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Atopic dermatitis has a substantial impact on work and activity impairment according to studies from Western communities. Prospective studies of work productivity and activity impairment in Asian patients with atopic dermatitis are lacking. The aims of this study were to investigate the impacts of atopic dermatitis on work productivity and activity impairment among Taiwanese patients, and to stratify the analyses by disease severity. One-third of employed participants reported missing work (absenteeism) in the preceding week due to atopic dermatitis, while 88.5% of the remaining two-thirds reported impaired work effectiveness (presenteeism). In addition, 92.5% of all participants reported impaired daily activities. Overall work impairment (aggregate productivity loss from absenteeism and presenteeism) was 1.8- and 2.6-fold greater in subjects with moderate and severe atopic dermatitis, respectively, compared with those with mild atopic dermatitis. Presenteeism, but not absenteeism, contributes to the majority of total work impairment in this cohort. Daily activity impairment was 1.5-fold greater in moderate atopic dermatitis, and 2.0-fold greater in severe atopic dermatitis, compared with mild atopic dermatitis. Both work and activity impairment showed significant positive correlations with atopic dermatitis severity scores (SCORing Atopic Dermatitis; SCORAD). In conclusion, work productivity and activity impairment is significantly correlated with disease severity in this Taiwanese atopic dermatitis cohort. In order to obtain a full picture of disease burden to patients and caregivers, patients with atopic dermatitis should be monitored for disease activity as well as corresponding impacts on quality of life.

Sir, It has been reported that lupus erythematosus (LE)-like adverse reaction is induced by various drugs, e.g. procainamide, hydralazine, isoniazid and diphenylhydantoin (1, 2). Antithyroid agents can also induce this syndrome. Propylthiouraci l has been reported to induce perinuclear antineutrophil cytoplasmic antibody (MPO-ANCA)positive vasculitis (3, 4). Methimazole and carbimazole, two other antithyroid drugs classiŽ ed with propylthiouracil as thionamides, can also cause ANCA-positive vasculitis, but much less frequently than propylthiouracil (4, 5). Other adverse eVects related to methimazole include fever, rash, arthralgia, hepatitis, agranulocytosis and lupus-like syndrome (4, 6). However, only a few reports have described the skin symptoms and the Fig. 1. Vesicles (arrows) and crusts are present on the lower leg. histological Ž ndings in detail in antithyroid agentinduced lupus-like syndrome. We report on a patient 62% segmental neutrophils and 1% eosinophils, a platelet with Graves’ disease who, after being treated with count of 470 109/l, a hemoglobin level of 6mg/dl, a reticulocyte count of 4.4%, a mean corpuscular volume of 87.6  , methimazole for one week, developed a blistering erupprothrombin time 9 s (control 10 s) and activated partial tion on the hands and legs. To our knowledge, this is thromboplastin time 25 s (control 30 sec). Urinalysis was the Ž rst report describing methimazole-induced lupusunremarkable. A chest X-ray Ž lm showed a bilateral, groundlike syndrome and ANCA-positive vasculitis with a glass appearance. Treatment with blood components and cutaneous feature of vesiculo-bullous systemic lupus methylprednisolone was given. Owing to persistent respiratory insuYciency, the patient was intubated. A skin biopsy specimen erythematosus (SLE). from the lower leg revealed a neutrophilic inŽ ltrate with nuclear dusts in the dermal papillae and tips of rete ridges, and vacuolar degeneration at the basement membrane zone CASE REPORT with subepidermal blister formation (Fig. 2). Direct immunoAn 18-year-old female with a 2-year history of hyperthyroid uorescence study showed linear deposition of IgG and IgA ism, which was treated with a 6-month course of propylthiouraat the basement membrane zone (Fig. 3). The indirect cil and propranolol, had discontinued the medications for one immuno uorescence study was negative. An open lung biopsy year until the recurrence of hyperthyroidism presented as specimen revealed an intra-alveolar hemorrhage and capillartremor, palpitation and heat intolerance. The patient did not itis, as suggested by focally expanded and disrupted alveolar have a history of systemic rheumatic disease or any previous septa replaced by a neutophilic inŽ ltrate. Further investigation complaint of photosensitivity and Raynaud phenomenon. The revealed PR3-ANCA (enzyme immunoassay, Pharmacia laboratory studies revealed the anti-thyroglobulin antibody Diagnostics GmbH & C. KG, Freiburg, Germany) 4 EU/ml (particle agglutination method, Fujirebio Co., Japan) level (normal

Contact dermatitis simulating erythema multiforme can be caused by many allergens. The chemical agent 1,2-ethanedithiol, which serves as a protective group in chemical synthesis, has hitherto only been implicated as an irritant. We report on a 22-year-old female chemistry student who developed widespread erythema multiforme-like lesions after local contact with 1,2-ethanedithiol. Many target lesions were observed bilaterally on her hands, forearms, arms, and on her forehead. One such lesion was histologically compatible with erythema multiforme. The patient had a positive patch test to 1,2-ethanedithiol, whereas none of 30 healthy subjects showed a positive reaction. However, eight of the 30 controls (26.7%) developed irritant reactions to 1,2-ethanedithiol. Cautious handling of the compound is a prudent precaution.

