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At least 73 records · Page 4Linked to original sources
PubMed2000

Case-control study of factors associated with nutritional rickets in Nigerian children.

OBJECTIVE: Because the causes of nutritional rickets in tropical countries are poorly understood, we conducted a case-control study to determine factors associated with rickets in Nigerian children. STUDY DESIGN: We compared 123 Nigerian children who had rickets with matched control subjects. Dietary, demographic, anthropometric, and biochemical data were collected to assess factors related to calcium and vitamin D status, which might predispose children to rickets. RESULTS: Mean (+/- SD) daily dietary calcium intake was low in both children with rickets and control children (217 +/- 88 mg and 214 +/- 77 mg, respectively; P =.64). Children with rickets had a greater proportion of first-degree relatives with a history of rickets (14.6% vs 3.1%; P <.001), a shorter mean duration of breast-feeding (16.0 vs 17.3 months; P =.041), and a delayed age of walking (14 vs 12 months; P <.001). Among children with rickets, biochemical features suggestive of calcium deficiency included hypocalcemia, extremely low calcium excretion, and elevated 1, 25-dihydroxyvitamin D and parathyroid hormone values. Median 25-hydroxyvitamin D concentrations were 32 and 50 nmol/L (13 and 20 ng/mL) in children with rickets and control children, respectively (P <.0001). Only 46 subjects with rickets (37%) had 25-hydroxyvitamin D values <30 nmol/L (12 ng/mL). CONCLUSIONS: Vitamin D deficiency appears unlikely to be the primary etiologic factor of rickets in African children. Moreover, low dietary calcium intake alone does not account for rickets. Insufficient dietary calcium probably interacts with genetic, hormonal, and other nutritional factors to cause rickets in susceptible children.

Adolescent↗
PubMed2005

The Chakaria food system study: household-level, case-control study to identify risk factor for rickets in Bangladesh.

OBJECTIVE: A comprehensive, multiround survey of local food systems in a rickets-endemic area of Bangladesh was conducted to identify household-level risk factors for rickets. DESIGN: A household-level, case-control study was conducted in a rickets-endemic area, Chakaria, with planned comparisons between households with one or more rachitic child and neighboring households with no affected children. SETTING: A rickets-endemic area of southeastern Bangladesh, Chakaria. SUBJECTS AND METHODS: An interview-based survey was conducted in six villages in Chakaria with 199 households with at least one child showing physical signs consistent with rickets and 281 households with no affected children. RESULTS: Households with rachitic children in Chakaria had more children, more pregnant or lactating women, and fewer adults than unaffected households in that community. Affected households tended to rely on farming for their livelihood and tended to have less economic activity as indicated by less outstanding debt than their neighbors. Households with rickets were at significantly greater risk of pneumonia than were other households. Calcium undernutrition was severe and widespread in Chakaria due to a food system that offered very little of the element in accessible forms. Household diets were based on cereals and starchy vegetables. Rice and fish constituted the major source of calcium for most households, although dairy products, when used, were very important calcium sources, particularly for young children. In fact, the use of dairy products was the only household choice that led to substantial increases in the calcium intakes of children, and households that used dairy products tended to show increased calcium intakes for all of their members. CONCLUSIONS: The risk of a Chakarian household having a child with rickets appeared to be related to its economic status. Although this might be expected to be manifest as limitations in food access and/or use, rickets households failed to show a dietary pattern associated with rickets. Calcium undernutrition was prevalent and, thus, would appear to be a predisposing factor for rickets; however, calcium undernutrition was prevalent in Chakarian households with and without rickets. Therefore, it is probable that another precipitating factor(s) play a role(s) in the etiology of rickets in Chakaria.

Adolescent↗
PubMed2005

A systematic review of nutritional rickets in Ethiopia: status and prospects.

