Polycyclic aromatic hydrocarbons in Ontario foundry environments.
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Biomedical subjects
Publications and source records attributed to J H Vogt.
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In two patients (father and daughter) with idiopathic hypoparathyroidism, one of whom was resistant to the action of vitamin D2 and AT-10, 1alpha-hydroxycholecalciferol (1alpha-(OH)D3) in doses of 2-5 mug/day restored the serum calcium concentration to the normal range. The calcemic effect of 1alpha (OH)D3 was in both patients due to an increased intestinal calcium absorption and increased calcium mobilization from bone. In one of the patients 1alpha-(OH)D3 also increased the renal tubular calcium reabsorption; in the other it did not have this effect, resulting in hypercalciuria as serum calcium rose. The lack of effect on tubular calcium reabsorption probably accounts for the relative resistance to the action of 1alpha-(OH)C3 in this patient compared with other.
The case history of a woman born in 1946 is given. In 1968 she developed a syndrome of headache, fever. elevated antistreptolysin titer, enlarged and ballooned sella turcica, hypothyroidism secondary to TSH deficiency, secondary amenorrhoea of pituitary genesis, probable growth hormone deficiency, and secondary adrenocortical insufficiency. From 1972 all the mentioned pituitary defects of function disappeared, and the sella turcica gradually became normal in size as shown by X-ray examination.
Intestinal 47Ca absorption has been determined from blood and stool radioactivity after oral administration of the isotope in nine patients before and during cellulose phosphate treatment. Oral administration of 5 g cellulose phosphate concomitant with 47Ca in 100 mg "carrier" calcium as CaCl2 decreased 47Ca absorption by 80 per cent. Cellulose phosphate, 5 g three times daily, decreased urinary excretion of non-radioactive calcium by 47 percent. Urinary magnesium excretion decreased by 47 percent whereas urinary phosphorus excretion increased by 67%. Calcium and magnesium excretion in urine decrease because cellulose phosphate binds divalent cations within the GI tract. The increased phosphorus excretion is probably due to partial hydrolysis of the substance in the gut.
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