Marked increase in bone mineral density with oral phosphate and calcitriol in tumour-induced osteomalacia.

Patients with osteomalacia have a low bone mineral density (BMD) and are often misdiagnosed as osteoporosis. A marked increase in BMD is noticed following successful treatment of osteomalacia. The biochemical hallmark of tumour-induced osteomalacia (TIO) is hypophosphatemia. Patients with TIO often have severe hypophosphatemic osteomalacia and dual-energy X-ray absorptiometry may demonstrate low BMD. Surgical removal of the phosphatonin-secreting lesion restores serum phosphate, corrects osteomalacia and is associated with a dramatic increase in BMD. We report two patients with TIO and low BMD, who were treated with oral phosphate and calcitriol supplementation. The percentage increase in BMD at 33 months was as high as 94.3% in areas with the lowest BMD at baseline. The BMD at 33 months was higher than the +2SD of the population-specific reference ranges, a finding not reported in surgically treated patients with TIO. An intermittent rise in parathyroid hormone following oral phosphate supplementation might have resulted in such findings.

X-Linked Familial Hypophosphatemia: A Case Report of 27-Year Old Male and Review of Literature.

X-linked hypophosphatemia (XLH) associated with short stature during childhood are mostly referred to the hospital and diagnosed as vitamin D deficiency rickets and received vitamin D before adulthood. A case is presented with clinical features of hypophosphatemia from childhood who did not seek medical care for diagnosis and treatment, nor did his mother or two brothers, who have short statures, bone pain, and fractures. The patient was assessed for sociodemographic, hematological, and biochemical parameters together with a genetic assessment. A DEXA scan and X-ray were done to determine the abnormalities and deformities of joints and bones despite clinical examination by an expert physician. All imaging, laboratory parameters, and the genetic study confirmed the diagnosis of XLH. A detailed follow-up of his condition was performed after the use of phosphate tablets and other treatments. X-linked hypophosphatemia needs a good assessment, care, and follow up through a complementary medical team including several specialties. Phosphate tablets in adulthood significantly affects clinical and physical improvement and prevention of further skeletal abnormality and burden on daily activity. The patients should be maintained with an adequate dose of phosphate for better patient compliance. More awareness is needed in society and for health professionals when conducting medical checkups during the presence of stress fractures, frequent dental and gum problems, rickets, short stature, or abnormality in the skeleton or walking to think of secondary causes such as hypophosphatemia. Further investigations including a visit to a specialist is imperative to check for the primary cause of these disturbances.

Refeeding Syndrome in Pediatric Age, An Unknown Disease: A Narrative Review.

Refeeding syndrome (RS) is characterized by electrolyte imbalances that can occur in malnourished and abruptly refed patients. Typical features of RS are hypophosphatemia, hypokalemia, hypomagnesemia, and thiamine deficiency. It is a potentially life-threatening condition that can affect both adults and children, although there is scarce evidence in the pediatric literature. The sudden increase in food intake causes a shift in the body's metabolism and electrolyte balance, leading to symptoms such as weakness, seizures, and even heart failure. A proper management with progressive increase in nutrients is essential to prevent the onset of this condition and ensure the best possible outcomes. Moreover, an estimated incidence of up to 7.4% has been observed in pediatric intensive care unit patients receiving nutritional support, alone or as an adjunct. To prevent RS, it is important to carefully monitor feeding resumption, particularly in severely malnourished individuals. A proper strategy should start with small amounts of low-calorie fluids and gradually increasing the calorie content and amount of food over several days. Close monitoring of electrolyte levels is critical and prophylactic use of dietary supplements such as thiamine may be required to correct any imbalances that may occur. In this narrative review, we aim to provide a comprehensive understanding of RS in pediatric clinical practice and provide a possible management algorithm.

Hypophosphatemia related to intravenous iron therapy with ferric carboxymaltose: A case series.

