Simultaneous Thoracic Spine Metastatic Melanoma and Pre-existing Prostate Adenocarcinoma: A Unique Case Presentation and Literature Review.

In melanoma patients, distant metastases frequently manifest in the skin, lung, brain, liver, bone, and intestine. Notably, bone metastasis predominantly occurs within the axial skeleton, with the lumbar and thoracic spines being the most affected regions. Conversely, prostate cancer often disseminates to the bone, lung, liver, pleura, and adrenal glands. The spinal column, particularly the lumbar region, frequently harbors metastases in prostate cancer cases. Given the proximity of axial lesions to the spinal cord, patients commonly experience pain, weakness, and urinary dysfunction. This article presents a compelling case report of a patient initially diagnosed with metastatic prostate cancer, who later exhibited a metastatic lesion in the thoracic spine, subsequently identified as originating from acral melanoma on the plantar surface of the right foot. Histopathological examination confirmed the presence of acral melanoma in both the spine and the right foot. The patient received comprehensive treatment for advanced melanoma from a multidisciplinary team comprising medical and radiation oncologists. Considering the overlapping pathophysiology of prostate cancer and melanoma, simultaneous screening for both diseases in cases where one is detected could yield significant benefits, including enhanced morbidity and mortality outcomes and the facilitation of early detection for secondary malignancies.

Antibodies to an Epstein Barr Virus protein that cross-react with dsDNA have pathogenic potential.

Pathogens such as the Epstein Barr virus (EBV) have long been implicated in the etiology of systemic lupus erythematosus (SLE). The Epstein Barr virus nuclear antigen I (EBNA-1) has been shown to play a role in the development of anti-nuclear antibodies characteristic of SLE. One mechanism by which EBV may play a role in SLE is molecular mimicry. We previously generated two monoclonal antibodies (mAbs) to EBNA-1 and demonstrated that they cross-react with double-stranded DNA (dsDNA). In the present study, we demonstrate that these mAbs have pathogenic potential. We show that they can bind to isolated rat glomeruli and that binding can be greatly diminished by pretreatment of glomeruli with DNase I, suggesting that these mAbs bind dsDNA in the kidney. We also demonstrate that these antibodies can deposit in the kidney when injected into mice and can induce proteinuria and elicit histopathological alterations consistent with glomerulonephritis. Finally, we show that these antibodies can cross-react with laminin and collagen IV in the extracellular matrix suggesting that direct binding to the glomerular basement membrane or mesangial matrix may also contribute to the antibody deposition in the kidney. In summary, our results indicate that EBNA-1 can elicit antibodies that cross-react with dsDNA, that can deposit in the kidney, and induce kidney damage. These results are significant because they support the role of a viral protein in SLE and lupus nephritis.

Clinical Features, Diagnosis, and Management of Patients With Anderson-Fabry Cardiomyopathy.

Anderson-Fabry disease (AFD) is an X-linked recessive, multisystem disease of lysosomal storage. A mutation in the gene encoding the hydrolase enzyme α-galactosidase A results in its deficiency, or complete absence of activity. Subsequent progressive intracellular accumulation of glycosphingolipids, predominantly globotriaosylceramide, in various tissues, results in progressive organ dysfunction and failure, most commonly affecting the kidneys, nervous system, skin, eyes, vascular endothelium, and the heart. Cardiac involvement in AFD represents a leading cause of morbidity and mortality. Globotriaosylceramide accumulation affects cardiomyocytes, smooth muscle cells, vascular endothelial cells, and fibroblasts leading to various pathologies including valvular regurgitation, conduction disease and arrhythmias, coronary microvascular dysfunction, and right and left ventricular hypertrophy (LVH) leading to early diastolic dysfunction and late-stage systolic impairment. Diagnosis is on the basis of decreased plasma α-galactosidase activity in men and positive genetic testing in women. Contemporary large-scale screening studies have revealed a prevalence of 1%-5% in patients with unexplained LVH in multiple cohorts. Cardiac magnetic resonance imaging, with its unique tissue characterization capabilities, is the most important imaging modality to assess for cardiomyopathy in patients with AFD. Enzyme replacement therapy is indicated in AFD patients with significant organ involvement, and has been shown to clear sphingolipids from endothelial cells in other organs, as well as to reduce left ventricular mass as early as 6 months after starting treatment. There is increasing evidence that enzyme replacement therapy might be more effective if given at earlier stages of disease, before the development of LVH and myocardial fibrosis.