Background: Sickle cell disease (SCD) significantly impacts diverse racial groups, particularly African American and Hispanic persons, who experience notable disparities in healthcare outcomes. Despite the extensive literature on SCD, studies focusing on in-hospital racial inequities remain limited. Methods: We conducted a retrospective analysis using the National Inpatient Sample (NIS) from 2016 to 2020, identifying adult hospitalizations for SCD (HbSS genotype). Hospitalizations were categorized by race—White, African American, Hispanic, and other, and analyzed for demographic variables, admission types, disposition outcomes, and complications. Statistical analyses included chi-square tests and multivariate logistic regression, adjusting for confounders. Results: Of the 1,089,270 identified hospitalizations, 90.31% were African American. African American and Hispanic patients exhibited significantly higher non-elective admissions compared to Whites (77.81%). In-hospital mortality was highest among Hispanics (0.82%). Multivariate regression analysis revealed that African Americans and others had higher odds of prolonged hospital stays (Adjusted Odds Ratio (AOR): 1.30 and 1.20, respectively). African Americans and Hispanics also had increased risks of in-hospital complications of SCD. Conclusions: This study highlights substantial racial disparities in SCD hospitalizations, with African Americans and Hispanics facing poorer outcomes compared to Whites. Hispanics also demonstrated increased mortality. These findings underscore the need for targeted healthcare interventions to address racial inequities in SCD management and improve outcomes for all affected populations.

Chronic lymphocytic leukemia (CLL) is an indolent malignancy characterized by the accumulation of dysfunctional B-cell lymphocytes. Complications such as hemophagocytic lymphohistiocytosis (HLH) can arise, particularly during disease progression. HLH has been increasingly reported as a complication of CLL, often triggered by factors such as superimposed infections, chemotherapy, Richter transformation, or disease progression. This case explores HLH as an initial presentation of undiagnosed CLL without any identifiable trigger. We present the case of a 65-year-old woman who presented with a high-grade fever, sore throat, and pancytopenia. Despite broad-spectrum antibiotic treatment, her condition deteriorated. Investigations revealed elevated ferritin levels, low natural killer cell activity, and other findings consistent with HLH. Flow cytometry and bone marrow biopsy ultimately confirmed the diagnosis of CLL. HLH is characterized by the hyperactivation of immune cells and is known to be triggered by a variety of factors, including infections and malignancies. In this case, the absence of identifiable triggers raises important questions about the underlying pathophysiology linking HLH with CLL. While previous reports have highlighted HLH as a complication of CLL, typically secondary to infection or treatment, this case is particularly noteworthy due to the unexplained onset of HLH in the absence of such triggers. This case underscores the need for heightened awareness of HLH as a potential manifestation of underlying malignancy, especially in non-septic patients presenting with unexplained fever and pancytopenia. In addition, the simultaneous presentation of normal pressure hydrocephalus emphasizes the complex interplay of inflammatory processes in CLL. Further research is needed to explore the relationship between inflammation and the pathogenesis of CLL.

Background: Non-islet cell tumor hypoglycemia is increasingly reported with gastrointestinal stromal tumors (GIST), but population-level estimates of its clinical impact are limited. We evaluated associations between hypoglycemia and inpatient outcomes among GIST hospitalizations. Methods: We conducted a retrospective cross-sectional study of the National Inpatient Sample (NIS) 2018–2020. Adult GIST discharges were identified by ICD-10-CM codes and stratified by hypoglycemia. Primary outcomes were in-hospital mortality and resource utilization—length of stay (LOS) and total hospital charge. Secondary outcomes included malnutrition, sepsis, ascites, peritonitis, bowel perforation, intestinal obstruction, gastrointestinal bleeding, and iron deficiency anemia. Analyses used survey-weighted logistic regression for binary outcomes and generalized linear models for continuous outcomes. A propensity score-matched sensitivity analysis balanced sepsis and malnutrition. Results: Among 61,725 GIST hospitalizations, 0.72% had hypoglycemia. Mortality was 12.6% with hypoglycemia vs. 3.1% without; adjusted odds of death were higher (aOR 4.16, 95% CI 2.06–8.37; p < 0.001). Hypoglycemia was also associated with malnutrition (aOR 5.63, 3.37–9.40), sepsis (aOR 4.00, 2.24–7.14), ascites (aOR 3.43, 1.63–7.19), and peritonitis (aOR 2.91, 1.17–7.22). LOS was 4.61 days longer on average (not significant; p = 0.185), and total hospital charge was $5218 higher (β = 19,116.8; p = 0.95). In the matched cohort, the mortality association attenuated but persisted (aOR 1.38, 1.27–1.49; p < 0.001); peritonitis remained significant (aOR 1.10, 1.04–1.17), intestinal obstruction (aOR 4.91, 3.44–7.05) and iron deficiency anemia (aOR 3.54, 1.62–7.74) became significant, while ascites and gastrointestinal bleeding were not significant. Conclusions: Hypoglycemia in GIST, although uncommon, marks a higher-risk inpatient trajectory with increased mortality and several complications; these signals largely persist after balancing severity proxies. Resource-use differences were directionally higher but not statistically significant. Recognition of hypoglycemia may aid risk stratification and inpatient management in GIST.

