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At least 325 records · Page 18Linked to original sources
PubMed2001

Vitamin D deficiency in mothers of infants with rickets.

OBJECTIVE: To identify infants treated for vitamin D deficiency rickets, and to determine the incidence of vitamin D deficiency in their mothers and their mothers' country of origin. DESIGN: A retrospective audit of the medical records of children diagnosed with vitamin D deficiency rickets. Inpatients were identified by discharge diagnoses of vitamin D deficiency or hypocalcaemia and outpatients by pharmacy dispensing of cholecalciferol. SETTING: The Women's and Children's Health Care Network and the Southern Health Care Network (Melbourne, VIC) from June 1994 to February 1999. PATIENTS: 55 children with vitamin D deficiency rickets. RESULTS: Fifty-four of the 55 children were born to mothers with ethnocultural risk factors for vitamin D deficiency. Vitamin D status had been assessed in 31 of the 55 mothers (56%): 25 (81%) had 25-hydroxyvitamin D3 concentrations < or = 25 nmol/L, consistent with osteomalacia. CONCLUSION: Vitamin D deficiency continues to occur in children of migrant families. When infants are diagnosed with vitamin D deficiency, vitamin D levels in their mothers and siblings should also be assessed.

Adolescent↗
PubMed1975

Rickets in Nigerian children--response to vitamin D.

The findings in 20 cases of nutritional rickets treated on an out-patient basis with oral calciferol and calcium gluconate are reported. Attention was paid to their clinical, biochemical and radiological responses. If was noted that presentation at the hospital out-patient department was always delayed until there were obvious and sometimes severe deformities in the children. Biochemical changes noted during the early phase of treatment showed an initial fall in the level of serum calcium and plasma phosohorus and a rise in the serum alkaline phosphatase. About three months after initiating treatment, calcium and phosphorus reverted to normal levels but serum alkaline phosphatase still remained high. Twelve of our cases (60 per cent) suffered from protein calorie malnutrition of the marasmic type and showed an apparent resistance to vitamin D therapy in what may be regarded as normal dosages. Response was however, achieved with substantial increase in the amount of vitamin given. There was a striking sex difference in the ratio of 15 males to five females indicating that males are more likely to develop nutritional rickets than females when subjected to predisposing environmental conditions. Vitamin D resistant type of rickets was not encountered in this study.

Alkaline Phosphatase↗
PubMedDate not supplied

[Rickets and tetany in the Spanish bibliography of the ninetenth century (author's transl)].

An historical study of the relationship between rickets and tetany through publications edited in Spain from 1800 to 1914 is presented. Twelve collections of journals, both pediatric and general medical, and likewise Medical Treatises, were used. In spite of the recognition of nervous phenomena accompanying rickets towards the beginning of the century, the clear relationship between rickets and tetany was not recognised until the beginning of this century. The causes of this delay are discussed, the main one being the limitations of an anatomoclinic mentality. The limited contribution and the low level of information of the Spanish author is emphasized.

History, 19th Century↗
PubMed1975

Vitamin D deficiency rickets. Two cases with faulty infant feeding practices.

Two cases of vitamin D deficiency rickets verify the occurrence of deficiency rickets in the United States in 1973. The two cases demonstrate the need for periodic reviews of feeding practices, especically when the possibility of so-called milk allergy is postulated. This may lead to avoidance of milk products. Fortification of various kinds of food with vitamin D does not ensure the protection from nutritional rickets of all children with peculiar feeding habits.

Alkaline Phosphatase↗
PubMed2002

Nutritional rickets and osteomalacia in school children and adolescents.

