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At least 19 recordsLinked to original sources
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↗
PubMed1976

Florid and subclinical rickets among immigrant children in Glasgow.

200 Asian 300 African, Chinese, or Scottish children were examined for clinical, biochemical, and radiological evidence of vitamin-D deficiency. Among the Asians there were 10 with florid rickets and 15 with subclinical rickets. Among the African, Chinese, and Scottish children there were no cases of florid rickets and only 7 cases of subclinical rickets (3 African, 3 Chinese, and 1 Scottish). Loss of metaphyseal definition is considered to be the radiological pattern of minimal active rickets and metaphyseal bands to represent the healing stage. Serum 25-hydroxycholecalciferol concentrations were low in clinical and subclinical minimal active rickets although there was some overlap with the wide range found in the "normal" group. Elevated serum-alkaline-phosphatase levels alone should not be regarded as indicating vitamin-D deficiency. The continuing prevalence of rickets in Asian children and in particular among schoolchildren warrants immediate action, which is long overdue.

Africa↗
PubMed1975

[Ten years' daily prophylaxis against rickets--review and outlook (author's transl)].

Ten years of experience with daily prophylaxis of rickets brought about isolated knowledge which corrected old mistakes and demands a revision of older attitudes towards the usual prophylaxis. Prophylaxis of vitamin D according to the most modern and reliable knowledge in the best way promotes the growth and mineralisation of the skeleton with dosages of 400 to 800 I.U. smaller or higher dosages are disadvantageous. By observing the above given dosage, rickets and hypercalcaemia are rare and only conceivable under special pathological conditions. The diagnosis of beginning rickets must be well known, otherwise unspecific symptoms of rickets may induce the administration of unnecessarily high amounts of vitamin D. The symptoms of rickets show a gradual increase: the increase of serum alkaline phosphatase precedes the clinical and radiological symptoms. The reliable radiographic deformities of the hand can first be seen at the Ulna, then at the Radius and later at the secondary centers of Metacarpals. Among the relatively reliable clinical symptoms there its first the rosary later the Marfan-sign and eventually the deformation of the long bones. For infants protected by vitamin D, craniotabes as a sign of rickets is completely unreliable as well as the Harrison grooves and rachitic kyphosis. If one observes all these rules and rachitic kyphosis. If one observes all these rules and criterions vitamin D is as reliable in the prophylaxis as in the therapy of vitamin D deficiency rickets.

Germany, West↗
PubMed1976

Diets and living conditions of Asian boys in Coventry with and without signs of rickets.

1. The diets and living conditions of nin Asian boys with biochemical, and in most instances also radiological, signs of rickets were compared with those of nine other boys who appeared to be normal. The groups were matched according to age, religion, place of father's origin and boy's own place of birth. 2. There were no outstanding differences between the diets of the boys with, and of those without signs of rickets. All had adequate to high calcium intakes. Most of the boys had low intakes of vitamin D, and those withsigns of rickets generally had lower intakes than the normal boys. The food tables used for making the calculations of vitamin D intakes report the amount of the vitamin in the lipid fraction of milk. If it proves to be true that most of the vitamin D activity of milk is in the aqueous fraction, the boys would have been getting considerably more vitamin D than the results suggested, and their average intake may have been about 3-5mug/d. 3. It was not possible to make any quantitative measure of the exposure of the boys to sunlight. All Asian boys studied appeared to have their bodies more completely covered than British or West Indian boys. 4. The problem of why nine boys had signs of rickets and nine had none has not been solved. It is suggested that those with signs of rickets may have had higher requirements for vitamin D than others. When the intake of vitamin D is low and exposure to sunlight is minimal, those with high requirements will be the ones to develop signs of rickets.

Adolescent↗
PubMed1976

Vitamin D deficiency and rickets.

Classical experimental rickets in the rat is a dual deficiency, resulting from both phosphate and vitamin D deficiency, with many of the features of rickets reproducible by simple phosphorus deficiency. Simple vitamin D deficiency differs markedly from experimental rickets, with only the absence of the vitamin D-dependent calcium-binding proteins common to both situations. The expression at the bone level of vitamin D deficiency differs in the two conditions, with rickets leading to profound structural and metabolic changes, whereas simple vitamin deficiency primarily compromises the regulatory function of bone, without obvious structural alterations. It is proposed that human nutritional rickets is the result of a nutritional vitamin D deficiency that aggravates the expression of a pre-existing metabolic defect in phosphate transport. Simple nutritional vitamin D deficiency, unaccompanied by rickets, may occur, but probably has always been rare.

Animals↗
PubMed1978

Case of tumour rickets.

A 10-year-old boy, with widespread soft tissue tumours of bone, developed hypophosphataemic rickets due to impaired renal tubular reabsorption of phosphate. Biopsy of the largest tumour showed a nonosteogenic fibroma. We believe this boy is another example of 'tumour rickets', as other causes of rickets were excluded clinically and biochemically. Cases of rickets or osteomalacia associated with a tumour, have generally been reported to be cured by surgical removal of the tumour, implicating it as the cause of rickets or osteomalacia. Owing to the large number of tumours in this boy, surgical removal was not possible, and he required large doses of vitamin D, together with oral phosphate, before his rickets healed. It is suggested that the tumour produces a phosphaturic hormone.

