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PubMed1990

[Rickets- and/or scurvy-like bone lesions in beta-thalassemia major].

Recently, a new type of skeletal lesions has been described in Cooley's anemia as a possible complication secondary to therapy. In 12 children affected with thalassemia major, who received an intensive transfusional regimen combined with continuous iron chelation therapy (desferoxamine-B: 50-80 mg/kg/day), some radiological abnormalities of the long bones were observed similar to those described in rickets and scurvy. These rickets and/or scurvy-like lesions had never been reported before the introduction of high-dose desferoxamine therapy. The pathogenesis of these lesions is uncertain, but the toxic effect of desferoxamine probably plays an important role in their development. The association of growth retardation and rickets and/or scurvy-like skeletal lesions in Cooley's anemia patients may be used as a valuable clinical criterion in long-term chelation management.

Adolescent↗

PubMedDate not supplied

[Phospholipids bound with plasma proteins in children with vitamin D-deficient rickets].

Composition of phospholipids bound with plasma proteins in the healthy children and in those with vitamin-D-deficient rickets are studied. It is found that the quantitative and qualitative content of phospholipids in the low- and high-density lipoproteins increases considerably with the rickets. At the same time the content of phospholipids which form complexes wit fibrinogen gets two times lower. The character of changes in the phospholipid composition in protein fractions and in the whole plasma in case of rickets is different.

Blood Proteins↗

PubMed1987

Etiology of rickets in Egyptian children.

Factors associated with the rickets found in children attending the Outpatients Department of Cairo Children's Hospital have been studied. All the children studied were small for their age with the rachitic children being significantly smaller than the controls. The clinical diagnosis of the disease was confirmed in 54 children by X-ray and plasma biochemistry. The best indicator of the disease was the enlarged epiphysis of the wrist and to a lesser extent that of the ankles. Some of the factors predisposing to rickets were assessed in the rachitic children and in age-matched controls. There was no difference in the nutrient intake of these two groups of children although intakes of energy, calcium and vitamin D, but not of protein, were lower than recommended dietary allowances. Although more of the rachitic children came from urban areas than the controls there were no significant differences in the environments to account for the occurrence of the disease. Factors contributing to the development of rickets are discussed with particular regard to aspects such as low body weight, low maternal vitamin D status and low calcium intakes which cause a high rate of utilization and metabolism of vitamin D.

Body Weight↗

PubMed1979

[Rickets-like changes in broiler chickens (author's transl)].

A disease in broiler chickens associated with rickets-like symptoms observed on post-mortem examination is described. The disease is not caused by deficiencies in the feed. Treatment with vitamin D3, calcium and phosphorus has little if any effect. There is evidence to suggest a relationship with the origin of the broilers. It also is an established fact that the disease is related to the farm. Particularly those broilers will develop rickets-like symptoms, which were housed on litter previously used for chickens with the same disease. It probably is an infectious disease. Non-purulent inflammation of the glandular stomach is constantly observed in chickens showing rickets-like symptoms. This disease is transmissible to SPF chickens. It is not clear whether this is an accidental finding or typical of this clinical picture.

Animals↗

PubMed1979

[X-linked familial hypophosphatemic rickets report of six cases (author's transl)].

X-linked familial hypophosphatemic rickets (X.L.F.H.R.) is one of the D resistant rickets. The inheritance pattern is related to the X chromosome. Most constant feature is hypophosphatemia. Pathogenesis is still a subject of controversy. There are three main theories: a) An abnormal vitamin D metabolism. b) Secondary hyperparathyroidism developping as a result of the diminished calcium absorption by gut. c) A primary deffect of phosphate transport al various levels. Authors study and comment six cases of X.L.F.H.R., three of which belong to the same family. Clinical, radiological and higtological findings correspond to those of severe rickets. It is a chronic disease which affects children during growth period, giving rise to deforming bones invalidism. Treatment consists on continuous administration of oral phosphate and vitamin D.

Adolescent↗

PubMed1979

Hypophosphatemic rickets: effect of 1 alpha, 25-dihydroxyvitamin D3 on growth and mineral metabolism.

Growth retardation nearly invariably accompanies hypophosphatemic rickets. Studies were conducted in an adolescent male with this disorder as follows. Protocol I: age, 6 to 16 years; treatment per day, 5,000 to 80,000 units vitamin D2, 1,760 to 2,200 mg phosphorus, orally as buffered phosphate; growth velocity, 5 to 6 cm/year. Protocol II: age 16 to 17 years; treatment per day, 1 alpha,25-dihydroxyvitamin D3, 1 microgram; 2,200 mg of phosphorus, orally as buffered phosphate; growth velocity, 14 cm/year. The height improved from less than third percentile for the decade during study protocol I to the 25th percentile during protocol II. Mineral balance studies showed a reduction of urinary and stool phosphorus during treatment protocol II, while the patient was receiving metabolic diet. The serum phosphorus improved from 2.2 to 4.3 mg/dl and radiologic healing of rickets was documented. No hypercalcemic episode was encountered. The data support the contention that 1 alpha,25-dihydroxyvitamin D3 is the treatment of choice for hypophosphatemic rickets.

