Oncogenic Osteomalacia

Edmister, Kelli Andresen; Sundaram, Murali

doi:10.1055/s-2002-36716

Cited by 24 publications

(6 citation statements)

References 23 publications

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“…Such instances have included Fanconi syndrome secondary to monoclonal gammopathy [10] and ifosfamide treatment [11]. Hypophosphataemia caused by malabsorption syndrome [12], parathyroid hormone-related protein-producing tumours or other tumours (so called oncogenic osteomalacia) [13][14][15] also produces a reversible osteomalacia, mediated via the phosphaturic hormones fibroblastic growth factor 23 (FGF 23) and matrix extracellular phosphoglycoprotein (MEPE), themselves controlled by the membrane metalloprotease PHEX [16]. In such cases the hypophosphataemia can lead to pathological fractures and tetany [15].…”

Section: Introductionmentioning

confidence: 99%

The development of hypophosphataemic osteomalacia with myopathy in two patients with HIV infection receiving tenofovir therapy

et al. 2005

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We report two cases in which osteomalacia developed in patients on tenofovir-containing highly active antiretroviral therapy (HAART) in the context of Fanconi syndrome with hypophosphataemia. Bone pain was the presenting feature and myopathy followed in one case. Disability was reversed with withdrawal of the drug and with mineral supplementation. The cases highlight the importance of considering the diagnosis of osteomalacia in patients treated with tenofovir. A possible association with incipient acute renal failure, particularly during nonsteroidal anti-inflammatory drug (NSAID) use, needs further investigation.Keywords: HIV infections, hypophosphataemia, myopathy, osteomalacia, tenofovir Received: 28 September 2004, accepted 18 February 2005 Introduction Reduced bone mineral density has become increasingly important within the HIV-infected cohort as longevity has increased. It has been documented in a number of studies [1,2] and is possibly linked to the use of highly active antiretroviral therapy (HAART) [3], although, in studying this effect, it is difficult to separate the relative contributions made by length of time since diagnosis and HAART use, the two being interdependent.Osteomalacia, however, has been documented in only a few cases [4] and the myopathy of osteomalacia not at all. Tenofovir causes recognized Fanconi syndrome and hypophosphataemia [5,6], although osteomalacia has rarely been linked to such treatment [7]. Osteomalacia has also occasionally been linked to cidofovir and adefovir, other nucleotide analogues [7]. In animal studies using high-dose tenofovir, osteomalacia was a frequent adverse event [8]. In other settings, however, Fanconi syndrome is known to cause osteomalacia and myopathy, which is reversible if the underlying cause can be corrected [9]. Such instances have included Fanconi syndrome secondary to monoclonal gammopathy [10] and ifosfamide treatment [11]. Hypophosphataemia caused by malabsorption syndrome [12], parathyroid hormone-related protein-producing tumours or other tumours (so called oncogenic osteomalacia) [13][14][15] also produces a reversible osteomalacia, mediated via the phosphaturic hormones fibroblastic growth factor 23 (FGF 23) and matrix extracellular phosphoglycoprotein (MEPE), themselves controlled by the membrane metalloprotease PHEX [16]. In such cases the hypophosphataemia can lead to pathological fractures and tetany [15]. Fractures or Looser's zones can be misdiagnosed as disseminated malignancy, leading to diagnostic delay and disability [17]. Case 1A 47-year-old homosexual man was diagnosed with AIDS in 1989. His past medical history had included Kaposi sarcoma (treated in 1999) and hepatitis B infection (now surface antigen negative), but no abnormality of blood pressure, of renal function, or of phosphate metabolism and no history of a concomitant potentially nephrotoxic agent. He had been on antiretroviral therapy since 1991, with a triple class resistant virus.In February 2002, as a result of virological failure on his previous salvage regime...

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Section: Introductionmentioning

confidence: 99%

The development of hypophosphataemic osteomalacia with myopathy in two patients with HIV infection receiving tenofovir therapy

et al. 2005

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“…It clinically mimics X-linked or autosomal dominant hereditary hypophosphatemic rickets. Approximately 100 cases of tumor-induced osteomalacia have been reported [129][130]. Patients affected are usually adults over the age of 30, with a maleto-female ratio of 1.2:1.…”

Section: Other Ectopic Hormone Syndromesmentioning

confidence: 99%

“…Laboratory and radiologic testing are essential for the diagnosis. Bone and indium-111 octreotide imaging are additional important diagnostic radiologic tools for small tumors not detected on routine physical examination or radiography [127][128][129][130]. Oral or intravenous supplementation of phosphate combined with vitamin D therapy is generally recommended in addition to the complete surgical removal of the tumor [131][132].…”

