Introduction: Concurrent chronic myeloid leukemia (CML) and chronic lymphocytic leukemia (CLL) in the same patient are rare and may be overlooked when leukocytosis is attributed to a single hematologic process. We report a case of synchronous CML and CLL identified at initial presentation, highlighting the diagnostic value of integrating morphology, immunophenotyping, cytogenetics, and molecular testing. Case Presentation: A 44-year-old man presented with progressive weight loss and back pain and was found to have leukocytosis with neutrophilia, absolute lymphocytosis, eosinophilia, and basophilia. Peripheral blood smear and flow cytometry supported CLL, whereas reverse-transcription polymerase chain reaction and cytogenetics demonstrated e13a2 BCR::ABL1 and t(9;22)(q34;q11.2), confirming concomitant CML in chronic phase. Bone marrow examination showed hypercellularity with granulocytic hyperplasia and nodular lymphoid infiltrates, and fluorescence in situ hybridization detected 13q14.3 deletion in the lymphoid clone. Imatinib 400 mg daily was initiated but was replaced with dasatinib 100 mg daily because of intolerance. At 14 months of follow-up, the patient remained clinically stable on dasatinib, with early molecular response at 3 months and major molecular response at 12 months, while the CLL remained under observation without indication for CLL-directed therapy. Conclusion: This case highlights the diagnostic complexity of synchronous hematologic malignancies and the importance of comprehensive multimodal evaluation when clinical, morphologic, and laboratory findings are not fully explained by a single diagnosis. Treating the clinically dominant clone while monitoring the second clone may be appropriate when the latter is asymptomatic.

Metformin-associated lactic acidosis (MALA) and euglycemic diabetic ketoacidosis (euDKA) are distinct causes of high anion gap metabolic acidosis, but their simultaneous occurrence is rare and may be overlooked when severe hyperlactatemia dominates the presentation. We report the case of a 68-year-old man with type 2 diabetes mellitus treated with basal-bolus insulin, metformin, and linagliptin who presented with vomiting, confusion, fatigue, hypotension, and reduced level of consciousness. Initial evaluation revealed profound acidemia (arterial pH 6.75), severe high anion gap metabolic acidosis (anion gap 51 mEq/L, bicarbonate 9.60 mmol/L), near-normal glucose (9.1 mmol/L), hyperkalemia (6.5 mEq/L), and severe acute kidney injury (creatinine 516 µmol/L). Ongoing metformin exposure in the setting of acute kidney injury supported MALA, while marked ketonemia with near-normal glucose supported concurrent euDKA, likely precipitated by vomiting and reduced oral intake. The patient was treated with intravenous fluids, vasopressors, sodium bicarbonate, insulin with concurrent dextrose, and sustained low-efficiency dialysis, with subsequent hemodynamic, metabolic, and renal recovery. This case emphasizes that marked hyperlactatemia does not exclude a concurrent ketotic process and that early ketone measurement can materially change management in metformin-treated patients with persistent high anion gap acidosis.

We report a 28-year-old man with alcohol-induced interstitial acute pancreatitis (AP) who developed rapidly progressive anemia and thrombocytopenia beginning on hospital day two. Hemoglobin decreased from 16.5 g/dL on presentation to a nadir of approximately 5.2 g/dL, and the platelet count declined from 309×103/µL to 12×103/µL. Laboratory evaluation showed hemolysis with markedly elevated lactate dehydrogenase, undetectable haptoglobin, hyperbilirubinemia, and a peripheral smear demonstrating polychromasia with rare schistocytes and spherocytes, while the direct antiglobulin test (DAT) was negative on two occasions. Renal function, coagulation studies, and ADAMTS13 activity were normal, and broad infectious and autoimmune evaluation was unrevealing. Given the temporal association with pancreatitis, exclusion of thrombotic microangiopathy (TMA), disseminated intravascular coagulation, infection, and other evaluated causes, and hematologic improvement after intravenous immunoglobulin (IVIG) and corticosteroids, the working diagnosis was a suspected Evans syndrome-like immune cytopenia (immune thrombocytopenia with DAT-negative immune hemolysis) triggered by AP. Extended serologic testing for DAT-negative autoimmune hemolysis was negative, so the diagnosis remained a clinical working diagnosis. The patient was treated with transfusion support, IVIG, and intravenous methylprednisolone, with gradual hematologic recovery. This case underscores the importance of early hematologic evaluation and consideration of immunomodulatory therapy after exclusion of TMA and other common causes of hemolysis in patients with AP and severe cytopenias.

Systemic lupus erythematosus can present with varied clinical features, and life-threatening serositis or autoimmune hemolysis may precede more typical findings. We report a 56-year-old woman who presented with progressive dyspnea, pleuritic chest discomfort, hypotension, and tachycardia and was found to have a large pericardial effusion with tamponade physiology requiring urgent pericardiocentesis. During hospitalization, worsening anemia with positive direct antiglobulin testing, peripheral spherocytes, reticulocytosis, hyperbilirubinemia, low haptoglobin, and splenomegaly supported the diagnosis of warm autoimmune hemolytic anemia. Infectious, malignant, and other causes of inflammatory pericardial effusion were excluded. The overall presentation, including serositis, autoimmune hemolysis, and positive lupus serologies, supported the diagnosis of late-onset systemic lupus erythematosus. She was treated with pericardiocentesis, corticosteroids, transfusion support, intravenous immunoglobulin, rituximab, and later hydroxychloroquine, with resolution of the pericardial effusion and improvement in anemia. This case emphasizes that systemic lupus erythematosus should be considered in adults with otherwise unexplained cardiac tamponade accompanied by hemolysis, even when classic mucocutaneous or musculoskeletal manifestations are absent at presentation.

Background: Cirrhosis and metabolic comorbidities frequently coexist. Both glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2i) have shown cardiometabolic and hepatic benefits, but their comparative effectiveness in established cirrhosis remains unclear. We compared 1-year clinical outcomes between adults with cirrhosis initiating either class. Methods: Using the TriNetX U.S. Collaborative Network, we identified adults with cirrhosis who initiated a GLP-1RA or SGLT2i after diagnosis and had no prior exposure to the comparator class. One-to-one propensity score matching balanced demographic, clinical, medication, and laboratory covariates. Primary outcomes at 1 year were all-cause mortality and inpatient hospitalization. Secondary outcomes included individual and composite cirrhosis decompensation events (ascites, paracentesis, spontaneous bacterial peritonitis, variceal bleeding, hepatic encephalopathy, hepatorenal syndrome) and adverse events (acute kidney injury, hypoglycemia, acute pancreatitis). Results: The matched cohorts comprised 8,016 patients per arm. GLP-1RA users had lower 1-year all-cause mortality (4.3% vs 5.3%; OR 0.80, 95% CI 0.69–0.93; p=0.003) and fewer composite decompensation events (5.3% vs 6.7%; OR 0.78, 95% CI 0.69–0.88; p<0.0001), driven by reductions in ascites and spontaneous bacterial peritonitis. Hospitalization did not differ (7.6% vs 8.2%; p=0.3). Variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome were comparable. AKI was less frequent with GLP-1RAs (4.8% vs 6.2%; p=0.001); rates of hypoglycemia and pancreatitis were similar. Conclusions: In this large real-world analysis of adults with cirrhosis, initiation of a GLP-1RA was associated with lower 1-year mortality and fewer ascites-related decompensation and AKI events compared with initiation of an SGLT2i.