A 54-year-old male with chronic osteomyelitis presented with new-onset hypercalcemia. Extensive initial evaluation did not reveal the underlying cause of his hypercalcemia. Subsequent biopsies revealed squamous cell carcinoma transformation consistent with Marjolin's ulcer. Timely surgery had been shown to be effective in achieving remission in patients with Marjolin's ulcers, even in the presence of hypercalcemia. Therefore, we recommend that patients with chronic wounds and new-onset or otherwise unexplained hypercalcemia should be evaluated for development of Marjolin's ulcers.

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BACKGROUND The eNOS 894G>T (Glu298Asp) polymorphism is significantly associated with the risk of cardiovascular diseases and a frequent insertion/deletion variant in the 5'‐UTR of prepro‐endothelin‐1 increases endothelin mRNA and protein expression. This study aimed to investigate the effect of eNOS 894G>T and ET‐1 +138I/D to the risk of stroke development. METHODS eNOS and ET‐1 genotypes were compared between 166 stroke patients (97 males, 69 females, median age 68 yrs) with angiographically verified intracerebral bleeding or ischemia and 166 disease‐free controls matched by age and gender and selected from the cross‐sectional Study of Health in Pomerania (SHIP). Genotyping was done by using a 5'‐exonuclease TaqMan® assay. RESULTS Genotype frequencies (heterozygous and homozygous) of the highly active ET‐1 +138I variant were similar among cases (40.4%) and controls (39.2%; p=0.82). Dysfunctional eNOS 894T genotypes did not differ between cases (43.4%) and controls (50.0%; p=0.23). Logistic regression revealed a significantly increased risk for stroke in patients with hypertension, hypercholesterolemia or history of myocardial infarction, while eNOS and ET‐1 genotypes were not predictive of stroke. CONCLUSIONS Our study clearly indicated lack of association between the known cardiovascular risk factor eNOS 894G>T (Glu298Asp) or the functionally relevant ET‐1 +138I variant and the risk of stroke development suggesting a minor role of these factors in cerebro‐vascular diseases. Clinical Pharmacology & Therapeutics (2005) 79, P66–P66; doi: