Paraneoplastic Syndromes


Article Author:
Bicky Thapa


Article Editor:
Kamleshun Ramphul


Editors In Chief:
Kranthi Sitammagari
Mayank Singhal


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
6/3/2019 8:03:48 PM

Introduction

Paraneoplastic syndromes are rare disorders with complex systemic clinical manifestations from underlying malignancy due to the altered immune system. In other words, malignant cells do not directly manifest symptoms with metastasis; rather they generate autoantibodies, cytokines, hormones, or peptides that affect the multiple organ systems such as neurological, dermatological, gastrointestinal, endocrine, hematologic, and cardiovascular system.[1]Symptoms can manifest before or after the diagnosis of cancer. Therefore, it is critical to recognize these syndromes to identify the hidden malignancy which can affect the clinical outcome in patients.

Etiology

Paraneoplastic syndromes are accompanied with underlying malignancy, but the exact mechanism remains unclear. The syndromes commonly manifest in lung cancer, breast cancer, hematological malignancies, medullary thyroid cancer, gynecological malignancies, and prostate cancer. [2][3]

Epidemiology

Precise incidence and prevalence of the paraneoplastic syndrome are unknown because of the rarity of disease; however, it can occur with any malignancy. A review of the literature suggests that paraneoplastic syndrome occurs in up to 8% of cancer patients.[4] Neurological manifestation in the form of neuropathies is common. Males and females are affected equally.

Pathophysiology

Tumor cells are immunogenic and lead to the activation of both cell-mediated and humoral immune systems. It has been observed that cytotoxic T cells recognize antigens on tumor cells and attack those cells or generate antibodies against tumor cells.[5] However, the body's immune system can also attack normal tissue with a similar antigen presentation and lead to symptoms. Most cases exhibit paraneoplastic syndrome with immunologic mechanisms; however, there are non-immunologic mechanisms of paraneoplastic syndrome. Paraneoplastic syndrome has heterogenous manifestations affecting multiple organ systems in the body, and clinical manifestation does not necessarily associate with the clinical or pathological stage of the underlying malignancy nor is it a prognostic indicator.[6]

Immunologic Mechanism

Cell-mediated immunity, T cells attack tumor cells antigens as well as similar antigens in normal cells.

Paraneoplastic antibodies, also known as onconeural antibodies, direct against target antigen (onconeural antigen) such as type-1 antineuronal nuclear antibodies (ANNA-1), type-2 antineuronal nuclear antibodies (ANNA-2), collapsing response mediator protein-5 (CRMP-5), Purkinje cell cytoplasmic antibody type-1 (PCA-1), anti-amphiphysin, anti-recoverin, anti-bipolar cells of the retina, N-methyl D-aspartate (NMDA) receptor antibodies, acetylcholine receptor antibodies, and gamma-aminobutyric acid A (GABA-A) receptor antibodies.

Non-Immunologic Mechanism

Tumor cells produce hormones or cytokines leading to metabolic abnormalities such as hyponatremia due to antidiuretic hormone or hypercalcemia due to the parathyroid-hormone related peptide. Hematological malignancies producing immunoglobulins affect the peripheral nervous system manifested as peripheral neuropathy.

History and Physical

Paraneoplastic syndrome involves multi-organ system in the body with heterogeneous and complex clinical manifestations in the setting of underlying malignancy.

Clinical presentations are categorized based on the organ system as follows.

Nervous System

Signs and symptoms are based on the part of the nervous system that is affected by a paraneoplastic syndrome, for example, central nervous system, neuromuscular junction, or peripheral nervous system. A patient may present with seizure, cognitive dysfunction, personality change, psychosis, insomnia, ataxia, dysarthria, dysphagia, cranial nerve deficits, and sensorimotor abnormalities.

Central Nervous System

Paraneoplastic encephalitis/encephalomyelitis

Diverse and complex symptoms arising from cerebellar encephalitis, brainstem encephalitis, limbic encephalitis, and myelitis. Characterized by cognitive dysfunction, depression, personality changes, hallucinations, seizures, somnolence, autonomic dysfunction, and less commonly endocrine dysfunction if the hypothalamus is involved.[7]

Subacute cerebellar degeneration

It is commonly associated with breast cancer, small cell lung cancer, Hodgkin lymphoma, and ovarian cancer. Clinically manifested as ataxia, dysarthria, dysphagia, diplopia, dizziness, nausea, and vomiting.

Opsoclonus-myoclonus syndrome

Clinically characterized by uncontrolled rapid eye movement, body jerks, ataxia, hypotonia, irritability and commonly affects children less than 4 years. Opsoclonus is the common manifestation in children whereas ataxia is more prominent in adults.

