Paraneoplastic Syndromes

Paraneoplastic syndromes are rare cancer-related disorders that occur when tumors trigger abnormal immune, hormonal, or inflammatory responses in the body. These syndromes can affect organs and tissues distant from the primary tumor or its metastases and may involve the neurologic, endocrine, dermatologic, rheumatologic, and hematologic systems.

Recent advances in oncology and immunology have improved the understanding, diagnosis, and treatment of paraneoplastic syndromes. These disorders may result from tumor secretion of hormones, peptides, or cytokines, or from immune cross-reactivity between malignant cells and normal tissues.

Paraneoplastic syndromes may develop before an underlying cancer is diagnosed and can occasionally serve as an early warning sign of an occult malignancy, particularly lung cancer, gastrointestinal cancers, lymphomas, and other solid tumors. Up to 20% of cancer patients may experience paraneoplastic manifestations, although many cases remain unrecognized.

Because paraneoplastic syndromes can cause significant morbidity and neurologic disability, early recognition and effective treatment are essential to improve quality of life, facilitate cancer therapy, and potentially prolong survival.

The most common cancers associated with paraneoplastic syndromes include:

• Lung carcinoma, especially small cell lung cancer (most common)
• Renal cell carcinoma
• Hepatocellular carcinoma
• Leukemias
• Lymphomas
• Breast cancer
• Ovarian cancer
• Neuroendocrine tumors
• Gastric cancer
• Pancreatic cancer
• Colorectal cancer
• Thymoma
• Multiple myeloma

Successful treatment of paraneoplastic syndromes is best achieved by controlling the underlying malignancy. Some manifestations may also respond to symptom-directed therapies such as cyproheptadine or somatostatin analogues for carcinoid syndrome, and bisphosphonates or corticosteroids for malignancy-associated hypercalcemia.

General paraneoplastic symptoms:

Patients with cancer may develop constitutional paraneoplastic symptoms such as fever, night sweats, anorexia, fatigue, and cachexia. These manifestations are often mediated by pro-inflammatory cytokines released during the immune or inflammatory response, including tumor necrosis factor-alpha (TNF-α), interleukins, and interferons. Tumor-related metabolic alterations, tissue catabolism, liver dysfunction, and abnormalities in steroidogenesis may also contribute to the development of these systemic symptoms.

Hematologic paraneoplastic syndromes:

Patients with malignancy may develop a wide range of hematologic paraneoplastic syndromes, including pure red cell aplasia, anemia of chronic disease, leukocytosis (leukemoid reaction), thrombocytosis, eosinophilia, basophilia, and disseminated intravascular coagulation (DIC).

Immune-mediated hematologic complications may also occur, particularly in lymphoid malignancies and Hodgkin lymphoma, including immune thrombocytopenia and Coombs-positive autoimmune hemolytic anemia.

Paraneoplastic erythrocytosis can develop in several solid tumors, most notably renal cell carcinoma and hepatocellular carcinoma, due to ectopic secretion of erythropoietin or erythropoietin-like substances. Monoclonal gammopathies may also be associated with certain malignancies.

The underlying mechanisms of hematologic paraneoplastic syndromes include tumor production of biologically active substances that stimulate or inhibit normal hematopoiesis, ectopic hormone or cytokine secretion, immune dysregulation, and the formation of autoantibodies that cross-react with hematopoietic cells or their receptors.

Cutaneous paraneoplastic syndromes:

Cutaneous paraneoplastic syndromes are dermatologic manifestations associated with underlying malignancy and may represent the earliest sign of an occult cancer. These skin changes can precede, accompany, or follow the diagnosis of malignancy and may also signal tumor recurrence or disease progression in patients previously treated for cancer.

Patients may develop a broad spectrum of cutaneous manifestations, ranging from nonspecific symptoms such as pruritus and flushing to characteristic paraneoplastic dermatoses including acanthosis nigricans, dermatomyositis, acquired ichthyosis, erythema gyratum repens, Leser-Trélat sign, and paraneoplastic pemphigus.

