The most common manifestation of an Erysipelothrix rhusiopathiae infection is the erysipeloid, a skin lesion that in most cases occurs after professional contact with infected animals. Bacteremia occurs in less than 1% of all cases of Erysipelothrix rhusiopathiae infections [1], but 90% of these cases demonstrate an association with endocarditis [2]. When preliminary identification shows the presence of gram-positive rods in blood cultures and when the patient is a member of the population at risk, this organism should be considered as a potential causal agent.We report a case of Erysipelothrix rhusiopathiae endocarditis involving the aortic valve in a 46-year-old man who had been working as a butcher and who had a history of alcohol abuse. He was referred to our hospital because of arthralgia affecting both shoulders, weakness in the left arm, paresis of the left lower extremity, and dizziness. Four weeks before admission he had experienced night sweats and daily-recurring chills. One week later he developed an erythema exsudativum multiformelike rash localized on the upper part of his body. He was treated with 16 mg methylprednisolone daily, with continuous dose reduction for 8 days. Following this treatment the efflorescences disappeared. Two weeks before admission to the hospital, arthralgia of both shoulders had developed. Physical examination provided no conspicuous findings. Nevertheless, abdominal sonography showed hepatosplenomegaly (liver: 16 cm diameter, spleen: 16×8×8 cm diameter, both homogeneous). On admission, a physical examination showed the patient to be in a state of reduced general health. His blood pressure was 100/80 mm Hg; his pulse was regular at 100/min; and his temperature was 39°C. Auscultatory investigation revealed a systolic murmur in the right second intercostal parasternal space and a conduction in both common carotid arteries. The liver was palpably slightly enlarged. Neurological examination revealed a left-sided hemiparesis, which was more marked on the left upper extremity, and increased deep-tendon reflexes on the left side. Cranial computed tomography revealed a small hemorrhagic infarction localized on the left cortical/subcortical side. The patient's leukocyte count was 14,640/mm 3 .An electrocardiogram showed sinus tachycardia at a rate of 100/min. Mild cardiomegaly without signs of congestion or infiltrates could be seen in the chest radiograph. Transthoracic and transesophageal echocardiography showed a thickened, calcified aortic valve with mild regurgitation but without vegetations; however, a round, hypodense paravalvular structure with a diameter of 11 mm was found that was interpreted as a paravalvular abscess. Contrast-enhanced abdominal computed tomography demonstrated splenomegaly of 15×6.8×14.3 cm with a subcapsular hypodense structure of 1.8×1.2 cm that was of irregular demarcation. Following this examination, a presumptive diagnosis of a septic embolus was formulated. Antibiotic therapy was initiated that consisted of 2.2 g amoxicillin/clavulanic acid intraven...
Reduction of ischemic injury during CPB is not achieved with ACE inhibitors. However, treatment of patients with ACE inhibitors before and during CPB is fully feasible without side effects affecting the kallikrein contact phase or significant influence on hemostasis.
The data suggest that leptin at low physiological concentrations is able to exert a partial insulin like effect on glucose uptake. We speculate that the effect might be mediated by both leptin receptor isoforms. This leptin effect is additive to the effect of insulin and might therefore contribute to the insulin independent basal glucose supply of the heart. It can not be completely excluded that the observed leptin effect on glucose transport is secondary to altered myocardial function.
The findings demonstrate that aprotinin in a moderate dose is effective in reducing postischemic troponin release in a non-blood perfused system. Measurement of myocardial high-energy phosphates after aprotinin use was performed for the first time and indicates that not a reduction in severity of direct myocardial ischemic intensity but a beneficial action on processes causing release of troponin is the mode of action of this effect.
Although PAI-1 activity levels are reduced after short-term treatment with ACE inhibitors in patients with stable angina pectoris while TPA antigen is unaffected, treatment with ACE inhibitors does not lead to a marked change in plasmin activation.
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