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confidence: 99%

Endocrine Paraneoplastic Syndromes: A Review

Arabi¹

2015

EMIJ

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It is important for the endocrinologist and oncologist to recognize these paraneoplastic endocrine syndromes since this may help in defining the cancer type and hence lead to the appropriate management. In addition, these syndromes are a major cause of morbidity and mortality. Moreover, AbstractParaneoplastic endocrine syndromes result from ectopic production of hormones by different tumors. Hypercalcemia of malignancy is the most common, mostly caused by ectopic parathyroid hormone related peptide (PTHrP) production which increases bone resorption. Other causes include the rare ectopic parathyroid hormone (PTH) production, ectopic production of 1, 25-(OH)2 vitamin D by the tumor and its adjacent macrophages and bone metastasis which by itself in addition to the local production of PTHrP at the level of the bone lead to bone resorption and thus hypercalcemia. Treatment includes extracellular fluid volume repletion, bisphosphonates or denosumab and calcitonin. Ectopic Cushing's syndrome caused by ectopic ACTH production results in hypokalemia, proximal muscle weakness, easy bruisability, hypertension, diabetes and psychiatric abnormalities including depression and mood disorders. Different diagnostic measures help to differentiate Cushing's disease from ectopic Cushing's syndrome. Treatment includes surgical resection of tumor and medical therapy to suppress excess cortisol production. Ectopic secretion of ADH has been associated with different tumor types. The best treatment options include removal of the underlying tumor, chemotherapy, or radiotherapy in addition to free water restriction, demeclocycline and vaptans. Ectopic growth hormone releasing hormone secretion has been identified with carcinoids, phechromocytoma and other tumors. Surgery is the mainstay of therapy with systemic therapy used in metastatic disease. Other rare ectopic hormone syndromes have also been identified including ectopic prolactin, ectopic erythropoietin, and thrombopoetin in addition to others. Keywords 2/12paraneoplastic endocrine syndromes may be the first presenting feature of malignancy [2,3]. This paper provides an overview on the common PNES, their prevalence, diagnosis, prognosis and response to treatment (Table 1). Methodology of Literature SearchEligible studies were identified by a search, from year 1920 up till February 2014, in Medline, PUBMED and EMBASE using a refined search strategy with several terms used including "endocrine paraneoplastic syndromes", "ectopic hormones", "humoral hypercalcemia of malignancy", "ectopic parathyroid hormone related peptide", "ectopic ACTH", "ectopic Cushing syndrome", "ectopic antidiuretic hormone", "syndrome of inappropriate ADH", "ectopic growth hormone releasing hormone", "ectopic growth hormone", "ectopic prolactin", "ectopic thyroid stimulating hormone" in addition to several others. In addition, searches of personal collections and the reference lists of eligible studies were identified with their full text papers being retrieved. A-Hypercalcemia of MalignancyHistorical Perspec...

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“…[1][2][3] Approximately, 120 cases of TIO have been reported in the literature. 1,3 Phosphate wasting and defect in 1,25 dihydroxyvitamin D synthesis in TIO is caused by humoral factors known as "phosphatonins" that are secreted by the mesenchymal tumors.…”

Section: Figurementioning

confidence: 99%

The Search for Primary Tumor in a Patient With Oncogenic Osteomalacia

Agrawal¹,

Jambhekar²,

Sarathi³

et al. 2010

Clinical Nuclear Medicine

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We report a case of oncogenic osteomalacia in which F-18 FDG PET imaging played a crucial role in detecting the occult neoplasm. A 39-year-old female patient presented with low backache and bilateral lower limb pain of 3-year duration. On evaluation, she was found to have hypophosphatemic osteomalacia and was referred for F-18 FDG PET scan because her initial clinical and radiologic evaluation failed to detect a tumor. F-18 FDG PET scan revealed a hypermetabolic focus in right popliteal fossa, which was correlated as a tumor in soft tissues of right popliteal fossa on magnetic resonance imaging. Following surgical excision of tumor, final histopathology revealed a benign phosphaturic mesenchymal tumor of mixed connective tissue origin. Postoperatively, her symptoms alleviated and serum phosphates normalized within 2 weeks. We suggest that F-18 FDG PET should be performed in such cases to localize occult neoplasm that may be otherwise missed on conventional radiologic imaging.

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Oncogenic Osteomalacia

Cited by 24 publications

References 23 publications

The development of hypophosphataemic osteomalacia with myopathy in two patients with HIV infection receiving tenofovir therapy

The development of hypophosphataemic osteomalacia with myopathy in two patients with HIV infection receiving tenofovir therapy

Endocrine Paraneoplastic Syndromes: A Review

The Search for Primary Tumor in a Patient With Oncogenic Osteomalacia

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