Objectives
The objective of this study was to use a decision-analytic model to examine the potential economic impact of establishing a remunerated programme for pharmacists prescribing for minor ailments (PPMA) in Ontario, Canada.
Methods
A novel decision tool was developed to assess the economic impact of pharmacists prescribing for upper respiratory tract infections (URTIs), contact dermatitis (CD) and conjunctivitis by performing a cost-minimization analysis from a public payer perspective. Two prescribing strategies were compared: (1) PPMA, where patients may seek care from pharmacists or physicians, and (2) the usual care model (UCM), where all patients receive care from physicians. Two remuneration models for the PPMA strategy were also compared: (1) a prescription-detached scenario (PDS), where pharmacists were remunerated CAD$18.00 for each consultation, and (2) a Prescription-Attached Scenario (PAS), where pharmacists were only remunerated if a decision to prescribe was made.
Key findings
At a service uptake rate of 38% for the PDS, the PPMA model led to savings of $7.51, $4.08 and $5.15 per patient for URTIs, CD and conjunctivitis, respectively. Per 30 000 patients, the PPMA model for these minor ailments was projected to lead to cumulative reductions in visits to the emergency department, family physician and walk-in clinics by 799, 3677 and 5090, respectively.
Conclusions
The results of the study strongly suggest that enabling community pharmacists to assess and prescribe for minor ailments could potentially lead to large savings for the government in Ontario, Canada. In 100% of the PAS scenarios simulated, pharmacists as prescribers led to cost savings.
egr1 is a primary response gene induced by prostaglandin E2, prostaglandin F2alpha and fluprostenol in OCCM cells through protein kinase C signaling, suggesting that Egr1 may be a key mediator of anabolic responses in cementoblasts. Cementum is vital for periodontal organ maintenance and regeneration. Periodontal ligament fibers (Sharpey's fibers) insert into bone and cementum, thereby supporting the tooth in the alveolus (1). If the periodontal organ is lost, its regeneration requires cementoblast differentiation in order to form new cementum for periodontal ligament fiber insertion. Early attempts to regenerate cementum have proven difficult and rarely generate sufficient tissue (2). A better understanding of the molecular and cellular regulators that promote cementoblast differentiation is critical for developing targeted periodontal regeneration.
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