Multiple Myeloma

By SWA

Multiple myeloma is a type of blood cancer that originates in the plasma cells, a kind of white blood cell responsible for producing antibodies. To understand the terms "Hx," "lytic lesion," and "mott cell with Russell bodies" in the context of multiple myeloma, let's break them down:

1. Hx

"Hx" is shorthand for "history." In medical contexts, it often refers to the patient's medical history. When diagnosing multiple myeloma, a thorough patient history is crucial, which may include:

  • Chronic back pain or bone pain.
  • History of frequent infections.
  • Symptoms of anemia, such as fatigue and pallor.
  • Kidney dysfunction signs, including changes in urine output or blood tests showing elevated creatinine.

2. Lytic Lesion

Lytic lesions are areas of bone destruction caused by the abnormal proliferation of myeloma cells. These cells stimulate osteoclasts (bone-resorbing cells), leading to the breakdown of bone tissue. Features of lytic lesions include:

  • Appearing as "punched-out" areas on X-rays.
  • Causing bone pain, fractures, and hypercalcemia (elevated calcium levels in the blood).
  • Commonly found in the skull, spine, ribs, and pelvis.

3. Mott Cell with Russell Bodies

Mott cells are abnormal plasma cells characterized by the presence of Russell bodies. Let's delve into these terms:

  • Mott Cell: A type of plasma cell that contains multiple inclusions or vacuoles filled with immunoglobulins.
  • Russell Bodies: These are eosinophilic, globular inclusions within the rough endoplasmic reticulum of plasma cells. They represent accumulations of immunoglobulins (IgGs) that the cell is unable to secrete properly. These are seen as large, round inclusions that stain positively with periodic acid-Schiff (PAS) and are typically associated with excess immunoglobulin production.

In multiple myeloma, the excessive production of abnormal immunoglobulins (monoclonal proteins or M-proteins) by malignant plasma cells can lead to the formation of Russell bodies. These inclusions are indicative of a high turnover of immunoglobulin synthesis and can be identified in bone marrow biopsy samples.

Understanding Multiple Myeloma

Multiple myeloma is characterized by the uncontrolled proliferation of malignant plasma cells in the bone marrow, leading to several key clinical features:

  • Bone disease: Osteolytic lesions, pathological fractures, and bone pain.
  • Hypercalcemia: Elevated calcium levels due to bone resorption.
  • Anemia: Due to bone marrow infiltration and kidney dysfunction.
  • Renal impairment: Caused by light chain deposition in kidneys, hypercalcemia, and hyperuricemia.
  • Infections: Due to immunodeficiency from the decreased production of normal immunoglobulins.

Diagnosis

Diagnosis typically involves:

Blood Tests Showing Elevated M-Protein Levels

  • M-Protein (Monoclonal Protein): M-proteins are abnormal antibodies produced in excess by malignant plasma cells. Blood tests can detect and quantify these proteins.
  • Serum Protein Electrophoresis (SPEP): This test separates proteins in the blood based on their electrical charge. In multiple myeloma, a sharp spike (M spike) in the gamma region indicates the presence of monoclonal proteins.
  • Immunofixation Electrophoresis (IFE): This test identifies the specific type of monoclonal protein (IgG, IgA, IgM, etc.).
  • Serum Free Light Chain Assay: Measures the amount of free light chains (kappa and lambda) in the blood. An abnormal ratio of kappa to lambda light chains is indicative of multiple myeloma.
  • Additional Blood Tests: Complete blood count (CBC) to check for anemia, renal function tests (creatinine and blood urea nitrogen), calcium levels (hypercalcemia), and beta-2 microglobulin levels for prognosis.

Urine Tests for Bence Jones Protein (Free Light Chains)

  • 24-Hour Urine Collection: Collecting all urine produced in 24 hours to measure the total amount of light chains excreted.
  • Urine Protein Electrophoresis (UPEP): Similar to SPEP, this test separates proteins in the urine. The presence of Bence Jones proteins, which are free light chains, is a key diagnostic marker.
  • Immunofixation of Urine Proteins: Identifies the specific type of light chains (kappa or lambda) in the urine.

Bone Marrow Biopsy Revealing Abnormal Plasma Cells

  • Bone Marrow Aspiration and Biopsy: A sample of bone marrow is taken, usually from the pelvis, to examine under a microscope.
  • Morphological Examination: Pathologists look for an increased number of plasma cells, which may constitute more than 10% of the marrow cells in multiple myeloma.
  • Cytogenetic and Molecular Testing: Tests like fluorescence in situ hybridization (FISH) can identify genetic abnormalities associated with multiple myeloma, such as translocations and deletions.
  • Histopathology: The biopsy may reveal Mott cells, which are plasma cells containing multiple Russell bodies. These are eosinophilic inclusions filled with immunoglobulins, indicating excessive production.

