Progress in characterizing ABC multidrug transporters in zebrafish.

Zebrafish have proved to be invaluable for modeling complex physiological processes shared by all vertebrate animals. Resistance of cancers and other diseases to drug treatment can occur owing to expression of the ATP-dependent multidrug transporters ABCB1, ABCG2, and ABCC1, either because of expression of these transporters by the target cells to reduce intracellular concentrations of cytotoxic drugs at barrier sites such as the blood-brain barrier (BBB) to limit penetration of drugs into privileged compartments, or by affecting the absorption, distribution, and excretion of drugs administered orally, through the skin, or directly into the bloodstream. We describe the drug specificity, cellular localization, and function of zebrafish orthologs of multidrug resistance ABC transporters with the goal of developing zebrafish models to explore the physiological and pathophysiological functions of these transporters. Finally, we provide context demonstrating the utility of zebrafish in studying cancer drug resistance. Our ultimate goal is to improve treatment of cancer and other diseases which are affected by ABC multidrug resistance transporters.

Parental experiences related to pediatric and adolescent chronic non-cancer pain: A qualitative exploration.

PURPOSE: To explore parental experiences in personal functioning and parenting associated with having a child experiencing chronic non-cancer pain. METHODS: Parents with children experiencing chronic pain were asked to fill out a survey prior to their initial Pediatric Pain Clinic or Pain Psychology appointment at a children's hospital in the southeastern United States. A retrospective analysis of qualitative data was conducted. Qualitative results from open-ended survey questions will be focused on within this manuscript. FINDINGS: A total of 288 surveys were collected in this study, with 243 participants answering at least one qualitative question. Of participants who responded to open-ended survey questions, there were 88 responses to a question related to parental change, 73 to parental impact, and 239 to goals of the visit. Through thematic analysis, five qualitative themes were identified: Pain Central: The Hub, Juggling Life, Suffering Side by Side, Unrealized Dreams, and Gettin' it Under Control. DISCUSSION: Parents do experience alterations in personal functioning and parenting as a result of having a child that experiences chronic non-cancer pain. Parents face struggles in many aspects of life including emotions, work, and interpersonal relationships. Theoretical considerations were discussed. APPLICATION TO PRACTICE: Understanding the experiences parents have in raising a child with chronic pain is important in helping health care providers to recognize that this population may need interventions. This also assists in informing patient treatment, improving patient and parent care outcomes, and educating clinicians on how to better support parents.

Modified Training Experiences for Psychology Interns and Fellows During COVID-19: Use of Telepsychology and Telesupervision by Child and Adolescent Training Programs.

Coronavirus (COVID-19) has affected opportunities available to psychology interns and postdoctoral fellows completing capstone training experiences during culminating training years. While research supports COVID-19 has increased the use of telepsychology services amongst psychologists, there is a paucity of research regarding how COVID-19 has altered training and use of telepsychology by psychology trainees. The current study includes survey responses from 59 psychology training directors and 58 psychology internship and postdoctoral fellowship trainees at pediatric sites throughout the United States. Results support changes in telepsychology training provided during COVID-19, including increased use of telepsychology for clinical service delivery and increased use of telesupervision for training. As expected, findings suggest novel training experiences in telepsychology for trainees within the last two years as a result of COVID-19. Given ongoing need for telepsychology services to assure access to psychological care during the pandemic and beyond, results provide support for graduate and advanced training programs to provide formal training in best-practices for utilization of telepsychology and telesupervision.

Pre-hospital qSOFA as a predictor of sepsis and mortality.

