BMI: does it predict the need for component separation?

PURPOSE: Patient optimization and selecting the proper technique to repair large incisional hernias is a multifaceted challenge. Body mass index (BMI) is a modifiable variable that may infer higher intra-abdominal pressures and, thus, predict the need for component separation (CS) at the time of surgery, but no data exist to support this. This paper assesses if the ratio of anterior-posterior (AP): transverse (TRSV) abdominal diameter, from pre-operative CT imaging, indicates a larger proportion of intra-abdominal fat and correlates with a hernia defect requiring a component separation for successful tension-free closure. METHODS: Ninety patients were identified who underwent either an open hernia repair with mesh by primary closure (N = 53) or who required a component separation at the time of surgery (N = 37). Pre-operative CT images were used to measure hernia defect width, AP abdominal diameter, and TRSV abdominal diameter. Quantitative data, nominal data, and logistic regression was used to determine predictors associated with surgical group categorization. RESULTS: The average hernia defect widths for primary closure and CS were 7.7 ± 3.6 cm (mean ± SD) and 9.8 ± 4.5, respectively (p = 0.015). The average BMI for primary closure was 33.9 ± 7.2 and 33.8 ± 4.9 for those requiring CS (p = 0.924). The AP:TRSV diameter ratios for primary closure and CS were 0.41 ± 0.08 and 0.49 ± 0.10, respectively (p < 0.001). In a multivariate analysis including both defect width and AP:TRSV diameter ratio, only AP:TRSV diameter ratio predicted the need for a CS (p = 0.001) while BMI did not (p = 0.92). CONCLUSION: Intraabdominal fat distribution measured by AP:TRSV abdominal diameter ratio correlates with successful tension-free fascial closure during incisional hernia repair, while BMI does not.

Expression of genes encoding Th1 cell-activating cytokines and lymphoid homing chemokines by chlamydia-pulsed dendritic cells correlates with protective immunizing efficacy.

We studied the expression of cytokines, chemokines, and chemokine receptors by the RNase protection assay in chlamydia-pulsed dendritic cells to better understand their potent anti-chlamydial immunizing properties. We found that chlamydia-pulsed dendritic cells express a complex profile of inflammatory and immunomodulatory molecules. These include CCR-7, interleukin-12, and interferon-induced protein 10, molecules that might influence the homing of pulsed dendritic cells to the site of chlamydial infection and the induction of a local protective CD4(+) Th1 cellular immunity.