Neuromuscular Junction

Myasthenia Gravis

Most commonly seen in patients with thymoma and is clinically manifested as a weakness of voluntary muscles and diaphragmatic weakness. Anti-AchR (acetylcholine receptor) antibody is positive in those patients, and electromyography (EMG) shows a decremental response to repetitive nerve stimulation.[8]

Lambert-Eaton myasthenic syndrome (LEMS)

It is caused due to impairment of voltage-gated calcium channels (VGCC) due to autoantibodies on the presynaptic membrane at neuromuscular junction which leads to decreased acetylcholine release. [8] LEMS is strongly associated with small cell lung cancer (SCLC), about 3% of patients develop LEMS, and it can occur at any stage of the disease. Clinically LEMS is characterized by weakness of the proximal muscles predominantly affecting thigh and pelvic muscles; patient generally have difficulty in strenuous activity; moreover, patients also have difficulties in basic activities such as climbing stairs, walking, and getting up from a chair. Symptoms are gradual in onset with slow progression. Patients also demonstrate autonomic symptoms such as dry mouth, decreased sweating, and constipation. Clinical examination is positive for diminished tendon reflexes.  The blood anti-VGCC antibodies are positive in approximately 85% of patients with LEMS.

Peripheral Nervous System

Autonomic neuropathy

Frequently associated with SCLC and thymoma. Autonomic neuropathy affects parasympathetic, sympathetic, and enteric nervous systems. Characterized by dry mouth, eyes, altered pupillary reflexes, bladder and bowel dysfunction, orthostatic hypotension. A patient may also manifest as chronic gastrointestinal (GI) pseudo-obstruction leading to constipation, nausea, vomiting, dysphagia, and abdominal distension.

Subacute sensory neuropathy

Characterized by paresthesia, pain, decreased sensation and deep tendon reflexes. It affects both upper and the lower extremities; distribution can be either multifocal, asymmetric or symmetric.

Endocrine

Cushing syndrome

Manifested as muscle weakness, weight gain, peripheral edema, centripetal fat distribution, and high blood pressure.[9] Blood workup significant for hypokalemia elevated cortisol level and elevated ectopic adrenocorticotropic hormone (ACTH) due to tumor cells.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

SIADH is more frequently seen in SCLC patients due to ectopic anti-diuretic hormone (ADH) by tumor cells.[10] Clinical manifestations vary from mild symptoms such as nausea, anorexia, fatigue, and lethargy to severe symptoms like confusion, seizures, respiratory depression, and coma. Laboratory findings are positive for hyponatremia, hyperosmolality and increased urine osmolality.

Hypercalcemia

It is frequently associated with lung cancer, multiple myeloma, and renal cell carcinoma. Hypercalcemia is mediated by different mechanisms such as the ectopic production of the parathyroid hormone-related peptide (PTHrP) by tumor cells, local osteolytic hypercalcemia and increased excess extrarenal vitamin D. Patients manifest as generalized weakness, lethargy, nausea, vomiting, altered mental status, bradycardia, acute renal failure, hypertonia, and hypertension.

Rheumatological

Paraneoplastic polyarthritis

Commonly involves large joints and is characterized by migratory, non-erosive, asymmetric polyarthritis.

Polymyalgia rheumatica

Manifested as pain and stiffness in the shoulder girdle, neck, and hip girdle.[11] It is most commonly associated with myelodysplastic syndrome.

Multicentric reticulohistiocytosis

Clinically characterized by papules, nodules, and destructive polyarthritis.

Hypertrophic osteoarthropathy

Clinically manifested as digital clubbing, joint swelling, and pain.

Hematological

Hematologic manifestations of the paraneoplastic syndrome are generally asymptomatic but can be manifested as pallor, fatigue, dyspnea, and venous thromboembolism. Hematologic syndromes are characterized by thrombocytosis, granulocytosis, eosinophilia, pure red cell aplasia, disseminated intravascular coagulation, and leukemoid reactions.

Dermatological

Acanthosis nigricans

Manifested as thickened hyperpigmented skin, usually in the axilla and neck region. Gastric adenocarcinoma is most commonly associated with acanthosis nigricans.[12]

Paraneoplastic pemphigus

Characterized by blistering and erosion of trunk, palms, and soles; also involves mucous membrane causing pain due to mucosal erosion. Commonly seen in patients with B-cell lymphoproliferative disorder.[13]

Sweet syndrome

This is also known as acute febrile neutrophilic dermatosis. It manifests as acute onset of painful, erythematous plaques, papules, and nodules accompanied by fever and neutrophilia.

