Protective effect of topical antibiotics in breast augmentation.

BACKGROUND: Previous studies indicate that antibacterial lavage and/or use of topical antibiotics may reduce infection in breast implant surgery and perhaps also reduce occurrence of capsular contracture. A retrospective analysis was performed to evaluate this effect. METHODS: The study participants included all women (n = 436) who underwent breast augmentation during two different time periods: 2000 to 2002 (n = 218) and 2005 to 2007 (n = 218). During the first period (2000 to 2002), cephalothin (Keflin), was added to the saline/epinephrine solution, which was used to irrigate the implant pocket and filled into the outer lumen of the saline/gel implants. In the second period (2005 to 2007), only saline/epinephrine was used. All women were operated on at the same clinic and by the same surgeon. Recorded postoperative complications included occurrence of infection, seroma, and capsular contracture. RESULTS: Medical records were identified for 414 women (94.9 percent): 2000 to 2002 (n = 203) and 2005 to 2007 (n = 211); 99.8 percent of all implants were placed in the submuscular position and 99.8 percent of all incisions were periareolar. Frequency of infection in the 2005 to 2007 cohort (12.8 percent) exceeded substantially the frequency among the 2000 to 2002 cohort (6.7 percent; p = 0.044), as did the frequency of seroma (7.6 percent versus 2.9 percent, respectively; p = 0.036). There was no significant difference in development of capsular contraction between the two groups (8.1 percent versus 5.9 percent; p = 0.393). CONCLUSION: The authors' data support the use of topical antibiotics in cosmetic breast surgery, because significant increases of both infections and seroma were seen in patients not treated with topical antibiotics compared with a cohort of similar patients where topical antibiotics were used.

Genetic evolution of HIV in patients remaining on a stable HAART regimen despite insufficient viral suppression.

Our objective was to investigate whether steadily increasing resistance levels are inevitable in the course of a failing but unchanged Highly Active Antiretroviral Therapy (HAART) regimen. Patients having an unchanged HAART regimen and a good CD4 response (100 cells/microl above nadir) despite consistent HIV-RNA levels above 200 copies/ml were included in the study. The study period spanned at least 12 months and included 47 plasma samples from 17 patients that were sequenced and analysed with respect to evolutionary changes. At inclusion, the median CD4 count was 300 cells/ml (inter-quartile range (IQR): 231-380) and the median HIV-RNA was 2000 copies/ml (IQR: 1301-6090). Reverse transcription inhibitor (RTI) mutations increased 0.5 mutations per y (STD = 0.8 mutations per y), while major protease inhibitor (PI) resistance mutations increased at a rate of 0.2 mutations per y (STD = 0.8 mutations per y) and minor PI resistance mutations increased at a rate of 0.3 mutations per y (STD = 0.7 mutations per y). The rate at which RTI mutations accumulated decreased during the study period (p = 0.035). Interestingly, the rate of mutation accumulation was not associated with HIV-RNA level. The majority of patients kept accumulating new resistance mutations. However, 3 out of 17 patients with viral failure were caught in an apparent mutational deadlock, thus the development of additional resistance during a failing HAART is not inevitable. We hypothesize that certain patterns of mutations can cause a mutational deadlock where the evolutionary benefit of further resistance mutation is limited if the patient is kept on a stable HAART regimen.

Tenofovir treatment in an unselected cohort of highly antiretroviral experienced HIV positive patients.

The aim of the present study was to explore the treatment effect of tenofovir as implemented in clinical practice. Data are presented on 34 patients. 11 patients had tenofovir added to a stable anti-retroviral treatment (ART) and 23 patients had drugs other than tenofovir. CD4 counts, HIV-RNA levels and genotypic resistance were determined at baseline and after 3 and 6 months. After initiation of tenofovir treatment, a mean decrease in HIV-RNA for all 34 patients was observed (-0.43 log1o copies/ml (+/- 1.22) and -0.49 log10 copies/ml (+/- 1.36) after 3 and 6 months, respectively, (p = 0.045)). However, the effect of tenofovir on HIV-RNA in the group of patients who had tenofovir added to a stable ART was limited, and the decrease in HIV-RNA was significantly higher in patients who had drugs other than tenofovir changed as well (p = 0.004 and p = 0.03 after 3 and 6 months, respectively). After initiation of tenofovir treatment, no significant increases in CD4 count were observed. All new NRTI-associated mutations could be explained by the background treatment. In conclusion, we observed a significant decrease in HIV-RNA only when tenofovir was prescribed, in conjunction with other anti-retroviral drugs, to patients on a failing highly active antiretroviral drug regimen (HAART).