Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FUSIDIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources
PubMed2002

[Cholestatic icterus induced by the administration of fusidic acid in a cirrhotic patient].

INTRODUCTION: Fucidic acid is an antibiotic essentially used to treat staphylococcal infections. Its chemical structure is very similar to that of bilary acids and hence implies competitive mechanisms between their elimination and metabolization. OBSERVATION: A patient with a past history of alcohol-induced cirrhosis was treated with fucidic acid for a Staphylococci aureus urinary infection. On day 2 of treatment a conjugate bilirubine icterus appeared. There was no argument to suggest a decompensation of the icterus. The icterus disappeared on suspension of fucidic acid. COMMENTS: The occurrence of an icterus in a cirrhotic patient may evoke decompensation of the hepatopathy and an extensive exploration must be made. A thorough survey of all drug administration must be made. Notably, the possibility of the occurrence of a connective bilirubin icterus during treatment with fucidic acid must be known. The icterus always regresses on withdrawal of treatment and this etiology must be evoked before conducting invasive examinations.

Anti-Bacterial Agents↗
PubMed1997

[Severe methicillin-resistant Staphylococcus aureus infections. Emergence of resistance to fusidic acid or fosfomycin during treatment with continuous infusion of vancomycin].

OBJECTIVES: To evaluate the development of resistance to fosfomycin or fucidic acid in severe infections caused by methicillin-resistant Staphylococcus aureus (MRSA) and to assess the relationship with serum levels of vancomycin METHODS: A retrospective study was performed in patients hospitalized in our intensive care unit during a 3-year period (1993-1995) who were treated for severe MRSA infection with continuous infusion vacomycin and fosfomycin or fucidic acid. We analyzed the development of resistance and serum levels of vancomycin. RESULTS: During this period, only 20 patients received continuous infusion vancomycin plus fucidic acid or fosfomycin. MSRA resistant to fucidic or fosfomycin developed in 9. Vancomycin serum levels were significantly lower in patients who developed resistance to focidic acid or fosfomycin, both during the first 5 days of treatment (16.68 +/- 1.07 micrograms/ml vs. 22.64 +/- 1.05 mg/ml, p < 0.01) and throughout treatment duration (17.29 +/- 1.07 micrograms/ml vs. 21.85 +/- 0.78 microgram/ml, p < 0.01). CONCLUSIONS: Our findings confirm that in spite of continuous vancomycin infusion at an initial rate of 2 g/24 h, Staphylococcus aureus resistance to fosfomycin or fucidic acid an develop during ongoing treatment. Vancomycin levels of at least 20 micrograms/ml should be obtained as rapidly as possible.

Anti-Bacterial Agents↗
PubMed1991

A study to compare the use of fusidic acid viscous eye drops and chloramphenicol eye ointment in an accident and emergency department.

A total of 300 patients attending an Accident and Emergency department with ophthalmic complaints needing topical antibiotic treatment were treated with fucithalmic or chloramphenicol (chloromycetin). Their compliance and the incidence of side effects were assessed. There was a 70.3% response rate to the questionnaire. Of the patients 51.3% using fucithalmic completed the 5 day course compared with 37.2% of those taking chloramphenicol. However, no patients were found to have suffered as a result of failing to complete the course. The incidence of side effects was similar in both groups.

Chloramphenicol↗
PubMed1998

Investigation of a rifampin, fusidic-acid and mupirocin releasing silicone catheter.

After strict hygienical measures have been exhausted the use of plastic materials with antibacterial activity may reduce catheter related-bacterial colonization. An antimicrobial silicone catheter was investigated by HPLC-measurement, SEM, antimicrobial assays and standard biocompatibility tests. The modified catheter was highly biocompatible and the antimicrobial leaching non-toxic. The initially release rate was governed by the drug solubility in the 'sink' and surface loading ('burst effect'). The second continuous period depended on the drug velocity in the silicone matrix and was extended up to 100 days with a proportionality to square root of t for each drug. Diffusion exponents were in range of 2 x 10(-8) to 1 x 10(-9) (cm2 sec(-1)). The lower diffusion exponent of mupirocin was explained by its higher cohesion energy and lower physico-chemical compatibility with the embedding silicone. The antimicrobial drugs were in a molecular-dispersed state with the silicone-matrix, whereas superficially located crystals of the antibiotics covering the catheter surface could be demonstrated by SEM.

