Eugene Jeong

Late-onset eccrine angiomatous hamartoma on the forehead.

A 71‐year‐old Korean man presented with a solitary erythematous plaque on his forehead ( Fig. 1 ). It was first noticed by the patient 1 year previously and had slowly increased in size over that time. Physical examination revealed a slightly elevated, 1.5 cm × 1.5 cm erythematous plaque on the upper midline of the forehead. Sweating was not evoked by physical work or emotional stress. There was no pain or tenderness associated with the lesion. The patient had no history of trauma to the forehead. Histopathologic examination of the lesion showed increased numbers of eccrine glands, as well as dilated vascular channels in the deep dermis and subcutaneous tissue ( Fig. 2 ). An immunohistochemical study showed that these eccrine glands stained positively for S‐100 and carcinoembryonic antigen (CEA), and the vascular channels for the antifactor VIII‐related antigens. These findings are consistent with eccrine angiomatous hamartoma. There was no change in the lesion during the 1‐year follow‐up period.

A case of idiopathic leuconychia totalis and partialis

SIR, Leuconychia is the most common chromatic disorder of the nail and is classified as pseudoleuconychia resulting from nail plate alteration due to an external origin, apparent leuconychia resulting from subungual and nail bed abnormalities, and true leuconychia where nail plate abnormalities originate in the nail matrix. True leuconychia includes four distinct categories according to distribution of white colour: leuconychia punctata, leuconychia striata, leuconychia partialis and leuconychia totalis. Most cases of true leuconychia may be congenital or, if acquired, may be associated with underlying systemic diseases such as typhoid fever, hepatic cirrhosis, ulcerative colitis or leprosy, and may also be associated with local trauma of the nail matrix, use of emetine, cytostatic agents or local exposure to salty solutions. Idiopathic true leuconychia is a very rare condition and only a few previous reports have described the findings in the progression from leuconychia partialis to leuconychia totalis. We report a 26-year-old man who presented with idiopathic leuconychia which demonstrated a progression from leuconychia partialis to combined leuconychia totalis and partialis. He had had asymptomatic white fingernails for 13 years, affecting the digits on both hands with the exception of the left thumb, with no family history of white fingernails (Fig. 1a). On examination, he had no hair, teeth or skin abnormalities. Leuconychia partialis was seen on the right thumb, left ring finger and both little fingers, with distal transverse white bands. The other fingers showed leuconychia totalis except for the left thumb nail, which showed yellow spikes unlike the other white fingernails. No toenail was involved. Pitting, splitting or ridging of the fingernails was not seen, and there was no subungual hyperkeratosis. Texture, shape and hardness were also normal. He denied taking any medication and having any other systemic illness. He also had experienced no specific trauma and no chemical exposures to his fingers or fingernails. According to the patient, he had had this condition for 13 years, during which period the whitening of the fingernails had progressed slowly. Repeated potassium hydroxide preparations and fungal cultures of the white nails were negative except for the left thumb nail. Potassium hydroxide preparation was positive at the left thumb nail and Trichophyton rubrum was cultured. Laboratory studies including full blood count, urinalysis, liver function tests, renal function tests, total protein, albumin, erythrocyte sedimentation rate and C-reactive protein were normal or negative. Microscopic examination of a white nail plate revealed a globular collection of large immature keratohyaline granules (Fig. 1b), whereas biopsy specimens from the nail bed and nail matrix were unremarkable. Interestingly, our patient also had onychomycosis of the left thumb, for which we prescribed itraconazole pulse therapy (two pulses of 400 mg daily for 7 days). Although no treatment is indicated or available for true leuconychia, we gave intralesional injections of corticosteroid (triamcinolone acetonide 5 mg mL at 1–2-week intervals) into the proximal nail fold for cosmetic reasons. Because true leuconychia is thought to be due to abnormal matrix keratinization, with persistence of keratohyaline granules in the nail plate, we considered that corticosteroid treatment might help to make these cells differentiate. After 2 months of treatment, the left thumb nail was somewhat improved, but the other fingernails showed no visible change. Our patient has shown persistence and ⁄or a slight progression in his nail whitening during 2 years of follow-up. b a

Leukaemic macrocheilia in acute myeloblastic leukaemia.

amounting to 11 kg. Histology showed a diffuse infiltrate of leukaemic cells in the dermis, extending into the subcutaneous fat (Fig. 2). The cells stained positively with chloroacetate esterase (Leder’s) and lysozyme stain, which showed them to be of myeloid lineage. Bone marrow examination was diagnostic for acute myeloblastic leukaemia. She was treated with cytosine arabinoside, daunorubicin and prednisone as induction chemotherapy. Her lips were markedly improved after chemotherapy (Fig. 1b). Our case shows an uncommon manifestation of leukaemia cutis presenting as macrocheilia.