Pruritus is among the most common cutaneous symptoms in malignancy, particularly in hematologic cancers such as Hodgkin lymphoma, non-Hodgkin lymphoma, and leukemias. It may result from cytokine release, immune dysregulation, or hypereosinophilia.

Flushing is often related to tumor secretion of vasoactive mediators such as serotonin, histamine, prostaglandins, or vasoactive intestinal peptide (VIP), especially in neuroendocrine tumors and carcinoid syndrome.

Pigmentary and keratotic skin lesions may also occur. Examples include acanthosis nigricans associated with gastrointestinal malignancies, generalized dermic melanosis linked to lymphoma, melanoma, and hepatocellular carcinoma, Bowen disease associated with lung, gastrointestinal, and genitourinary cancers, and the sudden appearance of multiple seborrheic keratoses (Leser-Trélat sign), commonly associated with gastrointestinal cancers and lymphomas.

Herpes zoster may occur because of immune dysfunction or immunosuppression in patients with malignancy.

Paraneoplastic endocrine syndromes:

Paraneoplastic endocrine syndromes result from ectopic hormone production by malignant tumors or from tumor-induced disturbances in normal endocrine regulation.

Hypercalcemia of malignancy is the most common endocrine paraneoplastic syndrome and is most frequently caused by ectopic production of parathyroid hormone-related peptide (PTHrP), particularly in squamous cell carcinoma of the lung, head and neck cancers, and bladder cancer. PTHrP stimulates osteoclastic bone resorption, leading to elevated serum calcium levels. Other mechanisms include the rare ectopic secretion of parathyroid hormone (PTH), ectopic production of 1,25-dihydroxyvitamin D by tumors or adjacent macrophages, and osteolytic bone metastases with local cytokine and PTHrP-mediated bone destruction. Clinical manifestations of hypercalcemia include polyuria, dehydration, constipation, confusion, fatigue, and muscle weakness. Treatment involves aggressive intravenous fluid replacement, bisphosphonates or denosumab, calcitonin, and management of the underlying malignancy.

Ectopic Cushing syndrome results from tumor secretion of adrenocorticotropic hormone (ACTH) or ACTH-like peptides, most commonly in small cell lung carcinoma. Excess cortisol production may lead to hypokalemia, proximal muscle weakness, easy bruising, central obesity, moon facies, hypertension, diabetes mellitus, immunosuppression, and psychiatric manifestations such as depression and mood disturbances. Biochemical and radiologic investigations are important to differentiate ectopic ACTH syndrome from pituitary Cushing disease. Treatment includes management of the underlying tumor together with medical therapies aimed at reducing cortisol excess, and surgical resection when feasible.

Ectopic secretion of antidiuretic hormone (ADH) can lead to syndrome of inappropriate antidiuretic hormone secretion (SIADH), resulting in water retention, dilutional hyponatremia, and electrolyte imbalance. SIADH is most commonly associated with small cell lung carcinoma but may also occur in non-small cell lung cancer and other malignancies. Management includes treatment of the underlying tumor with surgery, chemotherapy, or radiotherapy, together with fluid restriction, demeclocycline, hypertonic saline in severe cases, and vasopressin receptor antagonists (vaptans).

Ectopic secretion of growth hormone-releasing hormone (GHRH) has been reported in carcinoid tumors, pheochromocytomas, and other neuroendocrine neoplasms and may result in acromegaly. Surgical resection is the primary treatment when feasible, while systemic therapy may be required in metastatic disease.

Paraneoplastic hypoglycemia may occur because of ectopic insulin production or secretion of insulin-like growth factors (particularly IGF-2) by tumors such as pancreatic islet cell tumors, hepatocellular carcinoma, and hemangiopericytomas.

Conversely, refractory hyperglycemia may result from glucagon-secreting pancreatic neuroendocrine tumors (glucagonomas).

Paraneoplastic hypertension may develop because of excessive catecholamine secretion from pheochromocytomas or cortisol excess in ACTH-secreting tumors.