BACKGROUND: The quick sequential organ failure assessment score (qSOFA) has been proposed as a simple tool to identify patients with sepsis who are at risk for poor outcomes. Its utility in the pre-hospital setting has not been fully elucidated. METHODS: This is a retrospective observational study of adult patients arriving by ambulance in September 2016 to an academic emergency department in Fresno, California. The qSOFA score was calculated from pre-hospital vital signs. We investigated its association with sepsis, ED diagnosis of infection, and mortality. RESULTS: Of 2292 adult medical patients transported by ambulance during the study period, the sensitivity of qSOFA for sepsis and in-hospital mortality were 42.9% and 40.6%, respectively. Specificity of qSOFA for sepsis and mortality were 93.8% and 91.9%, respectively. Of those with an ED diagnosis of infection compared to all patients, qSOFA was more specific but less sensitive for sepsis. Increasing qSOFA score was associated with a discharge diagnosis of sepsis (OR 4.21, 95% CI 3.41-5.21, p < 0.001), in-hospital mortality (OR 3.30, 95% CI 2.28-4.78, p < 0.001), and ED diagnosis of infection (OR 1.37, 95% CI 1.18-1.58, p < 0.001). Higher qSOFA score was associated with triage to a higher acuity zone and longer hospital and ICU length of stay, but not up-triage during ED stay. CONCLUSIONS: Pre-hospital qSOFA is specific, but poorly sensitive, for sepsis and sepsis outcomes, especially among patients with an ED diagnosis of infection. Higher qSOFA score was associated with worse outcomes.

Exploring quality of life in postural orthostatic tachycardia syndrome: A conceptual analysis.

Postural Orthostatic Tachycardia Syndrome (POTS) is a complex autonomic disorder characterized by an abnormal increase in heart rate upon orthostatic change. While primarily described in its effect on the autonomic and cardiovascular system, it can cause significant functional impairment, leading to a diminished quality of life (QoL). This review paper aims to delve into the multifaceted dimensions of QoL in individuals with POTS by providing a conceptual model to discuss factors influencing QoL. Current QoL assessments used in the POTS population and their findings are described for each domain in this conceptual model. Limitations to this body of research include the literature having no consensus in the most appropriate measure of QoL to use for individuals with POTS, the absence of a POTS-specific measure of QoL, and current measures not assessing concerns germane to this population. The authors emphasize the necessity of a POTS-specific measure to be developed to improve our assessment and understanding of how living with POTS impacts QoL.

The Role of Psychology in Pediatric Rheumatic Diseases.

Pediatric rheumatic diseases (PRDs) are a heterogeneous group of diseases that can have a chronic unpredictable disease course that can negatively affect mood, functioning, and quality of life. Given the range of difficulties faced in managing PRDs, as well as the psychosocial issues youth with these diseases experience, pediatric psychologists can be well suited to address concerns that arise in care for youth with PRDs including adherence, cognitive assessment, pain management, functional disability, and mood. Potential ways that pediatric psychologists can address these concerns and be embedded within an interdisciplinary treatment plan for youth with PRDs are described.

Utilization of an Educational Liaison for Coordinated Care Between the Medical Home and School-Based Professionals for Students with Chronic Pain.

BACKGROUND: Pediatric programs focused on treating chronic pain often do not include an educational liaison (EL) to coordinate services between the patient's medical home and school. As chronic pain in youth can have deleterious effects on school functioning, collaboration between the medical home and the school system are needed to assure these students receive appropriate accommodations. CONTRIBUTIONS TO THEORY: This manuscript describes a model of coordinated care for students with chronic pain that includes a systemic strategy for collaborative care across settings. Specifically, the role of an EL is described in the context of advocating for the patient to receive appropriate educational accommodations. CONCLUSIONS: This paper provides a guide for caregivers and professionals to assure appropriate access to support services across settings. Recommendations are included for school accommodations and services to improve academic functioning and outcomes for students with chronic pain.

Abcg2a is the functional homolog of human ABCG2 expressed at the zebrafish blood-brain barrier.