OBJECTIVE: To review experiences of nutritional rickets and osteomalacia in school children and adolescents at King Khalid University Hospital, Riyadh, Kingdom of Saudi Arabia. METHODS: Records of children and adolescents aged 6-18 years, seen at King Khalid University Hospital, Riyadh, Kingdom of Saudi Arabia, during the period January 1994 through to December 1999, who were diagnosed to have rickets or osteomalacia were reviewed. The diagnosis was based on clinical, biochemical and radiological data. Data extracted and analyzed included age, sex, presenting symptoms and signs, dietary history and sun exposure, blood count, bone profiles, renal and liver profile, and 25-hydroxy vitamin D3 and 1, 25 dihydroxy vitamin D3. Hand and wrist x-rays were carried out for all patients while bone density of lumbar spine and 3 femoral sites and bone scan were performed on the majority of patients. RESULTS: Forty-two children and adolescents (25 females and 17 males) were diagnosed. Their age ranged between 6-18 years with a mean of 13.5. Non specific symptoms, such as bone pain and fatigue were the most presenting symptoms, while skeletal deformities and fractures were the presenting symptoms in only 5 and 3 patients. Lack of direct sun exposure and poor calcium intake was evident. Bone profiles at the time of diagnosis revealed mean serum calcium of 2.1 mmol/L, range 1.5 2.3 (Normal=2.2-2.7), phosphorus 1.1 mmol/L, range 0.7 1.9 (Normal=1.4 2.1) and alkaline phosphatase activities of 1,480 U/L, range 834-2,590 (N=<600). Serum concentrations of 25-hydroxy Vitamin D were low (<10 mg/L) while that of 1, 25 Dihydroxy Vitamin D varied between low to normal (<10-45 ng/L). Bone density of the lumbar spine and 3 femoral sites were performed in 26 patients and showed markedly reduced values, while bone scan demonstrated a high uptake of tracer throughout the skeleton "super scan". Multiple stress fractures were evident in 8 children. CONCLUSION: Although a community-based study to assess the magnitude of the problem is needed, it seems that rickets and osteomalacia of nutritional origin are not that uncommon and deserves special attention from all pediatricians and practicing physicians. They also suggested that further studies are needed to help understand the pathophysiology, and identify the contributing factors for the development of the disorder.

Adolescent↗
PubMed1998

A case-control study on determinants of rickets.

A case-control study on rickets was performed on 156 cases and 307 controls admitted to Birla pediatric wards, Yekatit 12 Hospital. The following factors were significantly (p < 0.05) associated with diagnosis of rickets in univariate analysis: male gender, being a twin, abnormal birth weight, malnutrition, higher birth order, higher number of siblings, having a caretaker who is not the mother, lower education of the caretaker, having a caretaker who is not housewife, and with protective effect, exposure to sunshine (in number of days per week, duration of daily exposure in minutes, and not wearing clothes during exposure). In multivariate analysis, the following factors remained independently associated with diagnosis of rickets in children: being a twin (OR = 5.86, 95% CI = 1.40-24.50), history of high birth weight (OR = 8.94, 95% CI = 2.30-34.70), moderate and severe malnutrition (OR = 5.64, 95% CI = 2.30-13.80 for severe malnutrition when compared to normal weight), having the grand mother as caretaker (OR = 19.80, 95% CI = 3.70-104.70), and with protective effect, exposure to sunshine (OR associated with an increase of one day of exposure per week = 0.65, 95% CI 0.55-0.77; OR associated with daily exposure of more than 30 minutes, when compared to less than 15 minutes = 0.24, 95% CI = 0.09-0.64; and OR associated with being nude while exposed to sunshine = 0.32, 95% CI = 0.14-0.73). There was no significant difference between cases and controls in marital status or religion of the caretakers.

Birth Order↗
PubMed2002

[Rickets in Asian immigrants during puberty].

Rickets usually occurs in the first two years of life and in puberty since metabolic demand is increased due to rapid growth in these two critical periods of life, when peak bone mass is achieved. Rickets remains one of the most prevalent pediatric diseases in developing countries. Although it is considered to have disappeared in developed countries, there is increasing evidence of widespread vitamin D deficiency among immigrants. There are many reports on rickets and osteomalacia in Asian infants, adolescents and pregnant women moving from India, Pakistan and Bangladesh to developed countries with a cooler climate. We describe three teenagers of Pakistani origin. Clinical presentation included limb pains, muscular weakness, knock-knees and seizures. In all three patients, biochemical findings included hypocalcemia, raised serum parathormone and alkaline phosphatase, and reduced 25-hydroxy vitamin D concentrations. After vitamin D treatment and dietary counseling, biochemical findings returned to normal and their symptoms improved. Given the recent increase in the number of immigrants to Spain, this forgotten disease will probably reappear.

Adolescent↗
PubMedDate not supplied

[Study of proteins of rat skeletal muscles in experimental rickets].

In dynamics of experimental rickets proteins of rat sceletal muscles were studied after and before physical exercises. Occurrence of rickets was estimated by following concentration of inorganic phosphorus and calcium in blood and by X-ray examination of knee joint. An increase in total amount of sarcoplasmic proteins was observed within the first week of development of the disease. After physical exercices the effect was noticed also within the second week of the development of rickets. Content of fractions of the sarcoplasmic proteins was similar in all animals and within all the periods studied. Within four weeks content of myofibrillar proteins was decreased in rickety rats, which were not subjected to physical exercices. In rats of the both experimental groups the ATPase activity of actomyosin was not distinctly altered within all the periods studied.

Actomyosin↗
PubMedDate not supplied

A case of dilated cardiomyopathy due to nutritional vitamin D deficiency rickets.

