fig. 1 Multiple well-demarcated depigmented patches on the dorsum of both hands (A) and of the right foot (B). Fig. 2 Biopsy specimen from the dorsum of the hand. (A, B) In the deep dermis, there is aggregation of multiple clear vacuoles and lipophages (HE A: ×40, B: ×400)