BACKGROUND: Nutritional rickets contributes to the high burden of illness and death among Ethiopian children below 5 years of age. Lack of adequate information appears to have negatively influenced the impact of prevention and treatment programs. OBJECTIVES: The objective of this systematic review is to review existing body of knowledge about nutritional rickets in Ethiopia and develop recommendations that will guide development of strategies for effective interventions and research. METHODS: Published and unpublished information on nutritional rickets in Ethiopia was collected systematically. The information was critically reviewed and discussed in the context of regional and global situation. RESULTS: The major cause of nutritional rickets in Ethiopian children is lack of exposure to sunshine and/or inadequate intake of vitamin D. Lack of awareness and traditional beliefs are major causes for not exposing infants to sunshine. The disease is associated with poor socioeconomic status, low birth weight, protein-energy malnutrition and common childhood infections. Severe form of rickets is commonly seen at about 18 months of age. Rickets predisposes Ethiopian children to pneumonia. Diagnostic criteria used in most studies include two or more clinical signs and a characteristic radiological or biochemical abnormality. There are critical gaps in our knowledge about the epidemiology, ecology, and potentially effective interventions to prevent and treat rickets in Ethiopian children. CONCLUSION: Most of the studies on nutritional rickets in Ethiopia have been conducted in hospital settings. There is a need for well designed epidemiological and ecological studies. The biologic basis for the striking association between PEM and active rickets seen in Ethiopia needs to be determined The role of calcium deficiency, the part played by genetic factors, the nature of the association between the duration of breastfeeding and rickets, and the role of complimentary feeds in Ethiopian children need to be explored. Studies are required to determine the amount of sunshine required to prevent rickets in Ethiopian infants. Studies are required to establish criteria for the diagnosis of clinical and sub clinical rickets, particularly in malnourished children. Prevention programs need to be pursued consistently and systematically and treatment options, including the single massive dose of vitamin D, need to be re-evaluated and optimal mode of treatment determined.

Child Nutrition Disorders↗
PubMed2006

Rickets: not a disease of the past.

Rickets develops when growing bones fail to mineralize. In most cases, the diagnosis is established with a thorough history and physical examination and confirmed by laboratory evaluation. Nutritional rickets can be caused by inadequate intake of nutrients (vitamin D in particular); however, it is not uncommon in dark-skinned children who have limited sun exposure and in infants who are breastfed exclusively. Vitamin D-dependent rickets, type I results from abnormalities in the gene coding for 25(OH)D3-1-alpha-hydroxylase, and type II results from defective vitamin D receptors. The vitamin D-resistant types are familial hypophosphatemic rickets and hereditary hypophosphatemic rickets with hypercalciuria. Other causes of rickets include renal disease, medications, and malabsorption syndromes. Nutritional rickets is treated by replacing the deficient nutrient. Mothers who breastfeed exclusively need to be informed of the recommendation to give their infants vitamin D supplements beginning in the first two months of life to prevent nutritional rickets. Vitamin D-dependent rickets, type I is treated with vitamin D; management of type II is more challenging. Familial hypophosphatemic rickets is treated with phosphorus and vitamin D, whereas hereditary hypophosphatemic rickets with hypercalciuria is treated with phosphorus alone. Families with inherited rickets may seek genetic counseling. The aim of early diagnosis and treatment is to resolve biochemical derangements and prevent complications such as severe deformities that may require surgical intervention.

Breast Feeding↗
PubMed2004

Nutritional rickets in ichthyosis and response to calcipotriene.

Nutritional rickets has occasionally been described in children with lamellar ichthyosis, but their vitamin D endocrine status has not been described. We report 3 cases of vitamin D-deficiency rickets associated with ichthyosis in African children. A 13-month-old Nigerian boy with lamellar ichthyosis had rib beading, elevated alkaline phosphatase, and rachitic changes on radiographs. His rickets did not resolve with calcium therapy, and his 25-hydroxyvitamin D level was low. His rickets resolved with parenteral vitamin D treatment, but his skin did not improve. Topical 0.005% calcipotriene (an analog of 1,25-dihydroxyvitamin D that has been useful in treating adults with psoriasis) was similarly ineffective in improving the child's skin condition. An 8-year-old Nigerian boy with life-long skin findings consistent with lamellar ichthyosis had windswept deformity of the legs with rib beading and enlargement of the wrists and ankles. Radiographs showed active rickets, and the boy had an elevated alkaline phosphatase level and a decreased calcium level. Before knowing that his 25-hydroxyvitamin D level was low, he was treated with calcium and showed radiologic improvement. The skin did not improve with resolution of the rickets but did improve with unilateral topical application of 0.005% calcipotriene. A 7-year-old South African girl presented with progressive windswept deformities of the legs and a 4-year history of skin disease (and a skin biopsy consistent with X-linked ichthyosis). Radiographs and biochemical data confirmed active rickets. Her rickets improved dramatically with vitamin D treatment. Thus, 3 African children with ichthyosis developed vitamin D-deficiency rickets, probably because of a combination of impaired skin production and sunlight avoidance. This is consistent with previous findings of hypovitaminosis D in adults with ichthyosis and other disorders of keratinization. Measurement of 25-hydroxyvitamin D may be indicated in children with ichthyosis to identify those at risk for vitamin D-deficiency rickets, because it is possible that the cutaneous synthesis of vitamin D in such children is impaired. Although the ichthyosis did not improve with resolution of vitamin D deficiency and rickets, 1 of 2 children treated with topical calcipotriene showed improvement in the treated areas of skin. Calcipotriene does not seem to be effective in reversing systemic vitamin D deficiency but can be effective in improving the severity of skin disease in children with ichthyosis.

