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Health condition · Clinically reviewed

Multiple myeloma, from MGUS to modern quadruplets, transplant and CAR-T.

A plasma cell cancer that has been transformed by the last decade of drug development. Understand the spectrum, the CRAB features and how UK treatment now looks.

Jump to treatment
A radiographer guides a patient onto the bed of an advanced 3 Tesla MRI scanner in a London imaging suite

Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against NICE, BSH, IMWG and peer-reviewed haematology sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK practice including quadruplet induction, BCMA CAR-T and bispecific antibodies.

Key facts

Myeloma at a glance.

The essentials, in plain English. Who gets it, what it does to the marrow and skeleton, and how UK haematology treats it today.

  • What it is

    A malignant plasma cell dyscrasia in the bone marrow producing a monoclonal immunoglobulin (paraprotein) and driving the CRAB features.

  • How common

    Around 6,000 new UK cases each year. The third most common haematological cancer. Median age at diagnosis is 70.

  • Who is at risk

    Older adults, men slightly more than women, and Black African-Caribbean people at 2 to 3 times the background risk.

  • The spectrum

    MGUS, smouldering myeloma, active multiple myeloma, solitary plasmacytoma and AL amyloidosis all sit on the same plasma cell disease spectrum.

  • Foundation therapy

    Quadruplet induction (anti-CD38 plus proteasome inhibitor plus immunomodulator plus dexamethasone) is now standard for most fit patients.

  • Newer options

    BCMA-directed CAR-T (cilta-cel, ide-cel) and bispecific antibodies (teclistamab, elranatamab, talquetamab) are transforming later-line care.

Why this guide matters

A spectrum, not a single disease.

MGUS, smouldering myeloma, active myeloma, solitary plasmacytoma and AL amyloidosis all sit on one plasma cell continuum. The right label matters because the treatment does.

  • MGUS is common and mostly stable

    A paraprotein under 30 g/L with fewer than 10 per cent marrow plasma cells and no CRAB features. The progression rate is around 1 per cent per year.

  • CRAB and SLiM CRAB define active MM

    Hypercalcaemia, renal impairment, anaemia and bone lesions, plus the SLiM biomarkers, mean treatment is needed rather than watchful waiting.

  • Modern therapy has changed outcomes

    Quadruplet induction, transplant where fit, lenalidomide maintenance and, at relapse, CAR-T and bispecifics have transformed survival.

How the diagnosis is made

From first symptoms to a full treatment plan.

The steps a UK GP, haematologist and specialist centre will normally follow, in order, so you know what to expect and why.

  1. 01

    Assessing

    History and examination

    Bone pain, fatigue, recurrent infections, weight loss and neurological symptoms. Ethnicity and family history noted.

  2. 02

    Assessing

    Baseline bloods

    FBC, U&Es, corrected calcium, albumin, LDH, urate and beta-2 microglobulin to look for CRAB features and staging inputs.

  3. 03

    Assessing

    Paraprotein screen

    Serum and urine electrophoresis with immunofixation, plus serum free light chains and the kappa/lambda ratio.

  4. 04

    Confirming

    Bone marrow biopsy

    Aspirate and trephine with immunophenotyping, cytogenetic FISH and an NGS panel to identify high-risk and targetable lesions.

  5. 05

    Confirming

    Whole-body imaging

    Whole-body low-dose CT (per IMWG guidance, replacing the skeletal survey), whole-body MRI and PET-CT for lytic lesions and extramedullary disease.

  6. 06

    Confirming

    Amyloid workup where suspected

    Congo red staining on fat pad, renal or bone marrow biopsy, plus BNP, troponin and cardiac MRI where AL amyloidosis is considered.

  7. 07

    Planning

    Staging and risk

    ISS and R-ISS staging combine beta-2 microglobulin, albumin, LDH and cytogenetics to define standard and high-risk disease.

Typical timeline: a suspected diagnosis to an agreed MDT plan in two to four weeks.

Symptoms

What myeloma actually feels like.

Bone pain, anaemia, recurrent infections, hypercalcaemia and kidney trouble are the classic mix. Some presentations are subtle and picked up on routine bloods.

  • Bone pain and fractures

    Back and rib pain, worse on movement, sometimes presenting as a pathological fracture or vertebral collapse.