Background: Cerebral venous sinus thrombosis (CVT) is a rare cause of stroke, constituting 0.5–3% of all strokes with an extremely varied spectrum of presentation, predisposing factors, neuroimaging findings, and eventual outcomes. A high index of suspicion is needed because timely diagnosis can significantly alter the natural course of the disease, reduce acute complications, and improve long-term outcomes. Due to its myriad causative factors, protean presentation, and association with several systemic diseases, CVT is encountered not only by neurologists but also by emergency care practitioners, internists, hematologists, obstetricians, and pediatricians. Discussion: Anticoagulation remains the mainstay of treatment for CVT. Heparin and warfarin previously had been the anticoagulation of choice. Recently there has been an increased interest in utilizing direct-acting oral anticoagulants in the treatment of CVT given comparable safety and efficacy with ease of utilization. However recent clinical guidelines given by multiple societies including the American Stroke guidelines and European guidelines do not include these agents so far in their treatment recommendations. Ongoing multicentric clinical trials are currently reviewing the role of these agents in both short-term as well as long-term. Our review of the literature supports the safety and reinforces the efficacy of DOAC in the treatment of CVT. Additionally, patient satisfaction has been shown to be better with the use of DOAC. In conclusion, DOAC continues to have a valid role in the management of CVT.

Immunotherapy-induced pseudomembranous colitis (PMC) is an uncommon but increasingly recognized adverse effect of immune checkpoint inhibitors, particularly in patients with advanced malignancies. We present a case of a 68-year-old male with gastric adenocarcinoma undergoing treatment with immunotherapy and chemotherapy, who developed symptoms of PMC. Workup for Clostridium difficile and other common etiologies was negative. Colonoscopy revealed severe mucosal congestion and yellowish-green exudates, consistent with PMC. Based on the biopsy results and clinical presentation, after excluding common etiologies, immunotherapy-induced PMC was suspected. The patient responded to steroid therapy, with gradual improvement and a tapering regimen upon discharge. This case underscores the diagnostic challenges in identifying the etiology of PMC, particularly when it presents with diffuse involvement of the colon, which is an uncommon presentation for immunotherapy-related colitis. The overlap in clinical, endoscopic, and histopathological findings with other forms of colitis, such as Clostridium difficile infection (CDI) and inflammatory bowel disease, highlights the need for heightened awareness among clinicians. This case highlights the diagnostic challenges in recognizing immunotherapy-induced PMC, particularly with atypical, diffuse colonic involvement. The overlapping features with other colitis make timely diagnosis difficult. Further research is needed to refine diagnostic criteria and management strategies for immunotherapy induced colitis (IMC).

Malignant pleural mesothelioma (MPM) is a rare but highly aggressive cancer, primarily caused by asbestos exposure, with limited diagnostic and therapeutic options. The disease is characterized by late-stage diagnosis and poor prognosis, necessitating advancements in early detection and treatment strategies. Biomarkers have emerged as vital tools in addressing these challenges, providing opportunities for early diagnosis, prognostic evaluation, and therapeutic guidance. This review explores the recent developments in MPM biomarkers, including soluble mesothelin-related peptides (SMRP), fibulin-3, osteopontin, and novel genetic and epigenetic markers. We also examine the potential of liquid biopsy technologies, encompassing circulating tumor cells (CTCs), cell-free DNA (cfDNA), and exosomal markers, in improving diagnostic precision and monitoring treatment response. Despite promising advancements, significant hurdles remain, including variability in biomarker sensitivity and specificity, lack of standardization in clinical settings, and the need for extensive validation studies. Recommendations for future research include integrating multi-omic approaches, leveraging artificial intelligence for biomarker discovery, implementing appropriate screening guidelines and fostering collaboration among research institutions to expedite translational efforts for personalized, biomarker driven treatment strategies. By addressing these gaps, biomarker research can pave the way for personalized medicine in MPM, improving early detection, treatment efficacy, and overall patient outcomes.