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1.
J Surg Res ; 243: 488-495, 2019 11.
Article in English | MEDLINE | ID: mdl-31377488

ABSTRACT

BACKGROUND: Prior studies of the impact of the Affordable Care Act on reimbursement for inpatient trauma care do not include disproportionate share hospital (DSH) funding. Because trauma centers and other safety-net hospitals are sensitive to any changes in financial support, it is essential to include DSH funding in evaluating overall reimbursement. This study analyzes the long-term financial trends, including DSH, of a level I trauma center in Ohio, a state that expanded Medicaid. METHODS: Charges, reimbursement, sources of insurance coverage, Injury Severity Scores, and DSH funding for the trauma patient population of an Ohio American College of Surgeons level 1 trauma center were studied from 2012 to 2017. Data were collected from Transition Systems, Inc. RESULTS: During 2012-2017, self-pay patient cases decreased from 15.0% to 4.1% and commercial insurance patients decreased from 34.2% to 27.6%. The percentage of Medicaid patients increased from 15.5% to 27.1%; however, Medicaid reimbursement average per case declined from $17,779 in 2012 to $10,115 in 2017 (a decline of 43.1%). Self-pay charges decreased from $22.0 million to $6.7 million. Total DSH funding, compensation given to hospitals that disproportionately treat underserved populations, decreased 17.4%. CONCLUSIONS: Self-pay charges and self-pay patients decreased dramatically; Medicaid patients and charges increased substantially in the years after the implementation of the Affordable Care Act at our trauma center. However, there was a decrease in commercial insurance, which had the highest reimbursement for our hospital, and a significant decline in DSH, a critical supplemental source of funding for safety-net hospitals.


Subject(s)
Injury Severity Score , Insurance Coverage/trends , Patient Protection and Affordable Care Act/economics , Reimbursement, Disproportionate Share/statistics & numerical data , Trauma Centers/economics , Humans , Trauma Centers/statistics & numerical data , United States
2.
Nephrol Dial Transplant ; 32(8): 1338-1344, 2017 Aug 01.
Article in English | MEDLINE | ID: mdl-26250434

ABSTRACT

BACKGROUND: Treatment response in lupus nephritis (LN) is defined clinically, without consideration of renal histology. Few studies have systematically examined histologic responses to induction therapy. In LN patients who underwent protocol kidney biopsies after induction immunosuppression, we describe the renal histology of the second biopsy and correlate histologic activity and damage with short- and long-term kidney outcomes. METHODS: Patients with suspected LN were biopsied for diagnosis (Biopsy 1), and those with proliferative LN were rebiopsied after induction (Biopsy 2). Histologic activity and damage at each biopsy were calculated as the National Institutes of Health activity and chronicity indices. Complete and partial renal responses after induction and after long-term follow-up were determined clinically. RESULTS: One-third of patients who achieved a complete clinical response after induction had persistently high histologic activity, and 62% of patients who had complete histologic remission on rebiopsy were still clinically active. Chronic renal damage increased after induction even in complete clinical responders. Chronicity at Biopsy 2 associated with long-term kidney function and development of chronic kidney disease. CONCLUSIONS: Early clinical and histologic outcomes are discordant in proliferative LN, and neither correlates with long-term renal outcome. The kidney accrues chronic damage rapidly and despite clinical response in LN. Preservation of kidney function may require therapeutic targeting of both chronic damage and inflammation during LN induction treatment.


Subject(s)
Inflammation/pathology , Lupus Nephritis/complications , Renal Insufficiency, Chronic/pathology , Adult , Biopsy , Female , Humans , Inflammation/etiology , Inflammation/surgery , Lupus Nephritis/therapy , Male , Remission Induction , Renal Insufficiency, Chronic/etiology , Renal Insufficiency, Chronic/surgery
3.
Arthritis Rheumatol ; 69(1): 169-175, 2017 01.
Article in English | MEDLINE | ID: mdl-27482943

ABSTRACT

OBJECTIVE: The Rituximab in ANCA-Associated Vasculitis (RAVE) trial compared rituximab to cyclophosphamide as induction therapy for the treatment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. We undertook the current study to determine whether known single-nucleotide polymorphisms (SNPs) for Fcγ receptors (FcγR) or cytochrome P450 (CYP) enzymes were associated with the response to treatment with rituximab and cyclophosphamide, respectively. METHODS: Functional SNPs for FcγR (FcγRIIa 519G>A, FcγRIIb 695T>C, FcγRIIIa 559T>G) and CYP enzymes (CYP2B6 1459C>T, CYP2C19 681G>A) were analyzed by direct sequencing of polymerase chain reaction-amplified genomic DNA. Each SNP was tested as a predictor of complete remission at 6 months or remission with continued prednisone administration using logistic regression and including the covariates of baseline Birmingham Vasculitis Activity Score for Wegener's Granulomatosis, ANCA type, and new versus relapsing disease. The associations of these SNPs with the secondary outcomes of time to complete remission, time to relapse, or time to B cell reconstitution were analyzed by Cox proportional hazard tests. RESULTS: No significant associations were identified between complete remission and any FcγR genotype in the rituximab group or any CYP genotype in the cyclophosphamide group. However, when the treatment groups were combined, an association was found between the 519AA genotype of FcγRIIa and complete remission (P = 0.01). The 519AA genotype predicted complete remission (P = 0.006) and a shorter time to complete remission (P < 0.001). CONCLUSION: The finding that the homozygous FcγRIIa 519AA variant was associated with complete response and a shorter time to complete response in the RAVE trial, independent of treatment type, implies that FcγRIIa may be broadly involved in disease pathogenesis and response to therapy.


Subject(s)
Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/drug therapy , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/genetics , Cyclophosphamide/therapeutic use , Cytochrome P-450 Enzyme System/physiology , Immunologic Factors/therapeutic use , Immunosuppressive Agents/therapeutic use , Receptors, IgG/physiology , Rituximab/therapeutic use , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/enzymology , Antibodies, Antineutrophil Cytoplasmic , Cohort Studies , Humans , Remission Induction
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