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The Role of Epigenetic Aberrations in The Cold Tumor Phenotype And Inflammatory Signaling in High-Risk Neuroblastoma
Full text linkNeuroblastoma (NB) is a highly aggressive, heterogeneous disease that arises from the sympathetic nervous system (SNS) and originates from neural crest cells (NCCs) (1). NB is the most common extracranial cancer in pediatric accounts for 15% of pediatric cancer deaths (2). This high mortality rate is the result of the metastatic, immune evasive, and treatment resistant characteristics of the disease (3). It has been proposed that NB arises from blocks in differentiation during development, resulting in a mixture of two distinct cell types within the tumor: mesenchymal and adrenergic (Figure 1.1) (4,5). The adrenergic cell type is more differentiated, and patients that exhibit more of this cell type have greater treatment success. The mesenchymal cell type is more stem like and is associated with the metastatic, immune evasive, and treatment resistant traits of NB (6,7). Because NB is considered a disease of development, many therapeutic strategies targeting epigenetic factors are being investigated in pre-clinical and clinical trials. Our work is currently focused on interrogating how the loss of ARID1A, a component of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex, affects NB’s oncogenesis and the immune evasive effects of the mesenchymal cell type. The successful completion of this project will 1) determine if ARID1A loss is a critical component for immune suppression by collapsing inflammatory signaling, and 2) examine three epigenetic therapies to develop better strategies for increasing immune infiltration and targets to immunotherapies common for NB. NB patient samples have been sequenced extensively (8), and it has been reported that there is a low median exonic mutation frequency as well as few recurrently mutated genes (9). This does not allow for many potential therapeutic targets, and even multimodal therapy can be unsuccessful and lead to relapse. Many recent studies focus on the chromosomal instability events that take place in NB and aberrant epigenetic regulation during NCC development (10). 1p36 loss of heterozygosity (LOH) occurs in around 29% of high-risk NB patients which has been linked to the treatment resistant (1-6) and immunologically suppressed phenotype. Previously, the Freeman lab established that one of the main tumor suppressors located in this area is ARID1A (5,11). Recent data reports that ARID1A has a role in initiating inflammatory signaling in adult cancers by opening areas of chromatin thereby enabling the transcription of Th1 signaling genes (13-19), but this immune impairment has not been sufficiently investigated in NB. NB is considered a cold tumor, a designation characterized by a lack of infiltrating CD8+ T cells, NK cells, and NK-T cells in the tumor microenvironment; low MHC-I expression; and lack of tumor antigens (20-22). These characteristics further decrease therapeutic options for patients (6, 11), and the few options that are available can lead to severe toxicities and adverse events. Disialoganglioside GD2 therapy is one form of immunotherapy for NB (11), which has only a 40% efficacy rate when paired with cytokine stimulation in NB patients (9). Strategies to improve treatment outcomes with anti-GD2 therapy are essential to limiting adverse reactions to the treatment and increase efficacy. One such strategy is combining common immunotherapies with epigenetic therapies. By overcoming aberrant epigenetic regulation, inflammatory sensing can increase leading to greater immunotherapy treatment outcomes. As stated previously, ARID1A loss has been linked in adult cancers to a decrease in Th1 signaling responses, specifically inflammatory signals, which lead to a lack of immune infiltration by NK cells and CD8+ T cells (28-30). Previously, the Freeman lab established that aberrant epigenetic regulation including ARID1A loss, not MYCN amplification, is a cause for cellular immaturity, developmental blocks, and cell state plasticity in NB;
LAI Antipsychotics vs. Oral Antipsychotics: Treatment adherence, Relapses, and Readmissions
Full text linkPurpose/Background
Schizophrenia is a lifelong illness with recurrent and often debilitating symptoms that may impair daily functioning, cognition, behaviors, socialization, emotions, and expression. It is recognized as a global mental health burden that affects the individual, their family, and society. Medication nonadherence and resulting relapse detrimentally affect the patient’s physical and mental health and quality of life. They are associated with increased hospitalization and emergency room visits, substance use, suicide, and homelessness. Current guidelines endorse second-generation antipsychotics such as Risperidone and Aripiprazole as the first-line treatment for most cases of psychosis. However, long-acting injectable (LAIs) atypical antipsychotics are a promising alternative to overcome noncompliance in treating Schizophrenia and help increase treatment adherence, decrease the likelihood of discontinuation, and provide better symptom management. The purpose of this project is to assess the benefits long-acting injectable antipsychotics have on treatment adherence, decreased re-hospitalizations, and relapses for treating individuals with schizophrenia.
