Disparities in Documentation: Evidence of Race-Based Biases in the Electronic Medical Record.

Personal implicit biases may contribute to inequitable health outcomes, but the mechanisms of these effects are unclear at a system level. This study aimed to determine whether stigmatizing subjective terms in electronic medical records (EMR) reflect larger societal racial biases. A cross-sectional study was conducted using natural language processing software of all documentation where one or more predefined stigmatizing words were used between January 1, 2019 and June 30, 2021. EMR from emergency care and inpatient encounters in a metropolitan healthcare system were analyzed, focused on the presence or absence of race-based differences in word usage, either by specific terms or by groupings of negative or positive terms based on the common perceptions of the words. The persistence ("stickiness") of negative and/or positive characterizations in subsequent encounters for an individual was also evaluated. Final analyses included 12,238 encounters for 9135 patients, ranging from newborn to 104 years old. White (68%) vs Black/African American (17%) were the analyzed groups. Several negative terms (e.g., noncompliant, disrespectful, and curse words) were significantly more frequent in encounters with Black/African American patients. In contrast, positive terms (e.g., compliant, polite) were statistically more likely to be in White patients' documentation. Independent of race, negative characterizations were twice as likely to persist compared with positive ones in subsequent encounters. The use of stigmatizing language in documentation mirrors the same race-based inequities seen in medical outcomes and larger sociodemographic trends. This may contribute to observed healthcare outcome differences by disseminating one's implicit biases to unknown future healthcare providers.

The weaponization of professionalism against physicians of color.

Though we have made ample advances in the field of medicine in recent years, our idea of professionalism continues to be based on the standard of how white men dressed in the nineteenth century. Such a standard of professionalism not only perpetuates gender bias, but also aims to remove the culture, traditions, and behaviors of minority groups with the goal of molding these individuals to resemble the majority, preventing 'Afro' heritage from entering medicine. By contextualizing our own experiences in the medical setting as physicians of color in the context of a variety of supporting literature, we provide an overview of professionalism, its role in medicine, the double standard faced by women, and how it continues to be weaponized against physicians of racial, ethnic, and religious minorities. We advocate for minority physicians to embrace their authenticity and for institutions to develop policies that openly, firmly, and enthusiastically welcome physicians of all ethnicities, religions, and genders. Positionality Statement: In the editorial you are about to read, we, the authors, collectively bring a rich tapestry of backgrounds and experiences to our discussion on healthcare disparities. Our team consists of two Hispanic/Latina oncologists, one Middle Eastern oncologist, one Black/Caribbean-American hematologist, and one White pre-medical student with Middle Eastern heritage. Our diverse backgrounds inform our perspectives and enhance our understanding of the complex and multifaceted nature of healthcare. We are united by a shared commitment to justice, equity, and the belief that every patient deserves high-quality care, regardless of their background. This editorial is informed by our professional expertise, personal experiences, and the diverse communities we serve, aiming to highlight the critical need for inclusivity and representation in healthcare. By acknowledging our positionality, we hope to provide a comprehensive and empathetic analysis that not only identifies the challenges but also offers actionable solutions to improve healthcare outcomes for all. We recognize the power of diversity in fostering innovation and driving positive change, and we are dedicated to using our voices and positions to advocate for a more equitable healthcare system.

Cold exposure induces vaso-occlusion and pain in sickle mice that depend on complement activation.

Vaso-occlusive pain episodes (VOE) cause severe pain in patients with sickle cell disease (SCD). Vaso-occlusive events promote ischemia/reperfusion pathobiology that activates complement. We hypothesized that complement activation is linked to VOE. We used cold to induce VOE in the Townes sickle homozygous for hemoglobin S (HbSS) mouse model and complement inhibitors to determine whether anaphylatoxin C5a mediates VOE. We used a dorsal skinfold chamber to measure microvascular stasis (vaso-occlusion) and von Frey filaments applied to the plantar surface of the hind paw to assess mechanical hyperalgesia in HbSS and control Townes mice homozygous for hemoglobin A (HbAA) mice after cold exposure at 10°C/50°F for 1 hour. Cold exposure induced more vaso-occlusion in nonhyperalgesic HbSS mice (33%) than in HbAA mice (11%) or HbSS mice left at room temperature (1%). Cold exposure also produced mechanical hyperalgesia as measured by paw withdrawal threshold in HbSS mice compared with that in HbAA mice or HbSS mice left at room temperature. Vaso-occlusion and hyperalgesia were associated with an increase in complement activation fragments Bb and C5a in plasma of HbSS mice after cold exposure. This was accompanied by an increase in proinflammatory NF-κB activation and VCAM-1 and ICAM-1 expression in the liver. Pretreatment of nonhyperalgesic HbSS mice before cold exposure with anti-C5 or anti-C5aR monoclonal antibodies (mAbs) decreased vaso-occlusion, mechanical hyperalgesia, complement activation, and liver inflammatory markers compared with pretreatment with control mAb. Anti-C5 or -C5aR mAb infusion also abrogated mechanical hyperalgesia in HbSS mice with ongoing hyperalgesia at baseline. These findings suggest that C5a promotes vaso-occlusion, pain, and inflammation during VOE and may play a role in chronic pain.