OBJECTIVES: This case series would like to highlight hypophosphatemia related to ferric carboxymaltose and its adverse clinical consequences. BACKGROUND: Intravenous iron supplementation is a good alternative to oral iron replacement in iron deficiency anaemia due to its ability to correct iron deficit with minimal infusions without incurring the gastrointestinal side effects of oral iron replacement. Ferric carboxymaltose is one common formula for intravenous iron supplementation. However, an increasingly recognised adverse side-effect of intravenous ferric carboxymaltose is hypophosphatemia. There has been increasing reports and studies highlighting hypophosphatemia related to intra-venous iron therapy. Though initially thought to be transient and asymptomatic, recent studies have shown that persistent hypophosphatemia in iron therapy can result in debilitating disease including myopathy, fractures and osteomalacia. METHODS: A retrospective analysis of all patients who had ferric carboxymaltose was performed. RESULTS: We highlight 3 cases where hyposphatemia affected the clinical outcomes. CONCLUSION: With the increased use of IV iron it is important to be aware of the high potential for hypophosphatemia secondary to ferric carboxymaltose.

Impact of Intravenous Iron Substitution on Serum Phosphate Levels and Bone Turnover Markers-An Open-Label Pilot Study.

The association between intravenous iron substitution therapy and hypophosphatemia was previously reported in patients with iron deficiency anemia. However, the extent of hypophosphatemia is thought to depend on the type of iron supplementation. We hypothesized that the intravenous application of ferric carboxymaltose and iron sucrose leads to a different longitudinal adaptation in serum phosphate levels. In this open-label pilot study, a total of 20 patients with inflammatory bowel diseases or iron deficiency anemia were randomly assigned to one of two study groups (group 1: ferric carboxymaltose, n = 10; group 2: iron sucrose, n = 10). Serum values were controlled before iron substitution therapy, as well as 2, 4, and 12 weeks after the last drug administration. The primary objective of the study was the longitudinal evaluation of serum phosphate levels after iron substitution therapy with ferric carboxymaltose and iron sucrose. The secondary objective was the longitudinal investigation of calcium, 25-hydroxyvitamin D (25(OH)D), intact parathyroid hormone, procollagen type 1 amino-terminal propeptide (P1NP), beta-CrossLaps (CTX), hemoglobin (Hb), iron, ferritin, and transferrin saturation levels. Two weeks after drug administration, phosphate levels were significantly lower (p < 0.001) in group 1 and ferritin levels were significantly higher (p < 0.001) in group 1. Phosphate levels (0.8-1.45 mmol/L) were below the therapeutic threshold and ferritin levels (10-200 ng/mL for women and 30-300 ng/mL for men) were above the therapeutic threshold in group 1. P1NP (15-59 µg/L) and CTX (<0.57 ng/mL) levels were above the therapeutic threshold in group 2. Four weeks after drug administration, significant differences were still observed between both study groups for phosphate (p = 0.043) and ferritin (p = 0.0009). All serum values except for Hb were within the therapeutic thresholds. Twelve weeks after drug administration, no differences were observed in all serum values between both study groups. Hb values were within the therapeutic threshold in both study groups. Serum 25(OH)D levels did not differ between both study groups throughout the whole study period and remained within the therapeutic threshold.

Uncovering genetic causes of hypophosphatemia.

BACKGROUND: Chronic hypophosphatemia can result from a variety of acquired disorders, such as malnutrition, intestinal malabsorption, hyperparathyroidism, vitamin D deficiency, excess alcohol intake, some drugs, or organ transplantation. Genetic disorders can be a cause of persistent hypophosphatemia, although they are less recognized. We aimed to better understand the prevalence of genetic hypophosphatemia in the population. METHODS: By combining retrospective and prospective strategies, we searched the laboratory database of 815,828 phosphorus analyses and included patients 17-55 years old with low serum phosphorus. We reviewed the charts of 1287 outpatients with at least 1 phosphorus result ≤2.2 mg/dL. After ruling out clear secondary causes, 109 patients underwent further clinical and analytical studies. Among them, we confirmed hypophosphatemia in 39 patients. After excluding other evident secondary causes, such as primary hyperparathyroidism and vitamin D deficiency, we performed a molecular analysis in 42 patients by sequencing the exonic and flanking intronic regions of a panel of genes related to rickets or hypophosphatemia (CLCN5, CYP27B1, dentin matrix acidic phosphoprotein 1, ENPP1, FAM20C, FGFR1, FGF23, GNAS, PHEX, SLC34A3, and VDR). RESULTS: We identified 14 index patients with hypophosphatemia and variants in genes related to phosphate metabolism. The phenotype of most patients was mild, but two patients with X-linked hypophosphatemia (XLH) due to novel PHEX mutations had marked skeletal abnormalities. CONCLUSION: Genetic causes should be considered in children, but also in adult patients with hypophosphatemia of unknown origin. Our data are consistent with the conception that XLH is the most common cause of genetic hypophosphatemia with an overt musculoskeletal phenotype.