Background: A principal protective component of the mammalian blood-brain barrier (BBB) is the high expression of the multidrug efflux transporters P-glycoprotein (P-gp, encoded by ABCB1) and ABCG2 (encoded by ABCG2) on the lumenal surface of endothelial cells. The zebrafish P-gp homolog Abcb4 is expressed at the BBB and phenocopies human P-gp. Comparatively little is known about the four zebrafish homologs of the human ABCG2 gene: abcg2a, abcg2b, abcg2c, and abcg2d. Here we report the functional characterization and brain tissue distribution of zebrafish ABCG2 homologs. Methods: To determine substrates of the transporters, we stably expressed each in HEK-293 cells and performed cytotoxicity and fluorescent efflux assays with known ABCG2 substrates. To assess the expression of transporter homologs, we used a combination of RNAscope in situ hybridization probes and immunohistochemistry to stain paraffin-embedded sections of adult and larval zebrafish. Results: We found Abcg2a had the greatest substrate overlap with ABCG2, and Abcg2d appeared to be the least functionally similar. We identified abcg2a as the only homolog expressed at the adult and larval zebrafish BBB, based on its localization to claudin-5 positive brain vasculature. Conclusions: These results demonstrate the conserved function of zebrafish Abcg2a and suggest that zebrafish may be an appropriate model organism for the studying the role of ABCG2 at the BBB.

Abcg2a is the functional homolog of human ABCG2 expressed at the zebrafish blood-brain barrier.

BACKGROUND: A principal protective component of the mammalian blood-brain barrier (BBB) is the high expression of the multidrug efflux transporters P-glycoprotein (P-gp, encoded by ABCB1) and ABCG2 (encoded by ABCG2) on the lumenal surface of endothelial cells. The zebrafish P-gp homolog Abcb4 is expressed at the BBB and phenocopies human P-gp. Comparatively little is known about the four zebrafish homologs of the human ABCG2 gene: abcg2a, abcg2b, abcg2c, and abcg2d. Here we report the functional characterization and brain tissue distribution of zebrafish ABCG2 homologs. METHODS: To determine substrates of the transporters, we stably expressed each in HEK-293 cells and performed cytotoxicity and fluorescent efflux assays with known ABCG2 substrates. To assess the expression of transporter homologs, we used a combination of RNAscope in situ hybridization probes and immunohistochemistry to stain paraffin-embedded sections of adult and larval zebrafish. RESULTS: We found Abcg2a had the greatest substrate overlap with ABCG2, and Abcg2d appeared to be the least functionally similar. We identified abcg2a as the only homolog expressed at the adult and larval zebrafish BBB, based on its localization to claudin-5 positive brain vasculature. CONCLUSIONS: These results demonstrate the conserved function of zebrafish Abcg2a and suggest that zebrafish may be an appropriate model organism for studying the role of ABCG2 at the BBB.

The thiol methyltransferase activity of TMT1A (METTL7A) is conserved across species.

Although few resistance mechanisms for histone deacetylase inhibitors (HDACis) have been described, we recently demonstrated that TMT1A (formerly METTL7A) and TMT1B (formerly METTL7B) can mediate resistance to HDACis with a thiol as the zinc-binding group by methylating and inactivating the drug. TMT1A and TMT1B are poorly characterized, and their normal physiological role has yet to be determined. As animal model systems are often used to determine the physiological function of proteins, we investigated whether the ability of these methyltransferases to methylate thiol-based HDACis is conserved across different species. We found that TMT1A was conserved across rats, mice, chickens, and zebrafish, displaying 85.7%, 84.8%, 60.7%, and 51.0% amino acid sequence identity, respectively, with human TMT1A. Because TMT1B was not found in the chicken or zebrafish, we focused our studies on the TMT1A homologs. HEK-293 cells were transfected to express mouse, rat, chicken, or zebrafish homologs of TMT1A and all conferred resistance to the thiol-based HDACIs NCH-51, KD-5170, and romidepsin compared to empty vector-transfected cells. Additionally, all homologs blunted the downstream effects of HDACi treatment such as increased p21 expression, increased acetylated histone H3, and cell cycle arrest. Increased levels of dimethylated romidepsin were also found in the culture medium of cells transfected to express any of the TMT1A homologs after a 24 h incubation with romidepsin compared to empty-vector transfected cells. Our results indicate that the ability of TMT1A to methylate molecules is conserved across species. Animal models may therefore be useful in elucidating the role of these enzymes in humans.

