Multiple myeloma

What it is

Multiple myeloma is a plasma cell cancer that makes abnormal monoclonal protein and accounts for about 10% of blood cancers. It starts in plasma cells, a type of white blood cell in the bone marrow that normally makes antibodies to fight infection. In myeloma, one abnormal clone of plasma cells grows out of control, crowds the marrow, and produces a monoclonal immunoglobulin or light chain, often called an M protein. This can damage bones, kidneys, and normal blood cell production.

Myeloma is usually not a single lump. It often affects multiple areas of bone marrow, which is why it is called multiple myeloma. Many patients are first found to have a precursor condition such as MGUS (monoclonal gammopathy of undetermined significance) or smoldering multiple myeloma before active disease develops.

A simple way to think about the spectrum is:

Condition	Main feature	Usual approach
MGUS	Low-level monoclonal protein, no organ damage	Monitoring
Smoldering multiple myeloma	Higher disease burden, still no myeloma-defining organ damage	Close monitoring, sometimes treatment in high-risk cases
Active multiple myeloma	Myeloma-defining events or organ damage present	Treatment needed

Doctors diagnose active myeloma when there are 10% or more clonal plasma cells in bone marrow or a biopsy-proven plasmacytoma, plus myeloma-defining features.

How it works

Myeloma develops when a clone of plasma cells acquires genetic changes that let it survive and multiply in the bone marrow. These cells interact with the marrow environment, including stromal cells, cytokines, and bone-remodeling pathways, which helps the cancer grow and weakens bone.

The main disease effects come from a few mechanisms:

1. Marrow crowding: Myeloma cells reduce normal blood cell production, causing anaemia and sometimes low platelets or low normal white cells.
2. Abnormal protein production: The M protein or free light chains can circulate in blood and urine. In some patients, these proteins injure the kidneys.
3. Bone breakdown: Myeloma increases bone resorption and suppresses normal bone formation, leading to lytic lesions, fractures, and high calcium.
4. Immune dysfunction: Even though plasma cells make antibodies, myeloma weakens normal immunity, so infections become more common.

Clinicians often remember the classic organ-damage pattern as CRAB:

• C: hypercalcemia
• R: renal impairment
• A: anemia
• B: bone lesions

Modern criteria also include certain biomarkers that predict near-term progression even before obvious CRAB damage appears.

Diagnosis / how it's measured

Diagnosis combines symptoms, blood and urine tests, bone marrow testing, and imaging. No single test is enough on its own.

Common tests include:

Test	What it looks for
Serum protein electrophoresis (SPEP) and immunofixation	Detects and types the M protein
Serum free light chain assay	Measures excess kappa or lambda light chains
24-hour urine protein studies or urine immunofixation	Detects light chains in urine
Complete blood count	Anaemia or other low blood counts
Creatinine and calcium	Kidney function and hypercalcemia
Bone marrow biopsy	Percentage of clonal plasma cells
FISH/cytogenetics	High-risk genetic features
Whole-body low-dose CT, PET-CT, or MRI	Bone lesions or plasmacytomas

Widely used diagnostic criteria include one of the following with clonal marrow plasma cells of at least 10% or a plasmacytoma:

• CRAB features attributable to myeloma
• 60% or more clonal bone marrow plasma cells
• Involved/uninvolved serum free light chain ratio of 100 or more with adequate absolute involved light chain level
• More than one focal lesion on MRI, each at least 5 mm

Risk stratification matters because some myelomas behave more aggressively than others. High-risk features can include certain cytogenetic abnormalities on FISH, such as del(17p), t(4;14), or t(14;16), though exact interpretation depends on the full clinical picture.

In India, diagnosis and treatment are usually led by a haemato-oncologist. Access to tests such as FISH, PET-CT, and transplant evaluation may vary by centre, so patients are often referred to tertiary cancer hospitals for complete work-up.

Evidence and uses

The main goal of treatment is to control the cancer, reduce symptoms and complications, and prolong survival. Treatment choice depends on age, fitness, kidney function, disease stage, genetic risk, and whether the patient is eligible for autologous stem cell transplant.

Common treatment components include:

Treatment type	Examples
Targeted/anti-myeloma drugs	Proteasome inhibitors such as bortezomib; immunomodulatory drugs such as lenalidomide
Steroids	Dexamethasone
Monoclonal antibodies	Daratumumab, isatuximab
Cell therapy / advanced therapy	Selected patients may receive CAR-T or bispecific antibodies in some settings
Stem cell transplant	Autologous transplant in eligible patients
Supportive care	Bisphosphonates, infection prevention, pain control, radiation for focal lesions

Most newly diagnosed patients receive a combination regimen rather than a single drug. Over the last two decades, outcomes have improved substantially because of proteasome inhibitors, immunomodulatory drugs, antibodies, better supportive care, and transplant strategies.

Supportive care is a major part of evidence-based treatment. Bone-strengthening drugs can reduce skeletal events. Vaccination, infection monitoring, treatment of anaemia, and kidney-protective measures are also important. Radiation may be used for painful bone lesions or spinal cord compression.

There is no established role for Ayurveda or herbal products as a replacement for standard myeloma treatment. Some patients in India use traditional remedies alongside cancer care, but evidence that these products control myeloma is limited or absent. Because many herbal products can affect the liver, kidneys, bleeding risk, or drug metabolism, patients should tell their oncology team about all supplements and AYUSH medicines they use.

When to see a clinician

See a clinician promptly if you have persistent bone pain, repeated infections, unexplained fatigue, weight loss, or abnormal blood test results showing high protein, anaemia, calcium elevation, or kidney dysfunction. Urgent assessment is needed for severe back pain with weakness, numbness, or bladder or bowel changes because spinal cord compression can occur.

People already diagnosed with MGUS or smoldering myeloma need regular follow-up because progression risk changes over time. During treatment, fever, reduced urine output, sudden confusion, dehydration, or new fractures should be reported quickly.

Limitations and open questions

Myeloma treatment has improved, but it is still usually considered a chronic, relapsing cancer rather than a disease that is cured in most patients. Some people respond for many years, while others have early relapse despite modern therapy.

Important open questions include how best to treat high-risk smoldering myeloma, how to sequence newer therapies, which patients benefit most from CAR-T or bispecific antibodies, and how to reduce long-term toxicity while maintaining disease control. Access and cost also remain major issues, including in India.

Evidence is strong for established anti-myeloma therapies and supportive care, but weaker for many complementary products marketed to patients with cancer. If a product claims to "boost immunity" or "cure" myeloma, that claim should be treated with caution unless it is supported by high-quality human studies and discussed with a qualified cancer specialist.