Related Experiment Video
Updated: Jul 17, 2026

06:35
An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
[Simultaneous multiple myeloma and giant cell arteritis without systemic amyloidosis]
Barbara C Finn1, Pablo Young, Emanuel D Silva
1Servicio de Medicina Interna, Hospital Británico de Buenos Aires. barbarafinn73@hotmail.com
Medicina
|January 24, 2007
Summary
Giant cell arteritis and multiple myeloma are known to be associated with amyloidosis. This study reports the first case of multiple myeloma and giant cell arteritis without amyloidosis, suggesting a direct link between these conditions.
Area of Science:
- Rheumatology
- Hematology
- Pathology
Background:
- Primary systemic amyloidosis is associated with giant cell arteritis.
- Multiple myeloma, a plasma cell malignancy, is also linked to primary amyloidosis.
- Giant cell arteritis (GCA) is a vasculitis affecting large arteries.
Observation:
- This report details the first documented case of a patient diagnosed with both multiple myeloma and giant cell arteritis.
- Crucially, this patient did not exhibit any signs or symptoms of systemic amyloidosis.
Findings:
- The co-occurrence of multiple myeloma and giant cell arteritis in the absence of amyloidosis challenges previous understandings.
- This unique case suggests a potential direct pathogenic relationship between multiple myeloma and giant cell arteritis, independent of amyloidosis.
Implications:
- This finding may necessitate a re-evaluation of the etiological factors contributing to giant cell arteritis.
- Further research into the shared pathways between multiple myeloma and giant cell arteritis could reveal novel therapeutic targets.
- Understanding this association could improve diagnostic approaches for patients presenting with either condition.
Related Concept Videos
Multiple Sclerosis l: Introduction
Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Myasthenia Gravis ll: Pathophysiology
The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...