Administration, Cutaneous↗
PubMed2005

Reemerging nutritional rickets: a historical perspective.

Recent case reports highlight the resurgence of rickets in certain groups of breastfed infants. Infants residing in the North, irrespective of skin color, and dark-skinned African American infants residing anywhere in the United States are most vulnerable to nutritional rickets if they are exclusively breastfed past age 6 months without vitamin D supplementation. At the turn of the 20th century, rickets was nearly universal among African American infants living in the North. The discovery of vitamin D, the initiation of public health campaigns to fortify infant foods with vitamin D, and the supplementation of vitamin D to breastfed infants were responsible for overcoming the rickets scourge. We review a classic nutritional study by Alfred F. Hess, one of the greatest clinical nutritional researchers of the early 20th century, in the context of the resurgence of rickets, especially among dark-skinned infants. The Columbus Hill district, a black community of New York, NY, served as the setting for the study. Sixty-five infants (aged 1-17 months) entered a 6-month open-label trial of daily cod liver oil therapy. Participants were assessed for signs of rickets at recruitment and at 2, 4, and 6 months. Cod liver oil prevented the development of rickets in 34 (92%) of 37 infants treated for 6 months and in 7 (58%) of 12 treated for 4 months. Of the 16 infants who did not take the prescribed treatment, rickets progressed unremittingly in 15. Hess translated his success into a public health campaign leading to the development of the first rickets clinic in 1917. This was the first step in the conquest of the rickets epidemic of the early 20th century.

Black or African American↗
PubMed2006

Association of swaddling, rickets onset and bone properties in children in Ulaanbaatar, Mongolia.

OBJECTIVES: To examine the influence of duration of completely or partially wrapped swaddling on rickets onset and bone properties in children of school age. STUDY DESIGN: Case-control study. METHODS: Subjects were 73 children aged 7-10 years with a history of rickets (cases) and 70 children with no history of rickets (controls) in Ulaanbaatar, Mongolia. The periods of completely and partially wrapped swaddling, rickets onset and age-standardized mid-tibial cortical speed of sound (TCSOS) were examined. The associations between swaddling duration and rickets onset and that between swaddling duration and TCSOS were analysed. RESULTS: All except one control child were completely wrapped from the first month after birth. The durations of completely wrapped and partially wrapped swaddling were similar among cases (3.6 and 4.7 months) and controls (3.1 and 4.4 months) (P=0.42 and P=0.65, respectively). Standardized TCSOS values of cases and controls were -0.572 and -0.038, respectively (P=0.06). The duration of swaddling did not show associations with rickets onset and standardized TCSOS among both cases and controls. Standardized TCSOS of cases with skeletal deformities at examination (-1.467, n=18) was lower than that of cases without skeletal deformities (-0.280, n=55) (P<0.01) and controls (-0.038, n=69) (P<0.001). CONCLUSIONS: The practice of swaddling itself neither influences rickets onset nor bone properties in school-aged children in Ulaanbaatar. Bone properties of school-aged children who had suffered from rickets and with skeletal deformities were poorer than those in children without skeletal deformities and children without a history of rickets. Prevention of persistent skeletal deformities among the children who have suffered from rickets is critical to promote healthy bone development in Mongolia.

Case-Control Studies↗
PubMed2003

Vitamin D, cod-liver oil, sunlight, and rickets: a historical perspective.

