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ObjectiveDetermine the association of incident antibiotic prescribing levels for common infections with infection-related complications and hospitalisations by comparing high with low prescribing general practitioner practices.Design retrospective cohort studyRetrospective cohort study.Data sourceUK primary care records from the Clinical Practice Research Datalink (CPRD GOLD) and SAIL Databank (SAIL) linked with Hospital Episode Statistics (HES) data, including 546 CPRD, 346 CPRD-HES and 338 SAIL-HES practices.ExposuresInitial general practice visit for one of six common infections and the proportion of antibiotic prescribing in each practice.Main outcome measuresIncidence of infection-related complications (as recorded in general practice) or infection-related hospital admission within 30 days after consultation for a common infection.ResultsA practice with 10.4% higher antibiotic prescribing (the IQR) was associated with a 5.7% lower rate of infection-related hospital admissions (adjusted analysis, 95% CI 3.3% to 8.0%). The association varied by infection with larger associations in hospital admissions with lower respiratory tract infection (16.1%; 95% CI 12.4% to 19.7%) and urinary tract infection (14.7%; 95% CI 7.6% to 21.1%) and smaller association in hospital admissions for upper respiratory tract infection (6.5%; 95% CI 3.5% to 9.5%) The association of antibiotic prescribing levels and hospital admission was largest in patients aged 18–39 years (8.6%; 95% CI 4.0% to 13.0%) and smallest in the elderly aged 75+ years (0.3%; 95% CI −3.4% to 3.9%).ConclusionsThere is an association between lower levels of practice level antibiotic prescribing and higher infection-related hospital admissions. Indiscriminately reducing antibiotic prescribing may lead to harm. Greater focus is needed to optimise antibiotic use by reducing inappropriate antibiotic prescribing and better targeting antibiotics to patients at high risk of infection-related complications.

Background Fetal growth restriction (FGR) is associated with glucocorticoid (GC) excess in human pregnancies and animal models. In mice and rats, GC treatment reduces placental angiogenesis and dysregulates the expression of angiogenic factors. It is not known whether GCs reduce angiogenesis in the human placenta. Hypothesis Glucocorticoid excess in the human placenta inhibits angiogenesis by dysregulating angiogenic factors. Methods Human umbilical vein endothelial cells (HUVECs) and human placental artery endothelial cells (HPAECs) were treated with hydrocortisone (HC), prednisolone (PRED) and dexamethasone (DEX) for 24–48 hours. Tube-like structure (TLS) formation on matrigel, cell migration, proliferation and apoptosis were assessed. Chorionic plate arteries (CPAs) from normal placentas (n = 10) were cultured for 48 hours with HC or DEX. mRNA expression of six angiogenic factors were quantified using real-time Q-PCR with normalisation to TBP. Results Pilot studies in HUVECs (n = 3, p Discussion GCs reduced tube formation and cell migration, key facets of angiogenesis, in HUVEC and HPAEC models. These findings indicate that GCs inhibit human placental angiogenesis, which could contribute to the pathogenesis of FGR. The downregulation of specific angiogenic factors by GCs identifies putative mechanistic pathways involved.