Thrombocytosis is the cause of various complications in myeloproliferative disorders. We present the case of a 54-year-old woman with chronic myelogenous leukaemia who developed large ulcers on both lower legs that were refractory to standard treatment. As concomitant thrombocytosis persisted despite treatment with hydroxyurea, the new megakaryocyte inhibitor anagrelide (Agrelin) was administered and led to normalization of the platelet count within 11 days. The leg ulcers started to heal after 2 weeks and disappeared over a period of 5 months. Our findings argue for a pathogenic role of platelets in the development of leg ulcers in patients with thrombocytosis due to a myeloproliferative disorder.

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Patients who died of a melanoma thinner than 1.5 mm within 96 months (group 1, n = 60) were compared with those having a tumor of the same thickness who had not died in this time period (Group 2, n = 300). Both groups were investigated with respect to differences in patient sex and age and to thickness, diameter, exophytic growth, and site of the melanoma as well as the number of mitoses/mm2 of tumor area. Relatively speaking, more men than women died of a thin melanoma: in Group 1 (deceased) there were 32 men and 28 women, in Group 2 (alive) 58 men and 242 women. The better survival rate of females did not depend on the difference in the predominating melanoma locations (female face and legs; male trunk): In both sites, on the legs and on the trunk, women had a significantly higher 8-year survival rate than men with equally thick tumors. Furthermore, melanomas on the arms and legs of females had a better prognosis than those on the trunk and face. Both the patient's sex and the tumor site seem to influence the survival of melanoma patients. Only in men was the median of mitoses/mm2 of tumor area found to be higher in the first group (2.2) than in the second group (0.75). In women, no marked difference in the mitotic count was found (Group 1:1.1; Group 2:1.15).

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Objective.Meconium aspiration induces acute lung injury (ALI) in neonates born through meconium-stained amniotic fluid. As yet, there is no specific therapy for improving the outcome. Recently, angiotensin-converting enzyme 2 (ACE2), which inactivates angiotensin II (Ang II), has been shown to ameliorate murine ALI.Design.To evaluate the therapeutic potential of this substance, we studied ACE2 in a piglet model of ALI induced by meconium aspiration.Subjects.Twelve anesthetized piglets were subjected in an animal research laboratory. ALI was induced by tracheal meconium instillation. Thereafter, six animals were randomly assigned to the ACE2 group, while another 6 served as control.Measurements.Systemic, pulmonary hemodynamic, and blood gas exchange parameters and Ang II levels were examined before ALI induction and at various time points after administering ACE2 or saline. In addition, ventilation-perfusion distribution of the lung was assessed by the multiple inert gas elimination technique (MIGET).Main Results.Animals treated with ACE2 maintained significantly higher arterial partial pressures of oxygen (Pao2) and lower arterial partial pressures of carbon dioxide (Paco2), respectively. Furthermore, Ang II, which was substantially increased, returned to basal values.Conclusion.In summary, ACE2 improves blood gas exchange in meconium-induced ALI in piglets.