Upcoding in medicare: where does it matter most?

Upcoding in Medicare has been a topic of interest to economists and policy makers for nearly 40 years. While upcoding is generally understood as "billing for services at higher level of complexity than the service actually pro- vided or documented," it has a wide range of definitions within the literature. This is largely because the financial incentives across programs and aspects under the coding control of billing specialists and providers are different, and have evolved substantially over time, as has the published literature. Arguably, the primary importance of analyzing upcoding in different parts of Medicare is to inform policy makers on the magnitude of the process and to suggest approaches to mitigate the level of upcoding. Financial estimates for upcoding in traditional Medicare (Medicare Parts A and B), are highly variable, in part reflecting differences in methodology for each of the services covered. To resolve this variability, we used summaries of audit data from the Comprehensive Error Rate Testing program for the period 2010-2019. This program uses the same methodology across all forms of service in Medicare Parts A and B, allowing direct comparisons of upcoding magnitude. On average, upcoding for hospitalization under Part A represents $656 million annually (or 0.53% of total Part A annual expenditures) during our sample period, while up- coding for physician services under Part B is $2.38 billion annually (or 2.43% of Part B annual expenditures). These numbers compare to the recent consistent estimates from multiple different entities putting upcoding in Medicare Part C at $10-15 billion annually (or approximately 2.8-4.2% of Part C annual expenditures). Upcoding for hospitalization under Medicare Part A is small, relative to overall upcoding expenditures.

Novel roles for ATP-binding cassette G transporters in lipid redistribution in Toxoplasma.

Toxoplasma is a protozoan parasite proficiently adapted to thrive in a parasitophorous vacuole (PV) formed in the cytoplasm of a large variety of mammalian cells. As an actively dividing organism, the parasite must adjust the lipid composition of its membranes to preserve organelle vitality and expand the size of the PV membrane to accommodate growing progeny. We showed that Toxoplasma takes up host lipids and can expel major lipids in an ATP-dependent process. In order to provide detailed mechanistic insights into lipid trafficking phenomena relevant to Toxoplasma biology, we characterized six parasite ATP-binding cassette (ABC) G family transporters and investigated their potential contribution to lipid homeostatic processes. All these transporters are expressed in the parasite and five of them are upregulated upon exposure to sterols. Four ABCG are localized to secretory organelles and the plasma membrane, and promote cholesterol and phospholipid efflux, reflecting the importance in exportation of large amounts of lipids into the PV. Interestingly, one ABCG that is associated with vesicles in the PV and the plasma membrane acts as a cholesterol importer. This last finding expands our current view on the role of some ABCG transporters in eukaryotic sterol influx.

Four distinct pathways of hemoglobin uptake in the malaria parasite Plasmodium falciparum.

During the bloodstage of malaria infection, the parasite internalizes and degrades massive amounts of hemoglobin from the host red blood cell. Using serial thin-section electron microscopy and three-dimensional reconstruction, we demonstrate four independent, but partially overlapping, hemoglobin-uptake processes distinguishable temporally, morphologically, and pharmacologically. Early ring-stage parasites undergo a profound morphological transformation in which they fold, like a cup, onto themselves and in so doing take a large first gulp of host cell cytoplasm. This event, which we term the "Big Gulp," appears to be independent of actin polymerization and marks the first step in biogenesis of the parasite's lysosomal compartment-the food vacuole. A second, previously identified uptake process, uses the cytostome, a well characterized and morphologically distinct structure at the surface of the parasite. This process is more akin to classical endocytosis, giving rise to small (<0.004 fl) vesicles that are marked by the early endosomal regulatory protein Rab5a. A third process, also arising from cytostomes, creates long thin tubes previously termed cytostomal tubes in an actin-dependent manner. The fourth pathway, which we term phagotrophy, is similar to the Big Gulp in that it more closely resembles phagocytosis, except that phagotrophy does not require actin polymerization. Each of these four processes has aspects that are unique to Plasmodium, thus opening avenues to antimalarial therapy.

Physician Incentive Compensation Plans in Academic Medical Centers: The Imperative to Prioritize Value.