MASP-2 and MASP-3 inhibitors block complement activation, inflammation, and microvascular stasis in a murine model of vaso-occlusion in sickle cell disease.

Patients with sickle cell disease (SCD) have ongoing hemolysis that promotes endothelial injury, complement activation, inflammation, vaso-occlusion, ischemia-reperfusion pathophysiology, and pain. Complement activation markers are increased in SCD in steady-state and further increased during vaso-occlusive crisis (VOC). However, the mechanisms driving complement activation in SCD have not been completely elucidated. Ischemia-reperfusion and heme released from hemoglobin during hemolysis, events that characterize SCD pathophysiology, can activate the lectin pathway (LP) and alternative pathway (AP), respectively. Here we evaluated the role of LP and AP in Townes sickle (SS) mice using inhibitory monoclonal antibodies (mAb) to mannose binding lectin (MBL)-associated serine protease (MASP)-2 or MASP-3, respectively. Townes SS mice were pretreated with MASP-2 mAb, MASP-3 mAb, isotype control mAb, or PBS before they were challenged with hypoxia-reoxygenation or hemoglobin. Pretreatment of SS mice with MASP-2 or MASP-3 mAb, markedly reduced Bb fragments, C4d and C5a in plasma and complement deposition in the liver, kidneys, and lungs collected 4 hours after challenge compared to control mAb-treated mice. Consistent with complement inhibition, hepatic inflammation markers NF-ĸB phospho-p65, VCAM-1, ICAM-1, and E-selectin were significantly reduced in SS mice pretreated with MASP-2 or MASP-3 mAb. Importantly, MASP-2 or MASP-3 mAb pretreatment significantly inhibited microvascular stasis (vaso-occlusion) induced by hypoxia-reoxygenation or hemoglobin. These studies suggest that the LP and the AP are both playing a role in promoting inflammation and vaso-occlusion in SCD. Inhibiting complement activation via the LP or the AP might inhibit inflammation and prevent VOC in SCD patients.

Improved Guideline Adherence With Integrated Sickle Cell Disease and Asthma Care.

INTRODUCTION: In children with sickle cell disease (SCD), concomitant asthma is associated with increased morbidity and mortality when compared with children with SCD without asthma. Despite the well-established burden of asthma in children with SCD, no paradigm of care exists for the co-management of these two diseases. METHODS: To address this gap, an integrated SCD and asthma clinic was created in a community health center that included (1) a dual respiratory therapist/asthma case manager; (2) an SCD nurse practitioner with asthma educator certification; (3) an onsite pulmonary function test laboratory; (4) a pediatric hematologist with expertise in managing SCD and asthma; and (5) application of the National Asthma Education and Prevention Program guidelines. A before (2010-2012) and after (2013-2014) study design was used to assess for improved quality of care with implementation of an integrative care model among 61 children with SCD and asthma followed from 2010 to 2014. RESULTS: Asthma action plan utilization after initial diagnosis increased with the integrative care model (n=16, 56% before, 100% after, p=0.003), as did the use of spirometry in children aged ≥5 years (n=41, 65% before, 95% after, p<0.001) and correction of lower airway obstruction (n=10, 30% before, 80% after, p=0.03). CONCLUSIONS: Although the use of an integrative care model for SCD and asthma improved evidence-based asthma care, longer follow-up and evaluation will be needed to determine the impact on SCD-related morbidity.