The Table 1 shows the summary of the mean data of vessel area, percentage of vascular area and vessel depth of each patient.

Vessel area

The mean vessel area in APWS was 1014.7 ± 782.5 //m2 and CPWS, 1341.5 ± 689.9 ^m2. The mean data was higher in CPWS, but there was no significant statistical difference between APWS and CPWS.

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Materials

The skin biopsies of 31 patients before treatment were included in this study. The patients consisted of 14 APWS and 17 CPWS. The mean age was 26.7 years in APWS and 25.7 years in CPWS. In APWS, the ages of the onset were from 2 to 40. Con­firmation of the acquired nature of the lesion was obtained in each case by reviewing photographs of the patient taken prior to onset of the lesion. If not available, then family members confirmed the time of onset. The details of these patients are shown in Table 1.

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INTRODUCTION

Port-wine stain (PWS) represents a type of congenital malformation involving mature dermal capillaries resulting in irreversible dilatation of capillaries. PWS is not only congenital but also acquired. All types are pathologically indistinguish­able and represent progressive ectasia of vessels located in the superficial dermal plexus. In contrast to well-known congenital port-wine stain (CPWS), acquired port-wine stain (APWS) is rare and its onset is generally after one year of age. The exact patho-mechanism of APWS is unknown, but trau- ma hormonal change, medication, and solar damage may contribute to its development. Pulsed dye laser (PDL) therapy is regarded as the treat­ment of choice in PWS. Some scientific researchers reported that APWS patients responded more favorably to PDL therapy, and required fewer treat­ments than those with CPWS.

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Therapy is generally supportive and consists of emollients and cold compressives. In some cases, bullous acral lesions can preclude further use of the causative agent due to severe pain and impairment of function. When future cycles of the agent are necessary, patient-controlled analgesia, systemic methylprednisone, pyridoxine, and supportive topi­cal treatments have been used to treat acral erythema. In patients with known bullous acral erythema, short courses of intravenous dexame- thasone given at each infusion of the causative agent seem to limit bullae formation, narcotic use, and functional impairment. But the data is anecdotal and no controlled studies have been performed. Our patient obtained substantial benefit from supportive topical steroids in the management of his acute symptoms.

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Chemotherapy-induced acral erythema (CIAE) is a localized cutaneous reaction to chemotherapeutic agents administered in patients with either hema- tologic malignancies or solid tumors. It is charac­terized by symmetrical, well-demarcated, painful erythema on the palms and soles which may pro­gress to bullae formation and desquamation. Occa­sionally extension to periungual areas and over the dosa of the hands and feet is observed. It usually occurs between 1 day and 3 weeks after the start of chemotherapy, and most cases are resolved within 1 to 2 weeks with desquamation of the skin followed by reepithelization. The histopathologic findings seen in CIAE include spongiosis, necrotic keratinocytes, nuclear pleomorphism, vacuolar changes and subepidermal bullae. It appears to be a dose-dependent, toxic reaction caused by chemo- therapeutic agents, but the pathogenesis remains unknown. Subsequent direct toxicity of the agent to the eccrine gland excretion has been proposed as a mechanism for the acral erythema. Morrell et al. reported that the occurrence of CIAE was dependent on the dose rate, implying not only the accumulated dose of drugs administered but the amount of drugs administered over time. Dimi­nished elimination of chemotherapeutic agents may be a potential risk factor for the development of bullous variant acral erythema. Although excretion of the methotrexate in our case was not delayed, he had completed his 2nd cycle of chemotherapy at the out-patient clinic with insufficient hydration. Moreover, he was hospitalized for insufficient hydra- tion, and completed 5 additional courses of MACOB-B without recurrence of the lesions. Therefore, the dehydrated state may be another potential risk factor.

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A 65-year-old man visited our hospital with a history of multiple palpable cervical lymph nodes for several months. The cervical lymph node biopsy was done and he was diagnosed as Non-Hodgkin’s lymphoma, diffuse large B-cell type, in November 2000. He was treated with combination chemo­therapy comprising 6 cycles of CHOP regimen (epirubicin, cyclophosphamide, vincristine and pre- dnisolone) for six months, and had been in a tolerable state for 4 years without any cutaneous symptom or sign of tumor recurrence. However, the tumor recurred on the terminal ileum in October 2004. He was again treated with combination chemotherapy comprising 2 cycles of MACOB-B regimen (epirubicin and cyclophosphamide for the 1st cycle, vincristine and methotrexate for the 2nd cycle) for 2 weeks. 1 day after the completion of the 2nd MACOB-B chemotherapy including vin­cristine 1.4 mg/m2 and methotrexate 360 mg/m2, painful erythema and bullous lesions developed on his soles (Fig. 1). There was no abnormal finding on physical examination except a dehydrated tongue. Initial laboratory investigations showed WBC 1,100/mm3(seg: 28%), BUN/Cr 44.3/1.65 mg/dL. The 24 hour urine chemistry was examined for the calculation of creatinine clearance rate, 58.1 mL/ min. The methotrexate level of the serum was 0.04 ymol/L.

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INTRODUCTION

Chemotherapy-induced acral erythema (CIAE) is an uncommon toxic reaction to a number of dif­ferent chemotherapeutic agents. It is characterized by symmetrical, well-demarcated, painful erythema on the palms and soles which may progress to bullae formation and desquamation. The drugs most often involved in this eruption are fluorouracil, cytosine arabinoside and doxorubicin. CIAE with bullous reaction in relation to methotrexate has been reported, but is not a common phenomenon. CIAE resolves without any aggressive management, and therapy is generally supportive. Therefore, the dif­ferential diagnosis of this condition from more serious conditions such as graft versus host disease or toxic epidermal necrolysis is essential.

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