Incidence, evolution and risk factors of hypophosphatemia in patients with solid tumors receiving ferric carboxymaltose: a retrospective cohort study.

OBJECTIVES: Ferric carboxymaltose (FCM) is increasingly used in the management of cancer-related anemia, yet it may cause hypophosphatemia. This retrospective study describes the incidence, evolution and risk factors of hypophosphatemia in a cohort of patients with solid tumors receiving FCM. METHODS: Serum phosphorus concentration was assessed longitudinally using a random intercepts model. The probability of developing hypophosphatemia, as graded by CTCAE version 4.0, was investigated using a multi-state model. Transition hazards were modeled non-parametrically and semi-parametrically by a Cox model. Causal marginal risk differences between baseline interventions on serum phosphorus and/or FCM dose were obtained via G-computation. RESULTS: In 174 ambulatory patients with solid tumors receiving FCM at two university hospitals between October 2020 and September 2021, the risk of developing moderate-to-severe hypophosphatemia was 36.0% (95% confidence interval (CI) 28.2-43.9%) and peaked within 16 days after first FCM administration. The average duration of moderate-to-severe hypophosphatemia was 12.4 days. After adjustment for confounders, lower baseline serum phosphorus (adjusted hazard ratio (aHR) 0.88 per 0.1 mmol/L increase, 95% CI 0.79-0.98) and higher FCM dose (first dose: aHR 1.12 per 1 mg/kg increase, 95% CI 1.01-1.25; second dose: aHR 1.06 per 1 mg/kg increase, 95% CI 1.00-1.13) significantly increased the hazard of moderate-to-severe hypophosphatemia. CONCLUSION: Approximately one out of three ambulatory patients with solid tumors may develop moderate-to-severe hypophosphatemia after FCM administration. Baseline serum phosphorus and FCM dose may be modifiable risk factors that should be considered for intervention in order to mitigate the risk of hypophosphatemia.

[Tumor-induced osteomalacia caused by an orbital tumor: a case report].

A 52-year-old patient was initially diagnosed as hypophosphatemic osteomalacia in the Department of Endocrinology due to knee, foot and lumbosacral pain. The symptoms were not significantly relieved after phosphorus and vitamin D supplementation. Later, the imaging examination showed an orbital tumor in the right eye. The tumor was surgically removed, and the symptoms of systemic bone pain were relieved.

Effect of hypophosphatemia on prognosis after spontaneous intracerebral hemorrhage: a retrospective study.

OBJECTIVE: Hypophosphatemia often occurs after spontaneous intracerebral hemorrhage, but the effect of hypophosphatemia on its prognosis is under debate. METHODS: Clinical data of patients with spontaneous intracerebral hemorrhage admitted to our neurosurgery department from January 2018 to June 2020 were retrospectively analyzed. The patients were divided into the hypophosphatemia group and the nonhypophosphatemia group according to the serum phosphorus test values obtained three times within 1 week after admission. The incidence of complications during hospitalization, 28-day mortality, and 6-month mRS score were compared between the two groups. The influence of low phosphorus in patients with hypophosphatemia on the 6-month mRS score was explored. RESULTS: A total of 133 patients were included, of which 85 had hypophosphatemia. Forty-two patients (21 in the hypophosphatemia group and 21 in the nonhypophosphatemia group) were enrolled after propensity score matching. There were no statistically significant differences in the incidence of complications during hospitalization, 28-day mortality, and 6-month mRS score between the two groups (P > 0.05). In 85 patients with hypophosphatemia, the minimum serum phosphorus was associated with the 6-month mRS score (B = - 3.153, 95% CI: - 5.842 ~ - 0.463, P = 0.022). The cutoff value of serumphosphorus for predicting 6-month mRS score was 0.505 mmol/l. CONCLUSION: Whether hypophosphatemia occurred during hospitalization in patients with spontaneous intracerebral hemorrhage showed no effect on the incidence of complications, 28-day mortality, and 6-month mRS score. A significant decrease in serum phosphorus during hospitalization (≤ 0.505 mmol/l) might correlate with a poor 6-month mRS score. Maintaining serum phosphorus stability after spontaneous intracerebral hemorrhage may improve prognosis.

