Prophylactic antibiotics in head and neck free flap surgery: A novel protocol put to the test.

OBJECTIVE: Recent evidence supports the use of ampicillin-sulbactam as a favored choice for antibiotic prophylaxis following head and neck free flap reconstructive surgery. However, there is a paucity of evidence guiding the optimal duration of antibiotic prophylaxis. The aim of this study is to compare the infection rates of short courses of ampicillin-sulbactam versus extended courses of various antibiotics in head and neck free flap reconstructive surgery. METHODS: This is a retrospective cohort study conducted from 2012 to 2017 at a tertiary academic center on 266 consecutive patients undergoing head and neck surgery with free flap reconstruction. The primary outcome measure was the rate of any infection within 30 days of surgery. RESULTS: There were 149 patients who received antibiotic prophylaxis for an extended duration of at least seven days. 117 patients received a short course of antibiotics defined as 24 h for non-radiated patients and 72 h for radiated patients. Postoperative infections occurred in 45.9% of patients, of which 92.6% occurred at surgical sites. There was no significant difference in terms of postoperative infection rate between patients receiving an extended duration of antibiotics versus a short duration (p = 0.80). This held true for subgroups of surgical site infections (p = 0.38) and distant infections (p = 0.59 for pneumonia and p = 0.76 for UTI). Risk factors for infections were identified as hypothyroidism (p = 0.047) and clean contaminated wound classification (p = 0.0002). CONCLUSION: Shorter duration of ampicillin-sulbactam prophylaxis in free flap reconstruction of head and neck defects does not negatively affect postoperative infection rates. LEVEL OF EVIDENCE: Level 2b.

C-Mpl Is Expressed on Osteoblasts and Osteoclasts and Is Important in Regulating Skeletal Homeostasis.

C-Mpl is the receptor for thrombopoietin (TPO), the main megakaryocyte (MK) growth factor, and c-Mpl is believed to be expressed on cells of the hematopoietic lineage. As MKs have been shown to enhance bone formation, it may be expected that mice in which c-Mpl was globally knocked out (c-Mpl(-/-) mice) would have decreased bone mass because they have fewer MKs. Instead, c-Mpl(-/-) mice have a higher bone mass than WT controls. Using c-Mpl(-/-) mice we investigated the basis for this discrepancy and discovered that c-Mpl is expressed on both osteoblasts (OBs) and osteoclasts (OCs), an unexpected finding that prompted us to examine further how c-Mpl regulates bone. Static and dynamic bone histomorphometry parameters suggest that c-Mpl deficiency results in a net gain in bone volume with increases in OBs and OCs. In vitro, a higher percentage of c-Mpl(-/-) OBs were in active phases of the cell cycle, leading to an increased number of OBs. No difference in OB differentiation was observed in vitro as examined by real-time PCR and functional assays. In co-culture systems, which allow for the interaction between OBs and OC progenitors, c-Mpl(-/-) OBs enhanced osteoclastogenesis. Two of the major signaling pathways by which OBs regulate osteoclastogenesis, MCSF/OPG/RANKL and EphrinB2-EphB2/B4, were unaffected in c-Mpl(-/-) OBs. These data provide new findings for the role of MKs and c-Mpl expression in bone and may provide insight into the homeostatic regulation of bone mass as well as bone loss diseases such as osteoporosis.

Inherited thrombocytopenia due to GATA-1 mutations.

The GATA family of transcription factors, including the founding member, GATA-1, have an important role in gene regulation. GATA-1 is integral to successful hematopoiesis. A wide variety of mutations in GATA-1 affect its function, as well as its interaction with its cofactors (especially Friend of GATA) and the genes upon which GATA-1 acts. Here we review the known mutations, focusing on the specific alterations within the amino acid sequence, the resulting effect on hematopoietic development, and the clinical manifestations that result. Attention is also paid to the relationship between Trisomy 21, also known as Down syndrome, and the phenomenon of a truncated GATA-1, named GATA-1s. The evidence for specific interaction between GATA-1 and chromosome 21, which may explain the correlation between these two mutations, is briefly reviewed.