Eil-Soo Lee

Differential in vivo cytokine mRNA expression in lesional skin of intrinsic vs. extrinsic atopic dermatitis patients using semiquantitative RT‐PCR

Background A small subgroup of atopic dermatitis (AD) patients with normal serum IgE levels and without specific IgE sensitization has been termed ‘intrinsic type of AD’ (ADi) as a counterpart to the term ‘extrinsic type of AD’ (ADe). However, there are neither molecular markers nor clinically diagnostic tools for distinguishing between ADi and ADe.

Characteristics of extrinsic vs. intrinsic atopic dermatitis in infancy: correlations with laboratory variables.

Background  Atopic dermatitis (AD) has been divided into the extrinsic type (ADe) and the intrinsic type (ADi) according to the serum IgE levels and the presence or absence of allergen‐specific IgE. Although previous studies have demonstrated differences in the various immunological parameters, the characteristics of AD in infancy have rarely been reported.

Immunophenotyping of inflammatory cells in lesional skin of the extrinsic and intrinsic types of atopic dermatitis

Background  There is a subgroup of atopic dermatitis (AD) patients with normal total and specific IgE levels and negative skin tests towards common allergens. This form of the disease has been referred to as the ‘intrinsic’ form of AD. Although previous studies have demonstrated differences in the cytokine profile between the extrinsic and intrinsic subtypes, the pathogenesis of both subtypes of AD remains unclear.

Treatment of extensive and recalcitrant viral warts with acitretin

45 Correspondence Toxic epidermal necrolysis caused by tetrazepam A 50-year-old man was referred to our department with toxic epidermal necrolysis (TEN). He had a history of Stevens– Johnson syndrome (SJS) due to phenobarbital, acute hepatitis with valproic acid, and severe neutropenia after carbamazepine. All treatments were given for secondary epilepsy which developed after a cerebral infarct, a consequence of carotid dissection. Nevertheless, no antiepileptic drugs had been required for 10 years, and he was only receiving chronic antiaggregant treatment with acetylsalicylic acid. As he was suffering from muscle contractures, he was given tetrazepam and thiocolchicoside. Whether he had taken these medicines before was unknown. Four days later, the patient presented with lip erosions and all drugs were stopped. Twelve days after the first intake, he was admitted to our department with a target-like generalized epidermal eruption in addition to epidermal necrolysis involving 5% of the skin surface. The mucous membranes were also involved, with the palate and genital areas presenting huge and painful erosions. Blistering spread over 3 days to up to 30% of the skin surface. Full dehydration, functional renal failure and sepsis occurred, and the patient died a few days later. TEN is quite rare, but severe, as the mortality rate is about 30–40% of cases. Numerous drugs have been reported as possible causes of TEN, mainly antiepileptic drugs, sulfonamides, and nonsteroidal anti-inflammatory drugs. Antibiotics and allopurinol are also known to induce such severe adverse events. 1

Alopecia neoplastica in a patient with gastric carcinoma

A well‐recognized but rare presentation of scalp metastasis is alopecia neoplastica, which occurs as a single or multiple areas of cicatricial alopecia. Alopecia neoplastica is usually a presentation of metastasis from breast cancer, and other primary sites are extremely rare. We report a 36‐year‐old woman with alopecia neoplastica due to metastasis from gastric carcinoma. She also had pelvic metastases. An asymptomatic erythematous alopecic plaque had developed 10 months before presentation and biopsy was consistent with scalp metastasis. Total abdominal hysterectomy and salphingo‐oophorectomy was performed and chemotherapy was proposed.

The use of dermoscopy for the diagnosis of plantar wart

© 2008 The Authors JEADV 2009, 23, 702–738 Journal compilation

Psoralen‐ultraviolet A‐induced erythema: sensitivity correlates with the concentrations of psoralen in suction blister fluid