Gemcitabine is considered to be a well-tolerated and safe cytostatic drug because of the relative lack of side effects. Cutaneous reactions due to gemcitabine treatment, including alopecia and maculopapular eruption, are well known. We report one patient with squamous cell carcinoma of the lung who developed a gemcitabine-induced cutaneous reaction mimicking acute lipodermatosclerosis. This case has never been reported in the literature before.

A 65-year-old woman with stage IIIA lung adenocarcinoma had received a right middleand lowerbilobectomy followed by six cycles of chemotherapy with gemcitabine and cisplatin. Docetaxel was administered because of poor response to the previous therapy. The treatment schedule for each cycle was intravenous infusion of docetaxel for 30 min on days 1, 8 and 15. The dosage was 36 mg/m weekly for each injection. After the first administration on day 1, extravasation of docetaxel into the dorsum of her left hand occurred. Local injection with hydrocortisone and ice packing were administered at that time. The lesion persisted and mild painful swelling was noted afterwards. She received a second injection of docetaxel on the right hand one week later – a smooth process without any complications. An erythematous swelling with tenderness and bulla formation developed on the dorsum of her left hand several hours after the second injection on the other hand. The next day she visited the oncological clinic of our hospital. Under the impression of cellulites, a prescription of cephalexin, acetaminophen and tramadol was given after intravenous injection of cefazolin 1g. The skin lesion continued to progress and extended to the whole left hand. She presented to us 14 days after the extravasation insult. On cutaneous examination, one palm-sized, welldemarcated, erythematous and slightly violaceous patch with flaccid bulla formation was noted on the dorsum of her left hand (Fig. 1) extending slightly to the volar aspect of the thenar region. She had neither palpable lymph nodes over the left anticubital fossa and the left axilla nor any systemic toxic signs. The range of motion of the left wrist was limited by tenderness and severe oedema. A vesicant-type reaction of docetaxel extravasation was diagnosed. The patient was instructed to use topical betamethasone valerate cream and chloramphenicol ointment to suppress the inflammation and for wound care.

Sir, Chemotherapy-induced ‘‘recall’’ is a phenomenon whereby the administration of a chemotherapeutic agent induces an inflammatory reaction at a previous injury site. Radiation recall is a phenomenon whereby the administration of a chemotherapeutic agent induces an inflammatory reaction at a previously irradiated site (1 – 3). These reactions are mostly seen in the skin, but they can also develop in organ systems such as the lungs, oesophagus, intestinal epithelium, oral mucosa, bladder mucosa and heart (1, 2, 4). In addition, reactivation of ultraviolet (UV) light-induced erythema (UV recall) is another well-documented sequela of methotrexate therapy (1 – 3). Both reactions are the prototypes of recall phenomena. However, the concept of ‘‘recall’’ has been extended to include reaction of tissue inflammation evoked by extravasations or phlebitis (2). Here we report a patient with acute myeloid leukaemia (AML) developing recall dermatitis on a previously scalded wound after chemotherapy.

Sir, infusion of gemcitabine and epirubicin. Furthermore, the patient had no clinical picture of acral erythema. Fixed erythrodysaesthesi a plaque (FEP) is a unique cutaneous reaction due to intravenous injection of doceOne skin biopsy undertaken on the left arm lesion showed epidermal dysmaturation, frequent dyskeratosis, taxel. It presents as Ž xed erythematous plaque(s) unrelated to extravasation or previous skin injury (1). interface dermatitis, pigment incontinence and a superŽ cial dermal perivascular mononuclear cell inŽ ltrate Gemcitabine (di uorodeoxycytidine , 2’,2’-di uorodeoxycytidine; dFdC) is a deoxycytidine analogue with (Fig. 2). Betamethasone valerate cream and salicylate ointment were given as topical therapy. The plaques structural and metabolic similarities to cytarabine (ara-C ) (2). It mimics the structure of the natural became desquamated, crusted and their colour darkened to brown. One month later, all the skin lesions resolved nucleoside and, following phosphorylation, is incorporated into DNA (3). Several previous reports have with only slight hyperpigmentation . No recurrence of the skin lesions was noted even though the patient shown that gemcitabine alone or in combination with cisplatin is active against non-small-cell lung cancer (NSCLC) with little cutaneous toxicities (4–6). Epirubicin is the 4’ epimer of the anthracycline antibiotic doxorubicin (7). A combination of epirubicin and gemcitabine has been reported to be eVective in treating patients with advanced NSCLC (8). We report the development of FEP on both forearms of a patient treated with gemcitabine and epirubicin.

