Coccidioidomycosis is an endemic fungal infection of the southwestern United States that may rarely produce mass-like pulmonary abnormalities mimicking malignancy. We describe a 70-year-old Hispanic woman with poorly controlled type 2 diabetes mellitus (HbA1c >14%) who presented after three days of generalized weakness, nonproductive cough, abdominal pain, nausea, vomiting, and progressive difficulty ambulating. CT demonstrated a 7.3 × 5.4 cm wedge-shaped necrotic right middle lobe mass with multiple bilateral pulmonary nodules. CT-guided biopsy of the mass demonstrated granulomatous inflammation with fungal elements, while subsequent serologic testing and bronchoalveolar lavage PCR supported pulmonary coccidioidomycosis. Her hospitalization was complicated by acute respiratory distress syndrome requiring invasive mechanical ventilation, prone positioning, and neuromuscular blockade; non-liposomal amphotericin B-associated acute tubular necrosis requiring hemodialysis; ventilator-associated Klebsiella pneumoniae pneumonia; and persistent encephalopathy with multifocal MRI abnormalities highly suggestive of central nervous system dissemination despite nondiagnostic cerebrospinal fluid studies. This case highlights how pulmonary coccidioidomycosis can mimic malignancy. It illustrates the multifactorial deterioration that may occur in susceptible hosts, emphasizing early tissue diagnosis, careful interpretation of suspected dissemination, and individualized antifungal and critical care management.

Cardiac implantable electronic device (CIED) pocket infection is the most common infectious complication following pacemaker implantation or generator replacement and generally requires complete device and lead extraction according to current international guidelines. Nevertheless, non-infectious disorders, including malignant disease, may closely mimic pocket infection, creating a challenging differential diagnosis and potentially leading to delayed diagnosis or unnecessary CIED extraction. Neoplastic involvement of the CIED pocket is exceptionally rare.

Oncocytic (Hurthle cell) carcinoma is an uncommon thyroid malignancy that tends to spread through the bloodstream and often concentrates radioactive iodine poorly. Spread to the brain is rare, and a solitary cerebellar deposit is rarer still. We describe a 44-year-old man who presented with neck swelling and was found to have a widely invasive oncocytic carcinoma with extensive vascular invasion and a minor classic papillary component (5%). He underwent total thyroidectomy with central neck dissection followed by radioactive iodine ablation with 150 mCi of iodine-131. The post-therapy scan showed uptake confined to the thyroid bed. Over the next 18 months, his serum thyroglobulin climbed steadily from 1.5 µg/L to 11.6 µg/L even though the thyroid-stimulating hormone (TSH)-stimulated diagnostic whole-body iodine scan remained negative. Fluorodeoxyglucose positron emission tomography/computed tomography then showed multiple hypermetabolic bilateral pulmonary nodules suspicious for metastases. Roughly 22 months after thyroidectomy, he developed progressive dizziness and headache. Magnetic resonance imaging (MRI) revealed a 3.3 × 3.2 × 3.1 cm mixed cystic and solid left cerebellar mass with surrounding vasogenic edema and mass effect on the brainstem. The mass was resected through a left suboccipital craniotomy. Histology showed a malignant epithelioid neoplasm with nested and trabecular growth, abundant granular eosinophilic cytoplasm, prominent nucleoli, scattered bizarre giant nuclei, and 8 mitoses per 2 mm[2] without necrosis. The tumor cells expressed cytokeratin AE1/AE3, CK7, TTF-1, and PAX-8 and were negative for CK20, CDX-2, synaptophysin, chromogranin, and S100, confirming thyroid origin. The metastasis fulfilled criteria for high-grade differentiated thyroid carcinoma with oncocytic features. His symptoms resolved after surgery, and stereotactic radiosurgery for the resection cavity was recommended. A rising thyroglobulin with negative iodine imaging represents a biochemical incomplete response and should prompt a search for structural disease recurrence. Because the brain lesion in our patient came to light only when symptoms appeared, brain MRI may be worth considering in patients with radiodiodine-refractory distant metastases.