Methods
This retrospective chart review was performed at Vanderbilt Adult Psychiatry Outpatient Clinic (VPH-OP) via electronic database access by an EMR Analysts (EStar), where participants were selected based on inclusion criteria for the long-acting injectables group and the oral antipsychotic group. Inclusion criteria included current establishment as a patient at the VPH-OP Clinic, greater than 18 years of age, a diagnosis of schizophrenia spectrum disorders and bipolar disorders per the DSM-5, and current treatment with antipsychotic medication. Participants who met criteria based on medication were randomized into the long-acting injectable group (n-15) and oral antipsychotic group (n=15). Data was collected in the Redcap data collection tool for deidentification and included age, race, gender, diagnosis, oral or long-acting injectable medication, missed appointments, in-patient hospitalizations, and whether the medication was changed, maintained, or discontinued. Data was collected from October 1, 2022, to October 31, 2023. The study was approved by the respective Institutional Review Boards.
Results
The study showed that there is no significant difference in inpatient hospitalization between oral antipsychotics and long-acting antipsychotics. 3 out of 15 LAIs compared to 3 out of 15 oral antipsychotics participants had inpatient hospitalizations. The study showed a slight significant difference in medication changes, discontinuation, and missed medication appointments. In 3 out of 15 LAIs compared to 4 out of 15 oral antipsychotic participants, medication was changed or discontinued. 9 out of 15 LAIs compared to 10 out of 15 oral antipsychotics out of 15 LAIs compared to 10 out of 15 oral antipsychotics participants missed medication appointments.
Implications for Nursing Practice
The study shows there are some beneficial aspects to using LAIs compared to oral antipsychotics. Future studies with a larger sample size would be beneficial to evaluate treatment adherence and examine statistical differences between LAIs and oral antipsychotics in patients with schizophrenia. Adherence to treatment for schizophrenia has been a difficult task due to the complicated symptomology of side effects associated with antipsychotic medications. Continuous studies to find the most efficient medications are imperative to help advance the treatment of individuals with schizophrenia
Loss of the SAC Components SldA Kinase or SldB or in vitro Adaptation to Triazole Produces Aneuploidy Associated with Triazole Heteroresistance in Aspergillus fumigatus
Full text linkThe opportunistic pathogen Aspergillus fumigatus represents the chief causative agent of human and animal invasive filamentous fungal infections. Triazoles, the primary therapeutic options to combat invasive aspergillosis (IA), target the fungal biosynthesis of ergosterol, a vital component of the fungal cell membrane. Unfortunately, resistance to this class of medical therapeutic has arisen globally and now threatens the future usefulness of these compounds for antifungal treatment. Infection with A. fumigatus that has acquired triazole resistance increases an already high associated mortality rate and reduces the limited arsenal of therapeutic options to combat IA. Moreover, how this specific fungal pathogen obtains resistance remains poorly understood. In this study, we show that loss of the previously uncharacterized A. fumigatus Spindle Assembly Checkpoint components SldA or SldB results in loss of susceptibility to multiple mold active medical triazoles. Furthermore, these mutants possess reduced susceptibility to antifungal compounds targeting ergosterol biosynthesis at points upstream of the triazole target Cyp51A. Loss of either component also results in signs of aneuploidy within uninucleate conidia in flow cytometry analyses for DNA content. Finally, exposure to voriconazole through laboratory experimental adaptation resulted in decreased triazole susceptibility, increased detection of sub populations of aneuploid spores in all samples of mutant as well as wild type lineages, and selection for a specific duplication in chromosome two in most lineages. Subsequent passages of adapted strains in drug-free media revealed adaptation to be unstable in most cases, with loss of adaptations typically occurring with simultaneous resolution of conidial aneuploidy, suggesting a correlation between aneuploidy and antifungal resistance in this pathogen. Together, these findings illustrate a previously unknown connection in A. fumigatus between defective function of the conserved surveillance system designed to prevent aberrant sorting of genomic material during nuclear division, and loss of susceptibility to antifungal compounds that target ergosterol biosynthesis. This knowledge helps to inform our understanding of how A. fumigatus survives and adapts to medical triazole antifungals
Evaluating Blood Pressure Methods in Non-traumatic Intracerebral Hemorrhage: A Two-site Prospective Observational Study