Adolescent↗

PubMed1984

[Hypophosphatemic rickets in premature infants weighing less than 1500 grams on oral and parenteral feeding].

The effect of mode of feeding on the development of rickets in very-low-birth-weight (VLBW) infants in spite of regular vitamin D supplementation was examined. Parenterally fed infants develop rickets more often than orally fed ones in spite of sufficient vitamin D supplementation. On total parenteral feeding hypophosphatemia was observed because phosphate supplementation was significantly lower than on oral feeding or in the intrauterine growing fetus of comparable gestational age. Adequate parenteral phosphate supplementation can prevent rickets.

Humans↗

PubMed1984

Is craniotabes a pathognomonic sign of rickets in 3-month-old infants?

Fifty-eight well Black infants between the ages of 10 and 15 weeks were examined for the presence of craniotabes and investigated for the presence of vitamin D deficiency and rickets. Thirty-five infants were found to have craniotabes and 5 of these had radiological evidence of rickets. No difference in dietary history, birth weight, weight gain, length or skull circumference was found between those with and those without craniotabes. Significantly more females than males had craniotabes. The majority of infants with craniotabes had normal biochemical values. Craniotabes is a common finding in 3-month-old infants and is of no help in diagnosing rickets in this age group.

Bone Diseases, Developmental↗

PubMed1983

Rickets as an unexpected x-ray finding.

Rickets, whether due to lack of proper nutrition or secondary to disease or medication, may be unexpectedly detected on radiographs obtained for other reasons. Several recent examples are reported here. It is important to be aware of the manifestations of rickets so that appropriate treatment is not delayed. Physicians should be alert for signs of rickets in the x-ray examination of any child.

Child, Preschool↗

PubMed1983

Ultrastructure of parathyroid glands of growing chickens with vitamin D deficiency rickets.

Ultrastructural studies were conducted on the parathyroid glands (PTG) of 2- to 7-week-old nontreated control growing broiler chickens (group A, 6 chickens); the same aged chickens with experimentally induced vitamin D deficiency rickets (18 morbid chickens each from groups B, C, and D); and in 4- to 9-week-old chickens naturally affected with rickets (group E, 8 chickens). Four types of principal cells were classified in the PTG of clinically normal birds and in PTG of birds with secondary hyperparathyroidism as follows: Type I cell (small cell in the resting phase); type II cell (medium-sized cell with well-developed rough-surfaced endoplasmic reticulum in the synthesizing phase); type III cell (large cell with well-developed Golgi apparatus and cytoplasmic organelles in the packaging and secretory phase); and type IV cell (medium-sized cell with poor cytoplasmic organelles in the involuting phase). Many coated vesicles were observed in type II and type III cells. In young control chickens, principal cells of the PTG were considered in the resting phase; in older control chickens, there were increased numbers of cells in the synthesizing phase. In the vitamin D deficiency groups, principal cells were in the synthesizing and packaging and secretory phases. In birds with naturally occurring rickets, principal cells were in packaging and secretory phases, with a small number of cells in the involuting phase. The ultrastructural changes of the PTG from the initial to final phases in growing chickens with secondary hyperparathyroidism were demonstrated.

Animals↗

PubMedDate not supplied

Rickets in turkey poults.

Fifteen outbreaks of rickets were diagnosed in turkey poults in Saskatchewan between 1978 and 1981. No relationship to farm, source of poults, or source of feed was apparent. Most outbreaks started when the poults were between 10 and 14 days of age, and they had recovered by 28 days of age. Losses varied from 1% to 14% of poults started. Skeletal lesions were characteristic of a vitamin D or calcium deficiency. On the basis of chemical analyses, adequate levels of calcium and phosphorus and proper amounts of vitamin premixes were present in the feed, but in five outbreaks biological feed tests implicated feed as a causative factor. The severity of rickets in poults fed defective feeds was markedly reduced by providing the poults with extra vitamin D in the drinking water or by injection. Two premixes used in different feeds contained adequate available vitamin D on the basis of biological testing. In some of the outbreaks, the rickets may have resulted from inadequate distribution of vitamin D in the feed, destruction of vitamin D during feed processing, or some unknown factor in the feed interfering with vitamin D utilization.

Animal Feed↗

PubMedDate not supplied

Field rickets in turkey poults: biochemical findings.