Hereditary hemorrhagic telangiectasia (HHT) is a rare genetic disease characterized by epistaxis, telangiectasias, and arteriovenous malformations (AVMs). Clinical diagnosis of HHT is typically guided by fulfillment of the Curaçao criteria. HHT is a known risk factor for brain abscesses in the pediatric population, particularly in those with pulmonary AVMs, where intrapulmonary right-to-left shunting permits septic emboli to seed the brain. We report the case of a 9-year-old girl with asthma and chronic sinusitis who presented with 5 days of congestion, cough, and worsening headache in the setting of Coronavirus Disease 2019 infection. Due to persistent hypoxia and transient altered mental status, further evaluation was pursued, with brain magnetic resonance imaging revealing multiple ring-enhancing lesions and chest computed tomography (CT) demonstrating multiple pulmonary nodules. CT angiography confirmed diffuse pulmonary AVMs. Culture from a brain biopsy grew Streptococcus intermedius. Whole-genome sequencing identified a de novo heterozygous SMAD4 variant, supporting a molecular diagnosis of juvenile polyposis/HHT syndrome. This case illustrates an atypical presentation and early diagnosis of this syndrome, prompted by the incidental finding of multiple subclinical brain abscesses. It underscores the value of maintaining a broad differential and performing targeted diagnostic studies when encountering brain abscesses of unclear origin. Pulmonary AVMs should be considered as a potential etiology of brain abscess, particularly in patients with concomitant hypoxemia and when endocarditis has been excluded. Furthermore, genetic evaluation for HHT should be considered in pediatric patients with unexplained or multifocal brain abscesses, even when the Curaçao criteria are not met, as early recognition may help prevent neurologic complications.

Accurate differentiation of benign and malignant pulmonary nodules on computed tomography (CT) is important for early lung-cancer assessment. However, classification remains challenging because benign and malignant nodules may exhibit subtle differences in texture, margin irregularity, boundary sharpness, and internal morphology that may not be fully represented by conventional convolutional feature extraction.

Granulomatosis with polyangiitis (GPA) is a subtype of ANCA-associated vasculitis that can have a heterogeneous clinical presentation. Although classically involving the respiratory tract and kidneys, GPA can rarely present with predominant skeletal muscle involvement. This is unique given that skeletal muscle involvement has predominantly been associated with eosinophilic GPA and microscopic polyangiitis in the literature. Here, we detail a patient who presented with acute, progressive bilateral proximal lower extremity weakness and thigh pain, along with weight loss and transiently elevated creatine kinase and aldolase. The clinical course was complicated by temporally distinct focal cerebral infarctions, alongside findings of rhinosinusitis and multiple pulmonary nodules. Serology was positive for PR3-ANCA antibodies, and magnetic resonance angiography of the brain utilising black blood sequence confirmed central nervous system (CNS) vasculitis. Crucially, targeted biopsies of the right vastus lateralis and lung nodule demonstrated fibrinoid necrosis and necrotizing granulomatous inflammation, respectively. Together, this histopathological evidence strongly suggests the proximal myopathy and CNS infarction as the result of profound, systemic microvascular ischaemia. This case highlights that GPA may initially manifest as muscle weakness. Recognising this atypical presentation is crucial to ensure timely initiation of treatment to reduce disease-associated morbidity and mortality.

Although thyroid metastasis from colorectal carcinoma (CRC) is exceedingly rare, with a reported clinical incidence of ~0.1-0.3%, its detection typically signifies advanced-stage systemic disease. This atypical metastatic pattern generally correlates with a terminal stage and a historically poor prognosis, with a reported 5-year survival rate of <15%. A 78-year-old female presented with advanced sigmoid adenocarcinoma complicated by a thyroid mass that caused significant tracheal compression and was accompanied by multiple pulmonary metastases. The patient's initial clinical manifestations included chronic hematochezia and diarrhea. Given the patient's advanced age and poor baseline status, a palliative thyroidectomy was performed to alleviate acute airway obstruction, followed by levothyroxine replacement therapy. Postoperative histopathological examination and immunohistochemical profiling, including SATB2 and CK19 positivity together with PAX8 and TTF-1 negativity, supported a diagnosis of metastatic adenocarcinoma of colorectal origin. In conclusion, clinicians should maintain a low threshold of suspicion for secondary malignancies when evaluating new thyroid nodules in patients with a known history of CRC. Although the findings from a single case study have limited generalizability, this report underscores the potential value of multidisciplinary systemic staging and individualized palliative management in optimizing supportive care for patients with rare metastatic patterns.