Rickets, a disease of vitamin D deficiency, is rarely confronted by the practicing pediatrician in the United States today. At the turn of the 20th century, rickets was rampant among the poor children living in the industrialized and polluted northern cities of the United States. With the discovery of vitamin D and the delineation of the anti-rachitic properties of cod-liver oil by the 1930s, it became possible to not only treat but also eradicate rickets in the United States. Rickets was a common disease in 17th century England. Frances Glisson's treatise on rickets published in 1650, a glorious contribution to English medicine, described the clinical and anatomic features of rickets in great detail. The exact etiology of rickets had been elusive until the 1920s. During the Glissonian era, rickets was a mysterious disease. By the late 19th and early 20th century, faulty diet or faulty environment (poor hygiene, lack of fresh air and sunshine) or lack of exercise was implicated in its etiology. Animal experiments, appreciation of folklore advocating the benefits of cod-liver oil, and the geographical association of rickets to lack of sunshine were all relevant factors in the advancement of knowledge in the conquest of this malady. In this article, the history of rickets pertaining to the discovery of vitamin D, cod-liver oil, and sunlight is reviewed.

Animals↗
PubMed2003

[Association of the vitamin D receptor gene start codon polymorphism with vitamin D deficiency rickets].

OBJECTIVE: Vitamin D deficiency rickets often causes growth retardation, impaired bone formation and hypocalcemia in children. It is well known that rickets is mainly caused by vitamin D deficiency, but whether there is hereditary susceptibility of children to develop vitamin D deficiency rickets is unknown. Vitamin D receptor (VDR) gene has been used as one of genetic markers in studying the metabolic diseases of bone. The present study aimed to explore the hereditary susceptibility of children to develop rickets through studying the association between VDR gene start codon polymorphism and vitamin D deficiency rickets, METHODS: The subjects were selected from Kunming city, every subject was of Han ethnic group. The subjects were composed of two groups, the patient group consisted of 48 children with active vitamin D deficiency rickets which was diagnosed clinically and confirmed radiologically; the control group was composed of 92 normal children. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), DNA sequence analysis and genetic analysis methods were used. A restriction fragment length polymorphism in the start codon of VDR gene (FokI) was tested in both groups. RESULTS: VDR gene start codon polymorphism was tested successfully for every subject. Frequencies of FF, Ff and ff genotypes were 46%, 33% and 21% in the rickets group, and 22%, 52% and 26% in the control group, respectively. A significant difference was found in the frequency distribution of VDR genotype between two groups (chi(2) = 8.912, P = 0.012). In the patient group, Ff and ff genotypes were less common than control group, but the FF genotype was more common than control group (OR = 3.046), indicating that FF genotype may be significantly associated with vitamin D deficiency rickets. Moreover, VDR allele frequencies of FokI polymorphism also showed significant difference between the two groups (chi(2) = 5.451, P = 0.020), F alleles were more common in patient group than in control group. DNA sequence analysis identified that the start codon of F allele was mutated from ATG to ACG. CONCLUSION: There is an association between VDR gene start codon polymorphism and vitamin D deficiency rickets. This study suggested the possibility that VDR gene polymorphism might be important in determining an individual's susceptibility to development of vitamin D deficiency rickets.

Base Sequence↗
PubMed1995

Rickets in black children beyond infancy in Natal.

