Topical lomefloxacin twice daily compared with fucidic acid in acute bacterial conjunctivitis.

Forty-five patients with presumed acute bacterial conjunctivitis were treated in an investigator-masked randomized multicenter study with either lomefloxacin 0.3% or fucidic acid 1% eye drops twice daily. Clinical signs and symptoms were rated by slit-lamp examination and conjunctival swab cultures were performed to evaluate clinical and microbiological efficacy. A total of 57 ocular isolates were tested for susceptibility to nine antibiotics. A significant decrease in clinical symptomatology was achieved by both treatments with a gradual improvement over the treatment period of 7-9 days. Bacteriological recovery was frequently achieved already at the first control visit (day 3-5), but the recovery rate was statistically significant (p = 0.014) only in the lomefloxacin group. The relatively high in vitro resistance rate (46%) to fucidic acid was not reflected by lower clinical efficacy. Two unrelated adverse events (one in each treatment group) and minimal local intolerance problems were observed in both treatment groups. A significantly higher incidence of burning sensation was observed with fucidic acid than with lomefloxacin (p < 0.01). All four treatment failures in the study occurred in the fucidic acid group. Lomefloxacin 0.3% ophthalmic solution demonstrated a high efficacy and good tolerance in the management of acute bacterial conjunctivitis.

The effect of ascorbate and ubiquinone supplementation on plasma and CSF total antioxidant capacity.

Free radicals are thought to be involved in the onset of neuronal disturbances such as Alzheimer's disease, Parkinson's disease, and neuronal ceroid lipofuscinosis. It is also assumed that they play a role in cerebral injury caused by ischemia or trauma. Plasma and cerebrospinal fluid (CSF), Total (peroxyl) Radical-trapping Antioxidant Parameter (TRAP), and the known antioxidant components of TRAP, for instance, ascorbic acid, uric acid, protein sulfhydryl groups, tocopherol, and ubiquinol were analyzed and the remaining unidentified fragment was calculated in five healthy volunteers before and after 4 weeks of ascorbate and ubiquinone (Q-10) supplementation. In CSF, TRAP was significantly lower than in plasma. The major contributor to plasma's antioxidant capacity was uric acid (UA), whereas in CSF it was ascorbic acid (AA). In CSF, AA concentrations were four times higher than in plasma. Oral supplementation of AA (500 mg/d first 2 weeks, 1,000 mg/d following 2 weeks) and Q-10 (100 mg/d first 2 weeks, 300 mg/d following 2 weeks) induced a significant increase in plasma AA and Q-10. Surprisingly, in spite of the high lipophilicity of Q-10, its concentration did not change in CSF. The supplementation of AA increased its concentration in CSF by 28% (p < .05). However, the increase in AA did not result in an increase in CSF TRAP. This indicates that AA had lost one-third of its radical trapping capacity as compared to that in plasma. The facts that AA is the highest contributor to CSF TRAP and its effect on TRAP is concentration dependent could indicate that the peroxyl radical-trapping capacity of CSF is buffered by AA.