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At least 973 records · Page 54Linked to original sources
PubMed1976

Sodium chloride restriction and extracellular fluid volume contraction in hyperphosphatiuric vitamin D resistant rickets in the Lowe syndrome.

A patient with a Lowe syndrome was observed from birth. Progressive hyperchloraemic renal tubular acidosis, hypophosphataemia, hyperphosphaturia and generalized hyperaminoaciduria had developed in infancy. Supplementary vitamin D, alkali and a high intake of dietary phosphate were unsuccessful in controlling the severe phosphate diabetes and rickets. Contraction of the extracellular fluid volume by dietary sodium restriction resulted in correction of the acidosis, hypophosphataemia, hyperaminoaciduria, and hyperphosphaturia, and healing of the rickets.

Acidosis, Renal Tubular↗
PubMed1976

[Mineral metabolism of the growing bone and its disturbances--methods of radiological examinations (author's transl)].

New possible interactions of vitamin D and its derivates are discussed with reference to metabolism of calcium and phosphorous and its effects on the skeletal system. The degree of osteoporosis and osteomalacia determined only by means of roentgenology depends on subjective factors. A survey is presented about objective determination which includes skeletal mineral content by radiology and nuclear medicine examination. Following a survey of our own investigative methods and results the follow-ups in various forms of vitamin D refractory rickets are reported.

Bone Development↗
PubMed1991

Impetigo herpetiformis associated with hypocalcemia of congenital rickets.

A 30-year-old woman with congenital rickets and autosomal recessive ichthyosis developed impetigo herpetiformis in the second trimester of her first pregnancy. This condition was temporally related to her discontinuation of vitamin D supplements and subsequent hypocalcemia. No associated systemic symptoms were observed, and a healthy baby was delivered prematurely at 34 weeks' gestation. This report supports the association between hypocalcemia and impetigo herpetiformis and raises theoretical questions regarding a relationship between vitamin D metabolism and various epidermal hyperproliferative states.

Adult↗
PubMed1991

Phosphate diabetes associated with bone metastases of oat cell lung cancer.

Although the link between phosphate diabetes and neoplasm or benign mesenchymal tumors has been well documented, the nature of the phosphaturia factor remains unknown. We describe two cases of phosphate diabetes associated with bronchogenic cancer. In these case reports, we suggest that fibroblasts or osteoblasts synthesize a phosphate eliminating substance.

Aged↗
PubMed1976

[Differential diagnostic problems resulting from massive doses of vitamin D and suspected pituitary dwarfism in the father of a child with vitamin-D-resistant rachitis (author's transl)].

A 1.8-year-old female child with retarded statomotor development and growth was reported. Radiologically and chemically, a rachitis was found which clearly improved following administration of 600,000 U. vitamin D3. Examination of the father who was thought to be suffering from pituitary dwarfism revealed hypophosphatemia and radiologic signs of osteomalacia. The diagnosis of a hypophosphatemic vitamin-D-resistant rachitis in this child could only be established with certainty during the course of the following months.

Adult↗
PubMedDate not supplied

[Hypocalcemic vitamin D-dependent renal rickets].

Two siblings, female 10 years old, and male 15 years old, with the diagnosis of vitamin D-dependent rickets were studied. Another sibling, also with the same diagnosis, died of bronchopnemonia at about 7 months of age. Both patients developed rachitic manifestations since the first year of life, which persisted despite the administration of massive doses of vitamin D intermitently. Severe hypocalcemia, moderate hypophosphatemia and elevated serum alkaline phosphatase were the most characteristic biochemical findings. Both patients showed diminished renal tubular reabsorption of amino acids and phosphates. These alterations were reversible during I.V. calcium gluconate administration. The clinical biochemical and X-ray manifestations disappeared completely after one year of treatment with dihydrotaquisterol. Vitamin D-dependent rickets is an autosomal recessive disease, characterized by a hydroxylation defect of 25 hydroxycholecalciferol at the carbon 1 level, due to abscence of 25 hydroxy-D1-hydroxylase. Thus 1-25 Dihydroxycholecalciferol, the active form of vitamin D3 is not formed, resulting in depression of intestinal calcium absorption and reabsorption from the bones.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