Defective Intestinal Phosphate Absorption in Familial and Non-familial Hypophosphataemia

Condon, J. R.; Nassim, J. R.; Rutter, A.C.

doi:10.1136/bmj.3.5715.138

Cited by 39 publications

(20 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The patients with vitamin D deficient osteomalacia had normal phosphate tolerance tests (normal maximum rise in plasma phosphate 1 * 59 ± 0 * 46 mg/100 ml). Details of the phosphate tolerance tests on the patients with familial hypophosphataemia have already been reported (Condon et al, 1970) det, 1952;Rupp, 1955). Defec-can be induced in subjects with familial hypophosrption of phosphate has also been phataemia by administration of large doses of of an nral nhn-rnhqte torlerance vitamin D.…”

Section: Resultsmentioning

confidence: 99%

“…The first is that it is due to a primary defect in renal tubular reabsorption (Dent, 1952;Fanconi and Girardet, 1952) and intestinal absorption of phosphate (Condon, Nassim, and Rutter, 1970 (Condon et al, 1970), was normal in vitamin D deficient osteomalacia (Condon et al, 1970 (Dent, 1962).…”

mentioning

confidence: 99%

“…The procedure for the phosphate tolerance test has previously been described in detail (Condon et al, 1970): 6 -9 g sodium phosphate (=-1 5 g P) was dissolved in 200 ml water and ingested by the patient who had fasted overnight. Venous blood samples collected in heparin were withdrawn 2 minutes before and 30, 60, 90, 150, and 210 minutes after ingestion of phosphate solution.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Pathogenesis of Rickets and Osteomalacia in Familial Hypophosphataemia

Condon¹,

Nassim²,

Rutter³

1971

Archives of Disease in Childhood

Self Cite

View full text Add to dashboard Cite

. The pathogenesis of rickets and osteomalacia in familial hypophosphataemia. Calcium and/or phosphate tolerance tests were performed on patients with familial hypophosphataemia, normal control subjects, and patients with vitamin D deficient osteomalacia.Intestinal calcium absorption was similar in patients with familial hypophosphataemia and control subjects. The phosphate tolerance test, which is known to be 'flat' in patients with familial hypophospbataemia, was normal in patients with vitamin D deficient osteomalacia.These findings suggest that rickets and osteomalacia in familial and some cases of non-familial hypophosphataemia are unrelated to abnormal metabolism of vitamin D. This hypothesis is supported by the fact that intestinal calcium absorption as measured by calcium tolerance test is normal in familial hypophosphataemia.It is suggested that the primary abnormality in familial hypophosphataemia is a partial metabolic block in the intestinal absorption and renal tubular reabsorption of phosphate. There are two main theories to account for the low plasma phosphate found in familial and nonfamilial hypophosphataemia. The first is that it is due to a primary defect in renal tubular reabsorption (Dent, 1952;Fanconi and Girardet, 1952) In order to verify or disprove this hypothesis, intestinal calcium absorption was assessed in patients with familial hypophosphataemia and normal control subjects by means of a calcium tolerance test. The calcium tolerance curves were similar in normal subjects and in patients with familial hypophosphataemia, suggesting that intestinal calcium absorption was normal in this disorder.

show abstract

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Pathogenesis of Rickets and Osteomalacia in Familial Hypophosphataemia

Condon¹,

Nassim²,

Rutter³

1971

Archives of Disease in Childhood

Self Cite

View full text Add to dashboard Cite

show abstract

“…Prior to the calcium and phosphorus balance studies, 500 mg oxytetracyclme per day was given to the test dog on two successive days. An oral phosphate tolerance test was done [5]. Since serum calcium and phosphorus values may be elevated in young growing animals, values for Great Danes were taken from the literature [lo].…”

Section: Methodsmentioning

confidence: 99%

Calcium Phosphate Deposition Disease in Great Danes

et al. 1982

View full text Add to dashboard Cite

Abstract.A new clinicopathologic syndrome, possibly familial, in Great Dane dogs, resembles the familial childhood variant of calcium pyrophosphate dihydrate deposit disease in man, except that the mineral deposits were composed of amorphous calcium phosphate or hydroxyapatite rather than pyrophosphate. The syndrome was characterized clinically by paraplegia and incoordination in very young puppies which was caused by concentric constriction of the posterior cervical spinal cord. Canal stenosis resulted from dorsal displacement of the seventh cervical vertebra and deformation of the vertebral articular processes. Mineral deposition in the diarthrodial joints of the axial skeleton could be seen on radiographs of weanling puppies, and the appendicular skeleton became involved as the dogs matured. Periarticular mineralization of the limbs was associated with shorter bones, a thin cortex, abnormal bone curvature, and increased medullary trabeculae. Bone alterations were associated with abnormalities of the growth plate, which had focal areas of cartilage calcification. Soft tissue mineralization, seen in all dogs, was a primary feature of the disease process. Serum calcium concentrations were within the normal range, but serum phosphorus concentrations were decreased.Crystal deposition disease is a current term for various types of crystal-induced synovitis. Gout was the first condition identified in which acute synovitis was associated with urate crystals in the synovial fluid. In calcium pyrophosphate dihydrate crystal deposition disease, the second form of the disease to be described, acute joint inflammation was associated with crystals of calcium pyrophosphate dihydrate rather than urates.

show abstract

“…The pictures revealed the tip of the tube was in the fundus and the injected contrast was found only in the stomach. The concentration of Pi used in the present study was based on previous studies conducted in rats (8,15,19) and humans (20). Studies have used concentrations that ranged from 0, i.e., tracer only (8,15) to 240 mM (20).…”

Section: Introductionmentioning

confidence: 99%