piperacillin-tazobactam, a widely used broad-spectrum antibiotic, carries a risk of severe adverse reactions, including rare but life-threatening hemophagocytic lymphohistiocytosis (HLH). Elevated procalcitonin (PCT), typically indicative of bacterial infection, can mask this diagnosis, leading to delayed recognition and potentially fatal outcomes. This case underscores the diagnostic challenge of drug-induced HLH mimicking infection. a 17-year-old female presented with community-acquired pneumonia (CAP) and severe iron deficiency anemia. Initial piperacillin-tazobactam therapy resolved her fever and respiratory symptoms. However, after 6 afebrile days, she developed recurrent high-grade fever (40.3°C), pancytopenia (WBC 1.81 × 109/L, ANC 0.23 × 109/L, Hb 80 g/L, platelets 74 × 109/L), hepatitis (AST 338 U/L, ALT 221 U/L), and rising serum ferritin (609.3 ng/mL) and PCT (3.057 ng/mL). comprehensive evaluation excluded new infections (bacterial, viral including EBV/CMV), malignancies, autoimmune disorders, and other HLH triggers. Bone marrow morphology revealed hemophagocytic cells. Based on HLH-2004 criteria, she fulfilled 5 diagnostic criteria: fever, ≥2 lineage cytopenias, hyperferritinemia, hemophagocytosis in bone marrow, and progressive splenomegaly. The temporal association with drug exposure and resolution upon withdrawal confirmed piperacillin-tazobactam-induced HLH. piperacillin-tazobactam was immediately discontinued upon suspicion of drug reaction. Despite elevated PCT prompting initiation of imipenem-cilastatin, the patient's fever resolved spontaneously carbapenem before administration, and liver enzymes began improving the next day. following piperacillin-tazobactam cessation, fever resolved permanently within hours. Cytopenias, liver dysfunction, elevated ferritin, and PCT normalized progressively without specific HLH-directed immunosuppressive therapy. The patient was discharged symptom-free. Normal complete blood counts were confirmed at outpatient follow-ups over 13 months. piperacillin-tazobactam can induce HLH, a critical diagnosis requiring immediate drug withdrawal. Elevated PCT in this context is a significant diagnostic pitfall, misleadingly suggesting bacterial infection progression. Unexplained fever and cytopenia during piperacillin-tazobactam therapy - even with elevated PCT - should prompt urgent evaluation for drug-induced HLH. Discontinuation of the causative agent is paramount for recovery and may obviate the need for unnecessary antimicrobial escalation or immunosuppressive therapy.

Hemophagocytic lymphohistiocytosis (HLH) is an aggressive and potentially life-threatening syndrome of aberrant immune hyperactivation characterized by excess cytokine release due to abnormal cytotoxic T-cell and macrophage activation. Secondary, or acquired, HLH occurs in the setting of underlying infection, malignancy, or autoimmune processes and often presents with systemic symptoms and multi-organ dysfunction that can initially be misattributed to infection, leading to a delay in diagnosis and management. Histoplasmosis-associated HLH is an infrequently described manifestation of secondary HLH that can occur in the setting of immunocompromised states. A 67-year-old woman with a history of granulomatosis with polyangiitis on active mycophenolate mofetil treatment initially presented with persistent flu-like symptoms in the setting of pancytopenia and elevated liver enzymes. Despite appropriate sepsis evaluation and extensive antimicrobial treatment, she remained persistently febrile and developed acute respiratory failure. Lab work revealed severely abnormal coagulation factors, hypofibrinogenemia, hyperferritinemia, and hypertriglyceridemia concerning for underlying hematologic disease process. Bone marrow biopsy obtained showed a hypercellular marrow with histiocytosis and hemophagocytic forms as well as intracellular narrow-based budding yeast, confirming an HLH diagnosis and suggestive of disseminated histoplasmosis. She was subsequently started on a high-dose steroid taper, intravenous immunoglobulin, and anti-fungal therapy with clinical improvement and stabilization of blood counts. Post-discharge follow-up has not involved repeat hospitalizations. Diagnosing HLH requires consideration of both clinical and laboratory criteria but there remains a lack of consensus use, especially in adult patients and those with associated autoimmune disease. Furthermore, the clinical presentation of HLH can overlap significantly with sepsis or other acute illnesses, thus delaying timely diagnosis and interventions for optimal patient outcomes. Our case emphasizes the importance of early consideration and comprehensive evaluation in this setting for HLH and secondary causes, including fungal etiologies. Additional clinical reporting of this rare presentation can increase clinician recognition and highlight potential diagnostic and treatment approaches. Subsequent close clinical observation with serial examinations and biochemical marker follow-up are needed to assess response and evaluate for changes in treatment approach.

Hemophagocytic lymphohistiocytosis (HLH) is a rare, life-threatening hyperinflammatory syndrome characterized by uncontrolled macrophage activation. Secondary HLH is more common in adults and may be triggered by infection, malignancy, or autoimmune disease. Dyslipidemia, particularly hypolipoproteinemia, has been described but remains underexplored. We retrospectively reviewed 18 adult HLH cases diagnosed between 2012 and 2020 at two institutions where complete lipid profiles were obtained at or near diagnosis. HLH was defined according to HLH-2004 criteria. Among 18 patients, 17 (94%) had secondary HLH, most commonly idiopathic (n = 5, 28%) or Epstein-Barr virus-associated (n = 3, 17%). Hypolipidemia was nearly universal: all (18/18) had HDL-C < 30 mg/dL, 15/18 (83%) had HDL-C < 20 mg/dL, and 12/18 (67%) had HDL-C < 10 mg/dL. LDL-C was <100 mg/dL in 12/18 (67%), with 6/18 (33%) undetectable. Triglycerides were variably elevated (median 279 mg/dL, range 96-1658 mg/dL). Three representative cases with profound hypolipoproteinemia demonstrated lipid normalization after HLH-directed therapy. Severe reductions in HDL-C and LDL-C appear to accompany HLH and may contribute to its pathophysiology by impairing antioxidant defenses, destabilizing membranes, and potentiating macrophage activation. This case series highlights a consistent association between hypolipoproteinemia and HLH, suggesting potential diagnostic value. However, the observational design and small cohort limit generalizability. Larger prospective studies are needed to clarify mechanisms and evaluate whether full lipid profiling should be incorporated into diagnostic algorithms.