Rapid renutrition improves health status in severely malnourished inpatients with AN - score-based evaluation of a high caloric refeeding protocol in severely malnourished inpatients with anorexia nervosa in an intermediate care unit.

OBJECTIVE: Refeeding syndrome is a feared complication of refeeding patients with anorexia nervosa. There are now a number of controlled studies showing that refeeding with an initial high calorie count is more beneficial than cautious refeeding and is safe under continuous monitoring. However, there have yet not been studies in severe anorexia nervosa. METHOD: We present an observational study in two different samples. The first sample consists of those 1075 out of a total of 3230 patients with anorexia nervosa treated in our hospital within 4 years for whom a complete admission laboratory was available and who had an age of at least 18 years at admission. A risk score was calculated from the number of pathological laboratory values out of 12 parameters indicating either refeeding syndrome or health hazards related to malnutrition. The second sample was obtained from a special ward for patients with eating disorders medically at-risk. During the period in question, 410 patients with anorexia nervosa were treated there. 142 patients had a BMI of 13 or less and at the same time a complete data set with the mentioned 12 laboratory parameters at admission and weekly in the following 4 weeks after admission. RESULTS: The risk represented by the laboratory parameters is significantly and negatively correlated to BMI and much higher for the group of patients with a BMI below 13 than for those with a higher BMI (χ2 sig < 0.000). The 142 patients in the special care unit gain an average of more than 4.1 kg within 4 weeks on the high-calorie diet. With this rapid weight gain, the risk score decreases highly significantly. Neither hypophosphatemia nor rhabdomyolysis is found under phosphate substitution. Hyperhydration occurred often, which manifests itself in the drop in haematocrit by the second week. DISCUSSION: Under thorough medical surveillance, supplementation of phosphate and thiamine, and substitution of electrolytes whenever necessary rapid renutrition appeared to be save even in extremely malnourished inpatients with anorexia nervosa. As measured by the laboratory values, the health status of the severely malnourished patients improves significantly on a high-calorie diet. Except for hyperhydration, there was no evidence of a refeeding syndrome.

Severe hypercalcemia associated with hypophosphatemia in very premature infants: a case report.

BACKGROUND: Severe hypercalcemia is rare in newborns; even though often asymptomatic, it may have important sequelae. Hypophosphatemia can occur in infants experiencing intrauterine malnutrition, sepsis and early high-energy parenteral nutrition (PN) and can cause severe hypercalcemia through an unknown mechanism. Monitoring and supplementation of phosphate (PO4) and calcium (Ca) in the first week of life in preterm infants are still debated. CASE PRESENTATION: We report on a female baby born at 29 weeks' gestation with intrauterine growth retardation (IUGR) experiencing sustained severe hypercalcemia (up to 24 mg/dl corrected Ca) due to hypophosphatemia while on phosphorus-free PN. Hypercalcemia did not improve after hyperhydration and furosemide but responded to infusion of PO4. Eventually, the infant experienced symptomatic hypocalcaemia (ionized Ca 3.4 mg/dl), likely exacerbated by contemporary infusion of albumin. Subsequently, a normalization of both parathyroid hormone (PTH) and alkaline phosphatase (ALP) was observed. CONCLUSIONS: Although severe hypercalcemia is extremely rare in neonates, clinicians should be aware of the possible occurrence of this life-threatening condition in infants with or at risk to develop hypophosphatemia. Hypophosphatemic hypercalcemia can only be managed with infusion of PO4, with strict monitoring of Ca and PO4 concentrations.

The Role of Phosphate in Alcohol-Induced Experimental Pancreatitis.

