Recognition and treatment of infective endocarditis.
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Anti-Bacterial Agents↗
Biomedical subjects
W R Wilson
Publications and source records attributed to W R Wilson.
Vancomycin therapy for infective endocarditis.
The use of vancomycin is increasing for the treatment of serious life-threatening staphylococcal and other bacterial infections, including infective endocarditis, in patients who are allergic to the penicillins. The literature through 1978 reveals approximately 55 cases of infective endocarditis treated with vancomycin alone or with combined antibiotic therapy. Many of these 55 patients were treated by different clinicians, were given variable regimens of therapy, received other therapy before vancomycin, had associated valve replacement; various amounts of data were provided for the reported cases. A summary of these reports indicates a cure in 48 (87%) of the 55 patients. Recent in vitro and in vivo animal and patient data indicate that vancomycin alone or as part of combined therapy is bactericidal and curative in patients allergic to penicillin for infective endocarditis caused by staphylococci and streptococci-both enterococcal and nonenterococcal (Streptococcus bovis and viridans group streptococci) infections. In this study, 10 patients with infective endocarditis were treated with vancomycin or combined therapy; seven were cured. Five of the 10 patients with infective endocarditis caused by viridans streptococci were cured with combined vancomycin-streptomycin given in short-term therapy for two weeks.
Adolescent↗
Short-term therapy for streptococcal infective endocarditis. Combined intramuscular administration of penicillin and streptomycin.
In a prospective study, 91 patients with penicillin-sensitive infective endocarditis (IE) were treated for two weeks with intramuscular (IM) penicillin G procaine, 1.2 million units every six hours, plus streptomycin sulfate, 500 mg IM every 12 hours. Viridans streptococci were isolated from 70 patients (77%); 21 patients (23%) had Streptococcus bovis infections. Eighteen patients (20%) had had symptoms of IE for three months or longer. Follow-up ranged from two months to 6.6 years. There were no relapses; mild vestibular toxic reactions occurred in two patients (2%). Two patients (2%) died--one of sudden-onset severe heart failure and one of cardiac arrest after aortic valve replacement. Twenty-six patients (19%) required cardiac valve replacement after completion of antimicrobial therapy. This therapy seems as efficacious as four weeks of parenteral antimicrobial therapy and is more cost-effective.
Adolescent↗
Suppression of serum tumour necrosis factor-alpha by thalidomide does not lead to reversal of tumour vascular collapse and anti-tumour activity of 5,6-dimethylxanthenone-4-acetic acid.
The antitumour agent 5,6-dimethylxanthenone-4-acetic acid (DMXAA), developed in this laboratory as a potent analogue of flavone acetic acid (FAA), has a novel antitumour action involving both immune and vascular components. DMXAA induces the synthesis of tumour necrossi factor-alpha (TNF) and it has been hypothesised that this mediates its selective reduction of tumour blood flow and consequent induction of tumour necrosis. Unexpectedly, the drug thalidomide, while reducing the serum TNF response to DMXAA, potentiates its antitumour effect. We have investigated this in the MDAH-MCa-4 mammary carcinoma model, comparing it to previous data with the Colon 38 adenocarcinoma. We have related DMXAA-induced blood flow changes in the MCa-4 tumour to tumour growth delay, serum TNF and extractable TNF from tumour tissue. We have also compared the effect of thalidomide (387 mumol/kg) on DMXAA (80 mumol/kg) with that of a monoclonal anti-TNF antibody (50 micrograms/mouse). We find that tumour blood flow reduction is strongly correlated with tumour growth delay. Coadministration of anti-TNF antibody abolishes serum TNF levels and slightly reduces the antitumour effects of DMXAA. While tumour growth delay is not correlated with serum induced TNF levels, it is related to tumour TNF levels. We conclude that while the data are consistent with TNF being the principal mediator of the action of DMXAA, serum TNF levels do not reflect the antitumour response.
Adenocarcinoma↗