Full text linkPurpose. Blood pressure (BP) management is difficult and complex in the treatment of acute non-traumatic intracerebral hemorrhage (ICH). Despite mean arterial pressure (MAP) being the most reliable measure of noninvasive automatic oscillometric (NIBP) in clinical practice, clinicians instead rely on systolic and diastolic blood pressure (SBP and DBP) values to guide clinical practice. Given the widespread use of NIBPs for obtaining BP values in the acute care setting, we determine the agreement between SBP, DBP, and MAP measured by NIBP, manual cuff, and Arterial lines (A-lines) in patients with ICH. Study Aims. To understand the agreement between SBP, DBP, and MAP measured by manual sphygmomanometry performed by trained healthcare providers with 1) NIBP, and, if applicable, 2) A-line measurements in patients with acute non-traumatic ICH. Secondary aims were to explore the relationship between BP values, hematoma expansion and outcomes in death and disability in patients with ICH. Methods. Using established guidelines for the assessment of agreement between devices, a prospective observational study of agreement between BP methods (NIBP, manual, and A-line) was conducted in patients with ICH within the first 24 hours of admission at two comprehensive stroke centers (CSC). Investigators used a dual auscultatory stethoscope to validate each manual BP variable. Calculation of MAP was done for manual BPs using the standard formula. A-line measures were zeroed, leveled to the phlebostatic axis, and checked for proper waveforms prior to use. Data were analyzed using the Bland-Altman (BA) analyses. Results. Our study found no agreement in SBP, DBP, and MAP for 650 paired manual and NIBP measurements. NIBP measures were consistently lower than manual, with DBP (p = \u3c .001) measuring in the least agreement between methods, followed by SBP (p = .005), and the closest was MAP (p = \u3c .001) using BA analysis. The differences were also analyzed for the percentage of measurements that fell within a difference of 5, 10, 15, and 20 mmHg for SBP, DBP, and MAP separately. For SBP, 58% of the 650 sets of measures fell within 10 mmHg. For DBP, 63% fell within 10 mmHg. For MAP, 76% fell within 10 mmHg. For the 25 paired manual, NIBP, and A-line measurements, there was no agreement in SBP, DBP, and MAP, with MAP being the closest value in agreement between the methods, followed by DBP and then SBP. The A-line measures were consistently higher than Aline with manual measures. For our secondary aims, we found no relationship between the NIBP vs manual values with outcomes in patients with ICH. Conclusion. Theoretically, lowering BP decreases the risk of hematoma, making blood pressure control a top priority in acute ICH care. Before we can set forth targeted BP goals for ICH, research must be guided by valid BP measurements to further our understanding of the utility of aggressive BP lowering, as well as its safety in the care of patients with ICH. It is imperative that proper BP measurements are performed and appropriate treatment goals are established, making examination of the agreement between devices and continued exploration of the use of MAP paramount in the management of acute intracerebral hemorrhage
Removal of common antimicrobial agents by sustained low- efficiency dialysis
Full text linkAdequate dosing of antimicrobials is paramount for treating infections in critically ill patients undergoing kidney replacement therapy; however, little is known about antimicrobial removal by sustained low-efficiency dialysis (SLED). The objective was to quantify the removal of cefepime, daptomycin, meropenem, piperacillin–tazobactam, and vancomycin in patients undergoing SLED. Adult patients ≥18 years with acute kidney injury (AKI) or end-stage kidney disease receiving one of the select antimicrobials and requiring SLED were included. Blood and dialysate flow rates were maintained at 250 and 100 mL/min, respectively. Simultaneous arterial and venous blood samples for the analysis of antibiotic concentrations were collected hourly for 8 hours during SLED (on-SLED). Arterial samples were collected every 2 hours for up to 6 hours while not receiving SLED (off-SLED) for the calculation of SLED clearance, half-life (t1/2) on-SLED and off-SLED, and the fraction of removal by SLED (fD). Twenty-one patients completed the study: 52% male, mean age (±SD) 53 ± 13 years, and mean weight of 98 ± 30 kg. Eighty-six percent had AKI, and 4 patients were receiving cefepime, 3 daptomycin, 10 meropenem, 6 piperacillin–tazobactam, and 13 vancomycin. The average SLED time was 7.3 ± 1.1 hours, and the mean ultrafiltration rate was 95 ± 52 mL/hour (range 10–211). The t1/2 on-SLED was substantially lower than the off-SLED t1/2 for all antimicrobials, and the SLED fD varied between 44% and 77%. An 8-hour SLED session led to significant elimination of most antimicrobials evaluated. If SLED is performed, modification of the dosing regimen is warranted to avoid subtherapeutic concentrations
