Leptomeningeal Enhancement due to Neurosarcoidosis Mimicking Malignancy

Saltijeral, Sahara N.; Grosu, Horiana B.; Garza, Henriette De La; O’Brien, Barbara; Iliescu, Gloria

doi:10.1155/2020/9513576

Cited by 5 publications

(3 citation statements)

References 8 publications

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“…Saltijeral et al have described a case of NS with leptomeningeal enhancement mimicking malignancy, similar to the patient in this case report. 9 ) Furthermore, Deguchi et al have reported a case of NS requiring differentiation from tuberculous meningitis. 10 ) Based on the finding by Kidd et al, who have reported that 14% and 40% of the patients with NS had pachymeningeal and leptomeningeal lesions, respectively, 2 ) NS can have pachymeningeal and leptomeningeal lesions mimicking malignant tumors or other diseases.…”

Section: Discussionmentioning

confidence: 99%

Isolated Neurohypophysial Sarcoidosis Involving the Cavernous Sinus Mimicking a Malignant Tumor

Kinoshita

Taguchi

Yamasaki

et al. 2022

NMC Case Report Journal

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Because of nonspecific clinical and radiological findings, it is difficult to diagnose isolated neurosarcoidosis without histological examination. Distinguishing neurosarcoidosis from neoplasm, infectious disease, or granulomatous disease can be challenging. In this study, we present a case of a 61-year-old female who presented with unilateral blindness. Magnetic resonance imaging (MRI) revealed a large invasive mass lesion located in the neurohypophysis with homogeneous enhancement after the injection of gadolinium. The lesion involved the bilateral cavernous sinus, which extended along the dura of the skull base with leptomeningeal lesions. Contrast-enhanced computed tomography (CT) and fluorodeoxyglucose positron emission tomography/CT of the entire body showed no other lesions. Biochemical examinations showed no useful data, including angiotensin-converting enzyme, β-glucan, soluble interleukin-2 receptor, and T-SPOT. Cerebrospinal fluid examination revealed only the elevation of total protein. Under the preoperative diagnosis of a malignant tumor or metastatic tumor, followed by tuberculosis, fungal infection, or granulomatous disease, a biopsy was performed to immediately determine the appropriate therapy, which revealed the histological diagnosis of sarcoidosis. After steroid therapy, the lesions had markedly shrunk as observed on MRI, and the eyesight of the patient's right eye was completely restored. In this case, without a biopsy, discriminating between sarcoidosis and a malignant tumor was difficult. We believe that a prompt histological diagnosis of an invasive isolated neurohypophysial mass lesion involving the bilateral cavernous sinus, which is similar to a malignant tumor, is essential for selecting the appropriate therapy.

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Section: Discussionmentioning

confidence: 99%

Isolated Neurohypophysial Sarcoidosis Involving the Cavernous Sinus Mimicking a Malignant Tumor

Kinoshita

Taguchi

Yamasaki

et al. 2022

NMC Case Report Journal

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“…At present, the diagnosis of LM mainly relies on MRI and cerebrospinal fluid (CSF) cytology, but their sensitivity is low ( 6 , 7 ). MRI findings of various diseases involving the leptomeningeal structures are similar to those of LM, with little distinctive capacity between some diseases and LM ( 8 , 9 ). CSF cytology remains the gold standard for the diagnosis of LM.…”

Section: Introductionmentioning

confidence: 95%

NSCLC Extracellular Vesicles Containing miR-374a-5p Promote Leptomeningeal Metastasis by Influencing Blood‒Brain Barrier Permeability

