Impact of Health Insurance Contract Timing on Breast Reconstruction Completion.

BACKGROUND: Cost of breast reconstruction can create a substantial burden for patients. As patients hope to maximize insurance plan benefits, it is crucial to receive efficient, cost-reducing care. This study analyzes the impact of insurance cycle [calendar-based insurance (CBI) versus non-calendar-based insurance (NCBI)] on breast reconstruction. METHODS: Between January of 2014 and 2018, patients undergoing postmastectomy breast reconstruction performed by two senior surgeons (N.T.H. and S.S.T.) at a single academic institution were retrospectively evaluated. Data were collected on insurance contract timing (CBI versus NCBI) and insurance payor. RESULTS: A total of 514 patients were included: 136 patients on NCBI and 378 patients on CBI. Individuals enrolled in CBI were more likely than NCBI patients to have their last operation toward the end of the calendar year ( P < 0.0005). In addition, individuals on private CBIs are more likely to have their last operation closer to the end of the year than those on public CBIs ( P < 0.0001). Individuals enrolled in CBI were less likely to receive autologous reconstruction than individuals on NCBI ( P = 0.011). Among patients on private CBIs, patients with all major revisions were more likely to start their reconstructive journey earlier in the year than patients who did not finish major revisions ( P = 0.011). Lastly, individuals on private insurance also undergo more revision procedures than those on public insurance ( P < 0.0001). CONCLUSIONS: Insurance contract cycle and payor impact the timing of breast reconstruction. This study emphasizes the importance of both patient and provider working toward maximizing health insurance plan benefits.

Sphingosine-1-phosphate promotes erythrocyte glycolysis and oxygen release for adaptation to high-altitude hypoxia.

Sphingosine-1-phosphate (S1P) is a bioactive signalling lipid highly enriched in mature erythrocytes, with unknown functions pertaining to erythrocyte physiology. Here by employing nonbiased high-throughput metabolomic profiling, we show that erythrocyte S1P levels rapidly increase in 21 healthy lowland volunteers at 5,260 m altitude on day 1 and continue increasing to 16 days with concurrently elevated erythrocyte sphingonisne kinase 1 (Sphk1) activity and haemoglobin (Hb) oxygen (O2) release capacity. Mouse genetic studies show that elevated erythrocyte Sphk1-induced S1P protects against tissue hypoxia by inducing O2 release. Mechanistically, we show that intracellular S1P promotes deoxygenated Hb anchoring to the membrane, enhances the release of membrane-bound glycolytic enzymes to the cytosol, induces glycolysis and thus the production of 2,3-bisphosphoglycerate (2,3-BPG), an erythrocyte-specific glycolytic intermediate, which facilitates O2 release. Altogether, we reveal S1P as an intracellular hypoxia-responsive biolipid promoting erythrocyte glycolysis, O2 delivery and thus new therapeutic opportunities to counteract tissue hypoxia.