Ectopic calcitonin production, reported in medullary thyroid carcinoma, breast cancer, and small cell lung carcinoma, may contribute to hypocalcemia, muscle twitching, tetany, and cardiac arrhythmias.

Additional rare ectopic hormone syndromes have also been described, including ectopic secretion of prolactin, erythropoietin, thyroid-stimulating hormone (TSH), and thrombopoietin. Gestational choriocarcinoma, for example, may rarely produce ectopic TSH.

Paraneoplastic Neurologic Syndromes:

Paraneoplastic neurologic syndromes (PNS) are a group of rare immune-mediated disorders affecting the central or peripheral nervous system, neuromuscular junction, or muscles in patients with cancer. These syndromes are not caused by direct tumor invasion, metastasis, infection, metabolic disturbances, or treatment-related toxicity, but rather by an autoimmune response triggered by the underlying malignancy.

In paraneoplastic neurologic syndromes, the immune system recognizes tumor-associated antigens as foreign and mounts an immune response involving autoantibodies and cytotoxic T lymphocytes. Because some tumor antigens resemble proteins normally expressed in neural tissues, this immune response may cross-react with the nervous system, leading to inflammation and neuronal damage. In some patients, the neurologic injury may be severe and can exceed the direct effects of the underlying tumor itself.

Paraneoplastic neurologic syndromes may involve the brain, spinal cord, peripheral nerves, autonomic nervous system, neuromuscular junction, or skeletal muscles. Early recognition is important because neurologic symptoms may precede the diagnosis of cancer and can occasionally serve as the first clinical manifestation of an occult malignancy.

Clinical outcomes vary widely. Some patients experience stabilization or improvement following treatment of the underlying cancer and immunotherapy, whereas others may develop permanent neurologic deficits because of irreversible neuronal damage.

Several forms of peripheral neuropathy may occur as part of paraneoplastic neurologic syndromes, although central nervous system manifestations such as paraneoplastic cerebellar degeneration, limbic encephalitis, and encephalomyelitis are also well recognized.

Peripheral neuropathy is among the most common neurologic paraneoplastic syndromes and typically presents as a distal symmetric sensorimotor polyneuropathy characterized by sensory loss, paresthesia, mild-to-moderate distal muscle weakness, and reduced or absent deep tendon reflexes. In some patients, neuropathy may be painful or predominantly sensory. The clinical presentation can resemble the peripheral neuropathy associated with other chronic systemic illnesses, making diagnosis challenging. Recognition of an underlying malignancy and associated paraneoplastic antibodies may help establish the diagnosis.

Subacute sensory neuropathy, also known as paraneoplastic sensory neuronopathy, is a rare but more specific form of paraneoplastic peripheral neuropathy. It results from degeneration of the dorsal root ganglia and typically presents with progressive sensory loss, paresthesia, and severe sensory ataxia with relatively preserved motor strength. The disorder may become profoundly disabling because of marked impairment of proprioception and coordination. Anti-Hu (ANNA-1) antibodies are detected in some patients, particularly those with small cell lung carcinoma, and may support the diagnosis. Neurologic recovery is often limited, although treatment of the underlying malignancy and immunotherapy may help stabilize disease progression in selected cases.

Guillain-Barré syndrome, an acute inflammatory demyelinating polyradiculoneuropathy characterized by ascending weakness and areflexia, has also been reported as a rare paraneoplastic neurologic manifestation. Although uncommon, it appears to occur more frequently in patients with Hodgkin lymphoma and other hematologic malignancies.

Lambert-Eaton myasthenic syndrome (LEMS) is an immune-mediated paraneoplastic disorder of the neuromuscular junction characterized by proximal muscle weakness and impaired acetylcholine release from presynaptic nerve terminals. The condition is caused by autoantibodies, most commonly directed against presynaptic voltage-gated calcium channels (VGCCs). Unlike myasthenia gravis, ocular and bulbar muscle involvement is usually less prominent.

LEMS may precede, accompany, or follow the diagnosis of malignancy and is most strongly associated with small cell lung carcinoma, which accounts for approximately 70% of paraneoplastic cases. It occurs more commonly in men and in patients with intrathoracic tumors.