Imaging Studies Showing Lytic Bone Lesions

  • X-rays (Skeletal Survey): A series of X-rays of the skull, spine, ribs, pelvis, and long bones to identify "punched-out" lytic lesions and fractures.
  • Magnetic Resonance Imaging (MRI): Provides detailed images of bone marrow and soft tissues, helpful in detecting early marrow infiltration, spinal cord compression, and subtle bone lesions not seen on X-rays.
  • Computed Tomography (CT) Scans: Detailed cross-sectional images of bones, useful for evaluating the extent of bone destruction and guiding biopsy needles.
  • Positron Emission Tomography (PET) Scans: Combined with CT (PET-CT), it can identify active myeloma lesions by detecting areas of increased glucose metabolism, which corresponds to cancer cell activity.

Comprehensive Diagnostic Approach

Diagnosing multiple myeloma involves integrating data from these various tests to confirm the presence of the disease and assess its severity. Key diagnostic criteria often referred to as CRAB features, include:

  • C: Hypercalcemia
  • R: Renal insufficiency
  • A: Anemia
  • B: Bone lesions

Summary

  • Blood Tests: Elevated M-protein levels, free light chain assay abnormalities.
  • Urine Tests: Detection of Bence Jones proteins.
  • Bone Marrow Biopsy: Reveals increased plasma cells, presence of Mott cells with Russell bodies.
  • Imaging Studies: Identifies lytic bone lesions, evaluates the extent of bone and marrow involvement.

Together, these diagnostic tools provide a comprehensive understanding of multiple myeloma, facilitating accurate diagnosis, staging, and treatment planning.

Summary

In summary, the terms "Hx + Lytic Lesion + Mott Cell with Russell Bodies" in the context of multiple myeloma refer to a patient history indicative of myeloma symptoms, the presence of destructive bone lesions, and specific pathological findings in plasma cells that indicate the overproduction and improper secretion of immunoglobulins. These elements collectively contribute to the diagnosis and understanding of the disease pathology in multiple myeloma.


Generated microscopic image depicting Mott cells with Russell bodies in a bone marrow sample. 

Note: By reading my blog, you acknowledge that I do not provide medical diagnoses or treatments. The information provided is meant to answer frequently asked questions and is gathered from reputable scientific papers.  

Comments

Post a Comment

Popular posts from this blog

Toxic Skin Condition Post-mRNA COVID-19 Vaccination

By SWA
Image
Identifying Severe Skin Conditions Post-Vaccination Following administration of the BioNTech mRNA vaccine, a small subset of individuals may develop severe and complex reactions. These reactions are often misdiagnosed or misunderstood due to their rarity and diverse presentation. This essay examines a case characterized by severe skin conditions, systemic symptoms, and complications such as hypercalcemia and crystal formation. It highlights the need for accurate diagnosis, holistic management, and increased awareness of these rare but significant vaccine-related adverse events. Initial Symptoms and Misdiagnoses Severe symptoms began shortly after the first dose of the BioNTech vaccine, initially presenting as petechiae, diagnosed by a rheumatologist. However, following the second dose, symptoms rapidly escalated, resulting in intense burning pain and thinning of the skin. The skin on the legs and thighs became paper-thin and could tear with the slightest touch, with the affected area e...
Read more

Dysferlin Protein: Key Roles, Genetic Locations

By SWA
Image
The purpose of this article is to share and discuss the details of a new discovery, which is highlighted within: CRISPR-Cas9: A Breakthrough Tool to Repair the DYSF Gene The dysferlin protein plays an essential role in maintaining the integrity of muscle cell membranes, particularly in tissues that endure significant mechanical stress, such as skeletal and cardiac muscles . Encoded by the DYSF gene , dysferlin is indispensable for repairing damaged cell membranes after injury caused by muscle contraction or external forces. This article explores the main locations where dysferlin is produced, its role in muscle repair, and supportive nutritional and therapeutic strategies for individuals with dysferlin deficiency, such as those affected by dysferlinopathies (e.g., Limb-Girdle Muscular Dystrophy Type 2B or Miyoshi Myopathy). Currently, there is no definitive answer as to why the severity of dysferlin protein expression or depletion varies. Do pathogens play a role in the methylation o...
Read more

Is ME CFS connected to Spinal Muscular Atrophy (SMA) or Post Polio?

By SWA
Image
Today, I understand why Spinal Muscular Atrophy (SMA) received little attention, particularly in the mid-50s. This complex and debilitating genetic illness was poorly understood, and patients' symptoms were often minimized or even dismissed. For more information, please visit the Spinal Muscular Atrophy (SMA) page on MalaCards . Even now, many neurologists lack detailed knowledge of SMA, and comprehensive examinations mentioned in research are rarely pursued. In 2008, while investigating permanent adrenal insufficiency, an MRI ordered by my endocrinologist unexpectedly revealed Chiari Malformation II. However, surgery in 2009 brought no improvement. In 2010, a DNA test showed a genetic marker in the ACTN3 gene: https://www.malacards.org/search/results?q=ACTN3%20gene%20and%20Spinal%20Muscular%20Atrophy%20(SMA) A 2015 MRI revealed ankylosing spondylitis, multiple Tarlov cysts, stenosis at L4 and L5, spinal canal narrowing, and widespread degenerative changes. Surgery on L4 and L5 ...
Read more