Leukocytoclastic vasculitis

Typically manifests as palpable purpura on the lower extremities, but a patient may also experience cyanosis, pruritus, pain, and ulceration of the affected skin.

Dermatomyositis

Characterized by a heliotrope rash on the upper eyelids, Gottron papules on phalangeal joints, and an erythematous rash on the face, neck back, chest, and shoulders.[12] Also involves muscles as inflammatory myopathy and is manifested as proximal muscle weakness and muscle tenderness.

Renal

Electrolyte imbalance (hypokalemia, hypo or hypernatremia, hyperphosphatemia) causing nephropathy and acid-base disturbance due to ectopic hormones produced by tumor cells such as ACTH and ADH.[14] Nephrotic syndrome can also be one of the manifestations of paraneoplastic syndrome.

Miscellaneous

Fever, cachexia, anorexia, dysgeusia

Evaluation

Diagnosis of the suspected paraneoplastic syndromes is based on the exclusion of other etiologies as there are heterogeneous clinical manifestations.

An international panel of neurologists developed criteria for paraneoplastic syndrome affecting the nervous system into definite and possible categories [15][16].

Definite paraneoplastic syndromes

A classical neurological syndrome and malignancy which develops within 5 years of neurological disorder. Classical syndromes are encephalomyelitis, limbic encephalitis, subacute cerebellar degeneration, opsoclonus-myoclonus syndrome, Lambert Eaton myasthenic syndrome, subacute sensory neuropathy, chronic gastrointestinal pseudoobstruction, and dermatomyositis.

  1. A nonclassical syndrome that improves significantly with the treatment of underlying malignancy and syndrome is not prone to spontaneous remission.
  2. A nonclassical syndrome with the detection of paraneoplastic antibodies and malignancy that develops within 5 years of diagnosis of the neurological syndrome.
  3. A classical or nonclassical neurological syndrome with well-recognized paraneoplastic antibodies. The well-recognized antibodies include anti-Hu, Yo, Ri, CV2/CRMP-5, Ma2, and amphiphysin.

Possible paraneoplastic syndrome

  1. A classical syndrome without paraneoplastic antibodies and cancer but at high risk for an underlying malignancy.
  2. A classical or nonclassical neurologic syndrome with partially characterized antibody but no cancer.
  3. A nonclassical syndrome without paraneoplastic antibodies but with cancer within 2 years of a neurological syndrome.

A patient should be evaluated with a complete panel of laboratory, imaging, electrodiagnostic studies and biopsy of specific tissues if required.

  • Complete blood count with differential
  • Comprehensive metabolic panel
  • Urinalysis
  • Tumor markers
  • Ectopic hormones level like PTHrP, ACTH, ADH
  • Cerebrospinal fluid analysis (CSF)
  • Protein electrophoresis o serum and CSF
  • Assay of paraneoplastic antibodies in blood and CSF
  • Skin biopsy
  • Muscle biopsy

Treatment / Management

Management of the patients is based on type, severity, and location of the paraneoplastic syndrome. First, therapeutic options are to treat underlying malignancy with chemotherapy, radiation, or surgery. 

Other therapeutic options are immunosuppression with corticosteroids or other immunosuppressive drugs, intravenous immunoglobulins, plasma exchange, or plasmapheresis.

Differential Diagnosis

  • Encephalopathy
  • Encephalitis
  • Personality disorder
  • Dementia
  • Myelitis
  • Anemia
  • Myelodysplastic syndrome
  • Bone marrow failure
  • Polycythemia Vera
  • Chronic fatigue syndrome
  • Mixed connective tissue disorder
  • Dermatomyositis
  • Scleroderma
  • Systemic lupus erythematosus
  • Polymyalgia rheumatica
  • Acute glomerulonephritis
  • Nephrotic syndrome

Enhancing Healthcare Team Outcomes

The diagnosis and management of paraneoplastic syndromes is difficult. In most cases, there is an underlying malignancy responsible. Because of the numerous causes, the condition is best managed by a multidisciplinary team that includes a pathologist, oncologist, radiologist, hematologist, nurse specialist, and an internist. Once the cause is discovered, it needs to be treated.

The management of the patients is based on type, severity, and location of the paraneoplastic syndrome. First, therapeutic options are to treat underlying malignancy with chemotherapy, radiation, or surgery. 

