Anabolic androgenic steroids (AAS) are a class of hormones that are used for hormonal replacement therapy in cases of male hypogonadism and for a few other medical conditions, mainly anemias, as well as for the female-to-male transition process. At the same time, AAS are widely abused for their muscle-building and strength-increasing properties. Among their side effects, androgens can exert a toxic effect on the liver, causing hepatotoxicity, but they can also induce hepatocyte proliferation and malignant transformation. Hepatocellular adenoma (HCA) and hepatocellular carcinoma (HCC) are two primary liver lesions that have been described as potentially related to AAS. This review provides an up-to-date analysis of how androgens can induce liver carcinogenesis and a comprehensive overview on the available data in the literature about AAS and primary liver tumors.

This report describes pulmonary nocardiosis in autoimmune pulmonary alveolar proteinosis (PAP), characterized by delayed microbiological diagnosis and a severe fluoroquinolone-associated adverse reaction. The autoimmune form, mediated by anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antibodies, predisposes patients to opportunistic infections due to impaired alveolar macrophage function. We describe a 48-year-old male smoker with a history of recurrent respiratory infections who presented with fever and hypoxemic respiratory failure. High-resolution CT demonstrated bilateral ground-glass opacities with superimposed interlobular septal thickening, consistent with a diffuse crazy-paving pattern predominantly involving the lower lobes, associated with focal consolidations in the left lower and right upper lobes. Despite initiation of broad-spectrum antimicrobial therapy, the patient exhibited clinical deterioration characterized by recurrence of fever, rising inflammatory markers (C-reactive protein (CRP) 298 mg/L), worsening hypoxemia with a decline in the PaO₂/FiO₂ ratio to 168, and radiological progression on repeat high-resolution computed tomography (HRCT), demonstrating increased areas of consolidation and expansion of ground-glass opacities. A milky-appearing bronchoalveolar lavage (BAL) initially yielded negative cultures; however, after 14 days of incubation, it revealed growth of Nocardia wallacei, identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). A diagnosis of autoimmune PAP was confirmed through the detection of anti-GM-CSF antibodies. The clinical course was complicated by relapse and a left-sided tendon rupture occurring after 10 days of fluoroquinolone therapy. The patient eventually achieved stability through a multidrug regimen followed by long-term secondary prophylaxis with cotrimoxazole for a total of 12 months. This case underscores the diagnostic challenge posed by slow-growing pathogens in patients with underlying rare lung diseases and highlights the necessity of maintaining a high index of suspicion for opportunistic infections when standard treatments fail.

Progressive supranuclear palsy (PSP) is a rare neurodegenerative tauopathy characterized by early postural instability, vertical supranuclear gaze palsy, axial rigidity, and poor response to levodopa therapy. Diagnosis remains challenging, particularly in the early stages, because of overlap with other Parkinsonian syndromes. We report the case of an 83-year-old woman who developed progressive gait instability, severe functional decline, dysphagia, and marked weight loss following a mild SARS-CoV-2 infection. Extensive investigations initially excluded metabolic, infectious, neoplastic, and structural causes. Neurological examination revealed axial and limb bradykinesia, hypomimia, hypophonia, apraxia, severe postural instability, and vertical gaze limitation. Oculomotor assessment also documented square wave jerks and eyelid opening apraxia. Levodopa therapy was ineffective. Brain MRI demonstrated marked midbrain atrophy with relative preservation of pontine volume, producing the characteristic hummingbird sign and Mickey Mouse sign. DAT-SPECT showed bilateral putaminal dopaminergic deficit, supporting a degenerative Parkinsonian syndrome. A diagnosis of probable PSP was established according to Movement Disorder Society criteria, clinical presentation, absence of levodopa responsiveness, and supportive imaging findings. This case highlights the diagnostic complexity of PSP when nonspecific systemic manifestations precede neurological deterioration and emphasizes the value of integrating clinical assessment with structural and functional neuroimaging.