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  1. Tong CV, Hussein Z, Noor NM, Mohamad M, Ng WF
    QJM, 2015 Jan;108(1):49-50.
    PMID: 25099611 DOI: 10.1093/qjmed/hcu166
    Matched MeSH terms: Paraneoplastic Syndromes/etiology
  2. Fadilah SA, Raymond AA, Cheong SK
    Postgrad Med J, 2001 Apr;77(906):268-269; discussion 277-8.
    PMID: 11264499
    Matched MeSH terms: Paraneoplastic Syndromes/etiology*
  3. Liam CK
    Med J Malaysia, 1997 Jun;52(2):186-7.
    PMID: 10968082
    Matched MeSH terms: Paraneoplastic Syndromes/etiology*
  4. Low JM, Basiam S, Ahlam Naila K
    Med J Malaysia, 2019 08;74(4):335-337.
    PMID: 31424045
    The acronym POEMS syndrome was coined for a unique multisystem disorder characterised by peripheral neuropathy, organomegaly, endocrinopathies, monoclonal gammopathy and skin changes. We report a male patient presenting to us with spinal plasmacytoma complicated with paraplegia. He was subsequently diagnosed to have POEMS syndrome and successfully treated with thalidomide and dexamethasone. Post treatment, he is able to ambulate independently.
    Matched MeSH terms: Paraneoplastic Syndromes/etiology*
  5. Nyanti L, Samsudin A, Tiong IK
    J Med Case Rep, 2019 Jun 21;13(1):188.
    PMID: 31221202 DOI: 10.1186/s13256-019-2122-8
    BACKGROUND: Leser-Trélat syndrome, which manifests as eruptive multiple seborrheic keratoses, is a rare paraneoplastic sign. Hyponatremia in the elderly population is an often overlooked but potentially sinister biochemical abnormality. Cancer-related causes of hyponatremia include syndrome of inappropriate antidiuretic hormone secretion, cerebral or renal salt wasting, and adrenal dysfunction. We report a case of an elderly man who presented with both syndrome of inappropriate antidiuretic hormone secretion and Leser-Trélat syndrome, and was eventually found to have renal malignancy.

    CASE PRESENTATION: A 74-year-old indigenous Malaysian man with underlying chronic kidney disease presented with recurrent admissions for hyponatremia with parameters indicative of syndrome of inappropriate antidiuretic hormone secretion, constitutional symptoms, and diffuse skin lesions suggestive of multiple seborrheic keratoses. A radiological workup revealed metastatic renal cell carcinoma with evidence of metastasis to the brain, adrenal glands, bone, and lungs.

    CONCLUSIONS: To the best of our knowledge, renal malignancy presenting as syndrome of inappropriate antidiuretic hormone secretion and Leser-Trélat concurrently is rare. The causes of hyponatremia in the elderly, approach to investigation, and value as a poor prognostic marker in malignancy are highlighted. We also discuss Leser-Trélat syndrome, its pathophysiology, and its possible implications on clinical practice.

    Matched MeSH terms: Paraneoplastic Syndromes/etiology*
  6. Stephen SE, Loong JLX, Hoong CK, Lim SM, Botross NP
    Am J Case Rep, 2018 Jul 23;19:858-863.
    PMID: 30033442 DOI: 10.12659/AJCR.909228
    BACKGROUND Acquired hemophilia is a rare but potentially dangerous bleeding disorder caused by autoantibodies against coagulation factors. It affects 1 to 1.5 per 1 million people each year. While 50% of cases could be idiopathic, other causes include malignancies, diabetes, pregnancy, infection, and autoimmune disorders. CASE REPORT We report a case of a 90-year-old male who developed a spontaneous hematoma on the dorsum of his right hand, with no prior history of trauma or any other mucosal bleeding. His activated partial thromboplastin time (aPTT) was found to be prolonged (>180 seconds) with a very low level of factor VIII (0.1%). CONCLUSIONS As workups did not identify the source, including malignancy and autoimmune diseases, of his acquired hemophilia, it is believed to be idiopathic. He was started on intravenous recombinant factor VIIa (NovoSeven) to control the bleeding in combination with an immunosuppressive therapy of cyclophosphamide and prednisolone. In approximately 10% of patients with acquired hemophilia, underlying malignancy, such as squamous cell cancer, chronic lymphocytic leukemia, non-Hodgkin lymphoma, and multiple myeloma can present and commonly develop in elderly patients. Therefore, patients diagnosed with idiopathic acquired hemophilia should be given long-term follow up.
    Matched MeSH terms: Paraneoplastic Syndromes/etiology
  7. Leow MKS, Dogra S, Ge X, Chuah KL, Liew H, Loke KSH, et al.
    J Clin Endocrinol Metab, 2021 04 23;106(5):e2299-e2308.
    PMID: 33462615 DOI: 10.1210/clinem/dgaa964
    CONTEXT: Literature suggests that oncogenic osteomalacia is usually caused by a benign mesenchymal tumor secreting fibroblast growth factor subtype-23 (FGF-23), but the involvement of other phosphatonins has only been scarcely reported. We have previously published a seemingly typical case of oncogenic osteomalacia. Following curative neoplasm resection, we now report unique molecular characteristics and biology of this tumor.

    CASE DESCRIPTION: A 25-year-old man had been diagnosed with severe oncogenic osteomalacia that gradually crippled him over 6 years. 68Ga-DOTA-TATE positron emission tomography/computed tomography scan localized the culprit tumor to his left sole, which on resection revealed a deep fibrous histiocytoma displaying a proliferation of spindle cells with storiform pattern associated with multinucleated giant cells resembling osteoclasts. Circulating FGF-23, which was elevated more than 2-fold, declined to undetectable levels 24 h after surgery. Microarray analysis revealed increased tumor gene expression of the phosphatonins FGF-23, matrix extracellular phosphoglycoprotein (MEPE) and secreted frizzled-related protein subtype 4, with elevated levels of all 3 proteins confirmed through immunoblot analysis. Differential expression of genes involved in bone formation and bone mineralization were further identified. The patient made an astonishing recovery from being wheelchair bound to fully self-ambulant 2 months postoperatively.

    CONCLUSION: This report describes oncogenic osteomalacia due to a deep fibrous histiocytoma, which coincidentally has been found to induce profound muscle weakness via the overexpression of 3 phosphatonins, which resolved fully upon radical resection of the tumor. Additionally, genes involved in bone formation and bone remodeling contribute to the molecular signature of oncogenic osteomalacia.

    Matched MeSH terms: Paraneoplastic Syndromes/etiology*
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