Hypophosphatemia in Patients With Multiple Myeloma
Hypophosphatemia is among the most common electrolyte abnormalities, especially among patients with underlying malignancies, and is frequently associated with adverse prognoses. Phosphorus levels are regulated through a number of mechanisms, including parathyroid hormone (PTH), fibroblast growth fac...
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Published in | Curēus (Palo Alto, CA) Vol. 15; no. 6; p. e40487 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
Springer Nature B.V
15.06.2023
Cureus |
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Abstract | Hypophosphatemia is among the most common electrolyte abnormalities, especially among patients with underlying malignancies, and is frequently associated with adverse prognoses. Phosphorus levels are regulated through a number of mechanisms, including parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23), vitamin D, and other electrolyte levels themselves. Clinically, the findings are nonspecific, and the diagnosis is frequently delayed. This article is a narrative literature review. The PubMed database was searched for relevant articles pertaining to hypophosphatemia causes and consequences in patients suffering from multiple myeloma. We found a variety of causes of hypophosphatemia in patients with multiple myeloma. Tumor-induced osteopenia, although more common among patients with small squamous cell carcinomas, can occur with multiple myeloma as well. Additionally, both light chains themselves and medications can trigger Fanconi syndrome, which leads to phosphorus wasting by the kidney. Bisphosphonates, in addition to being a possible cause of Fanconi syndrome, lead to a decrease in calcium levels, which then stimulates parathyroid hormone (PTH) release, predisposing the patient to significant hypophosphatemia. Additionally, many of the more modern medications used to manage multiple myeloma have been associated with hypophosphatemia. A better understanding of those mechanisms may give clinicians a clearer idea of which patients may need more frequent screening as well as what the potential triggers in the individual patient may be. |
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AbstractList | Hypophosphatemia is among the most common electrolyte abnormalities, especially among patients with underlying malignancies, and is frequently associated with adverse prognoses. Phosphorus levels are regulated through a number of mechanisms, including parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23), vitamin D, and other electrolyte levels themselves. Clinically, the findings are nonspecific, and the diagnosis is frequently delayed. This article is a narrative literature review. The PubMed database was searched for relevant articles pertaining to hypophosphatemia causes and consequences in patients suffering from multiple myeloma. We found a variety of causes of hypophosphatemia in patients with multiple myeloma. Tumor-induced osteopenia, although more common among patients with small squamous cell carcinomas, can occur with multiple myeloma as well. Additionally, both light chains themselves and medications can trigger Fanconi syndrome, which leads to phosphorus wasting by the kidney. Bisphosphonates, in addition to being a possible cause of Fanconi syndrome, lead to a decrease in calcium levels, which then stimulates parathyroid hormone (PTH) release, predisposing the patient to significant hypophosphatemia. Additionally, many of the more modern medications used to manage multiple myeloma have been associated with hypophosphatemia. A better understanding of those mechanisms may give clinicians a clearer idea of which patients may need more frequent screening as well as what the potential triggers in the individual patient may be. Hypophosphatemia is among the most common electrolyte abnormalities, especially among patients with underlying malignancies, and is frequently associated with adverse prognoses. Phosphorus levels are regulated through a number of mechanisms, including parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23), vitamin D, and other electrolyte levels themselves. Clinically, the findings are nonspecific, and the diagnosis is frequently delayed. This article is a narrative literature review. The PubMed database was searched for relevant articles pertaining to hypophosphatemia causes and consequences in patients suffering from multiple myeloma. We found a variety of causes of hypophosphatemia in patients with multiple myeloma. Tumor-induced osteopenia, although more common among patients with small squamous cell carcinomas, can occur with multiple myeloma as well. Additionally, both light chains themselves and medications can trigger Fanconi syndrome, which leads to phosphorus wasting by the kidney. Bisphosphonates, in addition to being a possible cause of Fanconi syndrome, lead to a decrease in calcium levels, which then stimulates parathyroid hormone (PTH) release, predisposing the patient to significant hypophosphatemia. Additionally, many of the more modern medications used to manage multiple myeloma have been associated with hypophosphatemia. A better understanding of those mechanisms may give clinicians a clearer idea of which patients may need more frequent screening as well as what the potential triggers in the individual patient may be. Hypophosphatemia is among the most common electrolyte abnormalities, especially among patients with underlying malignancies, and is frequently associated with adverse prognoses. Phosphorus levels are regulated through a number of mechanisms, including parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23), vitamin D, and other electrolyte levels themselves. Clinically, the findings are nonspecific, and the diagnosis is frequently delayed. This article is a narrative literature review. The PubMed database was searched for relevant articles pertaining to hypophosphatemia causes and consequences in patients suffering from multiple myeloma. We found a variety of causes of hypophosphatemia in patients with multiple myeloma. Tumor-induced osteopenia, although more common among patients with small squamous cell carcinomas, can occur with multiple myeloma as well. Additionally, both light chains themselves and medications can trigger Fanconi syndrome, which leads to phosphorus wasting by the kidney. Bisphosphonates, in addition to being a possible cause of Fanconi syndrome, lead to a decrease in calcium levels, which then stimulates parathyroid hormone (PTH) release, predisposing the patient to significant hypophosphatemia. Additionally, many of the more modern medications used to manage multiple myeloma have been associated with hypophosphatemia. A better understanding of those mechanisms may give clinicians a clearer idea of which patients may need more frequent screening as well as what the potential triggers in the individual patient may be.Hypophosphatemia is among the most common electrolyte abnormalities, especially among patients with underlying malignancies, and is frequently associated with adverse prognoses. Phosphorus levels are regulated through a number of mechanisms, including parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23), vitamin D, and other electrolyte levels themselves. Clinically, the findings are nonspecific, and the diagnosis is frequently delayed. This article is a narrative literature review. The PubMed database was searched for relevant articles pertaining to hypophosphatemia causes and consequences in patients suffering from multiple myeloma. We found a variety of causes of hypophosphatemia in patients with multiple myeloma. Tumor-induced osteopenia, although more common among patients with small squamous cell carcinomas, can occur with multiple myeloma as well. Additionally, both light chains themselves and medications can trigger Fanconi syndrome, which leads to phosphorus wasting by the kidney. Bisphosphonates, in addition to being a possible cause of Fanconi syndrome, lead to a decrease in calcium levels, which then stimulates parathyroid hormone (PTH) release, predisposing the patient to significant hypophosphatemia. Additionally, many of the more modern medications used to manage multiple myeloma have been associated with hypophosphatemia. A better understanding of those mechanisms may give clinicians a clearer idea of which patients may need more frequent screening as well as what the potential triggers in the individual patient may be. |
Author | Ilyas, Usman Nassar, Mahmoud Cancarevic, Ivan |
AuthorAffiliation | 2 Internal Medicine, Icahn School of Medicine at Mount Sinai, NYC Health + Hospitals/Queens, New York, USA 1 Internal Medicine, Icahn School of Medicine at Mount Sinai, Queens Hospital Center, New York, USA |
AuthorAffiliation_xml | – name: 1 Internal Medicine, Icahn School of Medicine at Mount Sinai, Queens Hospital Center, New York, USA – name: 2 Internal Medicine, Icahn School of Medicine at Mount Sinai, NYC Health + Hospitals/Queens, New York, USA |
Author_xml | – sequence: 1 givenname: Ivan surname: Cancarevic fullname: Cancarevic, Ivan – sequence: 2 givenname: Usman surname: Ilyas fullname: Ilyas, Usman – sequence: 3 givenname: Mahmoud surname: Nassar fullname: Nassar, Mahmoud |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37342302$$D View this record in MEDLINE/PubMed |
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Keywords | electrolyte disturbances multiple myeloma hypophosphatemia electrolyte phosphorus |
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SubjectTerms | Bisphosphonates Cancer Diabetes Disease Endocrine system Fibroblasts Growth factors Hypercalcemia Internal Medicine Kidneys Metabolism Multiple myeloma Nephrology Oncology Phosphates Phosphorus Regulation Squamous cell carcinoma Tomography Tumors |
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