During successive cell divisions of mortal cells the length of the telomeres (TTAGGG repeats in vertebrates) at the end of chromosomes decreases. It has been suggested that this process is responsible for cellular senescence. Expression of the ribonucleoprotein telomerase appears to prevent shortening of telomeres in germ-line cells and cancer cells. The purpose of this study was to investigate telomerase activity in melanocytic lesions and its possible role in the multi-step tumor progression model of malignant melanoma. To quantify the level of telomerase activity both in cultured cells and in fresh tissue samples the TRAP (telomeric repeat amplification protocol) ELISA was used. Eight cell lines of malignant melanoma, 3 primary cultures of fibroblasts, 36 melanocytic naevi, 5 atypical melanocytic naevi, 3 Spitz's naevi, 31 primary malignant melanomas and 13 metastases of malignant melanomas were investigated. Also 34 samples of skin (22 samples of perilesional skin and 12 samples of normal skin) were analysed. In our experiments all melanoma cell lines were strongly positive, whereas in fibroblasts telomerase activity could not be detected. Of the primary melanomas and metastatic melanomas, 90.3% and 92.3%, respectively, were strongly positive, and of the atypical melanocytic naevi, 80% were positive. Of the 36 common melanocytic naevi only 10 (27.7%) expressed weak telomerase activity and of the 34 samples of human skin, 4 (11.7%) expressed very weak telomerase activity. Our results indicate that telomerase activity increases from benign melanocytic naevi to atypical naevi and further to malignant melanoma and metastatic melanoma cells, and therefore may play a role in tumour initiation and progression.

Our report documents the necessity to look for early development of basal cell carcinomas in patients who show signs of the epidermal malformations described.

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A 57-year-old male patient suffered from polyarteritis nodosa. He presented with articular pain, polyneuropathy, subcutaneous nodules and nodes on the lower legs. After several immunosuppressive agents (methotrexate, mycophenolate mofetil and prednisolone) had proven to be ineffective, 2 g intravenous immunoglobulin (IVIG) per kilogram body weight were administered within 2 days in combination with 10 mg prednisolone per day. Subsequently, 6 cycles of IVIG were applied in increasing intervals from 4 to 6 weeks resulting in a minimum dosage of 0.33 g/kg/week IVIG. The polyarteritis improved within a few days after the first IVIG application. The intensity of polyneuropathy and arthralgia of polyarteritis decreased during the period of IVIG treatment. Finally, a dose reduction of less than 0.25 g/kg/week IVIG resulted in recurring polyarteritis nodosa, which could not be controlled by further administration of IVIG. Therefore, our data indicate that: (1) IVIG is partially effective in cases of polyarteritis nodosa, but the therapeutic effect is only transient; (2) the success of treatment may be correlated with the dose of IVIG per body weight and week; (3) the efficacy/cost ratio of IVIG in polyarteritis nodosa appears to be low.

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