Somatic-type malignant transformation (STM) is a rare but aggressive complication of nonseminomatous germ cell tumors (NSGCTs), most commonly arising from the teratomatous component and frequently occurring in metastatic sites. We report the case of a man in his 20s with a history of mixed NSGCT (50% yolk sac tumor, 40% teratoma, and 10% embryonal carcinoma) treated with left orchiectomy and chemotherapy in 2023, who initially responded to treatment but was subsequently lost to follow-up. He presented with one week of progressive dyspnea and pleuritic left-sided chest pain. Serum alpha-fetoprotein was markedly elevated at 2,966.7 ng/mL. Computed tomography demonstrated a progressive left hilar mass causing near-complete compression of the left mainstem bronchus with postobstructive consolidation, pulmonary vein tumor thrombus extending into the left atrium, a stable subcarinal metastatic mass, and a small left pleural effusion. Brain magnetic resonance imaging and transthoracic echocardiography were unremarkable except for normal cardiac function without intracardiac thrombus. CT-guided biopsy of the lung mass demonstrated adenocarcinoma consistent with a pulmonary phenotype. Following multidisciplinary evaluation, the lesion was determined to represent pulmonary adenocarcinoma arising from somatic-type malignant transformation of the teratomatous component of recurrent NSGCT. The patient remained clinically stable and was managed with close airway surveillance after Pulmonary and Critical Care Medicine consultation, with airway stenting or endobronchial debulking reserved for clinical deterioration. This case highlights the importance of recognizing STM in patients with recurrent NSGCT, as accurate diagnosis requires integration of clinical history, imaging, and pathology and has significant therapeutic and prognostic implications.
Neuropsychiatric systemic lupus erythematosus (NPSLE) is an uncommon but severe manifestation of systemic lupus with limited evidence to guide management when standard therapies fail. We report the case of a 19-year-old woman with new-onset SLE with myositis and nephritis overlap, positive for anti-Smith, anti-dsDNA, anti-PL7, and anti-Mi-2 antibodies with hypocomplementemia. Despite treatment with hydroxychloroquine and corticosteroids, she developed progressive weakness, catatonia and psychosis. MRI demonstrated diffuse cerebral volume loss. While hospitalized, she received IV methylprednisolone and mycophenolate mofetil, followed by cyclophosphamide, all with only transient improvement. Given her refractory disease, she underwent five sessions of therapeutic plasma exchange over eight days, which led to gradual resolution of catatonia and restoration of baseline mental and physical function without complications. This case underscores plasma exchange as a potential adjunctive therapy in severe, treatment-resistant NPSLE.
Polycythemia vera (PV) is a clonal myeloproliferative neoplasm primarily caused by the JAK2V617F mutation, present in 95% of patients. It results in erythropoietin-independent hematopoietic proliferation, erythrocytosis, increased hematocrit (Hct), leukocytosis, thrombocytosis, and hyperviscosity, predisposing patients to thrombotic events and neurologic deficits, including erythromelalgia and pruritus. Neurologic manifestations can occur, such as transient ischemic attack (TIA) and stroke. We report an 83-year-old woman, PV patient who presented with chorea and magnetic resonance imaging (MRI) of her brain showed pachymeningeal enhancement (dural-arachnoid enhancement); this radiological finding is most commonly described in intracranial hypotension, autoimmune conditions, infection, and neoplastic processes and has not been reported in PV. Laboratory findings included complete blood count (CBC) showed severe erythrocytosis, moderate leukocytosis with moderate, mild thrombocytosis; bone marrow (BM) aspiration and biopsy showed hypercellular BM and marked megakaryocytic hyperplasia; and positive JAK2V617F mutation with 80% JAK2 DNA, suggestive of PV as the underlying cause. The patient underwent phlebotomy and was started on Aspirin. Following treatment, she showed dramatic improvement in choreiform movements. Hydroxyurea 500 mg three times daily was subsequently added, leading to complete hematologic response and resolution of pachymeningeal thickening on follow up MRI. This case suggested association between polycythemia vera and choreiform movements and a possible mechanism is proposed.