Molecular Determinants of TRP Channel Gating
Full text linkTransient Receptor Potential (TRP) ion channels are a family of proteins that contribute to a myriad of physiological functions. They have been extensively studied since their discovery 35 years ago; however, there are still many questions regarding the mechanisms by which they function. This family of proteins is characterized by a generally shared structure: an intracellular N terminus featuring ankyrin repeats, six transmembrane helices including the pore domain, a re-entrant loop and TRP helix, and an intracellular C terminus with varying structure. Each of these regions has been implicated in the regular function of TRPs, while mutations that alter trafficking or function have been found throughout these domains. Here, I describe my contribution to uncovering the mechanisms by which several of these channels are governed in various pathophysiological conditions, including hyperalgesia, gut barrier dysfunction, and ataxia. Thermal hyperalgesia is a condition in which previously innocuous stimuli become painful as a result of inflammatory responses. TRP Vanilloid member 1 (TRPV1) is a contributor to this process due to its involvement in temperature sensing. Phosphoinositides, a component of the plasma membrane that modulate the activity of various ion channels (including TRPV1), are cleaved in response to inflammatory signals. Their role in regulating TRPV1 activity is controversial. To address this role in TRPV1 function in vivo, we leveraged dietary supplementation, genetic dissection, and functional assays. We found that phosphoinositides are a negative regulator of channel activity in vivo and influence channel activity through a putative interaction site on the distal C terminus. These findings are discussed in further detail in Chapter 2. Chronic alcohol use is associated with many symptoms, including dysbiosis and organ damage, which are a consequence of alterations to the gut barrier. The specific events leading to the development of a leaky gut due to chronic alcohol intake require further study. An initial step in this process is a rise in intracellular Ca2+ at the gut epithelium. Hence, we explored the role of TRPV6, a Ca2+-selective channel expressed in the intestinal epithelium. Using in vitro and in vivo models of the gut barrier, as well as biochemical and functional assays, we found that TRPV6 is essential for the development of alcohol-associated changes in gut barrier function, likely through a site within the channel’s N-terminal ankyrin repeat domain. Additional information regarding this topic can be found in Chapter 3. Ataxia is a condition characterized by a loss in coordination, which can result from damage or degeneration of the body’s central motor axis. The Canonical TRP member 3 (TRPC3) is highly expressed in the cerebellum, where it modulates neuronal activity. Mutation of this channel results in neurodegeneration and ataxia. However, the mechanism by which this occurs is unclear. Accordingly, we utilized functional, behavioral, and structural techniques to reveal that mutant-associated enhancement in channel activity results in neurodegenerative phenotypes through a combination of molecular determinants. Chapter 4 includes a detailed discussion of these results. Taken together, these findings provide new insight into the mechanisms underlying TRP channel function, as well as reveal potential targets for modulating the activity of these proteins. This is an important step in developing strategies against pathophysiological changes associated with dysfunction of these channels
The Impact of Candida albicans Glycogen on Fitness, Virulence and Host Response
Full text linkCandida albicans is an opportunistic human fungal pathogen that presents in healthy persons colonizing the oropharyngeal, esophageal, and gastrointestinal mucosa. This polymorphic fungal pathogen remains a leading cause of both invasive and superficial mycoses. C. albicans can cause oropharyngeal candidiasis (OPC) and disseminated candidiasis when normal host immunity is disturbed, while also causing vulvovaginal candidiasis (VVC) in healthy women. Adaptation to different host niches requires rapid and coordinated changes in Candida metabolism and physiology to cope with host immune surveillance and to counteract host-imposed constraints such as glucose limitation. Although largely unexplored in C. albicans, the glycogen metabolism pathway is a vital carbon assimilation and utilization system shown to be metabolically important in the model yeast Saccharomyces cerevisiae. Aside from the soluble glycogen that potentially contributes to Candida metabolism, glycogen has also been reported to be covalently linked to the immunogenic pathogen-associated molecular pattern (PAMP) b-(1,3)-glucan via a b-(1,6)-linked side chain to form a glucan-glycogen macromolecular complex at the cell wall