OBJECTIVE: To determine the clinical spectrum of rickets among black children admitted to King Edward VIII Hospital, Durban. DESIGN: Prospective study of black children with rickets beyond infancy. SETTING: Hospital-based population; King Edward VIII Hospital, Durban. PARTICIPANTS: A total of 37 patients, aged 1-12 years, were recruited over a 3-year period. None had been on vitamin D or calcium supplementation prior to investigation. OUTCOME MEASURES: Rickets was diagnosed clinically, radiologically and biochemically (by a raised alkaline phosphatase value of > 350 IU). Gastro-intestinal, hepatic and renal glomerular causes were excluded in all patients using standard clinical and laboratory criteria. RESULTS: Twenty-three patients were diagnosed as having privational rickets. Nine had 25-hydroxyvitamin D (25-OHD) levels of < 10 ng/ml while 14 had levels within the normal range and were suspected of having dietary calcium deficiency. Ten had a phosphopenic variety of rickets; the remaining 4 had healing or healed rickets on the basis of radiological assessment and normal biochemical values. Pain together with difficulty in walking and bowing of the lower limbs were the main reasons for presentation. The main clinical findings were thickened wrists and ankles and rickety rosary (100%), stunting (85%), anterior bowing of lower limbs (70%) and genu valgum (65%). The calcium and vitamin D deficiency group showed a much better clinical, biochemical and radiological response to therapy than the phosphopenic group on follow-up (18 patients). CONCLUSION: This is the first substantial report on rickets in the older child in Natal, which extends the findings from Transvaal, thereby establishing a recognisable pattern of rickets beyond infancy in South Africa. It draws attention to the common clinical presentations which may alert health professionals to the presence of this problem. This report demonstrates that the two commonest types are privational rickets (due to calcium and/or vitamin D deficiency) and phosphopenic rickets.

Calcium, Dietary↗
PubMed2004

The frequency of nutritional rickets among hospitalized infants and its relation to respiratory diseases.

This case control study was conducted to determine the frequency of nutritional rickets among hospitalized infants and to assess their relation to respiratory diseases. All infants between the age of 3 months and 2 years admitted to the pediatric ward of Queen Alia Military Hospital during the period February-October 2001 were examined and investigated to rule out nutritional rickets. Children admitted for the first time to hospital for acute illnesses were only included in the study. A special data collection sheet was designed for this study which includes information on the age, sex, causes of admission, family size, the rank of the child in the family, family monthly income, outdoor clothing habit of the mother, and the mode of feeding. Data were collected from the infant charts and/or by interviewing the child's mother or guardian. Clinical signs of rickets were also recorded, including rosary beads, craniotabes, wide anterior fontanel, delayed dentition, widening of epiphysis, bowing of the legs, and double malulous. Blood sample was collected for calcium, phosphorus, alkaline phosphatase, and hemoglobin level. Those infants with any clinical sign of rickets and/or abnormal chemical results had a wrist X-ray to confirm the diagnosis of rickets. The rachitic group (cases) was compared for statistical significance with the remaining non-rachitic infants (controls) for the data collected. Rachitic infants received intramuscular 600,000 IU of vitamin D; a follow-up wrist X-ray and blood sample for calcium, phosphorus and alkaline phosphatase was arranged 3 weeks later. Forty-seven infants (10.6 per cent) out of the 443 included in the study were found to have nutritional rickets. Forty (85.1 per cent) of the rachitic infants were admitted due to lower respiratory tract diseases compared with 30 per cent of the control group and the difference was statistically significant (p < 0.01). Duration of hospital stay in the rachitic infants was also significantly more prolonged than the non-rachitic control group (9.5 days vs. 7.4 days, p = 0.002). Rachitic infants were breastfed in 82.9 per cent, ranked second or more in the family in 87.2 per cent, and had mothers who wore head cover outdoors in 80.8 per cent compared with 60.8, 40.1, and 60.3 per cent, respectively, in the non-rachitic group (p < 0.01). High alkaline phosphatase, hypocalcemia, hypophosphatemia, and anemia was found in 100, 19, 50, and 78.7 per cent, respectively, in the rachitic group compared with 9.8, 2, 1.2, and 43.7 per cent, respectively, in the control group (p < 0.001). Nutritional rickets seems to be a common problem among infants in Jordan. Further studies at national level are needed to determine the prevalence of rickets in Jordan. Rachitic infants are commonly hospitalized due to lower respiratory tract infections, thus there is a high index of suspicion for rickets among hospitalized infants with lower respiratory tract diseases.

Age Distribution↗
PubMed2002

The usefulness of clinical features to identify active rickets.

To develop a clinical prediction rule that could accurately identify children with active rickets in countries where nutritional rickets is common, we prospectively recorded clinical features in 736 Nigerian children aged 18 months and older presenting with leg deformities or inability to walk. We scored radiographs of the wrists and knees for active rickets of the growth plates. Sensitivities and specificities of clinical variables for radiographically active rickets were calculated and, using logistic regression, we derived a clinical prediction rule. The prediction rule was tested in a validation set of 89 children. Wrists and costochondral enlargement were the clinical signs with the best combination of sensitivity (72% and 76%, respectively) and specificity (81% and 64%, respectively) for active rickets. Age < 5 years, height-for-age Z-score < -2, leg pain during walking, wrist enlargement and costochondral enlargement were independently predictive of active rickets (p < 0.01 for each in multivariate model). In the validation set, any three of these clinical features accurately identified 87% of children with active rickets, whereas only 24% of those without active rickets had three or more features. We conclude that clinical features can be used to identify children with active rickets.

