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The effects of hydrocortisone, dexamethasone, betamethasone 17-valerate and clobetasol propionate at concentrations of 10(-5)-10(-12) M on the proliferation of human dermal microvascular endothelial cells (HDMEC) were studied in vitro. In addition, confluent HDMEC were treated with TNF (1000 U/ml) or IL-1 beta (1000 U/ml) alone or in combination with the corticosteroids (10(-5) M, 10(-6) M) for 24 h, and cytokine-induced expression of intercellular adhesion molecule-1 (ICAM-1) was assessed by immunocytochemistry. Controls were treated either with growth medium or with the corticosteroids alone. All tested corticosteroids stimulated HDMEC growth after 4 and 6 days of treatment in a dose-dependent manner, as assessed by 3H-thymidine incorporation and the 4-methyl-umbelliferyl heptanoate (MUH) assay. The minimal effective concentration was 10(-9) M for hydrocortisone, 10(-10) M for dexamethasone and betamethasone, and 10(-12) M for clobetasol. In untreated and in corticosteroid-treated cultures, less than 5% of the cells expressed ICAM-1. TNF and IL-1 beta were strong inducers of ICAM-1 expression on 74% and 82% of the cells, respectively. None of the tested corticosteroids significantly influenced cytokine-induced ICAM-1 expression, suggesting that the anti-inflammatory effects of corticosteroids are not related to ICAM-1 modulation on HDMEC.

Superior vena cava syndrome (VCSS) develops because of a progressive reduction of venous return from the head, neck and the upper extremities. The presenting sign of this relatively rare condition is often a rapidly developing, often massive facial edema. As a consequence, such the patients are often seen initially by a dermatologist. Other clinical characteristics may include cyanotic facial erythema, dilatation of the neck veins, and a prominent venous pattern n the anterior chest. Today, primary lung cancers and other mediastinal tumours represent the most common cause of VCSS, which may take a slowly progressive or a more fulminant course. In these cases, the disease develops rapidly and becomes life-threatening, requiring intensive medial diagnosis and care. We describe three patients with superior vena cava syndrome due to a) bronchogenic carcinoma, b) bihilar sarcoidosis and c) metastasizing malignant melanoma. Since recognition of VCSS broadens the diagnostic spectrum of the dermatologist, an overview on its diagnostic and therapeutic implications is given based on our cases and the literature.