Gene/Protein Disease Symptom Drug Enzyme Compound
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 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors experimented Aloglutamol (an organic salt of aluminium) in uremic patients on dialysis to detect its phosphate-binding properties and study its use in the treatment of uremic osteodystropy. They report good results: predialysis Ca increased; serum PO4 and alcaline phosphatase levels decreased; Ca X PO4 was normalized; itch, muscular weakness and constipation decreased; no side-effects appeared, and the drug has a good taste. Therefore it is considered to be most useful in the treatment of hyperphosphatemia in uremia.
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PMID:[Use of Aloglutamol in uremic patients on dialysis (author's transl]. 70 77

A 17 year old man with longstanding hypocalcemia and hyperphosphatemia presented with incapacitating bone pain and progressive weakness nad bowing of the legs. The serum abnormalities were due to idiopathic hypoparathyroidism as evidenced by a decreased serum concentration of parathyroid hormone and an appropriate rise in urinary cyclic AMP and phosphate excretion, and serum calcium concentration, in response to exogenously administered parathyroid extract. The serum concentration of 1,25-dihydroxycholecalciferol was appropriately decreased. The bone findings were due to osteomalacia as documented by physical findings, bone roentgenograms, and bone biopsy. Normal renal tubular function, blood pH, and serum concentration of 25-hydroxycholecalciferol and elevated serum alkaline phosphatase excluded the common causes of osteomalacia. The data are consistent with the hypothsis that lack of parathyroid hormone causes both hypocalcemia and a decreased serum concentration of 1,25-dihydroxycholecalciferol which, in turn, limit the availability of calcium and cause defective synthesis of bone matrix resulting in abnormal mineralization.
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PMID:Hypoparathyroidism: a possible cause of osteomalacia . 87 58

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

Idiopathic hypoparathyroidism was diagnosed in five young to middle-aged cats of mixed breeding. Three of the cats were male and two were female. Historic signs included lethargy (n = 5), anorexia (n = 5), muscle tremors (n = 4), weakness (n = 4), generalized seizures (n = 3), ataxia (n = 3), mental dullness or disorientation (n = 3), panting (n = 2), pruritus (n = 1), ptyalism (n = 1) and dysphagia (n = 1). Weakness (n = 4), dehydration (n = 2), cataracts (n = 2), hypothermia (n = 1), and bradycardia (n = 1) were found on physical examination. Results of electrocardiography revealed a prolonged Q-T interval in two cats. Results of initial laboratory tests revealed profound hypocalcemia and severe hyperphosphatemia with normal renal function. The diagnosis of hypoparathyroidism was made on the basis of the history, clinical signs, and results serum biochemical testing (i.e., severe hypocalcemia and hyperphosphatemia); in two cats, the diagnosis was also confirmed by histologic examination of parathyroid glands. Initial treatment included intravenous administration of 10% calcium gluconate and oral administration of large loading doses of calcium and vitamin D (dihydrotachysterol). Successful long-term management with dihydrotachysterol and calcium was achieved in all cats. The final dosage of dihydrotachysterol required to maintain normocalcemia in the five cats ranged from 0.004 to 0.04 mg/kg/day (mean = 0.015 mg/kg/day). Long-term calcium supplementation was given to three of the cats in dosages ranging from 29 to 53 mg/kg/day (mean = 42 mg/kg/day) of elemental calcium. One cat died after 28 months of therapy from widely metastatic hemangiosarcoma; the other three cats are still alive and well after 5 to 37 months of treatment.
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PMID:Idiopathic hypoparathyroidism in five cats. 202 14

An 8 1/2-year-old girl presented with a long history of seizures, growth retardation, muscle weakness, gait disturbance, and hearing loss. Her evaluation revealed chronic moderate renal failure (serum creatinine 2.2 mg/dL), severe hypocalcemia (5 mg/dL), hyperphosphatemia (8.1 mg/dL), hypomagnesemia (1.5 mg/dL), increased urinary magnesium excretion (2 mg/kg/d), high fractional excretion of magnesium (21.7%), hypokalemia (3.2 mEq/L), and hyperkaliuria (26 mEq/L). Low circulating immunoreactive parathyroid hormone levels for the degree of the hypocalcemia (serum N-parathyroid hormone 212 pg/mL) and severe rickets without evidence of osteitis fibrosa cystica were found. The patient probably has primary renal leak hypomagnesemia (magnesuric hypomagnesemia) which caused impaired secretion of immunoreactive parathyroid hormone leading to severe hypocalcemia and calcium deficiency rickets. Treatment with magnesium and calcium supplements, calcitriol, and aluminum hydroxide resulted in marked clinical, biochemical, and radiologic improvement. Calcium deficiency rickets due to primary or secondary renal magnesium wasting in conjunction with moderate renal failure represents a largely unrecognized metabolic bone disease.
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PMID:Severe renal osteodystrophy without elevated serum immunoreactive parathyroid hormone concentrations in hypomagnesemia due to renal magnesium wasting. 382 40

Severe electrolyte disturbances developed after the administration of hypertonic phosphate enemas in 2 chronically obstipated cats. Hyperphosphatemia, hypernatremia, and hypocalcemia were detected in both cats. Physical findings included weakness, anxiety, tachycardia, hypothermia, and dehydration. Intravenous fluid and electrolyte therapy led to prompt, dramatic improvement in both cats. Although well tolerated by most healthy animals, hypertonic phosphate enemas should be avoided in small animals, especially those that are dehydrated, severely obstipated, or suffering from renal or colonic disease.
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PMID:Electrolyte abnormalities induced by hypertonic phosphate enemas in two cats. 408 55