  • Anaemia and fatigue

    Normocytic anaemia from marrow infiltration, causing tiredness, breathlessness and reduced exercise tolerance.

  • Recurrent infections

    Immunoparesis lowers normal immunoglobulins. Pneumococcal and viral infections are common at presentation.

  • Hypercalcaemia

    Thirst, polyuria, constipation, nausea and confusion. Corrected calcium above 2.75 mmol/L needs urgent treatment.

  • Renal impairment

    Rising creatinine, often from light chain cast nephropathy. Requires urgent haematology and renal input.

  • Spinal cord compression

    New back pain with leg weakness, sensory change or bladder disturbance. A neurosurgical and oncological emergency.

  • Hyperviscosity and neuropathy

    Blurred vision, headache, bleeding or peripheral neuropathy. More common in IgM and POEMS or AL amyloidosis.

  • Red flag - AL amyloid features

    Nephrotic-range proteinuria, cardiac failure with normal coronaries or unexplained autonomic neuropathy should prompt amyloid workup.

Treatment

How myeloma is treated in the UK.

Quadruplet induction, transplant where fit, lenalidomide maintenance, then a deep bench of relapse options including CAR-T and bispecific antibodies. Delivered through specialist haematology centres.

  • Quadruplet induction (transplant-eligible)

    D-VRd (daratumumab, bortezomib, lenalidomide, dexamethasone) or Isa-VRd for 4 to 6 cycles. Also DVTd or DaraKRd in selected pathways.

  • Autologous stem cell transplant

    High-dose melphalan conditioning followed by ASCT in fit patients, typically under 70. Deepens response and lengthens remission.

  • Lenalidomide maintenance

    Continuous lenalidomide, sometimes with daratumumab, until progression. Standard of care after ASCT.

  • Transplant-ineligible regimens

    Dara-Rd (MAIA), Dara-VMP (Alcyone) or VRd-lite. Chosen by fitness, frailty and comorbidity, with maintenance thereafter.

  • Later-line combinations

    Pom-dex, KRd (carfilzomib, lenalidomide, dexamethasone), ixazomib, elotuzumab, isatuximab, selinexor and venetoclax for t(11;14).

  • BCMA CAR-T therapy

    Cilta-cel (Carvykti) and ide-cel (Abecma). Approved from third or fourth line and moving into earlier settings on trial data.

  • Bispecific antibodies

    Teclistamab (Tecvayli) and elranatamab target BCMA; talquetamab targets GPRC5D. Approved for triple-class refractory disease.

  • Supportive care

    Bisphosphonates or denosumab, calcium and vitamin D, radiotherapy for painful lesions, infection prophylaxis, VTE prevention and renal support.

Specialist centres

Complex care, transplant, CAR-T and bispecifics are delivered through named units such as UCLH, The Christie, King’s College Hospital, The Royal Marsden, Queen Elizabeth Hospital Birmingham, Manchester Royal Infirmary, University Hospital of Wales in Cardiff and the Freeman Hospital in Newcastle.

What this guide is based on

The sources behind every claim on this page.

UK national guidance, international haematology consensus and specialist society standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your haematology team knows your bloods, your marrow biopsy and your comorbidities and can tell you which parts apply to you.

  • NICE. Myeloma: diagnosis and management (NG35) and technology appraisals (TAs) for daratumumab, isatuximab, teclistamab, ide-cel and cilta-cel.

  • British Society for Haematology (BSH). Guidelines for the diagnosis and management of multiple myeloma.

  • International Myeloma Working Group (IMWG). Updated criteria for the diagnosis of multiple myeloma and imaging recommendations.

  • Myeloma UK and Blood Cancer UK. Patient information and clinical practice resources.

Red flags

When myeloma needs urgent care.

Myeloma emergencies are not rare. Recognising them early keeps kidneys, spines and lives intact.

  • Spinal cord compression

    New back pain with leg weakness, saddle anaesthesia or bladder change. Same-day MRI, high-dose dexamethasone and urgent oncology or spinal referral.

  • Severe hypercalcaemia

    Corrected calcium above 3.0 mmol/L with confusion, dehydration or arrhythmia. Needs urgent IV fluids and bisphosphonate.

  • Acute kidney injury

    A rising creatinine or oliguria, often from light chain cast nephropathy. Requires urgent haematology, renal input and consideration of plasmapheresis.