Age Factors↗
PubMed2006

Nutritional rickets around the world: causes and future directions.

INTRODUCTION: Nutritional rickets has been described from at least 59 countries in the last 20 years. Its spectrum of causes differs in different regions of the world. METHODS: We conducted a systematic review of articles on nutritional rickets from various geographical regions published in the last 20 years. We extracted information about the prevalence and causes of rickets. RESULTS: Calcium deficiency is the major cause of rickets in Africa and some parts of tropical Asia, but is being recognised increasingly in other parts of the world. A resurgence of vitamin D deficiency has been observed in North America and Europe. Vitamin D-deficiency rickets usually presents in the 1st 18 months of life, whereas calcium deficiency typically presents after weaning and often after the 2nd year. Few studies of rickets in developing countries report values of 25(OH)D to permit distinguishing vitamin D from calcium deficiency. CONCLUSIONS: Rickets exists along a spectrum ranging from isolated vitamin D deficiency to isolated calcium deficiency. Along the spectrum, it is likely that relative deficiencies of calcium and vitamin D interact with genetic and/or environmental factors to stimulate the development of rickets. Vitamin D supplementation alone might not prevent or treat rickets in populations with limited calcium intake.

Africa↗
PubMed1994

Factors affecting the morbidity of vitamin D deficiency rickets and primary protection.

Rickets was investigated in 860 children in the 3 to 36 month age group in 21 villages attached to Sinik Health Centre, in northeastern Turkey. The blood calcium, phosphorus and alkaline phosphatase levels of suspect cases were determined following examination and wrist x-rays taken. The prevalence of cross-sectional rickets was determined, in the cohort group formed by removing the rickets cases (to the first group, advice was not given; to the second, 400 IU of vitamin D) and its incidence determined. The prevalence of rickets was calculated as 9.8% with no distinction observed between males and females (P > 0.05). It is higher in children in the 3-6 month group (23.97%) (P < 0.05); exposed rarely to the sun (P < 0.001); without fish in diet (P < 0.01); born to mother under 18 years old (P < 0.001); with a mother not using contraception (P < 0.01). The prevalence of acute respiratory infections (ARI) was calculated as 47.62% and 35.70% (P < 0.05) in children with and without rickets, respectively. The prevalence of enteritis was calculated as 29.76% and 18.43% (P < 0.05) in children with rickets and without rickets, respectively. Rickets was not seen where 400 IU of vitamin D was administered, while incidence for the twelve-month period was calculated as 3.8% in the other group. Combatting rickets is important in developing countries where deaths under five years are largely due to ARI and enteritis.

Causality↗
PubMed1987

Field rickets in turkeys: relationship to vitamin D.

Thirty-two outbreaks of leg disorders in turkeys were investigated during 1981-1985. Among them, 22 were characterized by a low percentage of bone ash and were considered as field rickets. Most of the field rickets cases exhibited reduced plasma calcium and inorganic phosphorus. Plasma 25-hydroxyvitamin D3 and intestinal calcium-binding protein were lower in the rachitic than in normal turkeys. These symptoms are typical of rickets resulting from vitamin D deficiency. The vitamin D3 equivalence of a diet that had been fed during field rickets outbreaks was assayed biologically and found to be 111 micrograms/kg diet, about eight times the minimal requirement. In two other cases no symptoms of rickets were observed in turkeys fed diets that had been previously consumed during field rickets outbreaks. The results indicate that in some cases of field rickets there was no involvement of dietary factors and confirm a previous suggestion that field rickets may result from defects in metabolism of vitamin D3, or in its expression.

Animals↗
PubMed2001

Nutritional rickets in young Nigerian children in the Sahel savanna.

