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Paraneoplastic syndromes
A paraneoplastic syndrome is caused by a substance the tumour secretes (a hormone or cytokine) or by an immune response against the tumour that also harms healthy tissue; it sometimes appears before the tumour itself, so a typical syndrome requires a focused search for the matching tumour.
Why it matters in the exam
Paraneoplastic syndromes are a classic exam topic — in oncology, internal medicine and neurology. The stem presents a patient with hyponatraemia, hypercalcaemia, proximal muscle weakness, ataxia, behavioural change or a rash, and asks to identify the associated tumour or antibody.
The key is fixed pairs: small cell lung cancer with SIADH, ectopic ACTH, Lambert-Eaton and Hu antibodies; squamous cancer with PTHrP; ovarian teratoma with NMDA antibodies; thymoma with myasthenia; and ovarian or breast cancer with Yo antibodies. In the neurological syndromes the damage is often irreversible, so tumour treatment should be fast.
Key points
- A paraneoplastic syndrome is caused by a substance the tumour secretes or by an immune response against it, and may precede the tumour diagnosis.
- Small cell lung cancer is linked to SIADH, ectopic ACTH, Lambert-Eaton and Hu antibodies.
- Squamous cancer causes hypercalcaemia through PTHrP secretion, and lymphoma through excess calcitriol production, even without bone metastases.
- NMDA antibodies are linked to ovarian teratoma, Yo antibodies to ovarian and breast cancer, and myasthenia to thymoma.
- Treatment is first of the tumour, and in neurological syndromes immune therapy is added — but the damage is often irreversible.
Summary table
| Syndrome | Typical tumour | Details |
|---|---|---|
| SIADH | Small cell lung cancer | Hyponatraemia with high urine osmolality; fluid restriction, tolvaptan in selected cases |
| Ectopic ACTH | Small cell, carcinoid | Hypokalaemia, alkalosis, hypertension and weakness, with few cushingoid signs |
| Hypercalcaemia from PTHrP | Squamous cancer (lung, head and neck), kidney, breast | In lymphoma — excess calcitriol production |
| Lambert-Eaton | Small cell | Antibodies against calcium channels; proximal weakness that improves with effort, dry mouth |
| Hu, Yo and Ri antibodies | Hu — small cell; Yo — ovary and breast; Ri — breast | Hu — sensory neuronopathy and encephalomyelitis; Yo — cerebellar degeneration; Ri — opsoclonus-myoclonus |
| NMDA antibodies and myasthenia | NMDA — ovarian teratoma in a young woman; myasthenia — thymoma | NMDA: behavioural change, seizures and involuntary movements; removing the teratoma helps |
| Skin and others | Dermatomyositis — ovary, lung and GI tract; acanthosis nigricans — stomach; hypertrophic osteoarthropathy — lung | Polycythaemia — kidney and liver; hypoglycaemia from IGF-2 — large fibrous tumours |
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Sources
- Graus et al., Updated diagnostic criteria for paraneoplastic neurologic syndromes, Neurology Neuroimmunology and Neuroinflammation, 2021 — High-risk antibodies and phenotypes
- Harrison's Principles of Internal Medicine, 21st ed. (2022) — Paraneoplastic syndromes: endocrinologic, hematologic and neurologic
- DeVita, Hellman and Rosenberg's Cancer: Principles and Practice of Oncology, 12th ed. (2023) — Paraneoplastic syndromes
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.