End-tidal carbon dioxide (ETCO 2 ) monitoring is the standard method for confirming endotracheal tube placement during emergency airway management. However, massive pulmonary embolism can create paradoxical capnography findings that complicate airway confirmation and resuscitation efforts. We present two cases of cardiac arrest where massive pulmonary embolism masked expected ETCO 2 changes despite confirmed endotracheal tube placement. In the first case, a 33-year-old male with diabetic ketoacidosis developed cardiac arrest with absent colorimetric ETCO 2 change despite direct visualization of correct tube placement, leading to suspicion of massive pulmonary embolism. In the second case, a 68-year-old male who underwent below-knee amputation for necrotizing fasciitis experienced recurrent cardiac arrests with persistently low ETCO 2 values despite confirmed intubation and adequate ventilation. Both patients had massive pulmonary embolism confirmed on computed tomography pulmonary angiography and received thrombolytic therapy. These cases highlight that massive pulmonary embolism increases alveolar dead space, preventing carbon dioxide delivery to the alveoli and resulting in absent or persistently low ETCO 2 despite adequate ventilation. Clinicians should maintain high suspicion for pulmonary embolism when ETCO 2 remains paradoxically low despite confirmed endotracheal tube placement and adequate ventilation during cardiac arrest, particularly in patients with risk factors for venous thromboembolism.
Primary central nervous system lymphoma (PCNSL) is a rare extranodal lymphoma most commonly involving the brain and leptomeninges. While high-dose methotrexate (HD-MTX)-based therapy has improved outcomes, relapse remains common and typically occurs within the CNS. Isolated ocular relapse after prolonged CNS remission is uncommon and diagnostically challenging. We report the case of a 78-year-old woman diagnosed in 2020 with PCSNL presenting with subacute constitutional and neurologic symptoms found to have a right frontal periventricular mass. She achieved complete radiographic remission following induction with HD-MTX and rituximab and remained free of CNS disease for nearly five years on serial surveillance imaging. Beginning in 2023, she developed progressive unilateral visual decline that was initially attributed to age-related macular degeneration, with repeatedly negative MRI studies of the brain and orbits. In 2025, further ophthalmologic evaluation with an ocular oncologist revealed vitreous and retinal involvement confirming isolated ocular relapse in the absence of systemic recurrence. She was retreated with HD-MTX and rituximab, resulting in clinical and fundoscopic improvement. This case highlights a rare pattern of delayed isolated ocular relapse following long-term remission in PCNSL. It underscores the limitations of neuroimaging in detecting ocular disease and emphasizes the importance of continued ophthalmologic surveillance with those specifically trained in ocular oncology in patients with persistent visual symptoms. Guideline-consistent systemic retreatment may provide effective disease control even in late relapse, particularly in patients with prior methotrexate sensitivity.
Human herpesvirus 6 (HHV-6) reactivation is a rare but serious complication of chimeric antigen receptor T-cell (CAR-T) therapy that can overlap with immune effector cell-associated neurotoxicity syndrome (ICANS) or cytokine release syndrome (CRS), making diagnosis and management challenging. We describe a 68-year-old man with relapsed/refractory IgA kappa multiple myeloma who received multiple prior therapies, including CyBorD, mVRD-lite, Dara-CyBorD, VD-ACE, and KPd, before undergoing lymphodepleting chemotherapy and CAR-T infusion. Early after infusion he developed grade 2 CRS and ICANS that improved with tocilizumab and corticosteroids, followed by recurrent encephalopathy with progressive neurologic decline. Initial infectious evaluation was negative, but repeat cerebrospinal fluid (CSF) and plasma polymerase chain reaction testing revealed HHV-6 reactivation. Antiviral therapy with foscarnet, later switched to ganciclovir, was initiated with corticosteroids and intravenous immunoglobulin. Although repeat CSF testing showed transient viral clearance, neurologic function continued to decline, and brain MRI demonstrated findings consistent with ICANS, including scattered white matter signal abnormalities and dural enhancement. Despite aggressive management, the patient developed multiorgan failure and died. This case illustrates the diagnostic complexity of HHV-6 reactivation during CAR-T therapy, where overlapping clinical and radiologic features with ICANS can obscure recognition; profound immunosuppression from prior treatment and CAR-T-induced immune dysregulation likely predisposed to viral reactivation. HHV-6 reactivation is a critical, underrecognized cause of neurotoxicity after CAR-T therapy, and clinicians should maintain a high index of suspicion in patients with delayed or atypical neurotoxicity, since early virologic testing and prompt antiviral therapy may improve outcomes in this vulnerable population.