Ibrutinib disrupts blood-tumor barrier integrity and prolongs survival in rodent glioma model.

In malignant glioma, cytotoxic drugs are often inhibited from accessing the tumor site due to the blood-tumor barrier (BTB). Ibrutinib, FDA-approved lymphoma agent, inhibits Bruton tyrosine kinase (BTK) and has previously been shown to independently impair aortic endothelial adhesion and increase rodent glioma model survival in combination with cytotoxic therapy. Yet additional research is required to understand ibrutinib's effect on BTB function. In this study, we detail baseline BTK expression in glioma cells and its surrounding vasculature, then measure endothelial junctional expression/function changes with varied ibrutinib doses in vitro. Rat glioma cells and rodent glioma models were treated with ibrutinib alone (1-10 µM and 25 mg/kg) and in combination with doxil (10-100 µM and 3 mg/kg) to assess additive effects on viability, drug concentrations, tumor volume, endothelial junctional expression and survival. We found that ibrutinib, in a dose-dependent manner, decreased brain endothelial cell-cell adhesion over 24 h, without affecting endothelial cell viability (p < 0.005). Expression of tight junction gene and protein expression was decreased maximally 4 h after administration, along with inhibition of efflux transporter, ABCB1, activity. We demonstrated an additive effect of ibrutinib with doxil on rat glioma cells, as seen by a significant reduction in cell viability (p < 0.001) and increased CNS doxil concentration in the brain (56 ng/mL doxil alone vs. 74.6 ng/mL combination, p < 0.05). Finally, Ibrutinib, combined with doxil, prolonged median survival in rodent glioma models (27 vs. 16 days, p < 0.0001) with brain imaging showing a - 53% versus - 75% volume change with doxil alone versus combination therapy (p < 0.05). These findings indicate ibrutinib's ability to increase brain endothelial permeability via junctional disruption and efflux inhibition, to increase BTB drug entry and prolong rodent glioma model survival. Our results motivate the need to identify other BTB modifiers, all with the intent of improving survival and reducing systemic toxicities.

The Methyltransferases METTL7A and METTL7B Confer Resistance to Thiol-Based Histone Deacetylase Inhibitors.

Histone deacetylase inhibitors (HDACi) are part of a growing class of epigenetic therapies used for the treatment of cancer. Although HDACis are effective in the treatment of T-cell lymphomas, treatment of solid tumors with this class of drugs has not been successful. Overexpression of the multidrug resistance protein P-glycoprotein (P-gp), encoded by ABCB1, is known to confer resistance to the HDACi romidepsin in vitro, yet increased ABCB1 expression has not been associated with resistance in patients, suggesting that other mechanisms of resistance arise in the clinic. To identify alternative mechanisms of resistance to romidepsin, we selected MCF-7 breast cancer cells with romidepsin in the presence of the P-gp inhibitor verapamil to reduce the likelihood of P-gp-mediated resistance. The resulting cell line, MCF-7 DpVp300, does not express P-gp and was found to be selectively resistant to romidepsin but not to other HDACis such as belinostat, panobinostat, or vorinostat. RNA-sequencing analysis revealed upregulation of the mRNA coding for the putative methyltransferase, METTL7A, whose paralog, METTL7B, was previously shown to methylate thiol groups on hydrogen sulfide and captopril. As romidepsin has a thiol as the zinc-binding moiety, we hypothesized that METTL7A could inactivate romidepsin and other thiol-based HDACis via methylation of the thiol group. We demonstrate that expression of METTL7A or METTL7B confers resistance to thiol-based HDACis and that both enzymes are capable of methylating thiol-containing HDACis. We thus propose that METTL7A and METTL7B confer resistance to thiol-based HDACis by methylating and inactivating the zinc-binding thiol.