Clinical manifestations include fatigability, progressive proximal limb weakness, reduced or absent deep tendon reflexes, autonomic symptoms such as dry mouth and erectile dysfunction, and occasionally ptosis or mild cranial nerve involvement. Some patients also experience paresthesia or muscle pain.

The diagnosis is supported by electrophysiologic studies demonstrating an incremental increase in compound muscle action potential amplitude following high-frequency repetitive nerve stimulation or brief exercise, reflecting facilitation of acetylcholine release.

Management primarily focuses on treatment of the underlying malignancy, which may lead to neurologic improvement or remission. Symptomatic therapies include amifampridine (3,4-diaminopyridine), which enhances acetylcholine release, and pyridostigmine in selected cases. Immunomodulatory treatments such as corticosteroids, intravenous immunoglobulin (IVIG), or plasma exchange may provide additional benefit in some patients. Guanidine has historically been used but is now less favored because of potential bone marrow and hepatic toxicity.

Paraneoplastic cerebellar degeneration is a rare but severe neurologic paraneoplastic syndrome characterized by rapidly progressive cerebellar dysfunction. Patients typically develop gait and limb ataxia, dysarthria, vertigo, and diplopia over weeks to months, often progressing to profound neurologic disability. Additional neurologic manifestations may include nystagmus, ophthalmoplegia, extensor plantar responses, brainstem signs, cognitive impairment, and occasionally dementia.

In many patients, neurologic symptoms precede the diagnosis of the underlying malignancy by months or even years and may therefore serve as an important clue to occult cancer. The syndrome is most commonly associated with breast cancer, ovarian cancer, small cell lung carcinoma, and Hodgkin lymphoma.

Anti-Yo antibodies (PCA-1) are detected in some patients, particularly women with breast or gynecologic malignancies, while other paraneoplastic antibodies such as anti-Hu, anti-Ri, or anti-Tr may also occur depending on the associated tumor type.

Brain MRI may initially appear normal but can later demonstrate cerebellar atrophy, especially in advanced disease. Cerebrospinal fluid analysis may show mild lymphocytic pleocytosis, elevated protein levels, or oligoclonal bands. Histopathologic findings characteristically include extensive Purkinje cell loss with inflammatory lymphocytic infiltrates surrounding cerebellar blood vessels.

Treatment primarily involves management of the underlying malignancy together with immunotherapy such as corticosteroids, intravenous immunoglobulin (IVIG), plasma exchange, rituximab, or other immunosuppressive therapies. Neurologic recovery is often limited because of irreversible neuronal damage, although early cancer treatment may help stabilize disease progression in some patients.

Opsoclonus-myoclonus syndrome is a rare paraneoplastic neurologic disorder characterized by spontaneous chaotic multidirectional eye movements (opsoclonus), cerebellar ataxia, and myoclonus involving the trunk and extremities. It is most commonly associated with neuroblastoma in children but may also occur in adults with breast cancer, small cell lung carcinoma, and other malignancies.

The disorder is believed to result from an autoimmune response directed against neuronal antigens, and anti-Ri antibodies may be detected in some patients. Neurologic symptoms can be severe and may significantly impair coordination, balance, speech, and motor function.

Treatment includes management of the underlying malignancy together with immunotherapy such as corticosteroids, intravenous immunoglobulin (IVIG), rituximab, or other immunosuppressive therapies. Clinical improvement may occur, particularly with early diagnosis and treatment.

Subacute motor neuronopathy is a rare paraneoplastic neurologic syndrome characterized by painless progressive lower motor neuron weakness affecting the upper and lower extremities. It is most commonly associated with Hodgkin lymphoma and other lymphoproliferative malignancies.

The disorder results from degeneration of anterior horn cells in the spinal cord, leading to muscle weakness, wasting, and reduced reflexes without significant sensory involvement. Clinical manifestations may resemble motor neuron disease, although the course is often more subacute and potentially reversible.

