Reduction in Healthcare Resource Utilization Following Treatment With a Home-Based Footworn Device in Patients With Knee Osteoarthritis: A Retrospective Claims Analysis.

Background: One in 7 US adults has knee osteoarthritis (OA) and almost two-thirds of them suffer from low back pain. OA is the third most rapidly rising condition associated with disability and leads to a significant burden on the healthcare system and society. Objective: This study looked at the healthcare resource utilization (HCRU) in patients with knee OA and low back pain before and after the utilization of a new, home-based, noninvasive, biomechanical intervention. Methods: This was a retrospective claims analysis of 585 patients treated with a personalized, noninvasive, home-based, biomechanical treatment that aims to alleviate knee pain and improve function (AposHealth®). The date of the first AposHealth claim was the index date. Data prior to the index date and post-index date were used to monitor changes in HCRU while in treatment. Descriptive statistics, including frequencies, means and standard deviations, were used to present patient characteristics. To standardize the results, an average monthly claims data rate was calculated and an expected annual rate was extrapolated. Annual HCRU rate per 1000 members was calculated. Results: HCRU decreased after utilizing the new intervention including a decrease of 79% in diagnostic claims, a 70% decrease in outpatient services, a 22% decrease in non-operative treatments, a 61% decrease in pain medications including an 85% drop in opioids use, and a 44% decrease in intra-articular injections. The pre-index estimated rate for total knee replacement (TKR), which is based on existing literature, was 15.1%, whereas the post-index rate of TKR was 0.9%. Conclusions: Patients with knee OA treated with a home-based, noninvasive, biomechanical intervention incurred fewer healthcare resources, leading to an overall reduction in the cost of care.

Insurance Coverage for Emerging Diabetes Technologies: Payers' Perspective.

Advances in glucose monitoring and insulin delivery technologies have led to the development of innovative self-management tools, such as continuous glucose monitoring, automated insulin delivery systems, and smart connected insulin pens. Although the clinical advantages of today's emerging diabetes technologies are well documented, the cost of integrating these tools into clinical practice must be considered to sustain the financial viability of both public and private insurers. Most clinicians are unfamiliar with the process the commercial insurers follow when making these decisions. This article reviews the key factors the insurers consider when determining eligibility criteria.

Profile of a population-based diabetic macular oedema study: the Liverpool Eye and Diabetes Study (Sydney).

PURPOSE: The population prevalence of diabetic macular oedema (DME) is unclear. Previous estimates have depended on photographic grading of clinically significant macular oedema, which is subjective and has resulted in widely varying estimates. With the advent of optical coherence tomography (OCT), the presence and severity of DME can now be assessed objectively and accurately. METHODS: The Liverpool Eye and Diabetes Study (LEADS) is a cross-sectional population-based study of patients with type 1 and type 2 diabetes in a multi-ethnic region of Sydney, Australia, to determine the population prevalence of OCT-defined DME, how this varies by ethnicity and association with systemic factors. This report describes the rationale, methodology and study aims. RESULTS: To date 646 patients out of an expected sample size of 2000 have been recruited. Baseline data are presented for patients with type 1 (n=75, 11.8%) and type 2 (n=562, 88.2%) diabetes recruited to date. Patients with type 1 diabetes were younger (39.5vs60.7 years), with longer duration of diabetes (18.1vs11.7 years), slightly worse glycaemic control (HbA1c 9.0vs8.3), and less likely to have hypertension (30.7vs71.4%), hypercholesterolaemia (33.3vs74.6%) and obesity (31.1vs51.5%, respectively, all p<0.05). CONCLUSIONS: The LEADS will provide objective estimates of the population prevalence of DME, how this varies with ethnicity and associations with systemic disease.

Growth-associated gene expression after stroke: evidence for a growth-promoting region in peri-infarct cortex.

Stroke induces axonal sprouting in peri-infarct cortex. A set of growth-associated genes important in axonal sprouting in peripheral nervous system regeneration and cortical development has recently been defined. The expression profiles of these growth-associated genes were defined during the post-stroke axonal sprouting response using a model of stroke in barrel field cortex. Stroke induces sequential waves of neuronal growth-promoting genes during the sprouting response: an early expression peak (SPRR1), a mid expression peak (p21, Ta1 tubulin, L1, MARCKS), a late peak (SCG10, SCLIP), and an early/sustained pattern (GAP43, CAP23, c-jun). These expression peaks correspond to specific time points in the sprouting response. The expression of the growth-inhibiting chondroitin sulfate proteoglycans aggrecan, brevican, versican, and phosphacan are induced late in the sprouting process; except neurocan, which is increased during the peak of the growth-promoting gene expression. The developmentally associated growth inhibitors ephrin-A5, ephB1, semaphorin IIIa, and neuropilin 1 are also induced in the early phases of the sprouting response. At the cellular level, chondroitin sulfate proteoglycans, in the form of peri-neuronal nets, are reduced in the region of axonal sprouting, during the peak of growth-promoting gene expression. These results identify a unique profile of growth-promoting gene expression in adult cortex after stroke, the inhibitory molecules that are present during the sprouting response, and a region in which growth-promoting genes are increased, growth-inhibitory proteins are diminished and axonal sprouting occurs. This region may be a growth-promoting zone after stroke.

Applications of microarrays with toxicologically relevant genes (tox genes) for the evaluation of chemical toxicants in Sprague Dawley rats in vivo and human hepatocytes in vitro.

Microarrays with toxicologically relevant genes (tox genes) have been developed in our laboratory for toxicogenomics studies in rat, dog and man. The genes were chosen using published information as well as a discovery process for genes responsive to toxic treatments using transcription profiling experiments conducted with rats and dogs. In addition to published information human tox genes were derived from rat tox genes based on gene homology. Using the microarray with rat-specific tox genes, a database containing gene expression, histopathology, and clinical chemistry findings has been generated for 89 compounds. Analysis of the database indicates that treatment with toxic compounds induces specific gene expression patterns. Dose- and time-dependent response relationships in gene expression were observed for treatment with toxic compounds. Gene expression at 24h was found to correlate well with organ toxicity observed at 72 h. Mining of the database led to the selection of specific groups of genes (predictive gene sets) whose expression patterns are predictive of organ toxicity with a high degree of accuracy (approximately 90%). The data also provide insight on toxic mechanism and gene regulation pathways. For instance, carbon tetrachloride and chloroform treatments were found to decrease the expression of the cytochrome P450 isoform 3A1 gene while enhancing the expression of the multiple drug resistance gene MDR1 in liver, clearly demonstrating that the CYP3A1 and MDR1 genes were not co-regulated as postulated by some researchers. This approach, the use of gene expression as an endpoint to define organ toxicity, is extended to the definition of human drug toxicity using primary human hepatocytes as a test system. Preliminary results demonstrate that the toxic drug, troglitazone, can be clearly distinguished from the less toxic analogues, rosiglitazone and pioglitazone based on their effects on tox gene expression in human hepatocytes. Our results with both rats in vivo and human hepatocytes in vitro suggest that microarrays with toxicologically relevant genes can be used routinely for the evaluation of chemical toxicity.