Other therapeutic options are immunosuppression with corticosteroids or other immunosuppressive drugs, intravenous immunoglobulins, plasma exchange, or plasmapheresis.


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Paraneoplastic Syndromes - Questions

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A 63-year-old male is seen in the clinic and found to have a metastatic cancer. Which of the following features is not associated with a malignancy?



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A patient with lung cancer has excessive production of calcium. Which of the following statements is incorrect?



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Which histologic type of lung cancer is most frequently associated with hypercalcemia?



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Which of the following hormones is not produced by paraneoplastic syndromes?



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Which of the following paraneoplastic syndromes is not seen with lung cancers?



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A 65-year-old smoker presents with a 10-pound weight loss over the past 2 months. Physical exam is unremarkable but the blood work reveals a sodium of 112 mEq/L, potassium of 3.8 mEq/L. chloride of 98 mEq/L, blood urea nitrogen of 12 mg/dL, creatinine of 0.8 mg/dL, glucose of 98 mg/dL, and bicarbonate of 18 mEq/L. What should be the next test ordered for this patient?



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Which of the following is not a manifestation of paraneoplastic syndrome?



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A 60-year-old smoking patient with a 5 cm central lung mass develops abdominal striae, moon facies, and a buffalo hump. The paraneoplastic syndrome is caused by a hormone secreted by the tumor that causes which reaction?



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Which of the following is least likely to accompany a mediastinal tumor?



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A 66-year-old smoker has a 4 cm central lung mass and later develops abdominal striae, moon facies, and a buffalo hump. The paraneoplastic syndrome is caused by a hormone secreted by the tumor that causes which reaction?



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A 66-year-old female presents with increasing bilateral shoulder and hip weakness that has been progressing over the last 3 months. Relevant medical history includes a diagnosis of breast cancer six months prior. What is her most likely diagnosis?



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An individual with lung cancer experiences weakness, confusion, ataxia, sensory loss, and nystagmus. What is the most likely diagnosis?



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Which of the following skin lesions are not associated with systemic malignancy?



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A patient with stage IIIB squamous cell carcinoma presents with confusion and has a calcium level of 18.5 mg/dL. Serum parathyroid hormone is low, but parathyroid-like hormone is positive. Treatment with large volumes of intravenous fluids and furosemide only lowers the calcium to 17.0. Select the most appropriate treatment.



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A patient with a right middle lobe lung mass has kidney stones and bone pain. Calcium is 17.2 mg/dL and phosphorus is 1.3 mg/dL. Select the appropriate laboratory test.



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A 65-year old presents with pain and swelling of his knee joints and lower legs that have been ongoing for the past 2 weeks. Last 2 days he has had a fever and extreme fatigue. To date, he lost 10 pounds in weight. He denies any trauma or past illnesses but does smoke and drink. Physical exam reveals clubbing of the fingernails and there is painful swelling of both lower legs. X-rays reveal periosteal thickening in the lower leg bones. Blood work reveals elevations in ESR and alkaline phosphatase. Based on this information, the most common cause of his pathology may be related to what type of pulmonary malignancy?



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Which of the following is a paraneoplastic syndrome?



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A 56-year-old male with a medical history significant for hypertension, smoking, chronic obstructive lung disease presented to the office with weight loss, loss of appetite, imbalance, a recent change in his speech and vision. Physical examination was remarkable for diminished bilateral lower extremity sensation, inability to perform point to point movement and rapid alternating movement, abnormal gait, positive Romberg sign. MRI brain was negative for mass or any acute process, CT scan chest revealed right upper lobe lung mass. Biopsy of the lung mass was positive for small cell lung cancer (SCLC). Which paraneoplastic antibody most likely will be positive for this patient?



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A 66-year-old man presents to the clinic accompanied by his daughter with a complaint of gradual onset of fatigue, anorexia, and constipation over the last five weeks. He also feels that he has been urinating more often and a larger volume. Over the last two days, he has experienced some confusion and lethargy. She also adds that her dad has a nagging cough with some tinge of blood that has not improved with over-the-counter medications and has lost 10 kg during that interval. He has a history of hypertension and for which he takes hydrochlorothiazide. He has been smoking 3 packs of cigarettes daily for 40 years and drinks socially. On physical examination, he appears somnolent and disoriented. His reflexes are reduced. Chest and cardiovascular examinations appear normal. Temporal wasting is noted. His serum calcium is 18.3 mg/dL, glucose 98 mg/dL, serum sodium 142 mEq/L, serum potassium 4.2 mEq/L. Which other metabolic abnormality do you expect in this patient given the underlying diagnosis?