Community-acquired pneumonia may occasionally be associated with unexpected respiratory deterioration despite apparent clinical, laboratory, and radiological improvement. We report a case of a previously healthy adult male who presented with progressive dyspnea, persistent cough, generalized weakness, malaise, and low-grade fever. Initial chest radiography showed no significant abnormalities despite marked respiratory symptoms, whereas chest computed tomography revealed bilateral bronchopneumonia with multiple centrilobular nodules and patchy ground-glass opacities. The patient was treated with intravenous meropenem, systemic corticosteroids, inhaled therapy, supplemental oxygen, and supportive care, with gradual improvement in inflammatory markers. On hospital day three, however, he developed sudden severe hypoxemic respiratory failure shortly after antimicrobial administration, requiring intensive care unit admission and high-flow nasal cannula oxygen therapy. Urgent CT pulmonary angiography excluded pulmonary embolism, follow-up imaging demonstrated partial regression of the pulmonary infiltrates, and cardiological evaluation showed no evidence of acute cardiac pathology. Meropenem was replaced with levofloxacin because a drug-related reaction could not be completely excluded. The patient's respiratory status subsequently improved rapidly with supportive treatment, and he was discharged without residual respiratory insufficiency. This case demonstrates that severe transient hypoxemic deterioration may occur during apparently successful treatment of bilateral bronchopneumonia and emphasizes the importance of promptly excluding pulmonary embolism, acute cardiac disease, drug-related reactions, and other potentially life-threatening causes of respiratory worsening.

Pulmonary tumour thrombotic microangiopathy (PTTM) is a rare but frequently fatal condition characterized by rapidly progressive pulmonary hypertension and right heart failure caused by tumour microemboli in the pulmonary vasculature. We report the case of a 64-year-old man who presented with rapidly progressive respiratory failure. Chest computed tomography demonstrated centrilobular nodules and a tree-in-bud (TIB) pattern. Pulmonary perfusion scintigraphy and transthoracic echocardiography suggested pulmonary hypertension with multiple peripheral perfusion defects, raising strong clinical suspicion for PTTM. Transbronchial lung biopsy (TBLB) revealed TTF-1-positive adenocarcinoma, although the primary tumour site remained undetermined. Based on these findings, clinically suspected PTTM was diagnosed and nivolumab monotherapy was promptly initiated as systemic treatment for the underlying malignancy. Despite transient severe deterioration, the patient's respiratory function improved markedly, and he has remained progression-free for more than 3 years. This case highlights the importance of early clinical recognition of PTTM and prompt initiation of appropriate systemic therapy, even before definitive identification of the primary tumour when clinically warranted.

Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is a systemic fibroinflammatory condition with highly variable pulmonary manifestations that frequently overlaps clinically, radiologically, and metabolically with primary malignancy, granulomatous disease, and vasculitis. Tissue diagnosis with immunohistochemical quantification of IgG4-positive plasma cells remains the diagnostic cornerstone. A 50-year-old male ex-smoker presented with a two-month history of progressive cough, dyspnoea, chest pain, and 8 kg of unintentional weight loss. Examination revealed digital clubbing and bilateral crepitations. Laboratory investigations showed mild normocytic anaemia, leukocytosis with neutrophilic predominance, and a markedly elevated erythrocyte sedimentation rate of 109 mm/h. Serum IgG4 was elevated at 2.23 g/L (reference range <1.35 g/L). Total IgG and comprehensive autoimmune and infectious serology were unremarkable. Positron Emission Tomography-Computed Tomography (PET-CT) demonstrated multiple bilateral pulmonary nodules (some cavitating) with an exceptionally high maximal standardised uptake value (SUVmax 20.1) and mediastinal lymphadenopathy, prompting strong initial suspicion of primary pulmonary malignancy. CT-guided lung biopsy revealed dense storiform fibrosis, a lymphoplasmacytic infiltrate rich in eosinophils, and features of fibroinflammatory change; however, immunohistochemistry did not demonstrate an increased number of IgG4-positive plasma cells, and formal histopathological criteria for IgG4-related disease were not fulfilled. In the context of compatible clinical, radiological, and serological findings, a diagnosis of probable IgG4-related lung disease was considered. Oral prednisolone at 0.6 mg/kg/day produced substantial clinical and radiological improvement, with near-complete resolution of opacities and reduction in nodule size by six months. This case illustrates the diagnostic pitfalls of IgG4-related lung disease, which can produce exceptionally high 18F-fluorodeoxyglucose (FDG) avidity on PET-CT, cavitating nodules, and constitutional features indistinguishable from malignancy. Histopathological evaluation with formal IgG4 cell quantification and ratio calculation is essential for accurate diagnosis; however, cases with supportive clinicoradiological features but non-diagnostic immunostaining may still pose significant diagnostic challenges. Early corticosteroid treatment yields excellent outcomes and prevents unnecessary oncological intervention.