Eriko Itoh

Pyoderma gangrenosum with increased levels of serum cytokines

A 66‐year‐old woman presented after an episode of accidental trauma with a painful ulcer on her scalp which rapidly enlarged in size, accompanied by central necrosis and undermining ulceration. The patients past history was negative for underlying systemic disease, although she had had a similar post‐traumatic intractable leg ulcer 3 years prior, which was unresponsive to surgical management but successfully treated with systemic steroids. A biopsied specimen from the scalp showed marked neutrophilic infiltrates in the dermis, compatible with a diagnosis of pyoderma gangrenosum (PG). The large ulcerative lesion responded very well to oral steroid therapy, showing rapid epithelialization. Serum levels of granulocyte colony‐stimulating factor and interleukin‐6 were significantly elevated prior to treatment, with decrease to normal levels after treatment. Serum tumor necrosis factor (TNF)‐α and granulocyte macrophage colony‐stimulating factor levels were within normal limits. The significance and pathogenic role of cytokine burst in PG is reviewed and discussed.

Changes in sebum levels and the development of acneiform rash in patients with non–small cell lung cancer after treatment with EGFR inhibitors

Background It has recently been shown that patients treated with epidermal growth factor receptor (EGFR) inhibitors often develop various cutaneous adverse events. While the pathogenesis underlying these events remains unclear, the relationship between skin toxicity induced by EGFR inhibitors and the sebaceous glands that express EGFR has been previously reported. Objectives The primary aim of this study was to determine the relationship between cutaneous sebum levels and acneiform rash, a typical skin toxicity of EGFR inhibitors, by measuring the sebum levels before and after EGFR inhibitor treatment. Methods Eight patients diagnosed with non–small cell lung cancer (NSCLC) (three men and five women with an average age of 69.3 years) who were initiated on treatment with EGFR inhibitors (either gefitinib [Iressa®] or erlotinib [Tarceva®]) were enrolled. Using a Sebumeter®, sebum levels in the face, chest, and back of each patient were measured before and after EGFR inhibitor treatment. The development of acneiform rash in each skin region was also assessed. Results Changes in sebum level along with the development of an acneiform rash were observed after patients were started on EGFR inhibitor treatment. Patients who developed an EGFR inhibitor–induced acneiform rash tended to have higher pretreatment sebum levels (baseline) than did patients who did not experience an acneiform rash. At each time point measurement, sebum levels were found to be significantly higher in patients who had developed an acneiform rash at that time. Patients who developed rash during treatment showed greater differences in sebum level compared with pretreatment baseline. Conclusion Patients who had increased levels of sebum or whose sebum levels showed greater change from pretreatment baseline developed an acneiform rash, suggesting that sebaceous gland activity may be involved in the mechanism underlying the development of acneiform rash, in patients treated with EGFR inhibitors.

Injury-induced acquired dermal melanocytosis arising on an operation scar.

represents a rare cutaneous congenital malformation syndrome, characterized mainly by the presence of capillary malformation and pigmentary nevi. Our patient showed ipsilateral atrophy of extremities and the typical lateralized speckled lentiginous nevus, which supports the diagnosis of SLNS. To our knowledge, the main features of previous reports of SLNS have been the distribution of SLN and the neurological abnormality mainly concentrating on the trunk, arm and leg. Our patient is unique because the neurological abnormality appeared on this patient’s tongue.

Case of autosomal recessive woolly hair/hypotrichosis with atopic dermatitis

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Late-onset self-healing Langerhans cell histiocytosis in a patient with atopic dermatitis

may trigger the disease. Generally, the involvement is bilateral. Sharma et al. reported a case of unilateral linear PPK, which was the first such case. In their case, only the left sole and hand were involved. Treatment is generally symptomatic. Topical keratolytics (e.g. salicylic acid, lactic acid), steroids, tretinoin, and psoralens can be used. Effective treatment with acitretin has been reported. Our case did not want to use systemic therapy. We treated him with 0.025% topical tretinoin for 1 month; the lesion got thinner but did not completely heal. The lesion recurred after 1 month. The patient didn’t want to use topical treatments and he didn’t use them regularly, so we suggested oral retinoids to our patient. The aetiology of this disease is unknown but genetic and environmental factors may trigger the disease. It has been described in a few autosomal dominant pedigrees. Martinez et al. reported that they have identified the locus for type I punctate PPK on chromosome 15q22–q24. In the family members of our patient there was no known skin disease, so our patient may have a mutation. PPKs can be associated with malignancies, so PPK patients must be examined and followed up carefully. Our patient had no other disease, and none of his relatives had similar lesions. Our patient’s laboratory tests and clinical examination were normal. All patients must be followed up carefully because of the association with malignancies. CONFLICT OF INTEREST: None.

Case of ossifying epithelioid hemangioendothelioma on the forearm.

removed were Lucilia sericata and the second maggots removed were Sarcophaga crassipalpis. It is remarkable that two different species of flies infested the patient’s vulvar SCC within a span of a few days. Cases of vulvar malignant wound myiases are rarely seen, especially in Japan. It is likely that the second species of maggot was deposited after removal of the first species of maggot. The former (L. sericata) is an oviparous species, while the latter (S. crassipalpis) is ovoviviparous. Female flies of the latter species deposit not eggs but larvae, which are visible as they are at least 1 mm just after deposition. Indeed, we did not notice the latter maggots when we observed the vulva for the first time. Generally, myiases of wounds or tumors are managed by treating the wounds or tumors. However, this patient’s recurrent vulvar SCC was terminal and incurable, and the patient was receiving palliative care. The tumor was worsening, and was sore to touch and difficult to wash. She was forced to leave it unclean and uncovered, even while sleeping. Thus, the odor of her exposed vulvar tumor could attract flies, especially during the summer. After removing the maggots from her vulvar SCC, we advised her to wear a disposable diaper because it might cause her less pain than common underwear. Since then, her myiasis has not recurred. CONFLICT OF INTEREST: None.