Malignant pleural effusions (MPEs) are almost always exudative, with only an estimated 3–4% meeting biochemical criteria for a transudate. Light’s criteria remain the standard method for classifying pleural effusions, and transudative effusions typically do not undergo cytologic evaluation. This may delay the diagnosis of malignancy in rare cases where malignant cells are present in a biochemically transudative effusion. We present a 41-year-old homeless man with no established primary care who presented with progressive muscle cramping and was found to have severe electrolyte abnormalities, leukocytosis, and a right-sided pleural effusion with new bilateral pulmonary nodules on computed tomography. Pleural fluid analysis met clear transudative criteria by Light’s criteria (protein ratio 0.24, LDH ratio 0.44). However, cytology revealed clusters of atypical cells consistent with pulmonary adenocarcinoma, confirmed by thyroid transcription factor-1 (TTF-1) positivity. The patient had no identifiable cause of transudative effusion, including heart failure, cirrhosis, nephrotic syndrome, or significant hypoalbuminemia. This case illustrates a rare presentation of malignant pleural effusion masquerading as a transudate in the absence of confounding systemic conditions. The mechanism likely involves early pleural metastatic involvement before the development of significant vascular permeability changes or lymphatic obstruction. This report underscores the importance of maintaining clinical suspicion for malignancy despite transudative biochemistry, particularly when features such as unilateral effusion, atypical imaging findings, or absence of an alternative systemic cause are present.
A young woman presented with left hip pain for one week. She had been admitted to another hospital one month prior for right ankle pain and was undergoing treatment for septic arthritis with home IV antibiotics. Imaging of the left hip and right ankle was consistent with septic arthritis, but washout of the left hip and right ankle yielded negative gram stain and bacterial cultures. Due to persistent fevers, further imaging revealed miliary tuberculosis, and AFB testing of the washout fluid from the right ankle eventually resulted positive for Mycobacterium tuberculosis. The patient was placed on airborne isolation and started on Rifampin, Isoniazid, Pyrazinamide and Ethambutol for a duration of one year.
Denosumab, a monoclonal antibody (mAb) targeting receptor activator of nuclear factor-κB ligand (RANKL), is commonly used in managing metabolic bone diseases and giant cell tumors (GCTs) of bone. Growing evidence suggests that RANKL inhibition may influence cardiovascular health by impacting endothelial function, inflammatory pathways, vascular smooth muscle cell behavior, and systemic calcium regulation. We report a case of a 48-year-old Caribbean-South Asian man with recurrent GCTs who received three subcutaneous doses of denosumab and soon thereafter developed an anterior ST-elevation acute coronary syndrome (STE-ACS). The patient had no traditional cardiometabolic risk factors. Coronary angiography revealed thrombotic occlusion of the proximal left anterior descending artery (LAD), which was successfully treated with primary percutaneous coronary intervention (PPCI) and guideline-directed medical therapy (GDMT). Given the lack of modifiable risk factors, a significant family history, and biologically plausible mechanisms linking RANKL inhibition to atherothrombotic events, a denosumab-associated myocardial infarction was considered the most probable cause.
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a well-recognized complication of end-stage kidney disease (ESKD), encompassing abnormalities in calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolism, and bone turnover. In advanced cases, secondary or tertiary hyperparathyroidism may lead to severe skeletal disease, including osteitis fibrosa cystica and brown tumors, which can mimic hematologic malignancies. We present the case of a 47-year-old man with childhood-onset focal segmental glomerulosclerosis (FSGS), two prior kidney transplants, and long-standing dialysis dependence who presented with bone pain, pancytopenia, neurologic symptoms, and imaging abnormalities initially concerning for multiple myeloma. Comprehensive evaluation revealed a single unifying diagnosis: severe tertiary hyperparathyroidism (parathyroid hormone 1,467 pg/mL) with advanced renal osteodystrophy and brown tumor-like skeletal changes, without evidence of plasma cell dyscrasia or marrow infiltration. This case highlights the diagnostic pitfalls posed by extreme manifestations of CKD-MBD and underscores the importance of prioritizing cohesive pathophysiologic reasoning in complex ESKD patients.