Vitamin D deficiency rickets was detected as the cause in a nine-month-old girl with dilated cardiomyopathy and signs of congestive heart failure. The patient responded to calcium and vitamin D supplementation promptly and left ventricular systolic functions normalized at the 3rd month of treatment. Nutritional rickets must be remembered in etiological assessment of dilated cardiomyopathy among infants living in regions in which nutritional rickets is still common.

Cardiomyopathy, Dilated↗
PubMed1992

Growth rate in children with vitamin-D-dependent rickets in relation to 1-alpha-hydroxyvitamin D3 dosage.

Growth rate of five children with vitamin D-dependent rickets was analyzed during the long-term treatment with an active analog of vitamin D3. Considerable increase in growth rate together with the improvement of biochemical values and radiological pattern took place during the initial phase of administration of 1-hydroxyvitamin D3. During the maintenance treatment of long duration with 1-hydroxyvitamin D3 both the acceleration of growth and catch-up growth persisted. However, in 4 among 5 children studied an inhibition of growth was observed during different periods of time. Only in one boy was this connected with the conclusion of the process of physiological growth. In three remaining children a slow-down in growth rate appeared during the pre-pubertal period or was the effect of lowering the dose of 1-hydroxyvitamin D3 as an countermeasure to hypercalciuria. In such cases inhibition of growth was caused by the administration of too small a dose of 1-hydroxyvitamin D3 in relation to the requirement. In all cases the appearance of biochemical features of rickets aggravation, such as low blood serum phosphate concentration and elevated alkaline phosphatase activity, preceded the observable inhibition of growth. The results obtained allow us to conclude that the inhibition of growth observed during the long-term treatment of rickets with 1-hydroxyvitamin D3 may be regarded as the first signal of inadequate dosage of 1-hydroxy vitamin D3.

Adolescent↗
PubMed1999

Rickets caused by excessive renal phosphate loss and apparent abnormal vitamin D metabolism in a cat.

Rickets was diagnosed in a 1-year-old cat with a history of weakness, osteopenia, and recurrent fractures. Processes causing rickets include vitamin D deficiency caused by inadequate, nutrition, lack of exposure to sunlight, defective metabolism of parent vitamin D to active metabolites, inherited vitamin D receptor defects, hypoparathyroidism, chronic renal failure, renal loss of phosphate, or malabsorptive states resulting from gastrointestinal or hepatic diseases. On the basis of analysis of serum 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D2 and D3 concentrations, serum biochemical analysis, and urinary fractional clearance of electrolytes, the causes of rickets in our cat, were most compatible with a combination of excessive loss of phosphorus via the kidneys and deficient or abnormal hepatic 25-hydroxylation of vitamin D. Calcifediol treatment and twice daily administration of phosphate salts resulted in clinical improvement and increases in mineralization of the skeleton, as evidenced on radiographic evaluation.

Animals↗
PubMed2005

Incidental finding of vitamin-D deficient rickets in an otherwise healthy infant--a reappraisal of current vitamin-D supplementation guidelines.

In an effort to prevent rickets and vitamin-D deficiency in healthy infants, the American Academy of Pediatrics recommends a supplement of 200 IU per day of vitamin D to all breastfed and nonbreastfed infants unless they consume at least 500 ml per day of vitamin-D-fortified formula or milk. Case reports of infantile vitamin-D-deficient rickets secondary to maternal vitamin-D deficiency have been reported but focused on mothers who had predictable risk factors for such a deficiency. We report on an infant with vitamin-D-deficient rickets who did not have nutritional risk factors and whose mother did not have nutritional or medical risk factors for such a deficiency. We conclude that the current vitamin-D supplementation guidelines be extended to all infants, regardless of feeding volume or source, or at least to all infants born to dark-skinned mothers.

Diagnosis, Differential↗
PubMed2005

[Clinicopathologic study of 10 cases of osteomalacia or rickets-associated mesenchymal tumors].

