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At least 19 recordsLinked to original sources
PubMed1972

25-Hydroxycholecalciferol. A comparative study in deficiency rickets and different types of resistant rickets.

The effects of 25-hydroxycholecalciferol were studied in 4 children with deficiency rickets and 22 children with D-resistant rickets, including patients with hereditary hypophosphatemic D-resistant rickets, "pseudo-deficiency" rickets, and rickets secondary to cystinosis or to tyrosinosis. Three protocols were used. (a) 8 days after a single oral dose of 16,000 IU of 25-hydroxycholecalciferol, normalization of all biological parameters was observed in all cases of deficiency rickets. A complete lack of response was observed in the different types of resistant rickets. (b) Under prolonged administration of 2,640 IU/day for 2 months, clinical-biological symptoms and X-ray lesions disappeared, and a catch-up growth pattern was observed in deficiency rickets; no relapse of rickets occurred up to 5 months after therapy was stopped. The same dose had no significant effect in 10 patients with hereditary hypophosphatemic D-resistant rickets. A bone biopsy performed in one case showed the persistence of characteristic lesions. (c) With increasing doses of 25-hydroxycholecalciferol varying from 6,000 to 30,000 IU/day and a follow-up of 6 months up to 2 yr duration, clinical-biological-radiologic recovery and catch-up growht was obtained in all cases of "pseudo-deficiency" rickets. In hypophosphatemic hereditary D-resistant rickets, 5 out of 13 patients' serum concentration of phosphorus reached at least 30 mg/liter, but a catch-up growth pattern was not observed. These results indicate that (a) 25-hydroxycholecalciferol is highly active in deficiency rickets; (b) a defect in the conversion of vitamin D(3) to its active 25-hydroxy metabolite is probably not the metabolic defect in any of the different types of vitamin D-resistant rickets studied.

Administration, Oral↗
PubMed1991

X-linked hypophosphatemic rickets without "rickets".

Wrist and knee radiographs from children with X-linked hypophosphatemic rickets were analyzed and compared with those from normal children and children with established rickets to assess whether radiographically apparent rickets is a consistent abnormality in X-linked hypophosphatemia. The absence or presence of rickets was correctly identified in 94.8% of wrist and knee films from normal and positive controls. In contrast, patients with X-linked hypophosphatemia exhibited rachitic abnormalities in only 5 of 11 wrist and 13 of 15 knee radiographs. As a result, 4 patients within this study group had rickets at the knee and not at the wrist, whereas 5 displayed classic defects at both sites. Perhaps more important, 2 patients, aged 3.8 and 5.2 years, displayed no evidence of rickets in either wrist or knee films, although relatives exhibited demonstrable rachitic abnormalities. Our data indicate that radiographically detectable rickets is a variable abnormality of X-linked hypophosphatemia and does not provide an unambiguous index for the diagnosis of this disease.

Adolescent↗
PubMed1982

Studies on the pathogenesis of avian rickets. I. Changes in epiphyseal and metaphyseal vessels in hypocalcemic and hypophosphatemic rickets.

Growth plate morphometry and measurements of serum chemistry were correlated to clarify the pathogenesis of hypocalcemic and hypophosphatemic avian rickets. Accumulation of proliferating and maturing cartilage in hypocalcemic chicks is accompanied by increased length and increased variation in length of perforating epiphyseal vessels, decreased number and abnormal arrangement of marrow spaces, an increased proportion of cells to blood vessels in marrow spaces, and a change in the distribution but not the total number of DNA-synthesizing chondrocytes per unit width of growth plate. Accumulation of hypertrophic cartilage in hypophosphatemic rickets is accompanied by no change in length, distribution, or number of perforating epiphyseal vessels, elongation but no change in number or arrangement of marrow spaces, an increase in the relative proportion of blood vessels to cells in the marrow spaces, and no change in distribution but a decrease in total number of DNA-synthesizing chondrocytes per unit width of growth plate. Both types of rickets have decreased amounts of calcified cartilage. These results provide further evidence that hypocalcemia and hypophosphatemia cause morphologically distinct types of rickets in birds. The data indicate that the thickness of the proliferating and maturing region and hence the distance of the hypertrophic zones from the epiphysis are anatomically and temporally related to length of perforating epiphyseal vessels and serum calcium levels. They indicate that in hypocalcemic rickets accumulation of proliferating and maturing cartilage is unlikely to be the result of increased chondrocyte replication and that the relative rates of chondrocyte hypertrophy and resorption of hypertrophic cartilage by marrow are equal. They support the concept that delayed chondrocyte hypertrophy is the major cause of growth plate thickening in hypocalcemic rickets. Data presented in this study, when considered together with data from the literature on hypophosphatemic rickets, support the long-held concept that growth plate thickening in this disease is caused primarily by a decreased rate of resorption of hypertrophic cartilage by marrow relative to the rates of chondrocyte proliferation, maturation, and hypertrophy. The data further support the concepts that growth of cartilage into marrow is a biphasic process including longitudinal growth effected mainly by blood vessels, and resorption of the lateral walls of marrow spaces effected mainly by marrow cells, and that it is the latter phase that is defective in hypophosphatemia.

