Cost-Effectiveness of Publicly Funded Treatment of Opioid Use Disorder in California

Background: Only 1 in 5 of the nearly 2.4 million Americans with an opioid use disorder received treatment in 2015. Fewer than half of Californians who received treatment in 2014 received opioid agonist treatment (OAT), and regulations for admission to OAT in California are more stringent than federal regulations. Objective: To determine the cost-effectiveness of OAT for all treatment recipients compared with the observed standard of care for patients presenting with opioid use disorder to California's publicly funded treatment facilities. Design: Model-based cost-effectiveness analysis. Data Sources: Linked population-level administrative databases capturing treatment and criminal justice records for California (2006 to 2010); published literature. Target Population: Persons initially presenting for publicly funded treatment of opioid use disorder. Time Horizon: Lifetime. Perspective: Societal. Intervention: Immediate access to OAT with methadone for all treatment recipients compared with the observed standard of care (54.3% initiate opioid use disorder treatment with medically managed withdrawal). Outcome Measures: Discounted quality-adjusted life-years (QALYs) and discounted costs. Results of Base-Case Analysis: Immediate access to OAT for all treatment recipients costs less (by $78 257), with patients accumulating more QALYs (by 0.42) than with the observed standard of care. In a hypothetical scenario where all Californians starting treatment of opioid use disorder in 2014 had immediate access to OAT, total lifetime savings for this cohort could be as high as $3.8 billion. Results of Sensitivity Analysis: 99.6% of the 2000 simulations resulted in lower costs and more QALYs. Limitation: Nonrandomized delivery of OAT or medically managed withdrawal. Conclusion: The value of publicly funded treatment of opioid use disorder in California is maximized when OAT is delivered to all patients presenting for treatment, providing greater health benefits and cost savings than the observed standard of care. Primary Funding Source: National Institute on Drug Abuse.

Glycemic Therapy for Type 2 Diabetes: Choices Expand, Data Lag Behind

Benefits and Harms of Osteoporosis Medications in Patients With Chronic Kidney Disease: A Systematic Review and Meta-analysis: Annals of Internal Medicine: Vol 166, No 9

Background: Complications of chronic kidney disease (CKD) include weak bones and increased fracture risk. Purpose: To review the benefits and harms of osteoporosis medications (bisphosphonates, teriparatide, raloxifene, and denosumab) compared with placebo, usual care, or active control in terms of bone mineral density (BMD), fractures, and safety in patients with CKD. Data Sources: PubMed and the Cochrane Central Register of Controlled Trials from December 2006 through December 2016. Study Selection: Paired reviewers independently screened abstracts and full-text articles for English-language, randomized, controlled trials that had at least 6 months of follow-up; evaluated osteoporosis medications among patients with CKD; and reported on BMD, fractures, or safety (mortality and adverse events). Data Extraction: Two reviewers serially abstracted data and independently assessed risk of bias and graded the strength of evidence (SOE). Data Synthesis: There were 13 trials (n = 9850) that included kidney transplant recipients (6 trials), patients who had stage 3 to 5 CKD or were receiving dialysis (3 trials), or postmenopausal women with CKD (4 trials). Evidence showed that bisphosphonates may slow loss of BMD among transplant recipients (moderate SOE), but their effects on fractures and safety in transplant recipients and others with CKD are unclear. Raloxifene may prevent vertebral fractures but may not improve BMD (low SOE). Effects of teriparatide and denosumab on BMD and fractures are unclear (very low SOE), and these medications may increase risk for some safety outcomes. Limitation: Unclear rigor of evidence, possible reporting biases, and scant evidence among patients with stage 3 to 5 CKD. Conclusion: Effects of osteoporosis medications on BMD, fracture risk, and safety among patients with CKD are not clearly established. Primary Funding Source: Kidney Disease: Improving Global Outcomes.

Cognitive Behavioral Therapy for Chronic Insomnia: Confronting the Challenges to Implementation

The History and Future of Treatment of Hypothyroidism

This article has been corrected. The original version (PDF) is appended to this article as a Supplement. Thyroid hormone replacement has been used for more than a century to treat hypothyroidism. Natural thyroid preparations (thyroid extract, desiccated thyroid, or thyroglobulin), which contain both thyroxine (T4) and triiodothyronine (T3), were the first pharmacologic treatments available and dominated the market for the better part of the 20th century. Dosages were adjusted to resolve symptoms and to normalize the basal metabolic rate and/or serum protein-bound iodine level, but thyrotoxic adverse effects were not uncommon. Two major developments in the 1970s led to a transition in clinical practice: 1) The development of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led to the discovery that many patients were overtreated, resulting in a dramatic reduction in thyroid hormone replacement dosage, and 2) the identification of peripheral deiodinase-mediated T4-to-T3 conversion provided a physiologic means to justify l-thyroxine monotherapy, obviating concerns about inconsistencies with desiccated thyroid. Thereafter, l-thyroxine monotherapy at doses to normalize the serum TSH became the standard of care. Since then, a subgroup of thyroid hormone–treated patients with residual symptoms of hypothyroidism despite normalization of the serum TSH has been identified. This has brought into question the inability of l-thyroxine monotherapy to universally normalize serum T3 levels. New research suggests mechanisms for the inadequacies of l-thyroxine monotherapy and highlights the possible role for personalized medicine based on deiodinase polymorphisms. Understanding the historical events that affected clinical practice trends provides invaluable insight into formulation of an approach to help all patients achieve clinical and biochemical euthyroidism.

Cytokine Inhibition in Patients With Chronic Fatigue Syndrome

Management of Acute and Recurrent Gout

Hepatitis C Virus Treatment and Persons Who Inject Drugs

Annals Video Summary - Efficacy and Safety of Bisphosphonates for Complex Regional Pain Syndrome: A Systematic Review and Meta-analysis

Chronic Coronary Artery Disease

Chronic coronary artery disease (CCAD) is a leading cause of death in the United States and many other countries. The defining pathobiology is an imbalance between the metabolic demands of the myocardium and oxygen supply, which most often results from coronary artery atherosclerosis. The classic presenting symptom of CCAD is angina, but clinical presentation varies greatly among patients. Since the last In the Clinic on CCAD (previously termed “stable ischemic heart disease”) in 2019, several new medications have been approved to reduce ischemic complications.