"You Look Perfectly Healthy to Me": Living With Postural Orthostatic Tachycardia Syndrome Through Adolescents' and Parents' Eyes.

Postural orthostatic tachycardia syndrome (POTS) is an autonomic dysfunction that impairs quality of life (QoL). Increased familiarity with the lived experiences of youth with POTS better informs our understanding of this condition and its impact on QoL, provides context and depth to existing research, and improves patient-centered care. Thus, this qualitative study seeks to develop a more robust understanding of QoL in this understudied population. Youth with POTS (N = 6) and their parents (N = 8) participated in semi-structured interviews. Following saturation, data were analyzed via conventional content analysis, including code/theme identification and member-checking. Four themes were identified (1) negative changes in functioning, (2) invalidation and difficulties living with an invisible condition, (3) trust and advocacy, and (4) need for increased resources and understanding. Findings suggest POTS negatively impacts adolescents' QoL across domains. Based on participants' responses, developing POTS-specific resources and integrating mental health services into interdisciplinary POTS treatment may improve youth's QoL.

The Multidrug Resistance Transporter P-glycoprotein Confers Resistance to Ferroptosis Inducers.

Ferroptosis is a form of cell death caused by direct or indirect inhibition of glutathione peroxidase 4 that leads to lethal lipid peroxidation. Several small molecule ferroptosis inducers (FINs) have been reported, yet little information is available regarding resistance mechanisms, particularly their interaction with the ATP-binding cassette (ABC) transporters P-glycoprotein (P-gp, ABCB1) and ABCG2. Given the role that ABC transporters play in absorption, distribution, and excretion of many drugs, characterizing these interactions could provide information regarding oral bioavailability and brain penetration and may predict drug-drug interactions. Using ferroptosis-sensitive A673 cells transfected to express P-gp or ABCG2, we found that P-gp overexpression was able to confer resistance to FIN56 and the erastin derivatives imidazole ketone erastin and piperazine erastin. Results were confirmed with OVCAR8-derived NCI/ADR-RES cells that overexpress P-gp, where the P-gp inhibitor valspodar completely inhibited resistance to the FINs. P-gp-mediated resistance to imidazole ketone erastin and piperazine erastin was also reversed in UO-31 renal cancer cells by CRISPR-mediated knockout of ABCB1. At a concentration of 10 µM, the FINs ML-162, GPX inhibitor 26a, and PACMA31 were able to increase intracellular rhodamine 123 fluorescence over 10-fold in P-gp-expressing MDR-19 cells and GPX inhibitor 26a was able to increase intracellular purpurin-18 fluorescence over 4-fold in ABCG2-expressing R-5 cells. Expression of P-gp may reduce the efficacy of these FINs in cancers that express the transporter and may prevent access to sanctuary sites such as the brain. The ability of some FINs to inhibit P-gp and ABCG2 suggests potential drug-drug interactions.

The thiol methyltransferase activity of TMT1A (METTL7A) is conserved across species.

Although few resistance mechanisms for histone deacetylase inhibitors (HDACis) have been described, we recently demonstrated that TMT1A (formerly METTL7A) and TMT1B (formerly METTL7B) can mediate resistance to HDACis with a thiol as the zinc-binding group by methylating and inactivating the drug. TMT1A and TMT1B are poorly characterized, and their normal physiological role has yet to be determined. As animal model systems are often used to determine the physiological function of proteins, we investigated whether the ability of these methyltransferases to methylate thiol-based HDACis is conserved across different species. We found that TMT1A was conserved across rats, mice, chickens, and zebrafish, displaying 85.7%, 84.8%, 60.7% and 51.0% amino acid sequence identity, respectively, with human TMT1A. Because TMT1B was not found in the chicken or zebrafish, we focused our studies on the TMT1A homologs. HEK-293 cells were transfected to express mouse, rat, chicken, or zebrafish homologs of TMT1A and all conferred resistance to the thiol-based HDACIs NCH-51, KD-5170 and romidepsin compared to empty vector-transfected cells. Additionally, all homologs blunted the downstream effects of HDACi treatment such as increased p21 expression, increased acetylated histone H3, and cell cycle arrest. Increased levels of dimethylated romidepsin were also found in the culture medium of cells transfected to express any of the TMT1A homologs after a 24 h incubation with romidepsin compared to empty-vector transfected cells. Our results indicate that the ability of TMT1A to methylate molecules is conserved across species. Animal models may therefore be useful in elucidating the role of these enzymes in humans.