BACKGROUND & AIMS: Heavy alcohol consumption is a common cause of acute pancreatitis; however, alcohol abuse does not always result in clinical pancreatitis. As a consequence, the factors responsible for alcohol-induced pancreatitis are not well understood. In experimental animals, it has been difficult to produce pancreatitis with alcohol. Clinically, alcohol use predisposes to hypophosphatemia, and hypophosphatemia has been observed in some patients with acute pancreatitis. Because of abundant protein synthesis, the pancreas has high metabolic demands, and reduced mitochondrial function leads to organelle dysfunction and pancreatitis. We proposed, therefore, that phosphate deficiency might limit adenosine triphosphate synthesis and thereby contribute to alcohol-induced pancreatitis. METHODS: Mice were fed a low-phosphate diet (LPD) before orogastric administration of ethanol. Direct effects of phosphate and ethanol were evaluated in vitro in isolated mouse pancreatic acini. RESULTS: LPD reduced serum phosphate levels. Intragastric administration of ethanol to animals maintained on an LPD caused severe pancreatitis that was ameliorated by phosphate repletion. In pancreatic acinar cells, low-phosphate conditions increased susceptibility to ethanol-induced cellular dysfunction through decreased bioenergetic stores, specifically affecting total cellular adenosine triphosphate and mitochondrial function. Phosphate supplementation prevented ethanol-associated cellular injury. CONCLUSIONS: Phosphate status plays a critical role in predisposition to and protection from alcohol-induced acinar cell dysfunction and the development of acute alcohol-induced pancreatitis. This finding may explain why pancreatitis develops in only some individuals with heavy alcohol use and suggests a potential novel therapeutic approach to pancreatitis. Finally, an LPD plus ethanol provides a new model for studying alcohol-associated pancreatic injury.

Consensus Recommendations for the Diagnosis and Management of X-Linked Hypophosphatemia in Belgium.

X-linked hypophosphatemia (XLH) is the most common genetic form of hypophosphatemic rickets and osteomalacia. In this disease, mutations in the PHEX gene lead to elevated levels of the hormone fibroblast growth factor 23 (FGF23), resulting in renal phosphate wasting and impaired skeletal and dental mineralization. Recently, international guidelines for the diagnosis and treatment of this condition have been published. However, more specific recommendations are needed to provide guidance at the national level, considering resource availability and health economic aspects. A national multidisciplinary group of Belgian experts convened to discuss translation of international best available evidence into locally feasible consensus recommendations. Patients with XLH may present to a wide array of primary, secondary and tertiary care physicians, among whom awareness of the disease should be raised. XLH has a very broad differential-diagnosis for which clinical features, biochemical and genetic testing in centers of expertise are recommended. Optimal care requires a multidisciplinary approach, guided by an expert in metabolic bone diseases and involving (according to the individual patient's needs) pediatric and adult medical specialties and paramedical caregivers, including but not limited to general practitioners, dentists, radiologists and orthopedic surgeons. In children with severe or refractory symptoms, FGF23 inhibition using burosumab may provide superior outcomes compared to conventional medical therapy with phosphate supplements and active vitamin D analogues. Burosumab has also demonstrated promising results in adults on certain clinical outcomes such as pseudofractures. In summary, this work outlines recommendations for clinicians and policymakers, with a vision for improving the diagnostic and therapeutic landscape for XLH patients in Belgium.

Refeeding syndrome in a woman with pancreatitis: a case report.

Refeeding syndrome can occur in malnourished patients with acute pancreatitis who have electrolyte imbalances. Refeeding syndrome is characterized by severe electrolyte imbalances (mainly hypophosphatemia, hypomagnesemia, and hypokalemia), vitamin deficiency (mainly thiamine deficiency), fluid overload, and salt retention resulting in organ dysfunction and cardiac arrhythmias. We herein report a case involving a patient with severe pancreatitis and gallbladder stones who developed refeeding syndrome with shock and loss of consciousness. The patient was treated by opportune vitamin and electrolyte supplementation therapy and showed substantial improvement after 2 weeks of hospitalization, gaining the ability to eat small bites of solid food orally. Early diagnosis and treatment of refeeding syndrome may reduce morbidity and mortality in patients with acute pancreatitis. Patients should be fasted only if alimentation is contraindicated, and electrolyte values must be closely monitored.

Mortality associated with new risk classification of developing refeeding syndrome in critically ill patients: A cohort study.