3. Jekler J, LarkoE O. Combined UVA-UVB versus UVB photo7. Hudson-Peacock MJ, DiŒey BL, Farr PM. Narrow-band UVB phototherapy for severe atopic dermatitis. Br J Dermatol 1996; therapy for atopic dermatitis: a paired comparison study. J Am Acad Dermatol 1990; 22: 49± 53. 135: 332. 8. Grundmann-Kollman M, Behrens S, Podda M, Peter RU, 4. El-Ghorr AA, Norval M. Biological eŒects of narrow-band (311nm TL01) UVB irradiation: a review. J PhotochemPhotobiol Kaufmann R, Kerscher M. Phototherapy for atopic eczema with narrow-band UVB. J Am Acad Dermatol 1999; 40: 995± 997. 1997; 38: 99± 106. 5. Coven TR, Burack LH, Gilleaudeau P, Keogh M, Ozava M, 9. Der-Petrossian M, Seeber A, HoE nigsmann H, Tanew A. Half-side comparison study on the e cacy of 8-metoxypsoralen bath-PUVA Krueger JG. Narrowband UV-B produces superior clinical and histopathological resolution of moderate-to-severe psoriasis in versus narrow-band ultraviolet B phototherapy in patients with severe chronic atopic dermatitis. Br J Dermatol 2000; 142: 39± 43. patients compared with broadband UV-B. Arch Dermatol 1997; 133: 1514± 1522. 10. Kunz B, Oranje AP, Labreze L, Stalder JF, Ring J, Taieb A. Clinical validation and guidelines for the SCORAD index: con6. George SA, Bilsland DJ, Johnson BE, Ferguson J. Narrow-band (TL01) UVB air-conditioned phototherapy for chronic severe sensus report of the European Task Force for Atopic Dermatitis. Dermatology 1997; 195: 10± 19. adult atopic dermatitis. Br J Dermatol 1993; 128: 49± 56.

In December 1998, a 72-year-old woman was given a diagnosis of non-small-cell lung cancer. Previous treatment included left upper lobectomy with lymph node dissection followed by 4 cycles of chemotherapy with gemcitabine and cisplatin. Docetaxel was administered because of disease progression. The dosage schedule of each cycle was intravenous infusion of docetaxel for 30min on days 1, 8 and 15 and the dosage was 45mg/m2 weekly for each injection. However, severe leukopenia following the Ž rst dose led to delayed administration of the second injection until day 19 after the Ž rst injection. Four days after the second injection, some peato bean-sized, itching, erythematous macules and patches developed on the right forearm and dorsum of the right hand. All of these lesions corresponded to the sites of pre-existing seborrheic keratoses (Fig. 1). The patient claimed that the seborrheic keratoses had been noted for more than 10 years and there was no history of eruptive appearance of new seborrheic keratoses. The injection sites of docetaxel therapy were on the Fig. 1. Some peato bean-sized, itching, erythematous macules and left, rather than right, forearm. There was no extravasation patches with scales were noted on the right forearm and dorsum of event during the docetaxel treatment. A skin biopsy was not the right hand. All of these lesions corresponded to the sites of preundertaken, owing to leukopenia. The patient’s skin condition existing seborrheic keratoses. was treated as eczema, with betamethasone valerate cream. The second cycle of docetaxel infusion was still administered, with the dosage reduced to 36mg/m2 because of the leukopenia. The in ammation of seborrheic keratoses ameliorated Both of these reports describe a patient with acute myelogenous one week later, but the patient complained of a tingling and leukemia who had a rapidly increasing number of seborrheic burning sensation over the area. One month after the onset of keratoses, compatible with Leser-Trelat sign. Following the lesions, an erythematous, palm-sized plaque with sensory chemotherapy, the seborrheic keratoses of Leser-Trelat became change was noted on the right forearm, partly localized to the in amed in both patients; with discontinuation of cytarabine keratoses. Fixed erythrodysesthesia plaque (FEP) due to docetherapy, the in ammatory reaction in the keratoses subsided taxel was diagnosed (3). One month later, the skin lesions in one of the patients (5). All the seborrheic keratoses of our resolved, but the pre-existing seborrheic keratoses remained. patient had been present for more than 10 years, which made The same skin reaction did not recur even though the patient Leser-Trelat sign unlikely. Besides, only a few seborrheic received a further 3 cycles of docetaxel therapy. keratoses on the right arm became in amed, while those on the other body sites were not involved. The above features are diVerent from those of the previous reports. The mechanism of this reaction is unknown (2). Susser DISCUSSION et al. (2) reviewed the mucocutaneous reactions to chemotherIn ammation of seborrheic keratoses is a rarely described apy and mentioned in ammation of keratoses. This syndrome cutaneous reaction to chemotherapy (2) and there are only 2 may or may not recur with the re-administration of the same chemotherapeutic agent(s). Discontinuation of chemotherapy previous reports mentioning this unique skin reaction (4, 5).