The multidrug resistance transporter P-glycoprotein confers resistance to ferroptosis inducers.

Aim: Ferroptosis is a non-apoptotic form of cell death caused by lethal lipid peroxidation. Several small molecule ferroptosis inducers (FINs) have been reported, yet little information is available regarding their interaction with the ATP-binding cassette (ABC) transporters P-glycoprotein (P-gp, ABCB1) and ABCG2. We thus sought to characterize the interactions of FINs with P-gp and ABCG2, which may provide information regarding oral bioavailability and brain penetration and predict drug-drug interactions. Methods: Cytotoxicity assays with ferroptosis-sensitive A673 cells transfected to express P-gp or ABCG2 were used to determine the ability of the transporters to confer resistance to FINs; confirmatory studies were performed in OVCAR8 and NCI/ADR-RES cells. The ability of FINs to inhibit P-gp or ABCG2 was determined using the fluorescent substrates rhodamine 123 or purpuin-18, respectively. Results: P-gp overexpression conferred resistance to FIN56 and the erastin derivatives imidazole ketone erastin and piperazine erastin. P-gp-mediated resistance to imidazole ketone erastin and piperazine erastin was also reversed in UO-31 renal cancer cells by CRISPR-mediated knockout of ABCB1. The FINs ML-162, GPX inhibitor 26a, and PACMA31 at 10 µM were able to increase intracellular rhodamine 123 fluorescence over 10-fold in P-gp-expressing MDR-19 cells. GPX inhibitor 26a was able to increase intracellular purpurin-18 fluorescence over 4-fold in ABCG2-expressing R-5 cells. Conclusion: Expression of P-gp may reduce the efficacy of these FINs in cancers that express the transporter and may prevent access to sanctuary sites such as the brain. The ability of some FINs to inhibit P-gp and ABCG2 suggests potential drug-drug interactions.

The Combination of Trametinib and Ganitumab is Effective in RAS-Mutated PAX-Fusion Negative Rhabdomyosarcoma Models.

PURPOSE: PAX-fusion negative rhabdomyosarcoma (FN RMS) is driven by alterations in the RAS/MAP kinase pathway and is partially responsive to MEK inhibition. Overexpression of IGF1R and its ligands is also observed in FN RMS. Preclinical and clinical studies have suggested that IGF1R is itself an important target in FN RMS. Our previous studies revealed preclinical efficacy of the MEK1/2 inhibitor, trametinib, and an IGF1R inhibitor, BMS-754807, but this combination was not pursued clinically due to intolerability in preclinical murine models. Here, we sought to identify a combination of an MEK1/2 inhibitor and IGF1R inhibitor, which would be tolerated in murine models and effective in both cell line and patient-derived xenograft models of RAS-mutant FN RMS. EXPERIMENTAL DESIGN: Using proliferation and apoptosis assays, we studied the factorial effects of trametinib and ganitumab (AMG 479), a mAb with specificity for human and murine IGF1R, in a panel of RAS-mutant FN RMS cell lines. The molecular mechanism of the observed synergy was determined using conventional and capillary immunoassays. The efficacy and tolerability of trametinib/ganitumab was assessed using a panel of RAS-mutated cell-line and patient-derived RMS xenograft models. RESULTS: Treatment with trametinib and ganitumab resulted in synergistic cellular growth inhibition in all cell lines tested and inhibition of tumor growth in four of six models of RAS-mutant RMS. The combination had little effect on body weight and did not produce thrombocytopenia, neutropenia, or hyperinsulinemia in tumor-bearing SCID beige mice. Mechanistically, ganitumab treatment prevented the phosphorylation of AKT induced by MEK inhibition alone. Therapeutic response to the combination was observed in models without a mutation in the PI3K/PTEN axis. CONCLUSIONS: We demonstrate that combined trametinib and ganitumab is effective in a genomically diverse panel of RAS-mutated FN RMS preclinical models. Our data also show that the trametinib/ganitumab combination likely has a favorable tolerability profile. These data support testing this combination in a phase I/II clinical trial for pediatric patients with relapsed or refractory RAS-mutated FN RMS.