Animals↗
PubMed1989

[Diagnostic significance of calcitonin analysis in children with rickets and rickets-like diseases administered calcium test].

The secretory activity of C-cells of the thyroid was investigated in 25 children with rickets and rickets-like diseases. There were 13 children with grades II and III rickets, 6 with vitamin D-dependent rickets, and 6 with Debre-de Toni-Fanconi disease. Five normal children constituted a control group. The basal concentration of calcitonin did not differ from the control parameter in all patients' groups. An increased release of the hormone to the blood was noticed in response to calcium stimulation. The rise of blood calcitonin was determined by the disease pattern, which made it possible to use the test with a one-minute intravenous calcium injection for differential diagnosis purposes. The maximal changes were discovered in children suffering from vitamin D-dependent rickets.

Calcitonin↗
PubMed1989

Two siblings with vitamin-D-dependent rickets type II: no recurrence of rickets for 14 years after cessation of therapy.

Rickets in a 3-year-old boy and his 1-year-old sister, both with alopecia, was cured by treatment with 50,000 IU of vitamin D2 daily for 2 years and did not recur within 14 years after cessation of therapy. A diagnosis of vitamin-D-dependent rickets type II was made in these patients at the ages of 20 and 18 years based on the findings that 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] did not inhibit DNA biosynthesis in phytohaemagglutinin-stimulated lymphocytes and that cultured skin fibroblasts showed impaired nuclear uptake and normal cytosol binding of [3H]1,25(OH)2D3. Surprisingly, the serum 1,25(OH)2D levels of these patients were high and their serum 24,25-dihydroxyvitamin D levels were low, although neither patient showed any symptoms except alopecia. The presence of vitamin D metabolite imbalances in the absence of rickets in these patients might be explained by differences in sensitivity to 1,25(OH)2D3 of bone formation and vitamin D metabolism. In addition, changes of sensitivity to treatment with vitamin D derivatives might be a consequence of differentiation of target cells. From the present findings, it is suggested that in this disease treatment with a sufficient dose of vitamin D derivatives should be initiated in the active phase of rickets.

Alopecia↗
PubMed1981

Policy for prevention of Asian rickets in Britain: a preliminary assessment of the Glasgow rickets campaign.

Evidence of continuing hospital admissions of patients with Asian rickets and osteomalacia led to a further attempt to provide more effective preventive measures for the Glasgow Asian community. Dose-response studies showed that the equivalent of 10 microgram of vitamin D daily would provide effective prophylaxis, and a general practice survey showed that self-administered vitamin D supplements would reduce the prevalence and severity of Asian rickets. A multidisciplinary working group devised a preventive campaign based on the free issue of vitamin D supplements on demand to children who required them. Supported by a health education programme for community health personnel and the Asian community, the first 16 months of the campaign produced an eight-fold rise in the issue of supplements to older Asian children and a 33% increase in their issue to infants of all ethnic groups. Because more children are receiving vitamin D supplementation the campaign seems likely to reduce the prevalence of Asian rickets in Glasgow.

Adolescent↗
PubMed1995

Healing of rickets during vitamin D therapy despite defective vitamin D receptors in two siblings with vitamin D-dependent rickets type II.

We report the healing of severe rickets despite hypocalcemia in two siblings with absent vitamin D receptors; long periods of treatment with excessive doses of vitamin D led to relative hypoparathyroidism and a return to normal of calcium metabolism during calcitriol treatment. This finding suggests that some other regulating factor may substitute for the defective vitamin D receptor.

Dose-Response Relationship, Drug↗