interface of C. albicans. However, the mechanism driving its incorporation, and the potential immunological consequence of cell wall glycogen content are still unclear. This work focuses on C. albicans glycogen, including its metabolism and regulatory mechanisms, closing knowledge gaps on their impact on Candida fitness, virulence and host-Candida interaction. In C. albicans, there are S. cerevisiae orthologs involved in glycogen metabolism but these proteins and pathways have not been functionally validated. We characterized glycogen metabolism pathways in C. albicans and investigated whether these impact C. albicans long-term survival both in vitro and in vivo during murine VVC or virulence during systemic infection. Genetic deletion and complementation of key genes involved in glycogen metabolism in S. cerevisiae confirmed that glycogen synthase (encoded by GSY1) and branching enzyme (encoded by GLC3), glycogen phosphorylase (encoded by GPH1) and debranching enzyme (encoded by GDB1) are essential for glycogen synthesis and catabolism in C. albicans, respectively. Potential compensatory roles for a glucoamylase encoded by SGA1 were also explored. Competitive survival assays revealed that gsy1∆/∆, gph1Δ/Δ and gph1∆/∆ sga1∆/∆ mutants exhibited long-term survival defects in vitro under starvation conditions and in vivo during vaginal colonization concomitant with reduced neutrophil recruitment. Complete inability to catabolize glycogen (gph1∆/∆sga1∆/∆) also rendered C. albicans significantly less virulent during disseminated candidiasis. Using nuclear magnetic resonance (NMR) profiling, we confirmed that dysregulation of glycogen synthesis ablated cell wall glycogen content that is typically covalently linked to the cell wall PAMP b-(1,3)-glucan. Challenge of human immune cells with fixed or live glycogen synthase mutant gsy1Δ/Δ led to exacerbated pro-inflammatory cytokine secretion (e.g., IL-1β) from macrophages or neutrophil swarming as compared to a WT or revertant strain. Antibody-mediated receptor neutralization confirmed that elevated cytokine release observed in human macrophages challenged with gsy1Δ/Δ was partially dependent on hDectin-1 signaling. To further establish translational impact of our findings, a collection of C. albicans clinical isolates was screened for glycogen content and significant intra-species heterogeneity between inflammatory status and level of glycogen content was revealed. Remarkably, overexpression of GSY1 in a subset of reduced glycogen accumulation isolates reversed their hyper-inflammatory phenotype and deletion of GSY1 in a subset of WT-like glycogen accumulation isolates induced a hyper-inflammatory phenotype during human macrophage challenge. Further analysis of cell wall components by fluorescence staining and flow cytometry revealed that levels of total glucan, total mannan and total chitin remained similar, while reduced glycogen content significantly correlated with increased cell wall β-(1,3)-glucan exposure. As the dysregulation of glycogen synthesis greatly affects C. albicans fitness both in vitro and in vivo and alters host innate immune recognition, we wished to further explore glycogen synthesis regulatory mechanisms in C. albicans. We determined that the protein encoded by the uncharacterized gene C1_01140C, and not the currently annotated C. albicans Gac1p, is the major type 1 protein phosphatase regulatory (PPP1R) subunit involved in glycogen synthesis. C1_01140Cp contains a conserved GVNK motif observed across multiple starch/glycogen binding proteins in various species and alanine substitution of each residue in this motif significantly impaired glycogen accumulation in C. albicans. Moreover, fluorescent protein tagging, microscopy, and co-immunoprecipitation (Co-IP) indicated that C1_01140Cp colocalized and associated with the PPP1 catalytic (PPP1C) subunit of the CaGlc7p phosphatase and CaGsy1p glycogen synthase CaGsy1p. We demonstrated that C. albicans retains a PPP1-mediated glycogen synthase regulatory mechanism that is highly orthologous to S. cerevisiae. Given these observations, we propose that C1_01140C be named as GAC1 and that C7_00660W (previously annotated GAC1) be renamed GAC2. Collectively, this work demonstrates the impact of C. albicans glycogen metabolism on fitness, virulence and host-Candida interaction. Glycogen catabolism positively impacts C. albicans long-term fitness in nutrient deficient environments and is important for full virulence. The dysregulation of glycogen synthesis in C. albicans also impacts host-Candida interactions through altering β-(1,3)-glucan exposure. C1_01140Cp was newly characterized and identified as the major PPP1R binding subunit that associates with PPP1C CaGlc7p to initialize glycogen synthesis in C. albicans
FtsK Regulates the Assembly of the Division Machinery in the FtsZ-less Chlamydia trachomatis