The emphasis on clinical volume in physician compensation plans has diminished professional vitality in academic medical centers and increased the cost of health care. Physician incentive compensation plans that focus on clinical volume can distort clinical encounters and fail to incorporate the professionalism and intrinsic motivators of clinicians. We assert herein that physician incentive compensation plans should reward clinical value (quality/cost) rather than clinical volume. The recommended change is compelled by the tenets of medical professionalism, the need to cultivate meaning in clinical practice, and the urgent financial and moral imperatives to improve health outcomes and reduce cost. The design of physician incentive compensation plans should incorporate accurate and valid measures of quality and cost, behavioral economic considerations, transparency and equity, prospective assessment of the impact on key outcomes, and flexible elements that encourage innovation and preserve fidelity to unique practice circumstances. Physicians should be recognized in compensation plans for enhancing the value of care, inspiring and educating the future clinical workforce, and improving public health through discovery.

Secretory traffic in the eukaryotic parasite Toxoplasma gondii: less is more.

Name a single-celled eukaryote that boasts a small genome size, is easily cultivated in haploid form, for which a wide variety of molecular genetic tools are available, and that exhibits a simple, polarized secretory apparatus with a well-defined endoplasmic reticulum and Golgi that can serve as a model for understanding secretion. Got it? Now name a cell with all these attributes that contains at least a dozen distinct and morphologically well-defined intracellular organelles, including three distinct types of secretory vesicles and two endosymbiotic organelles. Not so sure anymore?

Actin is required for endocytic trafficking in the malaria parasite Plasmodium falciparum.

The intra-erythrocytic stages of the malaria parasite endocytose large quantities of the surrounding erythrocyte cytoplasm and deliver it to a digestive food vacuole via endocytic vesicles. Digestion provides amino acids for parasite protein synthesis and is required to maintain the osmotic integrity of the host cell. The parasite endocytic pathway has been described morphologically by electron microscopy, but the molecular mechanisms that mediate and regulate it remain elusive. Given the involvement of actin in endocytosis in other eukaryotes, we have used actin inhibitors to assess the requirement for this protein in the endocytic pathway of the human malaria parasite, Plasmodium falciparum. Treatment of cultures with cytochalasin D did not affect haemoglobin levels in the parasites when co-administered with protease inhibitors, and neither did it affect the uptake of the endocytic tracer horseradish peroxidase, suggesting the absence of actin in the mechanism of endocytosis. However, in the absence of protease inhibitors, treated parasites contained increased levels of haemoglobin due to an accumulation of enlarged endocytic vesicles, as determined by immunofluorescence and electron microscopy, suggesting a role for actin in vesicle trafficking, possibly by mediating vesicle maturation and/or fusion to the digestive vacuole. In contrast to cytochalasin D, treatment with jasplakinolide led to an inhibition of endocytosis, an accumulation of vesicles closer to the plasma membrane and a marked concentration of actin in the parasite cortex. We propose that the stabilization of cortical actin filaments by jasplakinolide interferes with normal endocytic vesicle formation and migration from the cell periphery.

Differential effects of quinoline antimalarials on endocytosis in Plasmodium falciparum.

The effects of quinoline antimalarials on endocytosis by Plasmodium falciparum was investigated by measuring parasite hemoglobin levels, peroxidase uptake, and transport vesicle content. Mefloquine, quinine, and halofantrine inhibited endocytosis, and chloroquine inhibited vesicle trafficking, while amodiaquine shared both effects. Protease inhibitors moderated hemoglobin perturbations, suggesting a common role for heme binding.

A comprehensive space management model for facilitating programmatic research.