Anti-Bacterial Agents↗
PubMed2003

Fusidic acid-induced leukopenia and thrombocytopenia.

Fusidic acid is an active agent against a wide variety of gram-positive bacteria, and it has been increasingly used in methicillin-resistant Staphylococcus aureus infection. The major adverse effects are mild gastrointestinal discomfort and diarrhea. The hematological side effects such as granulocytopenia and thrombocytopenia have been rarely reported in western countries, but have not been documented in Asian population. Between January and April 2001, we identified 2 cases of fusidic acid-induced leukopenia and thrombocytopenia after 2 weeks of fusidic acid treatment. In both cases, hematological abnormality resolved in 3 to 6 days after discontinuation of fusidic acid. The published literature regarding hematological adverse effects caused by fusidic acid is reviewed in this report, and an immune-mediated mechanism possibly by drug-dependent antibody is speculated. We recommend periodic complete blood count check in patients receiving long-term fusidic acid treatment to avoid serious hematological adverse effects.

Aged↗
PubMed1982

Affinity labels for membrane components involved in the uptake of bile acids and of phallotoxins by hepatocytes. Development of covalently binding derivatives of bile acids and of compounds related to cholecystographic agents.

A series of covalently binding derivatives of bile acids, fusidic acid and of compounds similar to cholecystographic agents were synthesized. Nearly all of them inhibited the development of protrusions on the surface of isolated hepatocytes regularly seen after treatment with phalloidin. The same compounds inhibited the uptake of demethylphalloin and of cholate in a concentration dependent manner. Two kinds of effects could be distinguished: The irreversible part of the inhibition depended on the incubation period and could not be removed by washing procedures. The reversible one was independent on the duration of the preincubation. Final results indicated that the tested derivatives inhibited either both transports, and the phalloidin response of liver cells to the same degree and in the same manner, or were found to be ineffective in all tests. The above parallelism supports the hypothesis that phallotoxins may be translocated by a carrier system normally responsible for the uptake of bile acids from the portal blood.

Affinity Labels↗
PubMed1982

Template-free ribosomal synthesis of polypeptides from aminoacyl-tRNAs.

In the present paper it has been demonstrated that Escherichia coli ribosomes in the absence of messenger polynucleotides are capable of synthesizing some polypeptides from aminoacyl-tRNAs as substrates. EF-Tu induced binding of aminoacyl-tRNA, ribosomal peptidyl transferase and EF-G-promoted translocation are strictly required for this template-free elongation. Typical ribosomal inhibitors such as tetracycline, chloramphenicol, phenylboric acid, fusidic acid have been shown to inhibit the template-free synthesis of polypeptides. The synthesis requires GTP cleavage; a non-cleavable analog of GTP, guanyl-5'-yl methylenediphosphonate does not maintain the synthesis. Among sixteen different aminoacyl-tRNAs studied as substrates for the ribosomal template-free synthesis of polypeptides Lys-tRNA, Ser-tRNA, Thr-tRNA and Asp-tRNA were the best. Gly-tRNA, Glu-tRNA, Val-tRNA, Arg-tRNA, Ala-tRNA and Leu-tRNA as substrates gave relatively low levels of the polypeptide synthesis on nonprogrammed ribosomes. Pro-tRNA, Phe-tRNA, Asn-tRNA, Met-tRNA, Ile-tRNA and Gln-tRNA were practically inactive as substrates for the template-free elongation. No correlation has been found between the abilities of the aminoacyl-tRNAs to serve as substrates for the template-free elongation and their activities in template-free binding to ribosomes.