  • Hyperviscosity syndrome

    Blurred vision, mucosal bleeding, headache or altered consciousness. Plasmapheresis is a haematological emergency.

  • Neutropenic sepsis

    Fever on chemotherapy, especially with low neutrophils. Follow the sepsis six pathway and give broad-spectrum antibiotics within one hour.

  • Cardiac AL amyloidosis

    New heart failure with a thickened septum on echo, raised NT-proBNP and low voltages on ECG. Refer to a national amyloidosis centre.

  • Pathological fracture

    Vertebral collapse or long-bone fracture without significant trauma. Needs orthopaedic and oncology assessment.

  • New neurological deficit

    Focal weakness, cranial nerve palsy or rapidly progressive neuropathy. Consider plasmacytoma, cord compression or POEMS.

  • Tumour lysis on starting treatment

    High tumour burden regimens can cause hyperuricaemia, hyperkalaemia and renal failure. Rasburicase and IV hydration prevent it.

Living with it

A long-term condition, with more tools than ever.

Four things that make the biggest difference between treatment cycles: staying close to your team, protecting your bones, preventing infection and using the charities that exist for this exact disease.

A quiet reminder

Small habits, kept up, do more than heroics.

Regular blood tests, kept-up vaccines and a working relationship with a specialist nurse pay off more than any single change.

  1. 01 Team

    Stay connected to your unit

    Myeloma is a long-term condition with periods of active treatment and monitoring. Your specialist nurse is the single most useful contact.

  2. 02 Bones

    Protect your skeleton

    Bisphosphonates or denosumab, calcium and vitamin D, gentle strength work and dental checks before starting bone-modifying agents.

  3. 03 Infection

    Prevent infections

    Aciclovir with proteasome inhibitors, PJP cover with some regimens, plus pneumococcal, flu and COVID vaccinations kept up to date.

  4. 04 Support

    Use the charities

    Myeloma UK and Blood Cancer UK offer infoline support, printed guides and a patient community that understands the ups and downs.

Frequently asked

Everything we get asked about myeloma.

Quick answers on MGUS, the CRAB features, transplant, maintenance and the newer BCMA-directed therapies.

  • What is multiple myeloma?

    Multiple myeloma is a cancer of plasma cells in the bone marrow. The abnormal plasma cells make a single monoclonal immunoglobulin, called a paraprotein, and crowd out normal blood production. Over time this causes the CRAB features: hypercalcaemia, renal impairment, anaemia and bone lesions.

  • Is MGUS the same as myeloma?

    No. MGUS (monoclonal gammopathy of undetermined significance) is a premalignant condition. The paraprotein is under 30 g/L, marrow plasma cells are under 10 per cent and there is no end-organ damage. The risk of progressing to myeloma or a related disorder is around 1 per cent per year, so long-term monitoring is standard.

  • How is myeloma diagnosed?

    Diagnosis needs a paraprotein or abnormal free light chains, a bone marrow biopsy showing clonal plasma cells and evidence of end-organ damage (CRAB) or SLiM CRAB biomarkers. Whole-body low-dose CT or MRI looks for bone lesions, and cytogenetic FISH identifies high-risk features such as t(4;14), t(14;16), t(14;20) and del17p.

  • What does first-line treatment look like in the UK?

    For fit patients under about 70, standard care is a quadruplet induction such as D-VRd or Isa-VRd for 4 to 6 cycles, followed by an autologous stem cell transplant with high-dose melphalan and then lenalidomide maintenance until progression. For transplant-ineligible patients, Dara-Rd, Dara-VMP or VRd-lite are common choices with ongoing maintenance.

  • What are CAR-T and bispecific antibodies?

    BCMA-directed CAR-T therapies (cilta-cel and ide-cel) reprogramme a patient’s own T cells to attack myeloma. Bispecific antibodies such as teclistamab, elranatamab and talquetamab bring T cells and myeloma cells together off the shelf. Both are used in relapsed or refractory disease and are moving into earlier lines on trial data.

  • Can myeloma be cured?

    Multiple myeloma is not usually curable, but it is very treatable. Modern regimens produce long periods of good-quality remission, and outcomes have improved substantially over the past decade. Solitary plasmacytoma can sometimes be cured with radiotherapy alone, and a small proportion of transplant patients achieve very deep, sustained responses.

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