Full text linkIn evolving to obligate intracellular dependence, Chlamydia trachomatis serovar L2 (Ct), has eliminated several gene products essential for cell division in most other bacteria, including FtsZ, the central coordinator of divisome assembly. In the absence of FtsZ, we show that divisome assembly in Ct is initiated by FtsK, a chromosomal translocase. Chlamydial FtsK forms discrete foci at the septum and at the base of the progenitor mother cell, and our data indicate that FtsK foci at the base of the mother cell mark the location of nascent divisome complexes that form at the site where a daughter cell will emerge in the next round of division. The divisome in Ct has a hybrid composition, containing elements of the divisome and elongasome from other bacteria, and FtsK is recruited to nascent divisomes prior to the other chlamydial divisome proteins assayed, including the PBP2 and PBP3 transpeptidases, and MreB and MreC. Knocking down FtsK prevents divisome assembly in Ct and inhibits cell division and septal peptidoglycan (PG) synthesis. We further show that MreB does not function like FtsZ and serves as a scaffold for the assembly of the Ct divisome. Rather, MreB is one of the last proteins recruited to the chlamydial divisome, and it is necessary for the formation of septal PG rings. Our recent studies have demonstrated the critical role of localized cardiolipin (CL) synthesis in coordinating cell division in Ct. CL is concentrated at the poles and septum, where it promotes the recruitment of MreB during polarized cell division. The lipid’s unique structure helps induce membrane curvature and facilitates divisome protein assembly, making it essential for proper spatial organization of septal PG synthesis and MreB localization. This localized CL synthesis is required for MreB to support the formation of septal PG rings. Our studies further illustrate the critical function of chlamydial FtsK in coordinating divisome assembly and PG synthesis in this obligate intracellular bacterial pathogen. However, the mechanism that specifies the site of divisome assembly in Ct is unclear. In E. coli, the transient interaction of FtsK with XerD stimulates XerCD dependent recombination at the chromosomal dif site to decatenate chromosomes that become interlinked by homologous recombination during DNA replication. We show here chlamydial FtsK colocalizes with XerD during cell division. In addition, CRISPRi which uses a crRNA to target an inducible and defective Cas12 enzyme (dCas12) to a specific chromosomal sequence, has shown that chlamydial FtsK also colocalizes with a chromosomal sequence immediately adjacent to the dif site during cell division. However, when CRISPRi was used to target dCas12 to the XerD binding sequence at the chlamydial dif site, FtsK did not colocalize with Cas12 and cell division was blocked. Our data indicate that the site of divisome assembly in Ct is dependent upon the interaction of FtsK with XerD bound to the chromosomal dif site
The Impact of Patient and Provider Education on Statin Therapy Initiation and Adherence in Type II Diabetics
Full text linkPurpose/Background
Type 2 diabetes mellitus (T2DM) is a common, chronic disease that increases the risk of coronary artery disease and stroke fourfold, which makes protecting cardiac function a priority. The American Diabetes Association (ADA) and American Heart Association (AHA) recommend the prescription of statins to reduce cardiovascular complications. Unfortunately, provider and patient adherence to this recommendation is poor.This study aimed to determine if shared-decision making and patient follow-up within a 6 month period of being newly diagnosed with T2D has an effect on the initiation rate of statin therapy.
Methods
In this retrospective study we requested data from the University of Tennessee Family Medicine clinic on newly diagnosed diabetic patients from December 2021 to December 2023 that met criteria (40 years or older, eligible for statin therapy, new diagnosis of T2D, had at least one follow-up appointment within the last 2 years). Information requested included the patient’s sex, age, baseline HbA1C, referral date, and whether or not statin therapy was initiated within 6 months of diagnosis. The data was then analyzed for descriptive statistics using Intellectus statistical analysis software.
Results
Twenty-nine patients (8 male, 21 female) met inclusion criteria. The mean age of the participants was 52.8 years (female mean age: 54.9 years; male mean age: 47.5 years), and the mean baseline HgA1C was 9.16%. Of the 29 patients included in the study, 100% of them had statin therapy initiated within 6 months of diagnosis.
Implications for Nursing Practice
The results of this study are reassuring that patient follow up within 6 months of a new T2D diagnosis is key in initiating current statin therapy guidelines. These findings reinforce the essential role of nurse practitioners in the management of T2D and associated cardiovascular risk, highlighting the importance of patient education, regular monitoring, and collaborative care
