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“Purpose of review
The present review gives an update of the current management of Raynaud’s phenomenon and its
ischaemic Selleckchem Elacridar complications (digital ulceration and critical ischaemia) and discusses possible further developments in the next 5-10 years. New approaches to therapy are being driven by increased understanding of pathophysiology and by increased international networking of clinicians and scientists, facilitating clinical trials.
Recent findings
Key points include phosphodiesterase inhibitors most likely confer benefit, although clinical trials have given somewhat conflicting results, and have been short-term; a new topical, easy-to-use glyceryl trinitrate preparation has been shown to improve Raynaud’s Condition Score; the endothelin-1 receptor antagonist bosentan has now been shown to
reduce the number of new systemic sclerosis (SSc)-related digital ulcers in two multinational clinical trials; and although statin therapy is likely to confer benefit in SSc-related Raynaud’s phenomenon, further research is required to confirm this.
Summary
New therapeutic approaches in patients who do not respond to more traditionally used vasodilators include phosphodiesterase inhibitors and (for those with recurrent SSc-related digital ulcers) endothelin-1 receptor antagonism. Several other potential new therapies are being researched. Apoptosis inhibitor Optimal management of digital ulceration is multidisciplinary including tissue viability and (sometimes) surgical input.”
“An outbreak of Legionnaires’ disease with 113 confirmed cases was reported in the town of Matar, Spain, in August 2002. In this study, we compared three different typing methods and characterized the clinical isolates by comparing them with other clinical isolates with the same ST from our own database to further characterize the outbreak. In the outbreak, a total of 16 clinical (nine patients) and 32 environmental (from four environmental sources) Legionella pneumophila isolates were analyzed by pulsed-field
electrophoresis learn more (PFGE), sequence-based typing (SBT), and monoclonal antibody typing (MAb). We compared the MAb and SBT profiles of the outbreak clinical isolates and other unrelated clinical isolates showing the same ST profile. We obtained seven different PFGE and SBT profiles and six MAb patterns from the outbreak isolates. PFGE and SBT showed 100 % concordance during the outbreak. SBT proved to be highly discriminatory, particularly with the addition of the new neuA gene. One PFGE, SBT (ST-37), and Philadelphia profile was observed among the clinical isolates. Using PFGE, this ST37 Philadelphia profile was closely related to other unrelated clinical isolates. These findings suggest that the ST37 Philadelphia profile could be a virulence marker in our area. The combination of the three methodologies was useful to further characterize and obtain additional information on a very explosive outbreak.