Unlike many other paraneoplastic neurologic syndromes, spontaneous neurologic improvement or stabilization may occur, particularly following successful treatment of the underlying lymphoma.

Subacute necrotizing myelopathy is a rare but severe paraneoplastic neurologic syndrome characterized by rapidly progressive spinal cord dysfunction resulting from necrosis of both gray and white matter. Patients typically develop ascending sensory loss, motor weakness, sphincter dysfunction, and progressive paraplegia over days to weeks.

Because metastatic epidural spinal cord compression is a far more common cause of rapidly progressive myelopathy in patients with cancer, urgent spinal MRI is essential to exclude compressive lesions. In paraneoplastic necrotizing myelopathy, MRI may demonstrate spinal cord swelling, signal abnormalities, or areas of cord necrosis.

The prognosis is generally poor, and neurologic deterioration may progress despite treatment. Management focuses on treating the underlying malignancy together with supportive care and immunotherapy in selected cases.

Paraneoplastic encephalitis is an immune-mediated neurologic syndrome that may affect different regions of the brain and is most commonly associated with small cell lung carcinoma. Limbic encephalitis is a well-recognized form involving the medial temporal lobes and limbic system, presenting with anxiety, depression, memory loss, confusion, hallucinations, seizures, and behavioral changes.

The disorder results from an autoimmune response against neuronal antigens expressed by the tumor. Anti-Hu antibodies may be detected in serum or cerebrospinal fluid in some patients. Brain MRI may show edema, contrast enhancement, or hyperintense abnormalities involving the limbic structures. Early treatment of the underlying malignancy and immunotherapy may improve neurologic outcomes.

Anti-Yo Syndrome is a paraneoplastic neurologic disorder most commonly associated with breast and gynecologic malignancies, particularly ovarian cancer. It typically presents as paraneoplastic cerebellar degeneration with progressive ataxia, dysarthria, nystagmus, and other cerebellar deficits. Anti-Yo antibodies (PCA-1) may be detected in serum or cerebrospinal fluid.

Stiff Person Syndrome is a rare autoimmune neurologic disorder characterized by progressive muscle stiffness, rigidity, and painful spasms. It may occur as a paraneoplastic syndrome, particularly in association with breast cancer and small cell lung carcinoma. Anti-amphiphysin antibodies are frequently associated with paraneoplastic forms of the disease.

GI paraneoplastic syndromes:

Gastrointestinal paraneoplastic syndromes may result from tumor secretion of biologically active hormones, peptides, or inflammatory mediators. Profuse watery diarrhea with dehydration and electrolyte disturbances can occur because of ectopic production of vasoactive intestinal peptide (VIP), prostaglandins, or other secretory substances by tumors such as pancreatic neuroendocrine tumors and VIPomas.

Carcinoid tumors may produce excessive serotonin and other vasoactive mediators, leading to carcinoid syndrome characterized by flushing, secretory diarrhea, wheezing, bronchospasm, and abdominal cramping.

Protein-losing enteropathy may also develop as a paraneoplastic manifestation, particularly in association with lymphomas, because of intestinal lymphatic obstruction, mucosal infiltration, or tumor-related inflammatory changes.

Renal paraneoplastic syndromes:

Renal paraneoplastic syndromes may occur because of immune-mediated or tumor-related systemic effects of malignancy. Membranous glomerulonephritis is a recognized paraneoplastic manifestation associated with solid tumors such as colon and ovarian cancer as well as lymphomas, and is believed to result from deposition of circulating immune complexes within the glomeruli.

Secondary amyloidosis may also develop in association with plasma cell dyscrasias, multiple myeloma, lymphomas, and renal cell carcinoma because of chronic inflammatory activity and abnormal protein deposition. Renal involvement may present with proteinuria, nephrotic syndrome, progressive renal impairment, or edema.

Rheumatologic paraneoplastic syndromes:

Rheumatologic paraneoplastic syndromes are autoimmune or inflammatory musculoskeletal disorders that occur in association with underlying malignancy. These syndromes may precede, accompany, or follow the diagnosis of cancer and can affect the joints, muscles, connective tissues, or bones.

