Trends and risk factors for readmissions following press-fit total knee arthroplasty for the treatment of end-stage osteoarthritis of the knee: a five-year analysis.

INTRODUCTION: The development of new prostheses with improved osseointegration, bone preservation, and reduced cost has renewed interest in uncemented total knee arthroplasty (UCTKA). In the current study, we aimed to: (1) assess demographic data of patients who were and were not readmitted and (2) identify patient-specific risk factors associated with readmission. METHODS: A retrospective query from the PearlDiver database was performed from January 1, 2015, to October 31, 2020. International Classification of Disease, Ninth Revision (ICD-9), ICD-10, or Current Procedural Terminology (CPT) coding was used to distinguish cohorts of patients who had osteoarthritis of the knee and underwent UCTKA. Patients readmitted within 90 days were classified as the study population, while those who were not readmitted were classified as control. A linear regression model was utilized to analyze readmission risk factors. RESULTS: The query yielded 14,575 patients, with 986 (6.8%) being readmitted. Patient demographics such as age (P < 0.0001), sex (P < 0.009), and comorbidity (P < 0.0001) were associated with annual 90-day readmission. Patient-specific risk factors associated with 90-day readmission following press-fit total knee arthroplasty were: arrhythmia (OR: 1.29, 95% CI: 1.11-1.49, P < 0.0005), coagulopathy (OR: 1.36, 95% CI: 1.13-1.63, P < 0.0007), fluid and electrolyte abnormalities (OR: 1.59, 95% CI: 1.38-1.84, P < 0.0001), iron deficiency anemia (OR: 1.49, 95% CI: 1.27-1.73, P < 0.0001), and obesity (OR: 1.37, 95% CI: 1.18-1.60, P < 0.0001). DISCUSSION: This study demonstrates that patients with comorbidities, such as fluid and electrolyte problems, iron deficiency anemia, and obesity, were at an increased risk of readmission after having an uncemented total knee replacement. The risks of readmission following an uncemented total knee arthroplasty can be discussed with patients who have certain comorbidities by arthroplasty surgeons.

The Effects of Genetic Mutations and Drugs on the Activity of the Thiamine Transporter, SLC19A2.

A rare cause of megaloblastic anemia (MA) is thiamine-responsive megaloblastic anemia (TRMA), a genetic disorder caused by mutations in SLC19A2 (encoding THTR1), a thiamine transporter. The study objectives were to (1) functionally characterize selected TRMA-associated SLC19A2 variants and (2) determine whether current prescription drugs associated with drug-induced MA (DIMA) may act via inhibition of SLC19A2. Functional characterization of selected SLC19A2 variants was performed by confocal microscopy and isotopic uptake studies of [3H]-thiamine in HEK293 cells. Sixty-three drugs associated with DIMA were screened for SLC19A2 inhibition in isotopic uptake studies. Three previously uncharacterized SLC19A2 variants identified in TRMA patients exhibited disrupted localization to the plasma membrane along with near-complete loss-of-function. Ten of 63 drugs inhibited SLC19A2-mediated thiamine transport ≥ 50% at screening concentrations; however, with the exception of erythromycin, none was predicted to inhibit SLC19A2 at clinically relevant unbound plasma concentrations. Data from electronic health records revealed reduced levels of thiamine pyrophosphate (TPP) in patients prescribed erythromycin, consistent with inhibition of SLC19A2-mediated thiamine transport. Here, we confirmed the role of three SLC19A2 variants in TRMA pathology. Additionally, we report that inhibition of SLC19A2 is a potential, but uncommon mechanism for DIMA.