In FY04, the authors developed and implemented models to manage existing and incremental research space, and to facilitate programmatic research, at the University of Arizona College of Medicine. Benchmarks were set for recovery of total sponsored research dollars and for facilities and administrative (F&A) dollars/net square foot (nsf) of space, based on college-wide metrics. Benchmarks were applied to units (departments, centers), rather than to individual faculty. Performance relative to the benchmark was assessed using three-year moving averages, and applied to existing blocks of space. Space was recaptured or allocated, in all cases to programmatic themes, using uniform policies. F&A revenues were returned on the basis of performance relative to a benchmark. During the first two years after implementation of the model (FY05 and FY06), and for the 24 units occupying research space, median total sponsored research revenue/nsf increased from $393.96 to $474.46 (20.4%), and median F&A revenue/nsf increased from $57.42 to $91.86 (60.0%). These large increases in median values are driven primarily from redistribution and recapturing of space. Recruiting policies for unit heads were developed to facilitate joint hires among units. In combination, these policies created a comprehensive space management model for facilitating programmatic research. Although challenges remain in implementing the programmatic recruitment strategy, and selected modifications to the original policy were introduced later (e.g., research space for newly recruited junior faculty is now exempted from calculations for three years), overall, the models have created a climate of transparency that is now accepted and that allows efficient and equitable management of research space.

Are Teaching Hospitals Treated Fairly in the Hospital-Acquired Condition Reduction Program?

PURPOSE: To identify the factors associated with total Hospital-Acquired Condition Reduction Program (HACRP) score and with receiving a Centers for Medicare and Medicaid Services (CMS) penalty (1% reduction in payment to those hospitals in the lowest-performing quartile of HACRP scores) for fiscal years (FYs) 2015-2017 with a particular focus on trends over this period. METHOD: The authors evaluated the following variables: (1) type of hospital (teaching vs. nonteaching); (2) disproportionate patient percentage; (3) case mix index (CMI); (4) number of staffed beds; (5) length of stay (LOS); (6) gross patient revenue; and (7) region, using data from CMS and the American Hospital Directory. They conducted multivariate linear and logistic regressions. RESULTS: A total of 2,249 hospitals were included. The mean total HACRP scores across hospitals for FY15, FY16, and FY17 were 5.38, 5.35, and 5.18, respectively. In FY15, 21.2% (476/2,249) of hospitals received a penalty compared with 22.6% (508/2,249) in FY16 and 31.3% (704/2,249) in FY17 (P < .001). The logistic regression model showed that teaching hospitals, larger hospitals (> 400 beds), hospitals with high CMI or long LOS, and hospitals in the Northeast and Western United States were more likely to receive a penalty. Teaching hospitals and larger hospitals did not improve their scores over time compared with nonteaching and small hospitals. CONCLUSIONS: A reevaluation of the scoring methodology for the HACRP is needed. CMS could stratify hospitals into homogeneous categories and apply penalties to those that have the worst scores in each category.

Mohs Micrographic Surgery Volume and Payment Patterns Among Dermatologists in the Medicare Population, 2013.

OBJECTIVES: Mohs micrographic surgery (MMS) has expanded markedly in recent years but there is limited information on volume, practice patterns or reimbursement. This study characterizes MMS utilization in the Medicare population. MATERIALS AND METHODS: We analyzed the Medicare Provider Utilization and Payment Data: Physician and Other Supplier Public Use File Calendar Year 2013 data set for provider service volume and reimbursement for dermatologists who did and did not perform MMS procedures. RESULTS: Total Medicare-funded MMS procedures increased 25% from 2009 (558,447) to 2013 (700,262). Dermatologists who performed MMS had significantly more average services per provider (5419.4 vs. 3627.1, r=0.16, P<0.0001), were reimbursed significantly more in average total procedure-related compensation ($475,883.64 vs. $144,564.74, r=0.49, P<0.0001) than dermatologists who did not perform MMS, and made up 71.3% of the top decile of dermatologists ranked by total reimbursement received from Medicare. Total MMS service volume and reimbursement was concentrated among a subset of providers. Among MMS providers, a higher volume of MMS procedures was correlated with a greater likelihood of performing procedures on lesions located on the trunk, arms or legs (r=0.27, P<0.001). CONCLUSIONS: In 2013 reimbursement for MMS comprised almost 19% of the amount reimbursed by Medicare Part B Fee For Service to dermatologists and greater than half a percent of the total amount reimbursed to all physicians participating in the program. Further studies incorporating clinical and outcomes data are needed to evaluate appropriate utilization of this procedure.

Timing of revenue streams from newly recruited faculty: implications for faculty retention.