Paraneoplastic arthropathies, including inflammatory polyarthritis and polymyalgia-like syndromes, may occur in patients with hematologic malignancies and solid tumors such as colon, pancreatic, prostate, lung, and gynecologic cancers. Connective tissue diseases including systemic sclerosis and, less commonly, systemic lupus erythematosus (SLE) have also been reported in association with malignancy.

Hypertrophic osteoarthropathy is classically associated with intrathoracic malignancies, particularly lung cancer, and is characterized by painful joint swelling, periostitis, digital clubbing, and joint effusions commonly involving the knees, ankles, wrists, elbows, and metacarpophalangeal joints.

Dermatomyositis and, less frequently, polymyositis are well-recognized paraneoplastic inflammatory myopathies, especially in patients older than 50 years. These disorders typically present with progressive proximal muscle weakness associated with muscle inflammation and necrosis. Characteristic cutaneous findings in dermatomyositis include a violaceous heliotrope rash involving the eyelids with periorbital edema and an erythematous facial rash. Dermatomyositis is particularly associated with ovarian, lung, pancreatic, gastric, and colorectal cancers. Treatment of the underlying malignancy together with corticosteroids and immunosuppressive therapy may improve symptoms.

Summary:

Paraneoplastic syndromes are rare disorders caused by the systemic effects of cancer rather than direct tumor invasion or metastasis. These syndromes result from ectopic hormone production, immune-mediated tissue injury, cytokine release, or autoimmune cross-reactivity between malignant and normal tissues. Paraneoplastic syndromes can affect multiple organ systems including the neurologic, endocrine, hematologic, dermatologic, rheumatologic, gastrointestinal, and renal systems.

Neurologic paraneoplastic syndromes include Lambert-Eaton myasthenic syndrome, paraneoplastic cerebellar degeneration, limbic encephalitis, sensory neuropathy, opsoclonus-myoclonus syndrome, and stiff person syndrome. Dermatologic manifestations include acanthosis nigricans, dermatomyositis, Leser-Trélat sign, acquired ichthyosis, and paraneoplastic pemphigus. Endocrine syndromes may present with hypercalcemia, SIADH, ectopic Cushing syndrome, carcinoid syndrome, hypoglycemia, or ectopic hormone secretion.

Paraneoplastic syndromes are most commonly associated with small cell lung carcinoma, breast cancer, ovarian cancer, lymphomas, renal cell carcinoma, pancreatic tumors, neuroendocrine tumors, and gastrointestinal malignancies. In some patients, paraneoplastic manifestations may precede the diagnosis of an occult malignancy and therefore serve as an important early clinical clue to underlying cancer.

Early recognition and treatment of the underlying malignancy are essential and may improve symptoms, reduce morbidity, and prolong survival. Immunotherapy, corticosteroids, intravenous immunoglobulin, plasma exchange, bisphosphonates, and targeted supportive therapies may also play important roles depending on the specific syndrome involved.

Questions and Answers:

References:

Bilynsky BT, Dzhus MB, Litvinyak RI. Conceptual and clinical problems of paraneoplastic syndrome in oncology and internal medicine. Exp Oncol. 2015;37(2):82-88. PMID: 26146822.

Santacroce L, El-Deiry WS. Paraneoplastic syndromes. Medscape Reference. 2017. Available from: Medscape Reference – Paraneoplastic Syndromes

Chabner BA. Paraneoplastic syndromes. In: Hematology and Oncology. MSD Manual Professional Edition. 2013. Available from: MSD Manual – Paraneoplastic Syndromes

Höftberger R, Rosenfeld MR, Dalmau J. Update on neurological paraneoplastic syndromes. Curr Opin Oncol. 2015;27(6):489-495. doi:10.1097/CCO.0000000000000234

Ahmadieh H, Arabi A. Endocrine paraneoplastic syndromes: A review. Endocrinol Metab Int J. 2015;1(1):00004. doi:10.15406/emij.2015.01.00004

