Intravascular large B-cell lymphoma (IVLBCL) is a rare extranodal neoplasm in which malignant B cells proliferate predominantly within small blood vessels. Because lymphadenopathy, mass lesions, circulating malignant cells, and specific radiological findings may be absent, IVLBCL can closely mimic other medical conditions, resulting in delayed diagnosis. This case is notable for a prolonged culture-negative sepsis-like presentation with persistent unexplained hypoxemia due to predominant pulmonary microvascular involvement, further obscured by lupus-like autoimmune features and subsequent COVID-19 infection. An older woman in her early 70s presented with fever, lethargy, weight loss, back pain, hypotension, raised inflammatory markers, cytopenia, markedly elevated lactate dehydrogenase (LDH), and progressive hypoxemia. She was initially treated for presumed sepsis, but repeated microbiological investigations and serial imaging did not identify an infectious source, and clinical improvement was not sustained. A transient malar rash and a positive antinuclear antibody raised concern for a lupus-like autoimmune disease; however, testing for anti-double-stranded DNA and extractable nuclear antigen was negative, and the broader autoimmune workup did not support systemic lupus erythematosus as the unifying diagnosis. Subsequent severe acute respiratory syndrome coronavirus 2 infection further complicated the interpretation of hypoxemia and deterioration. Despite antimicrobial therapy, corticosteroids, antiviral treatment, and supportive care, she developed progressive multiorgan failure and died approximately six weeks after admission. Postmortem examination revealed widespread multiorgan IVLBCL involving the lungs, heart, kidneys, liver, spleen, and multiple additional extranodal sites. Pulmonary capillary involvement provided a clinicopathological explanation for persistent unexplained hypoxemia. This case demonstrates how IVLBCL may remain concealed when several plausible diagnoses coexist. Persistent culture-negative fever, constitutional decline, cytopenia, high LDH, nondiagnostic imaging, treatment nonresponse, and unexplained hypoxemia should prompt consideration of IVLBCL and early tissue-based investigation.

Autoimmune myelofibrosis (AIMF) is a rare, potentially reversible cause of bone marrow failure often linked to systemic autoimmune disease. We report a diagnostically challenging case of a 26-year-old woman from sub-Saharan Africa who presented with transfusion-dependent pancytopenia and an initial dry-tap marrow, with further testing limited by financial constraints. Seven months later, evolving clinical and immunologic features-including fever, leukopenia, thrombocytopenia, malar rash, positive ANA, and a sterile exudative pleural effusion-fulfilled the 2019 EULAR/ACR criteria for systemic lupus erythematosus (SLE). AIMF secondary to SLE was subsequently diagnosed, and she demonstrated a rapid hematologic response to glucocorticoids and hydroxychloroquine, remaining transfusion-independent for over five months. This case underscores the diagnostic complexity of AIMF in resource-limited settings and highlights the importance of sustained clinical suspicion and adaptable diagnostic strategies when evaluating unexplained pancytopenia.

Systemic lupus erythematosus (SLE) is a chronic, inflammatory, autoimmune disorder involving multiple systems. A 18-year-old female patient presented with complaints of headache, weakness, and tingling sensation in the left upper limb and lower limb. On magnetic resonance imaging (MRI), acute nonhemorrhagic infarct in right thalamo-capsular region was seen. The patient gave a history of malar rash and intermittent joint pains for which she had taken nonspecific treatment. Antineutrophilic antibody (ANA) by innumoflourescence and ANA blot was suggestive of SLE. Hence, the patient had central nervous system vasculitis and stroke due to SLE. The patient was started on antiplatelet therapy, tablet prednisolone 40 mg once daily, and tablet warfarin 5 mg once daily. The patient was readmitted after 2 weeks with menorrhagia and deranged INR. Tablet Warfarin was with-held, fresh frozen plasma transfusions were given. Repeat MRI did not show any new changes. Patient was given tablet nicoumalone and three doses of injection cyclophosphamide 800 mg. Hemiplegia has improved by 90%, her menstrual cycles are now regular.

An 18-year-old female with Systemic Lupus Erythematosus (SLE) presented with bilateral thigh pain, fever, and diarrhea three days before admission. Diagnosed with SLE one month earlier, she reported prior symptoms, including joint pain, malar rash, hair loss, and hyperpigmented lesions. Initial investigations revealed elevated transaminase levels (AST 355, ALT 132), positive ANA, decreased complement levels (C3 68, C4 16.8), and raised creatine kinase (619). A muscle biopsy confirmed myositis. The patient was treated with immunosuppressant (a combination of steroids and hydroxychloroquine) and supportive therapy. By the eighth day of hospitalization, her symptoms, especially thigh pain, resolved. Electromyocardiography was done, and the results were normal, indicating therapeutic success. This case highlights the importance of prompt diagnosis and management of myositis as a rare SLE manifestation to achieve favorable outcomes.