PURPOSE: To determine the timing and magnitude of revenues generated by newly recruited faculty, to facilitate configuration of recruitment packages appropriately matched to expected financial returns. METHOD: The aggregate of all positive cash flows to central college of medicine administration -- from research, clinical care, tuition, philanthropy, and royalties and patents, from all faculty newly recruited to the University of Arizona College of Medicine between 1998 and 2004 -- was quantified using the net present value (npv) methodology, which incorporates the time value of money. RESULTS: Tenure-track faculty and, in particular, those with laboratory research programs, generated the highest positive central cash flows. The npv for positive cash flows (npv[+]) during 6 and 10 years for newly recruited assistant professors with laboratory research programs were $118,600 and $255,400, respectively, and, for professors with laboratory research programs, $172,600 and $298,000, respectively (associate professors were not analyzed because of limited numbers). Faculty whose appointments at the University of Arizona College of Medicine exceeded 15 years in duration were the most productive in central revenue generation, far in excess of their numbers proportionate to the total. CONCLUSIONS: The results emphasize the critical importance of faculty retention, because even those newly recruited faculty who are most successful in central revenue generation (tenure track with laboratory research programs) must be retained for periods well in excess of 10 years to recoup the initial central investment required for their recruitment.

Phoenix rises, with Tucson's help: establishing the first four-year allopathic program in the nation's fifth largest city.

The authors describe the expansion of The University of Arizona College of Medicine from Tucson, Arizona, into Phoenix. They explain how the new Phoenix program, in partnership with Arizona State University, is one college of medicine for the state of Arizona, governed by a single accreditation by the Liaison Committee for Medical Education (LCME). The authors present 21 lessons to be considered early in a medical school expansion process: clearly establish responsibility, authority, and accountability; define activities under university purview and those that require broader engagement; delineate college-wide versus campus-specific functions; clearly define the intent of the new initiative; get frequent input from the LCME; use LCME input to ensure a student focus; be cautious in using consultants; use respected local "brokers"; create a single locus for input and concerns; educate constituencies about medical school requirements; engage leadership to create linkages across sites; encourage communication between leaders in both sites; discriminate between shared and distinctive local curriculum elements; consider the effort and experience required to develop a full curriculum versus those required to develop specific local curricular areas; create simple, transparent admission processes; define faculty profiles for the new program; ensure sufficient resources for core faculty; budget based on national metrics; create core mission-based principles to frame discussions and decisions; segregate clinical affiliation discussions from curriculum and recruitment of basic science faculty; and ensure sufficient land. Although these observations are most relevant to institutions planning expansions of already accredited programs, they derive from principles and practical considerations with wider applicability.

Host but not parasite cholesterol controls Toxoplasma cell entry by modulating organelle discharge.

Host cell cholesterol is implicated in the entry and replication of an increasing number of intracellular microbial pathogens. Although uptake of viral particles via cholesterol-enriched caveolae is increasingly well described, the requirement of cholesterol for internalization of eukaryotic pathogens is poorly understood and is likely to be partly organism specific. We examined the role of cholesterol in active host cell invasion by the protozoan parasite Toxoplasma gondii. The parasitophorous vacuole membrane (PVM) surrounding T. gondii contains cholesterol at the time of invasion. Although cholesterol-enriched parasite apical organelles termed rhoptries discharge at the time of cell entry and contribute to PVM formation, surprisingly, rhoptry cholesterol is not necessary for this process. In contrast, host plasma membrane cholesterol is incorporated into the forming PVM during invasion, through a caveolae-independent mechanism. Unexpectedly, depleting host cell plasma membrane cholesterol blocks parasite internalization by reducing the release of rhoptry proteins that are necessary for invasion. Cholesterol back-addition into host plasma membrane reverses this inhibitory effect of depletion on parasite secretion. These data define a new mechanism by which host cholesterol specifically controls entry of an intracellular pathogen.

Improving clinical productivity in the academic setting: a novel incentive plan based on utility theory.

