Livedoid vasculopathy - a thrombotic disease.

Livedoid vasculopathy is a rare, chronic occlusive disease of vessels supporting the upper layers of the skin. It is characterized by purpuric maculae and recurrent painful ulcerations mostly affecting the lower leg. These ulcerations occur episodically especially in summer time and heal slowly, leaving characteristic porcelain-white scars called ’atrophie blanche’.This review is focused on the current knowledge on livedoid vasculopathy and modern therapy strategies resulting from its etiopathogenetic associations with prothrombotic states. Livedoid vasculopathy and its pathophysiology are clearly distinguished from inflammatory vasculitis and thus require a different therapeutic approach. The prevention of irreversible residual scarring and improving the quality of life of patients in this often misdiagnosed disease is one of the main treatment goals.

Livedoid vasculopathy - current aspects of diagnosis and treatment of cutaneous infarction.

Livedoid vasculopathy is a rare, chronic, recurrent disease of the cutaneous microcirculation. Its typical clinical manifestation is a triad which consists of livedo racemosa of the skin, episodic painful ulcerations of the distal aspects of the legs and a healing process leaving small porcelain-white scars called atrophie blanche. As an important result of recent research, livedoid vasculopathy has been defined as a coagulation disorder classified as a vasculopathy different from inflammatory vasculitis. This differentiation adds to the current pathophysiologic understanding and supports the therapeutic rationale with respect to the use of new systemic anticoagulants. The prevention of irreversible residual scarring and the improvement of patientsí quality of life are the main goals in treating cutaneous infarction and require early and consequent treatment. This article presents current knowledge on diagnosing this rare disease and offers practical guidance on its therapy.

MRSA eradication in dermatologic outpatients - theory and practice.

BACKGROUND: The dissemination of methicillin resistant staphylococcus aureus (MRSA) is an increasing challenge in medical care. Apart from hospital acquired MRSA, there has also been an increase in community acquired and livestock associated MRSA. While the risks of MRSA (e. g. wound infections) and consequences (e. g. rejection of patients) are well known, there are little data on the effectiveness of eradication procedures. PATIENTS AND METHODS: 32 patients with proven MRSA colonization were monitored during eradication for the following aspects: (1) localization of MRSA (swabs from hairline, anterior nares, throat, axillae, groins, perineum, and wounds, if present), (2) presence of eradication-impairing factors, (3) length of time needed for eradication, (4) cost of eradication, (5) molecular fingerprint and risk assessment (spa-types). RESULTS: We describe the successful eradication of MRSA in all 32 patients. Most positive nasal swabs were obtained from the anterior nares and the throat and only rarely from the hairline or axillae. The greater the number of positive swabs, the more time was needed for eradication. In most patients (37.5%), eradication with topical antiseptics was successful. The average time for eradication was 12.97 (± 7.6) days. Twelve patients required systemic antibiotic therapy. Treatment costs associated with the use of systemic antibiotics were significantly higher. The most frequent spa types were t032 and t003. CONCLUSIONS: We report successful MRSA eradication in outpatients. Systemic antibiotics are unnecessary in the majority of patients. A combined anti-MRSA strategy for inpatients and outpatients is recommended.

Differential diagnosis and therapy of leg ulcers.

A leg ulcer is a symptom and the treating physician needs to find out its origin by differential diagnostic approaches and procedures. The correct diagnosis leads to a specific therapy that ideally accelerates the healing of the ulceration. Identifying the pathogenesis of a leg ulcer is the first and main step towards healing. Although vascular diseases are the major causes of leg ulcers, one needs to consider, in addition to venous and arterial disorders, autoimmune, infectious, metabolic and neoplastic causes. The simple truth that one can only make a diagnosis that was considered holds particularly true in leg ulcers. The differential diagnostic considerations presented here appear in the daily routine of a dermatologist and the article provides help in diagnostic approaches and therapeutic decisions.

The mechanism of melanoma-associated thrombin activity and von Willebrand factor release from endothelial cells.

Activation of the coagulation system in malignancy enables tumor spreading and is thus associated with poor prognosis for the patient. In this study, we analyzed the in vitro mechanisms by which two human metastatic melanoma cell lines, MV3 and WM9, transform the vascular endothelium into a prothrombotic activated state. We show that both melanoma cell lines activate prothrombin due to tissue factor (TF) expression by showing that thrombin generation was blocked with a TF-neutralizing antibody and TF-siRNA. In addition, using the cysteine protease inhibitor E-64, we excluded the formerly described cancer procoagulant (CP) as a major factor contributing to thrombin generation. Furthermore, we describe a direct thrombin-independent response of endothelial cells (ECs) to MV3-derived supernatant as measured by rapid release of VWF. We also show that two clinically approved LMWHs, tinzaparin and enoxaparin, are effective inhibitors of thrombin generation and thrombin activity in plasma. Furthermore, our data indicate a protective effect of heparins on EC activation as shown by reduced VWF release in response to MV3 supernatant. These promising effects of heparins on the melanoma-induced thrombotic conditions justify further clinical investigations in the field of oncology.