OBJECTIVE: To study the clinicopathologic features of osteomalacia or rickets-associated mesenchymal tumors. METHODS: The clinical and pathologic findings of 10 cases of osteomalacia or rickets-associated mesenchymal tumors were evaluated. Hematoxylin and eosin stain, immunohistochemistry and histochemistry were performed on the archival paraffin sections. RESULTS: Amongst the 10 patients studied, 6 were males and 4 were females. Their age at the time of operation ranged from 28 to 69 years ( mean = 45.6 years). A history of long-standing bone pain, arthralgia, limitation in movement, hypophosphatemia and hyperphosphaturia was present in all cases. The duration of symptoms ranged from 2 to 27 years (mean = 9.6 years). The tumor size ranged from 1 to 7 cm (mean size = 3.52 cm). Microscopically, the tumors were composed of various mesenchymal cells, including spindled fibroblast-like cells, adipocytes, chondroid cells and mucinous cells. The background was rich in blood vessels. In 8 of the 10 cases, there was also dystrophic calcification in an unusual flocculent or "grungy" pattern. Peripheral woven bone shell formation was noted in 2 cases and non-urate crystal deposition in 2 cases. Mitotic figures were rare in 9 cases. In 1 of the 10 cases however, mitotic figures and bizarre cells were commonly encountered. On immunohistochemical study, the tumor cells were all positive for vimentin. There was focal positivity for smooth muscle actin and CD34 in 5 and 3 cases respectively. The staining for desmin, S-100 and AE1/AE3 was negative. Ki-67 proliferation index was less than 4% in 8 cases and 30% in 1 case. Alcian blue-positive mucinous matrix and mucinous degeneration around vessels were noted in 8 cases. CONCLUSIONS: Most of the osteomalacia or rickets-associated tumors are either benign or low-grade malignant mesenchymal tumors. They can be mistaken as other neoplasms due to the morphologic heterogeneity present. Thorough understanding of the associated clinical features and laboratory investigation results is helpful in arriving at the correct diagnosis.

Actins↗
PubMed1991

Rickets of prematurity: a case report.

A case report is given, and an attempt made to summarize our knowledge about this disorder. An extremely premature infant (birth weight 750 grammes) developed progressive rickets resulting in fractures despite phosphate, calcium and calciferol (vitamin D) supplementation. The patient had mild respiratory distress syndrome but later developed broncopulmonary dysplasia. Initial biochemical evidence of rickets occurred by the 6th week of post-natal life (or 31 weeks post-conceptional age). Although the serum levels of vitamin D or 1-alphahydroxy vitamin D were not determined, it is assumed that the levels of the active metabolite was probably low since clinical, biochemical and radiologic cure of the rickets occurred following its usage.

Bronchopulmonary Dysplasia↗
PubMed1991

Reassessment on roentgenologic signs of early rickets. Roentgenopathologic correlations of 52 en block specimens.

Correlation of the X-ray manifestation and the en bloc sections of 52 wrists of infants and children aged from 0-4 years from autopsy was carried out to identify the real X-ray signs of rickets. Simple ill-defined provisional calcified zone (PCZ), enlargement of head of ulna, shallow saucer-shaped and undulant or multilaminar PCZ are normal in variation. The signs of early rickets included marginal spur, saucer-shaped deformity, ill-defined and disordered trabeculae under PCZ, mild brush appearance and osteoporosis. However, only when five of the above mentioned criteria were met at the same time, can early rickets be diagnosed.

Child, Preschool↗
PubMedDate not supplied

[Hyperparathyroidism in deficiency rickets. Changes after vitamin therapy].

The study concerned 16 cases of deficiency rickets observed over 3 years. The level of serum parathyroid (IPTH) hormone was always increased in the late stages of rickets, but was normal in 3 cases of early rickets with hypocalcaemia and monophosphataemia. There was no statistical correlation between the level of IPTH and monophosphataemia. There was no statistical correlation between the level of IPTH and calcaemia. After vitamin D-therapy, the levels if IPTH returned to normal in 5 to 21 days in most cases. No obvious difference was noted in this evolution between children treated by vitamin D2 and 25 OH D. The excretion of urinary cyclic adenosine monophosphate decreases in parallel with blood IPTH.

Cyclic AMP↗
PubMed1990

Nutritional rickets.

Nutritional rickets was diagnosed in 18 infants aged eight to 24 months. Clinical features included progressive leg bowing, poor linear growth, a diet deficient in vitamin D, seizures, and abnormal serum calcium, phosphate and alkaline phosphatase levels. Wrist radiographs and serum alkaline phosphatase levels were the most useful confirmatory tests. Breast milk may not contain enough vitamin D to protect infants, particularly dark-skinned children and those living in cloudy, northern U.S. cities, from rickets after six months of age. As breast feeding becomes more widely practiced, care is required to ensure that infants at high risk for rickets receive appropriate vitamin D supplementation.

Breast Feeding↗
PubMed1990

Alopecia with rickets: an end organ unresponsiveness to 1,25-dihydroxyvitamin D--a case report.

Two siblings of a rare syndrome of vitamin D dependent type II rickets are reported for the first time from India. The clinical and biochemical picture was characterised by florid rickets, alopecia, hypocalcemia and resistance to therapy with high dosages of vitamin D3. Due to lack of facilities for estimation of 1,25(OH)2D, alopecia remains the only clue to the diagnosis of this rare syndrome in association with resistant rickets.

Alopecia↗