Escherichia coli↗
PubMed2000

Nitric oxide and neuronal and pancreatic beta cell death.

Neural cells are found in all organs of the body and play an important role in the maintenance of the internal milieu. The pancreatic beta cell is the most numerous cell types in the endocrine pancreas. It is particularly important because of its role in insulin secretion, a crucial hormone in glucose metabolism. In view of this, the significance of the survival of neural and pancreatic beta cell cannot be over emphasised. Neural and pancreatic beta cell death occurs in a variety of ways. The destruction of neural cells can be induced with (1) free radicals (H(2)O(2), O(2)(-)(,) HO(-)) and nitric oxide; (2) Cytokines (tumour necrosis factor, interleukin-1 beta, interferon-gamma); (3) Glutamate; (4) Amphetamine analog (Ecstasy); (5) S100 protein; (6) Ammonia; (7) Iron ions; (8) Resins, e.g. methylmethycrylate. Pancreatic beta cell can be destroyed by (1) free radicals (H(2)O(2), O(2)(-)(,) HO(-)) and nitric oxide; (2) Cytokines (tumour necrosis factor, interleukin-1 beta, interferon-gamma); (3) alkylating agents (streptozotocin, alloxan, N-methyl-nitrosourea N-ethyl-N-nitrosourea, Methylmethanesulphonate and ethylmethanesulphonate); (4) hyperglycaemia; (5) islet amyloid poplypeptide; and (6) Inositol Monophosphate dehydrogenase inhibitors. There is enough evidence that most of these agents involved in neural and pancreatic beta cell death exert their toxic effects through the nitric oxide pathway. Neuroprotective agents include vitamin B12 analogs and alpha-tocopherol, NOS inhibitors, antioxidants (e.g. glutathione, superoxide dismutase), metals like cobalt, neurotrophic receptors (Akt kinase) and growth factors. The pancreatic beta cell death induced by these toxic agents can be prevented and or delayed by nicotinamide (vitamin B3), heat shock, copper, alpha-tocopherol (vitamin E), succinic acid, dihydroxylipoic acid, fusidic acid, glucocorticoids, cyclosporin A, growth factors and gene therapy.

Animals↗
PubMed1978

[The bactericidal power of antibiotic combinations. Application in the treatment of osteo-articular infections due to Staphylococcus aureus (author's transl)].

Study of the bactericidal power of antibiotic combinations against 18 strains of staphylococcus aureus causing osteoarthritis showed that the combinations most often synergistic or indifferent were: rifampicin + lincomycin or synergistine, rifampicin + fusidic acid, synergistine + fusidic acid or trimethoprim-sulphamethoxazole, cephalosporins + gentamycin, rifampicin or fusidic acid + gentamycin, trimethoprim-sulphamethoxazole + rifampicin or fusidic acid. Study of the antibiotic therapy used here was based upon the inhibitory power of serum and the measurement of antibiotic concentrations in healthy bone. Combinations which are synergistic or indifferent in vitro endow the serum with a high level of bactericidal activity. Certain antagonisms (cephalosporins or penicillin M + rifampicin) found in vitro may be reflected neither clinically nor in study of the inhibitory power of the serum.

Adolescent↗
PubMed2001

Biological cost and compensatory evolution in fusidic acid-resistant Staphylococcus aureus.

Fusidic acid resistance resulting from mutations in elongation factor G (EF-G) of Staphylococcus aureus is associated with fitness costs during growth in vivo and in vitro. In both environments, these costs can be partly or fully compensated by the acquisition of secondary intragenic mutations. Among clinical isolates of S. aureus, fusidic acid-resistant strains have been identified that carry multiple mutations in EF-G at positions similar to those shown experimentally to cause resistance and fitness compensation. This observation suggests that fitness-compensatory mutations may be an important aspect of the evolution of antibiotic resistance in the clinical environment, and may contribute to a stabilization of the resistant bacteria present in a bacterial population.

Amino Acid Sequence↗