May-Thurner Syndrome (MTS) is an underrecognized anatomic cause of left-sided deep vein thrombosis (DVT) resulting from compression of the left common iliac vein by the overlying right common iliac artery. Although it accounts for approximately 2-5% of DVT cases, it may be overlooked when other provoking risk factors are present, leading to incomplete treatment and risk of recurrence. We report a 61-year-old woman with no prior history of venous thromboembolism who presented with one week of progressive left lower extremity swelling and pain following recent femoral venous catheterization during a prior hospitalization. Imaging demonstrated extensive proximal iliofemoral DVT involving the left external iliac, common femoral, and superficial femoral veins. Despite initiation of intravenous anticoagulation, the significant clot burden prompted aspiration mechanical thrombectomy. Post-procedural venography revealed persistent residual stenosis of the left common iliac vein, raising suspicion for underlying iliac vein compression. The distribution of thrombosis and focal stenosis was consistent with MTS. Balloon venoplasty was unsuccessful, and definitive management was achieved with placement of a 16 mm × 80 mm venous stent, resulting in restoration of inline venous flow. The patient was transitioned to oral anticoagulation with dual antiplatelet therapy and experienced clinical improvement without complications. This case highlights MTS as an important and potentially underdiagnosed cause of extensive left-sided DVT, particularly when thrombus burden appears disproportionate to apparent provoking factors. Recognition of this anatomic variant is essential, as anticoagulation alone may be insufficient and endovascular intervention is often required to prevent recurrence and long-term venous morbidity.
Epilepsia partialis continua is an uncommon form of focal status epilepticus characterized by continuous focal motor activity with preserved awareness. In adolescents with psychiatric comorbidity, these movements may be mistaken for functional or compulsive behavior, a phenomenon that may reflect diagnostic overshadowing, the misattribution of neurological or medical symptoms to a preexisting psychiatric condition. A 15-year-old boy with anxiety disorder, obsessive compulsive disorder, and panic disorder presented with a two week history of persistent right toe and foot tapping that spread proximally and became painful. His family reported that the movements continued during sleep, although inpatient observation showed that they occasionally paused or disappeared. This inconsistency contributed to an early impression of a psychogenic process and led to the deferral of neuroimaging. Continuous video EEG subsequently demonstrated frequent, rapidly recurring epileptiform discharges over the left central region that corresponded to the right foot movements, confirming epilepsia partialis continua. Treatment with lacosamide and clobazam led to complete resolution of the movements and pain within 24 hours. Subsequent brain MRI was unremarkable, and symptoms remained controlled on follow up. This case illustrates how psychiatric history can shape diagnostic reasoning and delay recognition of epilepsia partialis continua. Persistent focal motor activity, even when intermittently suppressible or behaviorally ambiguous, should prompt early consideration of this diagnosis and escalation to prolonged video EEG when routine evaluation is inconclusive, enabling accurate diagnosis and effective seizure control.
Griscelli syndrome type 2 (GS2) is a rare autosomal recessive immunodeficiency disorder characterized by silver-colored hair, fair skin, and an increased risk of developing hemophagocytic lymphohistiocytosis (HLH). Systemic juvenile idiopathic arthritis (sJIA) is an autoinflammatory condition distinguished by daily fevers, transient rash, and arthritis, with macrophage activation syndrome being a known complication. We present a case involving an 18-month-old female with persistent fever, rash, and joint inflammation. Laboratory findings revealed elevated inflammatory markers and hyperferritinemia, prompting concern for HLH, though full diagnostic criteria were not satisfied. A unique clinical sign led to extended evaluation, and genetic testing confirmed the presence of GS2. Concurrent clinical features also met the requirements for sJIA. To the best of our knowledge, this is the first reported instance of GS2 co-occurring with sJIA. This case highlights a potential shared susceptibility to immune dysregulation and raises the possibility that immunodeficiency may reveal or influence the manifestation of autoinflammatory diseases. Prompt recognition is essential in managing atypical and treatment-resistant inflammatory presentations.