Metz S. Ectopic hormones from tumors. Ann Intern Med. 1975;83(1):117-118. doi:10.7326/0003-4819-83-1-117

Catalano M. Amiloidosi. Medicina e Chirurgia Online (MedMedicine). 2016. Available from: MedMedicine – Amiloidosi

Darnell RB. Onconeural antigens and the paraneoplastic neurologic disorders: At the intersection of cancer, immunity, and the brain. Proc Natl Acad Sci U S A. 1996;93(10):4529-4536. doi:10.1073/pnas.93.10.4529

Graus F, Delattre JY, Antoine JC, Dalmau J, Giometto B, Grisold W, et al. Recommended diagnostic criteria for paraneoplastic neurological syndromes. J Neurol Neurosurg Psychiatry. 2004;75(8):1135-1140. doi:10.1136/jnnp.2003.034447

Anderson NE, Rosenblum MK. Autoimmune neuropathology of the central nervous system. Curr Opin Neurol. 2011;24(5):484-490. doi:10.1097/WCO.0b013e32834a9e3f

Manupati S, Paymaneh F. Paraneoplastic pemphigus. DermNet NZ. 2023. Available from: DermNet NZ – Paraneoplastic Pemphigus

Sandhu NP, Zakaria S, Degnim AC, et al. Dermatomyositis presenting as a paraneoplastic syndrome due to underlying breast cancer. BMJ Case Rep. 2011;2011:bcr1020103416. doi:10.1136/bcr.10.2010.3416

Kumari P, Yeung P, Medani A, Klani AN. Hypertrophic osteoarthropathy: Uncommon presentation of lung cancer. Cleve Clin J Med. Available from: Cleveland Clinic Journal of Medicine – Hypertrophic Osteoarthropathy

Wick MR, Wei SS. Medullary thyroid carcinoma. Pathology Outlines. Available from: Pathology Outlines – Medullary Thyroid Carcinoma

Keywords:

paraneoplastic syndromes, paraneoplastic syndrome symptoms, paraneoplastic syndrome diagnosis, paraneoplastic syndrome treatment, paraneoplastic neurological syndromes, neurologic paraneoplastic syndromes, endocrine paraneoplastic syndromes, hematologic paraneoplastic syndromes, cutaneous paraneoplastic syndromes, rheumatologic paraneoplastic syndromes, renal paraneoplastic syndromes, gastrointestinal paraneoplastic syndromes, paraneoplastic cerebellar degeneration, Lambert-Eaton myasthenic syndrome, Eaton-Lambert syndrome, limbic encephalitis, anti-Hu antibodies, anti-Yo syndrome, stiff person syndrome, opsoclonus myoclonus syndrome, paraneoplastic neuropathy, paraneoplastic encephalitis, small cell lung cancer paraneoplastic syndrome, lung cancer paraneoplastic syndromes, ovarian cancer paraneoplastic syndrome, breast cancer paraneoplastic syndrome, renal cell carcinoma paraneoplastic syndrome, lymphoma paraneoplastic syndromes, Hodgkin lymphoma paraneoplastic syndrome, dermatomyositis and cancer, acanthosis nigricans cancer, Leser-Trélat sign, paraneoplastic pemphigus, hypertrophic osteoarthropathy, SIADH in cancer, ectopic Cushing syndrome, hypercalcemia of malignancy, carcinoid syndrome, ectopic ACTH syndrome, paraneoplastic hypercalcemia, autoimmune neurologic syndromes, occult malignancy signs, cancer-related autoimmune disorders, neuroendocrine tumors, carcinoid facial flushing, cerebellar atrophy MRI, renal amyloidosis, multiple myeloma amyloidosis, cancer-related skin manifestations, cancer-related neurologic disorders, cancer-related endocrine disorders, paraneoplastic antibodies, onconeural antibodies, cancer immune syndromes, paraneoplastic disorders in oncology, cancer-associated syndromes, paraneoplastic manifestations, cancer complications, oncology syndromes, hematology oncology disorders