BACKGROUND & AIMS: Although refeeding syndrome (RFS) has been recognized as a potentially fatal metabolic complication, the definition of RFS has remained unclear. Recently, European researchers suggested an evidence-based and consensus-supported algorithm that consisted of a new RFS risk classification and treatment strategies for medical inpatients. The classification was based on the National Institute for Health and Clinical Excellence (NICE) criteria for patients at risk of developing RFS. In this study, we aimed to investigate the frequency of each applied new risk group and the association between the new classification and mortality in critically ill patients. METHODS: This cohort study was conducted at a Japanese metropolitan tertiary-care university hospital from December 2016 to December 2018. We included critically ill adult patients who were admitted to the intensive care unit (ICU) via the emergency department and who stayed in the ICU for 24 h or longer. We applied the new risk classification based on the NICE RFS risk factors on ICU admission. The main exposure was risk classification of RFS: no risk, low risk, high risk, or very high risk. The primary outcome was in-hospital mortality censored at day 30 after ICU admission. We performed a multivariable analysis using Cox proportional hazard regression. RESULTS: We analyzed 542 patients who met the eligibility criteria. The prevalence of the four RFS risk classification groups was 25.8% for no risk, 25.7% for low risk, 46.5% for high risk, and 2.0% for very high risk. The 30-day mortality was 5.0%, 7.2%, 16.3%, and 27.3%, respectively (log-rank trend test: p < 0.001). In the multivariable Cox regression, adjusted hazard ratios with no risk group as a reference were 1.28 (95% CI 0.48-3.38) for low risk, 2.81 (95% CI 1.24-6.35) for high risk, and 3.17 (95% CI 0.78-12.91) for very high risk. CONCLUSIONS: Approximately half the critically ill patients were categorized as high or very high risk based on the new risk classification. Furthermore, as the risk categories progressed, the 30-day in-hospital mortality increased. Early recognition of patients at risk of developing RFS may improve patient outcomes through timely and optimal nutritional treatment.

Hypophosphatemic Hypovitaminosis D Induces Osteomalacia in the Adult Female Rat.

Osteomalacia is a bone-demineralizing disease of adulthood, often caused by hypovitaminosis D. Current animal models of the disease mimic osteomalacia as a consequence of gastric bypass or toxic exposure to metals, but a relevant model of diet-induced osteomalacia is lacking. For that purpose, 7-month-old female Sprague Dawley rats were randomly assigned into 2 weight-stratified groups and maintained for 4 months on synthetic diets containing negligible or normal levels of vitamin D. The dietary regimen resulted in vitamin D deficiency as measured by 25-hydroxyvitamin D serum levels; however, hypovitaminosis D per se did not affect biomarkers of calcium metabolism and bone turnover, nor did it result in increased osteoid. Thus, vitamin D depletion through the diet was found to be insufficient to induce an osteomalacia-like phenotype in the adult rat. After 4 months, the phosphate content of the vitamin D-depleted diet had decreased to 0.16% (calcium:phosphorus ratio of 5.85), resulting in an osteomalacic-like condition (trabecular osteoid surface/bone surface constituted 33%; CI, 26-40). The diet change also affected both metabolic and bone turnover biomarkers, including significantly suppressing serum fibroblast growth factor 23. Furthermore, decreased dietary phosphate in a vitamin D-depleted diet led to microarchitectural changes of trabecular and cortical bone, lower bone mass density, lower bone mass content and decreased bone strength, all indicating reduced bone quality. Taken together, our results show that osteomalacia can be induced in the adult female rat by depleting vitamin D and lowering phosphate content in the diet.

The Association of Hypophosphatemia With Resistant Lactic Acidosis in Critical Care Illness.

Critically ill patients are known to have a variety of electrolyte abnormalities. Lactic acidosis can frequently be seen secondary to shock states and is usually treated with aggressive volume resuscitation. Interestingly, hypophosphatemia is a potential cause of resistant lactic acidosis, which may not be as commonly identified or considered. We present a case of a 42-year-old man admitted twice over a span of 6 months with an elevated lactate level that did not resolve with volume resuscitation. It was ultimately determined that his lactic acidosis was due to hypophosphatemia after ruling out other potential causes. Phosphate replacement therapy resulted in the normalization of his lactate. In the literature, multiple theories have indicated the association of hypophosphatemia with lactic acidosis though no prior cases exist supporting a direct relationship. In this case, we set forth to evaluate the complicated relationship between all of these factors and to highlight the importance of early detection and treatment of hypophosphatemia, which may be beneficial in treating lactic acidosis.