A 53-year-old man with retinitis pigmentosa, who had two years' complaints of general malaise and muscle weakness, noticed occasional attacks of the cramps of the lower legs about three months prior to admission. At that time, hypocalcemia (7.6 mg/dl) and hyperphosphatemia (5.2 mg/dl) were pointed out. On admission, serum potassium was high-normal or high (4.4 - 4.9 mEq/l). Endocrinological studies revealed the findings of pseudohypoparathyroidism (PHP) type II, including a normal urinary cyclic AMP but blunted phosphaturic response to synthetic human parathyroid hormone (PTH), a high level of serum amino-terminal fragment of PTH with a low level of serum calcium and its ionized form, and a high-normal level of nephrogenous cyclic AMP. This patient also had selective hypoaldosteronism, as shown by intermittent hyperkalemia, low plasma and urinary levels of aldosterone and normal glucocorticoid levels. Plasma renin activity was normal but responded to a greater extent to furosemide plus upright posture. Plasma aldosterone was low and responded poorly to furosemide plus upright posture and graded angiotensin II infusions. The possible explanations for the association of PHP type II and selective hypoaldosteronism in this patient with retinitis pigmentosa are discussed.
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PMID:Pseudohypoparathyroidism (PHP) type II and selective hypoaldosteronism in a patient with retinitis pigmentosa. 632 73

Acute accidental vitamin D2 (ergocalciferol) toxicosis was diagnosed in a 6-month-old foal with extensive lesions of soft tissue mineralization. In an experimental study, three 18-month-old horses were given ergocalciferol per os at a rate of 9,300, 22,200, or 47,200 IU/kg of body weight/day for 21 days. Clinical signs or lesions were not seen in horses given the low and intermediate doses, whereas the horse receiving the highest dose developed clinical signs and lesions similar to those noted in the foal. Signs included depression, loss of appetite, weakness, limb stiffness with impaired mobility, and cessation of growth or weight loss. Gross and histologic lesions of mineralization of various soft tissues, especially of the endocardium and wall of large blood vessels, were seen in the foal and the horse given the high dose. Marked, persistent, hyperphosphatemia (7.0 to 13.0 mg of P/dl of serum) developed in each horse. The horse given the intermediate dose remained normocalcemic. Horses given the low and high doses became hypercalcemic (13.6 to 14.5 mg of Ca/dl of serum), but serum calcium concentrations varied from day to day and both horses were normocalcemic at necropsy (12.4 to 12.7 mg of Ca/dl of serum). Distal metacarpal bone ash concentrations of calcium, phosphorus, and magnesium of the foal were mg/g of bone ash) 400.5, 180.5, and 5.30, respectively. In the horses, treatment with ergocalciferol also had no significant effect on serum magnesium (1.88 to 2.18 mg/dl of serum) or distal metacarpal bone ash concentrations of calcium (352.5 to 362.5 mg/g of bone ash), phosphorus (182.5 to 184.0 mg/g of bone ash), or magnesium (5.48 to 6.02 mg/g of bone ash).
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PMID:Acute vitamin D2 (ergocalciferol) toxicosis in horses: case report and experimental studies. 697 34

Between January 1996 and June 1998, 24 children with symptomatic hypomagnesemia were enrolled for analysis of their symptomatology, causes, and treatment outcome. Hypocalcemia and hyperphosphatemia suggesting impaired parathyroid function were the most common electrolyte disorders. Hypokalemia was also frequently noted. The related symptoms including seizure, tetany, and weakness were common. Drug-induced renal magnesium wasting was the most common cause of symptomatic hypomagnesemia, and tended to occur in older children using aminoglycoside, furosemide, and amphotericin-B. The associated gastrointestinal causes might add a minor contribution to the development of hypomagnesemia. Analyses of PTH levels in 13 children suggested that inhibition of PTH synthesis or secretion was responsible for hypomagnesemic hypocalcemia in most patients. However, peripheral PTH resistance might also account for the mechanism in a few patients. In most patients, symptomatic hypomagnesemia was transient, and improved after magnesium provision. Only one child with congenital renal magnesium wasting and two with primary hypomagnesemia needed long-term magnesium treatment.
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PMID:Symptomatic hypomagnesemia in children. 992 14

Abnormalities in serum phosphate levels are more prevalent in certain subsets of Emergency Department patients than in the general population. Patients with diabetic ketoacidosis, chronic obstructive pulmonary disease, alcoholism, malignancy, and renal failure are at increased risk. Multiple factors, including nutritional intake, medications, renal or intestinal excretion, and cellular redistribution, are potential etiologies. The clinical manifestations of mild hypophosphatemia or hyperphosphatemia are typically minor and nonspecific (myalgias, weakness, anorexia). When the imbalance is severe, critical complications may occur (tetany, seizures, coma, rhabdomyolysis, respiratory failure, ventricular tachycardia). Mild asymptomatic hypophosphatemia can be treated with oral phosphate supplementation (15 mg/kg daily) on an outpatient basis. Patients with severe or symptomatic hypophosphatemia should be treated with IV phosphate therapy (0.08-0.16 mg/kg over 6 h) and admitted for monitoring and subsequent serum electrolyte testing. Mild asymptomatic hyperphosphatemia is commonly managed in renal failure by limiting dietary intake and reducing absorption with phosphate-binding salts. Hemodialysis may be required for severe hyperphosphatemia with symptomatic hypocalcemia.
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PMID:Serum phosphate abnormalities in the emergency department. 1248 22


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