OBJECTIVES: To determine the prevalence of clinical and biochemical rickets in an under-five out-patient population, relate the prevalence of biochemical rickets (BR) to the sociocultural characteristics of families and determine the response of nutritional rickets to vitamin D therapy. DESIGN: Prospective cross-sectional and retrospective case-series surveys. SETTING: Paediatric general out-patient and consultant clinics. SUBJECTS: One hundred and ninety eight out-patients and twenty two patients aged >1 to 60 months treated for nutritional rickets. INTERVENTIONS: Clinical examination, interview with mothers and determination of biochemical abnormalities of under-fives and management of patients with rickets using stosstherapy. MAIN OUTCOME MEASURES: Prevalence of BR and response to stosstherapy. RESULTS: Eight (4%) patients in the survey had clinical and biochemical rickets while 33 (17%) had biochemical rickets only; 92 (47%) other patients had isolated hypocalcaemia and/or hypophosphataemia. The prevalence of BR was higher in males (p <0.05), and increased with age (p <0.001). The prevalence was lower in families who were indigenous to the area (p <0.05), children of Moslem families (p <0.05) and children whose mothers were full-time housewives, unskilled or traders (p <0.01), and who lacked any formal western education (p = 0.157). Three of the seven evaluable patients who received stosstherapy responded late. CONCLUSION: The results support the hypothesis that deficiency or reduced availability of dietary calcium may be of at least equal importance with vitamin D deficiency in the aetiology of nutritional rickets in the Sahel savanna.

Calcium, Dietary↗
PubMed2002

Primary care pediatrician knowledge of nutritional rickets.

OBJECTIVE: The purpose of this study is to determine primary care pediatricians' level of awareness in the diagnosis and management of rickets. The information will be useful in assessing the need for provider education related to appropriate advice regarding vitamin D supplementation for infants. STUDY DESIGN: A one-page questionnaire was sent to a sample of 510 pediatricians in states surrounding the Great Lakes. These physicians were chosen depending based on practice listings from local telephone directories. Results were analyzed using the Chi-squared (chi2) test. RESULTS: Of the 248 respondents, 43% (n = 105) had encountered at least one actual or suspected case of rickets in the past five years. Sixty-nine percent of respondents chose vitamin D deficiency rickets-specific diagnostic tests, 24% chose rickets-specific tests, and 7% chose tests that are not specific to diagnosing rickets. Ninety-four percent of respondents chose treatments specific to vitamin D deficiency rickets, while 6% chose treatments not specific to rickets. CONCLUSION: Most primary care pediatricians from major metropolitan areas in the Great Lakes region are aware of the appropriate methods to diagnose and treat vitamin D-deficiency rickets. However, educational interventions are still necessary for both physicians and parents to promote widespread use of vitamin D supplementation in all breastfed infants.

Adult↗
PubMed2004

Rickets in the Dairy State.

BACKGROUND: Nutritional vitamin D deficiency rickets occurs when children do not receive adequate vitamin D, which can be obtained from diet or manufactured in the skin when there is adequate sun exposure. A number of reports have described cases of vitamin D deficiency rickets in breastfed infants, but the public health significance of this problem in Wisconsin is unknown. OBJECTIVES: Our objectives were to identify cases of vitamin D deficiency rickets in Wisconsin infants and to determine the percentage of these infants participating in the Wisconsin Women, Infant and Children (WIC) program. METHODS: All cases of rickets due to nutritional vitamin D deficiency seen at Children's Hospital of Wisconsin or its associated outpatient clinics were identified by retrospective chart review. Data collected included date of birth, age at presentation, race, clinical presentation, diet history, history of vitamin supplementation, x-ray findings, and biochemical studies. The children with nutritional vitamin D deficiency rickets were cross-referenced with the Wisconsin WIC database. RESULTS: Fifty-one definite cases of nutritional vitamin D deficiency rickets were identified. Skeletal deformities, failure to thrive, fractures, seizures, incidental lab finding, tetany, and refusal to walk were the most common reasons for identifying rickets. All of the children were breastfed and did not receive vitamin supplementation. The infants had a mean age of 13.6 months and 46 (90%) were African American. Thirty-seven out of 51 children (73%) were enrolled in the Wisconsin WIC program. CONCLUSION: Vitamin D deficiency nutritional rickets is an important public health problem in Wisconsin. The Wisconsin WIC program may be an important site for intervention strategies.

Female↗