森 墾

We report a case of a man in his 60s with ROS1 fusion-positive lung adenocarcinoma who developed multiple cystic lesions in both the kidneys and liver during crizotinib treatment. The patient presented with fever, abdominal pain, and oliguria. Contrast-enhanced CT revealed new cystic lesions in both the kidneys and liver, with some showing thick walls, septa, and hyperdense contents. MRI demonstrated heterogeneous signal intensities on T2-weighted images and mixed low to high signal intensities on T1-weighted images. Some cysts displayed T2 hypointense and T1 hyperintense areas along the cyst walls, with diffusion restriction predominantly at the periphery of the masses. Percutaneous drainage of the cysts was performed, and cytology revealed an increase in the number of cells, including neutrophils. However, no malignant cells or microorganisms were detected. Based on these imaging findings and laboratory results, the patient was diagnosed with crizotinib-associated renal and hepatic cysts. Symptoms improved after crizotinib discontinuation, and follow-up imaging showed cyst regression. This is the first report describing MRI findings for crizotinib-associated hepatic cysts. Characteristic MRI findings, such as T2 hypointensity/T1 hyperintensity along the cyst walls and diffusion restriction predominantly at the periphery of the masses, suggesting hemorrhagic components, may help differentiate crizotinib-associated cysts from other lesions, including metastases and abscesses.

Mucosa-associated lymphoid tissue (MALT) lymphoma commonly arises from chronic inflammation or autoimmune diseases, such as Sjögren syndrome (SjS). Although rare, amyloid deposition in MALT lymphoma has been reported. We present a rare case of parotid gland MALT lymphoma in a 49-year-old woman, in whom preoperative diagnosis was challenging due to atypical imaging findings resulting from amyloid deposits. MRI showed T2-hypointense and T1-iso- to slightly hyperintense masses in the left parotid gland and right sublingual gland, with predominant marginal contrast enhancement and no significant diffusion restriction. Additionally, atrophy and fatty replacement of the parenchyma were noted in bilateral parotid glands, suggesting SjS. Left superficial parotidectomy was performed and pathological findings confirmed MALT lymphoma with extensive amyloid deposition. Histopathological findings of the resected parotid gland parenchyma also suggested SjS. MALT lymphoma should be considered in the differential diagnosis of multiple salivary gland masses in patients with suspected SjS. If MRI reveals atypical imaging findings for malignant lymphoma, particularly T2-hypointensity with no significant diffusion restriction, the possibility of amyloid deposition in MALT lymphoma should be considered.

We herein report a case of reversible cerebral vasoconstriction syndrome (RCVS) with an unusual presentation of hyperdense blood vessels. A 53-year-old woman developed thunderclap headache. Brain computed tomography (CT) showed hyperdensity of the anterior cerebral artery. Brain magnetic resonance imaging revealed cerebral infarctions in the left anterior cerebral artery (ACA) territory and cerebellum. The left ACA presented with a hyperintense vessel sign, although magnetic resonance angiography (MRA) appeared normal. One week later, stenotic changes were confirmed using MRA. The vasoconstriction disappeared on day 20, and the patient was diagnosed with RCVS. CT-defined hyperdense vessel signs can be observed at an early stage of RCVS, leading to ischemic events.

We herein report a novel de novo KCNH5 variant in a patient with refractory epileptic encephalopathy. The patient exhibited seizures at 1 year and 7 months old, which gradually worsened, leading to a bedridden status. Brain magnetic resonance imaging (MRI) showed cerebral atrophy and cerebellar hypoplasia. A trio whole-exome sequence analysis identified a de novo heterozygous c.640A>C, p.Lys214Gln variant in KCNH5 that was predicted to be deleterious. Recent studies have linked KCNH5 to various epileptic encephalopathies, with many patients showing normal MRI findings. The present case expands the clinical spectrum of the disease, as it is characterized by severe neurological prognosis, cerebral atrophy, and cerebellar hypoplasia.