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A 62-year-old male comes to the clinic complaining of gradual onset weakness involving the lower extremities and fatigue for the past three months. He has a persistent cough with blood-tinged sputum at times. He denies any recent international travels. He also complains that he has difficulties getting up after sitting and has lost 5 kg over the last two months. He drinks two beers daily and has smoked 1 pack of cigarettes per day over the past 50 years. On examination, the patient has decreased strength in his lower extremities, and his lower deep tendon reflexes are also diminished. CT shows a mass in his lungs, and a biopsy reveals the presence of a chromogranin positive lung malignancy. Which of the following best explains the pathophysiology behind this patient's muscle weakness?



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A 67-year-old man comes to the clinic with an initial complaint of fatigue, muscle weakness in his extremities, and weight loss over the last five months. He has a history of hypertension that has been under control with diet and denies any other medical history. He has been a long term smoker for 45 years and consumes about 2-3 packs of cigarettes daily. He does not drink alcohol or use any illicit drugs. On physical examination, muscle strength of 3/5 is noted in the proximal muscle groups bilaterally and symmetrically. Reflexes are normal, and no other sensory abnormality is seen. Erythematous papules are noted in his fingers. He denies having been in contact with any animals recently and having any history of allergy. No other major abnormal findings are seen. Chest x-ray shows a mass in the right lower lobe, and a biopsy is done to search for malignancy. Muscle biopsy shows perimysial inflammation. Which other specific findings can be seen in this patient's muscle biopsy?



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Paraneoplastic Syndromes - References

References

Paraneoplastic glomerulopathies associated with hematologic malignancies., Dhanapriya J,Dineshkumar T,Sakthirajan R,Surendar D,Gopalakrishnan N,Balasubramaniyan T,, Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia, 2018 Mar-Apr     [PubMed]
The real evidence for polymyalgia rheumatica as a paraneoplastic syndrome., Muller S,Hider S,Helliwell T,Partington R,Mallen C,, Reumatismo, 2018 Mar 27     [PubMed]
Cell-mediated immune responses in paraneoplastic neurological syndromes., Zaborowski MP,Michalak S,, Clinical & developmental immunology, 2013     [PubMed]
Paraneoplastic syndromes: an approach to diagnosis and treatment., Pelosof LC,Gerber DE,, Mayo Clinic proceedings, 2010 Sep     [PubMed]
Paraneoplastic dermatological manifestation of gastrointestinal malignancies., Dourmishev LA,Draganov PV,, World journal of gastroenterology, 2009 Sep 21     [PubMed]
Recommended diagnostic criteria for paraneoplastic neurological syndromes., Graus F,Delattre JY,Antoine JC,Dalmau J,Giometto B,Grisold W,Honnorat J,Smitt PS,Vedeler Ch,Verschuuren JJ,Vincent A,Voltz R,, Journal of neurology, neurosurgery, and psychiatry, 2004 Aug     [PubMed]
Recommended diagnostic criteria for paraneoplastic neurological syndromes., Greenlee JE,, Journal of neurology, neurosurgery, and psychiatry, 2004 Aug     [PubMed]
Baijens LW,Manni JJ, Paraneoplastic syndromes in patients with primary malignancies of the head and neck. Four cases and a review of the literature. European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery. 2006 Jan;     [PubMed]
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Honnorat J,Viaccoz A, New concepts in paraneoplastic neurological syndromes. Revue neurologique. 2011 Oct;     [PubMed]
Grisold W,Giometto B,Vitaliani R,Oberndorfer S, Current approaches to the treatment of paraneoplastic encephalitis. Therapeutic advances in neurological disorders. 2011 Jul;     [PubMed]
van Sonderen A,Wirtz PW,Verschuuren JJ,Titulaer MJ, Paraneoplastic syndromes of the neuromuscular junction: therapeutic options in myasthenia gravis, lambert-eaton myasthenic syndrome, and neuromyotonia. Current treatment options in neurology. 2013 Apr;     [PubMed]
Barbosa SL,Rodien P,Leboulleux S,Niccoli-Sire P,Kraimps JL,Caron P,Archambeaud-Mouveroux F,Conte-Devolx B,Rohmer V, Ectopic adrenocorticotropic hormone-syndrome in medullary carcinoma of the thyroid: a retrospective analysis and review of the literature. Thyroid : official journal of the American Thyroid Association. 2005 Jun;     [PubMed]
Peri A,Grohé C,Berardi R,Runkle I, SIADH: differential diagnosis and clinical management. Endocrine. 2017 Jan;     [PubMed]
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