Report of Dialysis-Induced Hypophosphatemia Leading to Reversible Encephalopathy Prevented by Adding Phosphorus to the Dialysate.

Patients with advanced chronic kidney disease have an inability to excrete phosphorus normally leading to high serum concentrations of phosphorus. The hyperphosphatemia is even more pronounced in dialysis patients who often require large doses of phosphorus binders to combat the problem. Hemodialysis is able to remove fair amount of the extra phosphorus; however, the removal is often hampered by the fact that the phosphorus is removed only from the extracellular compartment and phosphorus is mainly intracellular. The end result being a high serum phosphorus concentration at the beginning of dialysis, a sharp decline in the value by the end of dialysis and significant rebound of serum phosphorus concentration a few hours after stopping dialysis as phosphorus moves out of the cells. Here, we describe 2 hemodialysis patients with normal predialysis serum phosphorus concentration and preexisting conditions that made them at risk for developing encephalopathy who developed recurrent obtundation toward the end of the dialysis treatments. After confirming critical postdialysis hypophosphatemia, phosphorus was added to the dialysate baths and the episodes of encephalopathy associated with dialysis ceased.

Ventricular bigeminy and trigeminy caused by hypophosphataemia during diabetic ketoacidosis treatment: a case report.

BACKGROUND: Hypophosphatemia has many causes, and is often encountered during DKA (Diabetic Ketoacidosis) treatment. However, it rarely requires clinical intervention. CASE PRESENTATION: Ventricular arrhythmia was observed in a 10-year-old girl with newly diagnosed type 1 diabetes mellitus and hypophosphatemia while undergoing treatment for ketoacidosis. Oral phosphate supplementation ceased ventricular arrhythmia almost completely. CONCLUSIONS: The clinical signs of hypophosphatemia are potentially life-threatening. Therefore, physicians should be vigilant when treating patients who are at risk of hypophosphatemia. Severe hypophosphatemia accompanied by clinical symptoms requires oral or intravenous supplementation of phosphate.

Reliability of calcium-phosphorus (Ca/P) ratio as a new, accurate and inexpensive tool in the diagnosis of some Ca-P disorders.

PURPOSE: The serum calcium/phosphorus (Ca/P) ratio is an accurate tool to differentiate patients with primary hyperparathyroidism (PHPT) from healthy subjects. However, other disorders of the Ca-P metabolism might impair the Ca/P ratio, such as hypophosphatemia (HypoP) not PHPT related. The aim of this study is to examine the diagnostic value of Ca/P ratio in the diagnosis of PHPT and HypoP not PHPT related. METHODS: Single-center, retrospective, case-control study, including 150 patients with PHPT and 306 patients with HypoP, compared with 150 controls. HypoP patients were enrolled among HIV-infected patients by selecting those with Fanconi-like syndrome due to antiretroviral treatment. Parameters which were measured were serum Ca, P, parathyroid hormone (PTH), 25-OH vitamin D, albumin and creatinine). RESULTS: The Ca/P ratio was significantly higher in PHPT and HypoP patients, compared to controls (p < 0.0001). At receiver operator characteristic (ROC) curve analysis, the cut-off of 3.56 (2.75 SI) for Ca/P ratio was able to identify patients with PHPT and HypoP (sensitivity 95%; specificity 93%). Among patients with Ca/P ratio above 3.56, the thresholds of 10.3 mg/dL (2.6 mmol/L) for serum Ca (sensitivity 93%; specificity 98%) and 80.5 pg/mL for PTH (sensitivity 91%; specificity 91%) were defined for the specific diagnosis of PHPT. CONCLUSIONS: The Ca/P ratio above 3.56 (2.75 SI) is a highly accurate tool to identify PHPT and HypoP not PHPT-related patients. Thanks to its simplicity, this index can be proposed as a screening and first-line examination in the diagnostic work-up when a disorder of Ca-P metabolism is suspected or should be ruled out.