Jin,

Cui,

Niu

et al. 2024

Molecular Cancer Research

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Leptomeningeal metastasis (LM) is a devastating complication of advanced non-small cell lung cancer (NSCLC). Diagnosis and monitoring of LM can be challenging. Extracellular vesicles (EVs) microRNAs (miRNAs) have become a new noninvasive diagnostic biomarker. The purpose of this study was to examine the clinical value and role of EVs miRNAs in NSCLC-LM. According to next-generation sequencing (NGS), miRNAs with differential expression of EVs in serum of NSCLC patients with LM and non-LM were detected to find biological markers for the diagnosis of LM. Cellular and in vivo experiments were conducted to explore the pathogenesis of EVs miRNA promoting LM in NSCLC. In the present study, we first demonstrated the serum level of EV-associated miR-374a-5p in patients with LM of lung cancer was much higher than that in patients without LM and was correlated with the survival time of patients with LM. Further studies showed that EVs miR-374a-5p efficiently destroys tight junctions and the integrity of the cerebral microvascular endothelial cell barrier, resulting in increased blood-brain barrier (BBB) permeability. Mechanistically, miR-374a-5p regulates the distribution of ZO-1 and occludin in endothelial cells by targeting ADD3, increasing vascular permeability and promoting LM. Implications: These results suggest that serum NSCLC-derived EVs miR-374a-5p is involved in premetastatic niche formation by regulating the permeability of BBB to promote NSCLC-LM, and can be used as a blood biomarker for the diagnosis and prognosis of NSCLC-LM.

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“…Various diseases may present with leptomeningeal involvement, mimicking LMD. Currently, these have been sparsely described in the literature, primarily in the context of case reports, including rare instances of neuroborreliosis, giant cell arteritis, and sarcoidosis [ 148 , 149 , 150 ].…”

Section: Leptomeningeal Mimicsmentioning

confidence: 99%

Leptomeningeal Metastasis: A Review of the Pathophysiology, Diagnostic Methodology, and Therapeutic Landscape

Nguyen

Dada

et al. 2023

Current Oncology

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The present review aimed to establish an understanding of the pathophysiology of leptomeningeal disease as it relates to late-stage development among different cancer types. For our purposes, the focused metastatic malignancies include breast cancer, lung cancer, melanoma, primary central nervous system tumors, and hematologic cancers (lymphoma, leukemia, and multiple myeloma). Of note, our discussion was limited to cancer-specific leptomeningeal metastases secondary to the aforementioned primary cancers. LMD mechanisms secondary to non-cancerous pathologies, such as infection or inflammation of the leptomeningeal layer, were excluded from our scope of review. Furthermore, we intended to characterize general leptomeningeal disease, including the specific anatomical infiltration process/area, CSF dissemination, manifesting clinical symptoms in patients afflicted with the disease, detection mechanisms, imaging modalities, and treatment therapies (both preclinical and clinical). Of these parameters, leptomeningeal disease across different primary cancers shares several features. Pathophysiology regarding the development of CNS involvement within the mentioned cancer subtypes is similar in nature and progression of disease. Consequently, detection of leptomeningeal disease, regardless of cancer type, employs several of the same techniques. Cerebrospinal fluid analysis in combination with varied imaging (CT, MRI, and PET-CT) has been noted in the current literature as the gold standard in the diagnosis of leptomeningeal metastasis. Treatment options for the disease are both varied and currently in development, given the rarity of these cases. Our review details the differences in leptomeningeal disease as they pertain through the lens of several different cancer subtypes in an effort to highlight the current state of targeted therapy, the potential shortcomings in treatment, and the direction of preclinical and clinical treatments in the future. As there is a lack of comprehensive reviews that seek to characterize leptomeningeal metastasis from various solid and hematologic cancers altogether, the authors intended to highlight not only the overlapping mechanisms but also the distinct patterning of disease detection and progression as a means to uniquely treat each metastasis type. The scarcity of LMD cases poses a barrier to more robust evaluations of this pathology. However, as treatments for primary cancers have improved over time, so has the incidence of LMD. The increase in diagnosed cases only represents a small fraction of LMD-afflicted patients. More often than not, LMD is determined upon autopsy. The motivation behind this review stems from the increased capacity to study LMD in spite of scarcity or poor patient prognosis. In vitro analysis of leptomeningeal cancer cells has allowed researchers to approach this disease at the level of cancer subtypes and markers. We ultimately hope to facilitate the clinical translation of LMD research through our discourse.

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Leptomeningeal Enhancement due to Neurosarcoidosis Mimicking Malignancy

Cited by 5 publications

References 8 publications

Isolated Neurohypophysial Sarcoidosis Involving the Cavernous Sinus Mimicking a Malignant Tumor

Isolated Neurohypophysial Sarcoidosis Involving the Cavernous Sinus Mimicking a Malignant Tumor

NSCLC Extracellular Vesicles Containing miR-374a-5p Promote Leptomeningeal Metastasis by Influencing Blood‒Brain Barrier Permeability

Leptomeningeal Metastasis: A Review of the Pathophysiology, Diagnostic Methodology, and Therapeutic Landscape

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