Two clinical cases of field rickets and one of nutritional rickets in turkey poults were studied. Plasma levels of calcium, phosphorus, alkaline phosphatase, and vitamin D metabolites were determined. Concentrations of calcium, phosphorus, and alkaline phosphatase in affected poults were typical of nutritional rickets. The mean plasma calcium concentration in rachitic poults was not significantly different from that in controls. Mean values for plasma phosphorus were 1.5 to 2.4 mg/dl lower in the rachitic poults, and values for alkaline phosphatase activity were 1.3-1.7 times greater. In assays of vitamin D metabolites, mean 24, 25 dihydroxyvitamin D3 values were consistently lower in rachitic poults.

24,25-Dihydroxyvitamin D 3↗

PubMed1982

Early biochemical findings in familial hypophosphataemic, hyperphosphaturic rickets and response to treatment.

Regular biochemical measurements were made in 4 babies, each of whom had one parent with familial hypophosphataemic, hyperphosphaturic rickets. Hypophosphataemia developed by 2 months and levels of alkaline phosphatase had increased by 3 months in all four. Decreased tubular reabsorption of phosphate and x-ray changes of rickets did not develop until 6 months in 3 of the babies. In the fourth these abnormalities developed at 9 days and 3 months. The babies were treated with oral phosphate and small doses of 1-alpha-hydroxy-cholecalciferol. The rickets healed readily in 3 babies and their linear growth kis within the normal range. Healing took much longer in the remaining child and his linear growth is below the 3rd centile. Hypercalcaemia has not been a problem of treatment.

Alkaline Phosphatase↗

PubMed1980

Unsuspected nutritional rickets.

Based on the presentation and clinical features of four cases of nutritional rickets, it is suggested that particular groups of children, namely vegetarians, children breast-fed for an unusually long time, and black children, are at risk to develop the nutritional deficiencies of vitamin D and calcium that lead to clinical rickets. The diagnoses in these cases were made by fortuitous radiologic examination, even though the children had been receiving regular pediatric supervision, indicating a lack of awareness of the condition. This report is intended to emphasize the reemergence of nutritional rickets and to illustrate the different modes of its clinical presentation.

Breast Feeding↗

PubMed1995

Cod-liver oil, vitamin D and the fight against rickets.

Although rickets has all but disappeared as a medical problem, the disease caused serious concern in turn-of-the-century England, where it reached epidemic proportions. The connection between rickets and a lack of vitamin D wasn't made until shortly after World War I, when it was determined that regular exposure to sunlight would eliminate the problem; another solution was to provide vitamin D supplements in milk. The problem hasn't disappeared entirely, however. Seventeen cases of rickets have been diagnosed at Toronto's Hospital for Sick Children in the past 5 years.

Cod Liver Oil↗

PubMed1975

Rickets associated with long-term anticonvulsant therapy in a pediatric outpatient population.

Over a 12-month period, an ambulatory pediatric population receiving long-term anticonvulsants was surveyed for the presence of biochemical and radiologic rickets. There were 74 treated children and 95 matched controls. Elevations of serum alkaline phosphatase activity occurred in 31 of the 74 (42%) treated children (23 of 47 children between 2 and 10 years and 8 of 21 children between 10 and 16 years). This frequency of abnormal values was significantly greater than that which occurred in our control population. Calcium and phosphorus abnormalities were minimal in both treated and control populations. Radiologic rickets occurred in 6 of the 74 (8%) of the treated children and in none of the control population. Neither the severity of the rickets nor the degree of hyperalkaline phosphatasemia were correlated with age of the patient, duration, and/or dose of anticonvulsant therapy.

Adolescent↗

PubMedDate not supplied

A case of transient hyperphosphatasaemia following vitamin D-deficient rickets.

A seven-month-old boy with a diagnosis of vitamin-D deficiency rickets is presented. After treatment with vitamin-D, biochemical and radiological improvement was noted. At 14-months of age the plasma akaline phosphatase activity valve was found to be elevated even though rickets was not present. A diagnosis of hyperphosphatasemia was established. Although rare in infancy, transient hyperphospha tasemia may occur following vitamin-D deficient rickets. This possibility should be considered when evaluating laboratory results in such cases.

Alkaline Phosphatase↗

PubMedDate not supplied

Growth hormone and insulin-like growth factor I plasma levels in patients with hypophosphatemic rickets.

The cause of the growth retardation present in patients with hypophosphatemic rickets has not been totally elucidated. There has been a previous report of a growth hormone deficit in a group of these patients. To verify this abnormality we studied two groups of patients with hypophosphatemic rickets, one with (n = 6) and the other without (n = 7) treatment with calcitriol and oral phosphates. All patients in both groups showed a normal growth hormone response (> 10 micrograms/l) to standard stimulatory tests and normal IGF-I plasma levels. Mean IGF-I plasma levels were not significantly different (untreated 1.46 +/- 0.80 U/ml, treated 1.25 +/- 0.69 U/ml) and the mean logarithmic deviation of IGF-I plasma levels from both groups did not differ from normal. In summary, we found no abnormalities of the growth hormone-IGF-I axis in our patients with hypophosphatemic rickets.

Absorption↗