The Role of Psychology in Pediatric Rheumatic Diseases.

Pediatric rheumatic diseases (PRDs) are a heterogeneous group of diseases that can have a chronic unpredictable disease course that can negatively affect mood, functioning, and quality of life. Given the range of difficulties faced in managing PRDs, as well as the psychosocial issues youth with these diseases experience, pediatric psychologists can be well suited to address concerns that arise in care for youth with PRDs including adherence, cognitive assessment, pain management, functional disability, and mood. Potential ways that pediatric psychologists can address these concerns and be embedded within an interdisciplinary treatment plan for youth with PRDs are described.

Implementation of telehealth during COVID-19: Implications for providing behavioral health services to pediatric patients.

The coronavirus pandemic and in-person contact restrictions necessitated rapid implementation of telehealth, specifically videoconferencing, to provide essential care to patients. This study surveyed 25 pediatric behavioral health providers at a single center during their first month of utilizing telehealth during coronavirus disease 2019 (COVID-19). Twenty-one participants completed a pre-questionnaire distributed prior to telehealth service delivery, and 23 providers completed a post-questionnaire approximately three weeks later. Results indicate the majority of behavioral health providers had no experience providing telehealth services prior to COVID-19. The majority of participating behavioral health providers utilized telehealth to provide pediatric patient care within the first month of access to telehealth. Participants' confidence in their ability to provide telehealth services significantly increased within the first month of implementation, regardless of previous training in telehealth. This study identified differences between anticipated and actual barriers to treatment, with technological issues identified as the largest actual barrier to service delivery. Participants indicated a preference for in-person service delivery, which they reported allows for better rapport-building, behavioral observations, reduced technological barriers, and fewer distractions. However, most participants reported they intend to continue utilizing telehealth for certain types of behavioral health services (e.g., diagnostic interviews and outpatient therapy) after the pandemic has subsided.

Preappointment surveys and reminder calls to improve show rate.

OBJECTIVES: To assess the impact of preappointment surveys and reminder phone calls on show rate and time spent in new patient appointments at a multidisciplinary pediatric chronic pain clinic. STUDY DESIGN: We examined show rates and appointment length during the 1-year period before and 1-year period after a preappointment survey and phone reminders were implemented. Fisher exact test was used for categorical variables and Student's t test with equal variances was used for continuous variables. METHODS: The setting was a multidisciplinary pediatric chronic pain management clinic in Florida. Participants were 362 patients scheduled for an initial pain clinic evaluation 1 year prior to and after the implementation of a preappointment survey on August 19, 2019. Our main outcome measures were show rate and appointment length. RESULTS: Patients who completed a preappointment survey were significantly more likely to attend their clinic appointment than noncompleters (97.2% vs 36.2%) and spent significantly less time in their appointment. CONCLUSIONS: With new patients, preappointment surveys can improve clinic show rate and decrease time spent in initial appointments. Clinics may consider policies targeting completion of preappointment surveys to assist with show rate, but they must consider their patients' barriers to completing surveys so access to care is not limited.