Hemophagocytic lymphohistiocytosis (HLH), a rare and deadly disease, is typically classified as either primary (familial) or secondary (acquired), depending on the etiology and underlying cause. Secondary HLH often develops in the presence of infectious, malignant, rheumatologic, or metabolic conditions, with infections, especially Epstein-Barr virus (EBV) infection, being among the leading causes. Brucella infection-induced HLH is relatively rare, with only eight cases reported in the past decade, all of which had a favorable prognosis following timely diagnosis and treatment. A 53-year-old man with brucellosis who developed secondary HLH and multiple organ dysfunction presented to our hospital with a 2-month history of fever and abnormal liver enzymes. Initial blood culture following admission confirmed Brucella spp. in the aerobic bottle after ⁓87.85 h of incubation. However, after the initial discharge, the patient did not adhere to the prescribed antibiotic therapy and subsequently developed symptoms of fever and abdominal discomfort, and was readmitted to our hospital. Laboratory examination also revealed pancytopenia. An additional blood culture further revealed the growth of Brucella spp. in the aerobic bottle after ⁓113.67 h of incubation. Other findings included decreased fibrinogen, increased ferritin, increased soluble IL-2 receptor α chain (sCD25), decreased Natural Killer (NK) cell activity, presence of hemophagocytic cells in the bone marrow smear, splenomegaly, and abnormal liver and kidney functions. The HScore score was 230 points. A thorough assessment was made, which led to the exclusion of other possible diseases, culminating in the identification of Brucella infection as the most probable cause of HLH. Consequently, the patient was given anti-infection (doxycycline, levofloxacin, etimicin, and rifampin), glucocorticoids (GCs), human immunoglobulin (HIG), and other symptomatic supportive treatments, which ultimately improved his condition. Despite the generally poor prognosis of HLH patients, those with Brucella-induced HLH may have a favorable outcome with prompt intervention. Conversely, a delayed treatment could increase the risk of HLH onset and progression, leading to death in severe cases.

Pneumonia caused by Chlamydia abortus (C. abortus) is uncommon, particularly when complicated by severe acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS). Hemophagocytic lymphohistiocytosis (HLH) is a rare and potentially fatal disease characterized by the uncontrolled activation and non-malignant expansion of macrophages and T lymphocytes. This report describes a case of severe pneumonia complicated by hemophagocytic lymphohistiocytosis, caused by Chlamydia abortus. A 42-year-old female with no history of underlying medical conditions, no known exposure to poultry or avian animals, and no consumption of undercooked sheep or ewes contaminated with infected placenta, presented to the respiratory medicine department with a 3-day history of fever, cough, and sputum production. Initially diagnosed with community-acquired pneumonia, she was treated with piperacillin-tazobactam for 5 days. However, despite 12 h of high-flow oxygen therapy, her oxygenation did not improve, and she was transferred to the ICU, where she received additional treatments, including moxifloxacin and methylprednisolone. Her condition worsened further, prompting the initiation of veno-venous extracorporeal membrane oxygenation (VV-ECMO) and bronchoalveolar lavage for metagenomic next-generation sequencing (mNGS) analysis. The mNGS results identified Chlamydia abortus with a count of 180,791, leading to the cessation of moxifloxacin and the addition of omadacycline to her regimen. After 13 days of ECMO therapy, her condition improved, and the ECMO was discontinued. The endotracheal tube was successfully removed 15 days after intubation. However, 3 days later, the patient developed recurrent fever, pancytopenia, elevated ferritin, blood lipids, soluble CD25, and decreased natural killer cell activity, leading to a diagnosis of hemophagocytic lymphohistiocytosis (HLH). She was treated with ruxolitinib, etoposide, and other supportive medications. Despite treatment, her condition continued to deteriorate. Three days later, the family opted to discontinue therapy due to financial constraints. She passed away 12 h later. Chlamydia abortus infection can result in severe acute respiratory distress syndrome (ARDS), necessitating prompt diagnosis and active clinical intervention. This case is unique due to the rare occurrence of HLH following Chlamydia abortus infection, a pathogen not commonly associated with this condition. Metagenomic next-generation sequencing (mNGS) offers a distinct advantage in rapidly and accurately identifying rare pathogen infections, while extracorporeal membrane oxygenation (ECMO) can be an effective treatment for severe pneumonia caused by Chlamydia abortus. It highlights the importance of early recognition and management of HLH in patients with severe, unexplained infections, particularly in those with unusual pathogens. Additionally, Chlamydia abortus infection may be complicated by HLH. Clinicians should remain vigilant for patients presenting with unexplained high fever, hepatosplenomegaly, and pancytopenia, and HLH screening should be initiated promptly. Early intervention can significantly improve patient survival rates.