Peritoneal tuberculosis (PT) is a rare form of extrapulmonary Mycobacterium tuberculosis infection that may closely mimic Crohn’s disease (CD) or intra-abdominal malignancy, leading to diagnostic delay, particularly in endemic areas. We report two illustrative cases complicated by localized abscess formation. The first case involved a 40-year-old woman presenting with chronic right lumbar pain. Computed tomography (CT) revealed a large right psoas abscess associated with circumferential thickening of the cecal base and terminal ileum, along with necrotic mesenteric and iliac lymphadenopathy. Colonoscopy showed ulcerative ileocolitis, and histology demonstrated chronic granulomatous inflammation suggestive of either tuberculosis or CD. CT-guided biopsy of the abscess wall was performed, and polymerase chain reaction testing for Mycobacterium tuberculosis was positive. Histopathology examination was consistent with tuberculosis. The patient responded well to anti-tuberculous therapy with complete radiological resolution. The second case concerned a 17-year-old male admitted with right iliac fossa pain, fever, weight loss, and night sweats. CT showed a right pelvic collection adjacent to the ileocecal junction with distal ileal and cecal thickening, initially suggesting CD. Colonoscopy revealed ulcerative ileitis with granulomatous inflammation. As radiological drainage was not feasible, laparoscopy was performed and showed a friable micronodular peritoneum with terminal ileitis. Peritoneal biopsies demonstrated non caseating granulomatous inflammation, consistent with peritoneal and ileocecal tuberculosis. These cases highlight that PT may present as localized abdominal or psoas abscesses and closely mimics CD. Early integration of imaging, endoscopy, tissue sampling, and microbiological or molecular testing is essential for prompt diagnosis and appropriate curative treatment.
Melanoma is an aggressive malignancy with a high propensity for metastasis; however, clinically apparent involvement of the gastrointestinal tract is uncommon. We report a case of metastatic melanoma involving the stomach that presented as gastrointestinal bleeding shortly after initial diagnosis. A patient with recently diagnosed melanoma with nodal metastasis presented with melena and symptomatic anemia. Esophagogastroduodenoscopy revealed multiple gastric mucosal lesions that were notably amelanotic, lacking the characteristic pigmentation typically associated with melanoma. Histopathological and immunohistochemical evaluation confirmed metastatic melanoma, and imaging findings were concerning for advanced disease. The presence of pneumatosis raised suspicion for mucosal compromise and possible early perforation, highlighting the potential severity of gastrointestinal involvement. Gastrointestinal metastases from melanoma are often clinically silent and may present with nonspecific symptoms, leading to delayed diagnosis. This case is notable for early symptomatic presentation and the presence of amelanotic lesions, which may be easily overlooked during endoscopic evaluation. The absence of pigmentation can pose a diagnostic challenge and requires a high index of suspicion in patients with a history of melanoma. Early endoscopic evaluation and tissue diagnosis are essential for timely recognition and management. Clinicians should maintain a high index of suspicion for gastrointestinal metastases in melanoma patients presenting with unexplained anemia or bleeding, even in the absence of classic endoscopic features.
Myeloproliferative neoplasms (MPNs) are commonly linked to driver mutations in the JAK2, MPL, and CALR genes. In contrast, SH2B3 (LNK) mutations are uncommon and remain an under-characterized contributor to dysregulated JAK-STAT signaling. The clinical features and treatment responsiveness of SH2B3-mutated MPNs are not well defined, and data on outcomes with ropeginterferon alfa-2b in this molecular subgroup are limited. We report a 75-year-old man who presented for evaluation of headache, generalized bone pain, and night sweats and was found to have abnormal blood counts including persistent leukocytosis, erythrocytosis, and thrombocytosis. Prior molecular testing was negative for JAK2, MPL, and CALR mutations. Bone marrow examination showed hypercellularity with panmyelosis, mild megakaryocytic atypia, and WHO grade 1 reticulin fibrosis. Hematologic next-generation sequencing identified a pathogenic SH2B3 c.1481C>G (p.Ser494*) nonsense mutation, predicted to result in a loss of SH2B3’s C-terminal regulatory domain. Given the tri-lineage cytoses and marrow findings, a diagnosis of SH2B3-mutated MPN was established. He was started on ropeginterferon alfa-2b, resulting in resolution of his symptoms and complete hematologic response (WBC ≤ 10 × 10 3 /μL, Hct ≤ 45%, and PLT ≤ 400 × 10 3 /μL) within 12 weeks, without the need for phlebotomy or treatment-limiting adverse effects. This case underscores the clinical significance of SH2B3 mutations as a driver of triple-negative MPNs and supports their inclusion in molecular evaluation when classical mutations are absent. The favorable clinical and hematologic response to ropeginterferon alfa-2b suggests that interferon-based therapy may be effective in SH2B3-mutated MPNs.