Since the advent of psoralen‐ultraviolet A (PUVA) therapy, the value of plasma 8‐methoxypsoralen (8‐MOP) concentrations to predict PUVA‐induced erythema has been widely investigated. Plasma 8‐MOP concentrations have not been proportional to, and cannot alone predict, the degree of PUVA‐induced erythema. We assumed that PUVA‐induced erythema was related more closely to psoralen concentrations in the skin tissue rather than those within blood vessels. This study was designed to investigate the correlations between the 8‐MOP concentrations in suction blister fluid (SBF) and in plasma, with the degree of PUVA‐induced erythema. 8‐MOP concentrations in plasma and SBF were measured in 15 vitiligo patients and 11 volunteers. Blood and SBF samples were collected 2 h after taking 8‐MOP, and 8‐MOP concentrations in plasma and SBF were quantified using reverse‐phase high‐performance liquid chromatography. Eleven volunteers were phototested using a series of doses of ultraviolet A at the time of sampling. The erythema responses were estimated visually to determine the minimal phototoxic dose (MPD). SBF 8‐MOP concentrations showed a weak positive correlation with plasma 8‐MOP concentrations, which means that we could not predict the exact SBF 8‐MOP concentrations using the plasma 8‐MOP concentrations. The MPD showed a better correlation with the log of the SBF 8‐MOP concentration than with that of the plasma 8‐MOP concentration. These results show that plasma 8‐MOP concentration cannot represent the exact SBF 8‐MOP concentration, and that SBF 8‐MOP concentrations, which are representative of the skin tissue 8‐MOP level, are more closely related to the erythemal sensitivity during PUVA therapy.

Arginine in the beginning of the 1A rod domain of the keratin 10 gene is the hot spot for the mutation in epidermolytic hyperkeratosis.

Keratin intermediate filaments are expressed in specific type I/type II pairs in the stage of differentiation of keratinocytes. The mutations in the keratin genes expressed in the epidermis are etiologically responsible for several epidermal genetic skin diseases, such as epidermolysis bullosa simplex, epidermolytic hyperkeratosis (EHK), ichthyosis bullosa of Siemens, palmoplantar keratoderma, pachyonchia congenita and white sponge nevus. The mutations of keratins 1/10 which are expressed in spinous and granular layers are confirmed to cause EHK. There are several trials to correlate between the clinical phenotypes and sites of mutations of the keratin genes. One of these is that EHK is divided into two groups: the palms and soles involvement (PS) group and the non-palms and soles (NPS) group. So far the PS group had the mutations in the keratin 1 and the NPS group in keratin 10. Most of the mutations of the NPS group were reported in the beginning of the 1A rod domain and over 2/3 of the mutations in the 1A rod domain were the base pair substitution of arginine. Here we find two different mutations in two unrelated Korean kindreds classified as NPS group-R156C and R156H-in the 1A rod domain of keratin 10. Our results are compatible with the above classification and suggest that the arginine in the beginning of the 1A rod domain is the hot spot for the mutation of the keratin 10 gene.

Dermatomyositis associated with generalized subcutaneous edema and Evans syndrome

Although periorbital edema is a common manifestation of dermatomyositis (DM), generalized subcutaneous edema associated with DM is extremely rare. Evans syndrome is an autoimmune disease in which an individuals antibodies attack ones own red blood cells and platelets. Evans syndrome is rarely a presenting feature of DM. DM has been rarely reported to be associated with either generalized edema or Evans syndrome. We report the case of a 52-year-old Korean woman who presented with generalized subcutaneous edema, an erythematous rash, dysphagia, and proximal muscle weakness, and subsequently developed features of Evans syndrome. Treatment with high-dose glucocorticoids and an immunosuppressive agent controlled the DM, the generalized subcutaneous edema, and the Evans syndrome.

CD10 is expressed in dermal sheath cells of the hair follicles in human scalp.

SIR, Hyperhidrosis of the anal fold may become a severe problem for the patient, with possible development of eczema or mycosis. Moreover, social and professional disadvantages due to visible sweat marks are frequent. In contrast to focal hyperhidrosis of the palms or axillae, diagnostic procedures such as gravimetry or iodine-starch test are difficult to perform and standard values for sweating rates (mL min) are not available. To evaluate the degree of hyperhidrosis of the anal fold and to assess therapeutic effectiveness we use a modified iodine-starch test with specially prepared copy paper. Although this technique has been described for palmar and plantar hyperhidrosis, it has not been described for the anal fold. ISO-A4 copy paper is intermingled with nonpulverized iodine crystals for 5 days in a sealed container (1 g jodum purum per 50 pages copy paper). Before application of the prepared paper the anal fold is completely dried. The paper is folded in the middle and placed in the anal fold of the patient, either standing or positioned face-down, for 60 s. The hyperhidrotic area appears on the copy paper, revealing a violet-blue colour, similar to the colouring of standard iodine-starch tests. For quantification we use a plastic foil with standardized grids (1 · 1 cm) that is placed on the copy paper, enabling an exact measurement of the hyperhidrotic area in cm; alternatively, the grid is directly copied on the prepared paper. The extent of sweating areas before and after therapy is thus clearly visualizable (Fig. 1a,b). In summary, the method described above allows a fast, easy to perform and cost-effective evaluation of focal hyperhidrosis of the anal fold and enables a visual representation of therapy, thus being a useful tool both for doctor and for patient.