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Hypophosphatemia as a prognostic value in acute exacerbation of COPD.

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BACKGROUND Phosphorus (P) is an essential element in all living cells, it is extremely important in the process of production of adenosine triphosphate, main element in the structure of nucleic acids. Low levels of phosphorus in blood is very rare, however, it may be caused by unbalance between

Hypophosphatemia in A Specialized Intestinal Failure Unit: An Observational Cohort Study

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Background: Patients with intestinal failure (IF) are prone to hypophosphatemia and shifts in magnesium and potassium levels. While these shifts are often attributed to refeeding syndrome (RFS), the incidence of electrolyte shifts among

Hypophosphatemia on the intensive care unit: individualized phosphate replacement based on serum levels and distribution volume.

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BACKGROUND Hypophosphatemia occurs in about 25% of patients admitted to the intensive care unit. To date, a safe and validated phosphate replacement protocol is not available. OBJECTIVE To evaluate an individualized phosphate replacement regimen. METHODS Fifty consecutive intensive care unit

Ventricular tachycardia in acute myocardial infarction: the role of hypophosphatemia.

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The relationship between serum concentration of certain electrolytes and the pathogenesis of ventricular arrhythmia in myocardial infarction has been the subject of frequent review. The role of hypophosphatemia in the pathogenesis of arrhythmia in patients with acute myocardial infarction has not

Extremely preterm infants who are small for gestational age have a high risk of early hypophosphatemia and hypokalemia.

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OBJECTIVE Electrolyte balances have not been sufficiently evaluated in extremely preterm infants after early parenteral nutrition. We investigated the risk of early hypophosphatemia and hypokalemia in extremely preterm infants born small for gestational age (SGA) who received nutrition as currently

Predictors of Hypophosphatemia and Outcomes during Continuous Renal Replacement Therapy.

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Hypophosphatemia occurs in up to 80% of patients undergoing continuous renal replacement therapy (CRRT) and has been associated with poor outcomes. Whether preemptive phosphate supplementation is warranted in select patients has not been adequately explored. This single-center,

A potential role of hypophosphatemia for diagnosing convulsive seizures: A case-control study.

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Transient loss of consciousness (TLOC) is a common presentation in the emergency room, where patient history can usually differentiate syncope from generalized tonic-clonic (GTC) seizures. Several serum markers, such as creatine kinase and lactate, can be helpful, especially when

High-dose intravenous phosphorus therapy for severe complicated hypophosphatemia.

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To evaluate the efficacy and safety of a simple approach to intravenous phosphorus therapy, we prospectively studied ten adult patients with severe hypophosphatemia (less than or equal to 1 mg/dl), two or more clinical reasons for the hypophosphatemia, and normal renal function. They were treated

The defect in transcellular transport of phosphate in the nephron is located in brush-border membranes in X-linked hypophosphatemia (Hyp mouse model).

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We purified renal cortex brush-border membranes from mutant hemizygous hypophosphatemic (Hyp/Y) mice and male control (+/Y) littermates. Tenfold purification of mutant and wild-type membranes was obtained. Phosphate enters +/Y brush-border membrane vesicles by a saturable Na+-dependent

Clenbuterol ingestion causing prolonged tachycardia, hypokalemia, and hypophosphatemia with confirmation by quantitative levels.

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BACKGROUND Clenbuterol is a long acting beta2-adrenergic agonist used in the treatment of pulmonary disorders. Acute clenbuterol toxicity resembles that of other beta2-adrenergic agonists. Most previously reported cases of clenbuterol toxicity describe patients who ate livestock illicitly treated

[Hypophosphatemia and refeeding syndrome: a severe and underdiagnosed adverse effect].

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A 68-year-old woman was hospitalised because of generalised weakness and development of confusional state, related to severe hyponatremia, probably due to an eating disorder with malnutrition. During the first days of hospitalisation the patient eats surprising large amounts of food. The worsening

Severe hypokalemia and hypophosphatemia presenting with carpopedal spasm associated with rhabdomyolysis.

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Background Severe hypokalemia, defined as serum potassium < 2.5 mEq/L, may lead to neuromuscular, gastrointestinal, and ECG abnormalities. Neuromuscular consequences of hypokalemia include weakness, cramps, rarely paralysis, eventually progressing to rhabdomyolysis. Case presentation We report a

Vanadate-Induced Renal cAMP and Malondialdehyde Accumulation Suppresses Alpha 1 Sodium Potassium Adenosine Triphosphatase Protein Levels.

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It has been demonstrated that vanadate causes nephrotoxicity. Vanadate inhibits renal sodium potassium adenosine triphosphatase (Na, K-ATPase) activity and this is more pronounced in injured renal tissues. Cardiac cyclic adenosine monophosphate (cAMP) is enhanced by vanadate, while increased cAMP

Hypophosphatemia.

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Hypophosphatemia, defined as serum phosphate levels less than 2.5 mg%, is a relatively common disorder that can affect virtually every organ system. Phosphate deficiency can result from decreases in phosphate intake or absorption, increased loss from renal and nonrenal pathways, and transcellular

Severity of postoperative hypophosphatemia in relation to glucose administration and renal handling of phosphate.

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Major surgery is associated with fall in the concentration of inorganic phosphate in serum, as is intravenous infusion of glucose. Hypophosphatemia during different forms of postoperative dextrose administration was evaluated in patients who had undergone colorectal surgery. They were randomized to

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