Antiphospholipid syndrome is a systemic autoimmune disorder characterized by thrombotic events in the presence of antiphospholipid antibodies including lupus anticoagulant, anticardiolipin, and anti-β2-glycoprotein I antibodies. Catastrophic antiphospholipid syndrome is a rare but life-threatening variant, accounting for less than 1% of antiphospholipid syndrome cases, and is characterized by rapid progressive microvascular thrombosis and multiorgan failure. We report the case of a middle-aged man who developed catastrophic antiphospholipid syndrome associated with systemic lupus erythematosus, presenting with diffuse alveolar hemorrhage, acute kidney injury, vasculitis skin lesions, and severe thrombocytopenia. Management requires intensive care support, immunosuppressive therapy, intravenous immunoglobulin administration, cyclophosphamide administration, and delayed plasmapheresis. Despite multi-organ involvement and guarded prognosis, the patient survived following multidisciplinary management. This case highlights the importance of early recognition, rapid therapeutic intervention, and coordinated interdisciplinary care to improve survival in patients with catastrophic antiphospholipid syndrome.
Autoimmune pericarditis is commonly idiopathic but may represent the initial manifestation of systemic autoimmune disease. Hepatic autoimmune disorders rarely present with primary cardiac involvement, and recognition of extrahepatic presentations is essential for early diagnosis and prevention of organ damage. Autoimmune hepatitis-primary biliary cholangitis (AIH-PBC) overlap syndrome is an uncommon entity characterized by combined hepatocellular and cholestatic immune-mediated injury. A previously healthy young woman presented with progressive pleuritic chest pain and dyspnea and was found to have a large pericardial effusion causing hemodynamic compromise requiring surgical drainage. Pericardial pathology demonstrated acute and chronic fibrinous pericarditis. Initial evaluation revealed elevated inflammatory markers and mild transaminitis with positive autoimmune serologies including antinuclear antibody and anti-smooth muscle antibody. Following clinical improvement, she developed recurrent pericarditis accompanied by worsening liver enzyme abnormalities. Liver biopsy demonstrated chronic active hepatitis with bile duct injury and bridging fibrosis, consistent with autoimmune hepatitis-primary biliary cholangitis overlap syndrome. Cardiac magnetic resonance imaging confirmed active pericardial inflammation without myocarditis. Immunosuppressive therapy with corticosteroids followed by azathioprine resulted in clinical stabilization. This case highlights autoimmune pericarditis as the presenting manifestation of AIH-PBC overlap syndrome and underscores the importance of evaluating unexplained pericarditis for systemic autoimmune disease. Early recognition of cardio-hepatic autoimmune overlap allows timely immunosuppressive therapy and may prevent progression to advanced hepatic fibrosis.
Autoimmune pancreatitis (AIP) is an uncommon inflammatory condition of the pancreas characterized by glandular enlargement and ductal narrowing arising from dysregulated immune activity. Its clinical and imaging overlap with pancreatic malignancy makes accurate distinction essential. We describe a case series of four patients who initially presented with a pancreatic mass suspicious for malignancy, but received a confirmed diagnosis of AIP following thorough diagnostic evaluation. The cohort comprised three male patients (aged 32, 55, and 68 years) and one female patient (aged 73 years). The predominant presenting features included abdominal pain (n=2), scleral icterus (n=3), and pruritus (n=1). Laboratory workup demonstrated elevated total and direct bilirubin in all patients, and serum IgG4 levels were above the normal range in every case. Cross-sectional abdominal imaging with contrast-enhanced CT or MRI identified a pancreatic mass in each patient. All four patients underwent endoscopic ultrasound (EUS)-guided fine needle biopsy (FNB) with rapid on-site evaluation (ROSE), none of which revealed evidence of malignancy. Histopathologic examination showed intact pancreatic acinar architecture in all cases; chronic inflammation and fibrosis were noted in three patients. IgG4 and CD138 immunohistochemical staining was non-reactive in three patients. All patients underwent endoscopic retrograde cholangiopancreatography (ERCP) with biliary stent placement to address biliary obstruction. Interval ERCP confirmed resolution of the obstruction, enabling stent removal without subsequent recurrence. Following establishment of an AIP diagnosis, all patients were treated with a corticosteroid taper, resulting in symptomatic resolution and complete radiologic clearance of the pancreatic mass, with removal of biliary stents thereafter. Patients remained asymptomatic with no evidence of relapse at 3-, 6-, and 12-month follow-up intervals.