PURPOSE: Academic internal medicine practices face growing challenges to financial viability due to high overhead, competing institutional missions, and suboptimal physician productivity. The authors describe the development of a clinical incentive plan for a group of academic subspecialty physicians at the Dana Clinic, an outpatient setting at Yale School of Medicine, and report on results of the first year's experience under the plan. METHOD: Utility theory was used to assess the risk profile of clinic faculty and identify incentive payments that would optimize faculty benefit or "utility" while minimizing departmental costs. Under the plan, physicians who reached a productivity target based on work Relative Value Units (wRVUs) between October 2003 and November 2004 had overhead costs covered and received a fixed payment to support salary; additional incentive payments were available for those exceeding the target. Physicians failing to reach the target were responsible for their own overhead costs and received no fixed payment. Physician productivity as measured by wRVU per full-time equivalent (FTE) was compared for the year prior to, and the year following, incentive plan introduction. RESULTS: Forty-seven members of eight academic sections were included in the analysis. Median productivity improved by 34%, with 42 of 47 physicians showing improvement. Significant improvements were also noted in collections (62%) and visit volume (23%), and shifts were observed in coding patterns. CONCLUSIONS: The unique threshold-based structure of the incentive plan, as determined through utility theory modeling, as well as permitting physicians to choose how to achieve the wRVU target were key features of its success, resulting in improved productivity without increasing practice resources or faculty salaries.

Toxoplasma gondii is capable of exogenous folate transport. A likely expansion of the BT1 family of transmembrane proteins.

Folates are key elements in eukaryotic biosynthetic processes. The protozoan parasite Toxoplasma gondii possesses the enzymes necessary for de novo folate synthesis and has been suggested to lack alternative mechanisms for folate acquisition. In this paper, we present a different view by providing evidence that Toxoplasma is capable of salvaging exogenous folates. By monitoring uptake of radiolabeled folates by parasites in axenic conditions, our studies revealed a common folate transporter that has a high affinity for folic acid. Transport of this compound across the parasite plasma membrane is rapid, biphasic, temperature dependent, bi-directional, concentration dependent and specific. In addition, morphological evidence demonstrates that fluorescent methotrexate, a folate analog, is internalized by Toxoplasma and shows localization reminiscent to the mitochondrion. The presence of putative folate transporter genes in the Toxoplasma genome, which are homologous to the BT1 family of proteins, suggests that Toxoplasma may encode proteins involved in folate transport. Interestingly, genome analysis suggests that the BT1 family of proteins exists not only in Toxoplasma, but in other Apicomplexan parasites as well. Altogether, our results not only have implications for current therapeutic regimens against T. gondii, but they also allude that the folate transport mechanism may represent a novel Apicomplexan target for the development of new drugs.

The not-for-profit form and translational research: Kerr revisited?

Translational research conducted in academic health centers is confounded by the organizational structure in which the work is performed. Investigators must obtain research funding and appropriate recognition as a part of a research team in a not-for-profit environment which has more readily rewarded basic work, and individual accomplishments. What results is a unique form of conflict of interest, best understood by relating the basic principles underlying the not-for-profit form to the conduct of translational research in the AHC setting.

A strategy for allocating central funds to support new faculty recruitment.

Requests for central funding for recruiting new faculty in academic health centers (AHCs) typically exceed available resources. The administration's prioritization of the requests, therefore, involves implicit or explicit predictions of the value of the potential faculty member to the institution. Optimal management dictates that the value of the recruit be assessed both on the extent to which they contribute to the organization's mission and on their capacity to generate revenues. The first premise of this article is that faculty recruits can be considered as "projects," and their potential value to the organization can be estimated in this context. The second premise is that the best way to determine a project's financial worth is by determining the net present value of each potential faculty recruit. The author models the combination of these premises and demonstrates that the approach allows for the more systematic prioritization of resource allocation for faculty recruitment in AHCs.

Strategies for defining financial benchmarks for the research mission in academic health centers.

