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Osteomalacia
Published in Charles Theisler, Adjuvant Medical Care, 2023
Common causes of osteomalacia are: Vitamin D deficiency (e.g., from lack of sunshine plus inadequate intake). Also, if the body cannot absorb fats properly, they are passed directly out of the body in the stool (steatorrhea). As a result, vitamin D, which is a fat-soluble vitamin, and calcium are poorly absorbed.The kidneys do not function properly (tubular acidosis), causing metabolic acidosis. The increased acid helps to dissolve the skeleton.Digestive organs do not adequately function for proper absorption of calcium.2Chronic liver disease that interferes with vitamin D metabolism.Deficient intake of calcium or lack of phosphate.3
PerformLyte—A Prodosomed PL425 PEC Phytoceutical-Enriched Electrolyte Supplement—Supports Nutrient Repletion, Healthy Blood pH, Neuromuscular Synergy, Cellular and Metabolic Homeostasis
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi
Dietary phosphates are available in milk, egg yolks, chocolate, and soft drinks, and excreted in the urine and stool. Phosphorous deficiency symptoms include anxiety, fatigue, irregular breathing, irritability, joint stiffness, numbness, weakness, and irregular changes in body weight.142,144
Laboratory evaluation of parathyroid gland function
Published in Pallavi Iyer, Herbert Chen, Thyroid and Parathyroid Disorders in Children, 2020
Phosphate is second to calcium in abundance; this anion is present in DNA and RNA nucleotides, essential for the generation of energy as adenosine triphosphate (ATP), and a component of cell membranes, signal transduction pathways, and the bone mineral—hydroxyapatite. It is absorbed by the intestinal duodenum and jejunum, filtered through the renal glomerulus to be reabsorbed by the proximal renal tubule or excreted in urine, and deposited into bone linked to calcium as hydroxyapatite from which site it may be reabsorbed by PTH and calcitriol. Under usual circumstances, the serum concentrations of calcium and phosphate are reciprocally related, and the calcium × phosphate product approximates 30. Serum concentrations of phosphate decrease with age: between 0 and 5 days serum phosphate levels range between 4.8 and 8.2 mg/dL; 1–3 years: 3.8–6.5 mg/dL; 4–11 years: 3.7–5.6 mg/dL; 12–15 years: 2.9–5.4 mg/dL; 16–19 years: 2.7–4.7 mg/dL; adult: 2.5–4.5 mg/dL.
Developments in FGFR and IDH inhibitors for cholangiocarcinoma therapy
Published in Expert Review of Anticancer Therapy, 2023
Zachary J Brown, Samantha M. Ruff, Timothy M Pawlik
Preclinical studies have demonstrated that knockdown of FGFR2 can suppress cell growth and colony formation in CCA cells with G2/M cell cycle arrest and downregulation of STAT3, cyclin AA, and cyclin B [30]. In addition, inhibition of FGFR2 can enhance the suppressive effect of gemcitabine on cell migration and invasion. The combination of infigratinib, an FGFR inhibitor, and gemcitabine interrupted cell growth, migration, and invasion [30]. In a phase I study dose-escalation trial, futibatinib – which is an oral, irreversible, highly selective FGFR 1–4 inhibitor – was assessed in 71 patients who had tumors with an FGFR GA [31]. The most common GAs were FGFR1 amplifications and FGFR2 fusions. Five patients had a partial response: three patients with ICC harboring FGFR2 fusions and two patients with primary brain cancer harboring other FGFR GAs; 41 patients had stable disease. Among patients with CCA, 75% of patients had either partial response or stable disease. The most common treatment-related adverse events were hyperphosphatemia, diarrhea, and constipation; 48% of patients experienced grade 3 adverse events [31]. Hyperphosphatemia is one of the most common adverse events associated with FGFR inhibitors and can be effectively managed with phosphate lowering drugs, reducing phosphate intake in food and dose adjustments. As a result, serum phosphate levels should be routinely checked during treatment [32].
An update on phosphate binders for the treatment of hyperphosphatemia in chronic kidney disease patients on dialysis: a review of safety profiles
Published in Expert Opinion on Drug Safety, 2022
Hiroaki Ogata, Akiko Takeshima, Hidetoshi Ito
Hyperphosphatemia is an inevitable complication among patients with advanced chronic kidney disease (CKD) because impaired kidneys cannot excrete urinary phosphate commensurate to the dietary load [1,2]. Hyperphosphatemia is associated with various complications; therefore, nephrologists manage serum phosphate concentrations using restriction of dietary phosphorus intake, phosphate removal by dialysis, and drug therapy to ensure they stay within the optimal range. There is little evidence based on large-scale prospective cohorts or randomized control trials to know whether dietary intervention can improve clinical outcomes in CKD patients [3]. Strict restriction of dietary phosphate intake should not always be applied to all hyperphosphatemic patients [4]. Most foods inevitably contain phosphate; particularly, high-protein foods are rich in phosphate. Interestingly, the bioavailability of phosphate varies widely depending on foods [5]. In general, phosphate derived from meat, fish, and dairy products is likely to be absorbed in the gastrointestinal tract as compared with that from plants. Inorganic phosphate derived from food additives is thought to be absorbed almost completely. Therefore, in contrast to simply restricting the intake of phosphate or protein, the type of food might be more important in CKD patients with hyperphosphatemia.
Toxicity of phosphate enemas – an updated review
Published in Clinical Toxicology, 2022
Rosa Hamilton Smith, Michael Eddleston, D. Nicholas Bateman
A potential weakness of all the reports we identified is the lack of data on serum magnesium, which is likely to be depressed by excess phosphate. There was no systematic attempt to assess treatment for the metabolic changes observed and all patients were treated based on their clinical and biochemical features. The blood results we report were those observed and reported but may not precisely coincide with features of acute toxicity. From a treatment perspective, haemodialysis tended to be reserved for severe cases but was not always successful in preventing death, 2 of the 4 patients haemodialyzed died [19,20]. Thus, apart from standard care with fluid and intravenous calcium as indicated on blood results or clinical and ECG features, and haemodialysis in those with associated severe renal impairment, no firm treatment recommendations can be clearly derived.