Valid financial benchmarks are needed for the research mission in academic health centers (AHCs). Databases listing institutional success in obtaining sponsored research funding are publicly available. However, these databases are generally not adjusted for AHC size, confounding useful comparisons between institutions. The authors suggest simple strategies, which depend on a form of ratio analysis, to circumvent this limitation. Annual rates of growth (rates of return, R(f)) are determined for total National Institutes of Health research grant dollars, number of research grants, and average dollars per research grant for 15 U.S. AHCs. Selected institutions are compared to one another and to the total pool of medical school funding. Performance is evaluated over a ten-year period (1992-2001) to illustrate the advantages, limitations, and applications of the ratio analysis approach. Alternative strategies are suggested for individual AHCs to evaluate their departmental and organizational performance, again without regard to institution size, and also dependent on ratios. Application of these strategies, especially when individualized to the particular AHC, permits more accurate assessment of past performance and more accurate and effective planning for future growth.

Neutral lipid synthesis and storage in the intraerythrocytic stages of Plasmodium falciparum.

In eukaryotic cells the neutral lipids, steryl esters and triacylglycerol, are synthesized by membrane-bound O-acyltransferases and stored in cytosolic lipid bodies. We show here that the intraerythrocytic stages of Plasmodium falciparum produce triacylglycerol using oleate and diacylglycerol as substrates. Parasite membrane preparations reveal a synthesis rate of 4.5 +/- 0.8 pmol x min(-1)mg(-1) of protein with maximal production occurring in the mid- and late-trophozoite stages in both, membrane preparations and live parasites. In contrast to other eukaryotic cells, no discernable amounts of steryl esters are produced, and the parasite is insensitive to cholesterol esterification inhibitors. Synthesized neutral lipids are stored as lipid bodies in the parasite cytosol in a stage specific manner. Their biogenesis is not modified upon incubation with excess fatty acids or lipoproteins or after lipoprotein depletion of the culture medium. We investigated on the enzymes involved in neutral lipid synthesis and found that only one gene with significant homology to known members of the membrane-bound O-acyltransferase family is present in the P. falciparum genome. It encodes a microsomal transmembrane protein with a predicted size of 78.1 kDa, which we named PfDGAT because of its close identity with various known acyl-CoA:diacylglycerol acyltransferases. PfDGAT is expressed in a stage specific manner as documented by Western blotting and immunoprecipitation assays using antibodies against Toxoplasma DGAT, suggesting that PfDGAT is the most likely candidate for plasmodial triacylglycerol synthesis.

On the biogenesis of lipid bodies in ancient eukaryotes: synthesis of triacylglycerols by a Toxoplasma DGAT1-related enzyme.

In mammalian cells, the main stored neutral lipids are triacylglycerol and cholesteryl esters, which are produced by two related enzymes, acyl-CoA:diacylglycerol acyltransferase (DGAT) and acyl-CoA:cholesterol acyltransferase (ACAT), respectively. Very little is known about the metabolism, intracellular storage and function of neutral lipids in many pathogenic lower eukaryotes. In this paper, we have characterized the activity of an important triacylglycerol synthetic enzyme in the protozoan Toxoplasma gondii. A full-length cDNA and gene encoding a T. gondii DGAT1-related enzyme were identified and designated TgDGAT1. The gene is composed of 15 exons and 14 introns, and encodes a protein with a predicted M(r) 63.5kDa, containing signature motifs characteristic of the DGAT1 family. The native protein migrates at 44kDa under reducing conditions. TgDGAT1 is an integral membrane protein localized to the parasite cortical and perinuclear endoplasmic reticulum, with the C-terminus oriented to the lumen of the organelle. When a Saccharomyces cerevisiae mutant strain lacking neutral lipid production is transformed with TgDGAT1 cDNA, a significant DGAT activity is reconstituted, resulting in triacylglycerol synthesis and biogenesis of cytosolic lipid inclusions, resembling lipid bodies in T. gondii. No production of steryl esters is observed upon TgDGAT1 expression in yeast. In contrast to human DGAT1 lacking fatty acid specificity, TgDGAT1 preferentially incorporates palmitate. Our results indicate that parasitic protozoa are also neutral lipid accumulators and illustrate the first example of the existence of a functional DGAT gene in an ancient eukaryote, demonstrating that diacylglycerol esterification is evolutionarily conserved.