Bone Neoplasms↗
PubMed1976

Two types of nutritional rickets in infants.

In 100 infants with nutritional rickets, i.e., responsive to vitamin D therapy, we found a close inverse relationship between serum phosphorus, on the one hand, and serum alkaline phosphatase and the presence of radiological signs of rickets, on the other. There was no correlation between serum calcium and the severity of bone lesions. It is concluded that hypophosphatemia but not hypocalcemia is typical of rickets. Since hypophosphatemia and rickets can be produced experimentally by phosphate deficiency alone, we suggest our infants can be divided into two groups, one with true vitamin D deficiency that leads to hypocalcemia and no or mild bone lesions, and one with primary phosphate deficiency, resulting perhaps from a defect in phosphate transport, which leads to rickets and hypophosphatemia.

Age Factors↗
PubMed1977

Vitamin D-resistant rickets associated with epidermal nevus syndrome: demonstration of a phosphaturic substance in the dermal lesions.

A 5-year-old boy was found to have severe rickets in association with hyperpigmented, linear, verrucous, epidermal tumors, typical of the epidermal nevus syndrome. Normocalcemia (9.6 mg/dl), hypophosphatemia (2.0 mg/dl), elevated serum alkaline phosphatase concentration (313 IU), decreased renal tubular reabsorption of phosphorus (35%), radiologic evidence of rickets, and lack of response to usual therapeutic doses of vitamin D suggested hypophosphatemic vitamin D-resistant rickets. Therapy with vitamin D in doses to 750,000 IU and oral phosphate, 2.0 gm/day, failed to induce healing of the rickets. A subtotal parathyroidectomy performed when the patient was 9 years old was also without effect. When he was 12 years old several fibroangiomas on the face and left lower limb were excised. Within three months all biochemical abnormalities resolved and radiologic evidence of healing was observed. A portion of excised tissue was homogenized and injection of the supernate into a 6-week-old puppy induced excessive phosphaturia. The data suggest that the rickets was induced by a phosphaturic substance extractable from the tumors.

Calcium↗
PubMed1976

Origin, diagnosis, and treatment of the dental manifestations of vitamin D-resistant rickets: review of the literature and report of case.

Previous discussions center on early diagnosis, initial treatment, and follow-up therapy for the patient with vitamin D-resistant rickets. Both the medical and dental aspects of treatment for these patients has a long-range effect on the normal developmental patterns. Although treatment is begun at an early age, some rachitic skeletal effects such as minor bowing of the legs and bossing of the skull will invariably be noticed. In patients with controlled rickets the alveolar processes undergo normal development, with apparent normal dental eruption. The poor development and calcification of the alveolus seen in the untreated patient leads to loss of the lamina dura and periodontal ligament of the teeth. Patients with resistant rickets possess a functional dentition, although not without inherent defects. Various degrees of fracture and attrition of enamel can be seen, and hypoplasia of dentin is nearly a universal result. Defects extending to the dentinoenamel junction have been shown in repeated cases. Cementum, because of its close relationship with dentin calcification, also appears abnormal. Pulp tissue may undergo abberations of physiology in resistant rickets, although further work in this respect is needed. With respect to the possible dental pathoses seen in this disease, the dental history of the patient with resistant rickets discussed in this report showed that several of the deciduous teeth, possibly the mandibular left second premolar and right first molar, and definitely the maxillary right second premolar and canine and the mandibular left canine had all undergone pulpal degeneration of apparently unknown causation. In the maxillary right second premolar and the mandibular left canine, enamel fractures were clinically and radiographically apparent. However, the maxillary right canine originally had an acute abscess with no defects other than normal, minimal wear facets. No causative factor for its necrosis could be found. Overt enamel fractures in the maxillary right second premolar and the mandibular left canine may have led to microexposures of the pulp with subsequent bacterial pulpal contamination. Suppuration present in several of the pulps when first entered during endodontic treatment, as well as chronic fistulas in several areas, support the conclusion that contamination by some means does indeed occur.

Abscess↗
PubMed1991

Mineral content of different areas of human dentin in hypophosphataemic vitamin D-resistant rickets.

Calcium, phosphorus, fluoride, sodium, magnesium and zinc estimations were carried out on teeth from a patient with hypophosphataemic vitamin D-resistant rickets (HVDRR) and from a patient with acquired rickets with the aim of determining differences in the composition of dentine in these two types of rickets. Normal deciduous teeth served as controls. Mineral analyses were carried out using an electron probe micro-analyser after carefully polishing the hemisected specimens. After the analyses the specimens were coated with gold-palladium for more detailed SEM studies. The Ca, P, F and Zn contents of the calcospherites were normal, while there was more Na and less Mg in the dentine of HVDRR teeth than of controls. The significance of this remains unexplained. The mineral content of the interglobular spaces was very limited, but there was more Zn in these than in other parts of the HVDRR teeth, in the acquired rickets teeth or in the control teeth. The excess of Zn in the interglobular spaces is thought to have an effect on the mineralisation process in HVDRR teeth. The globular nature of HVDRR teeth is thought to be genetically controlled and the result of a reduction in the number of calcification nuclei. The globular nature of the HVDRR teeth was not due to lack of Ca and P, as the serum levels of these minerals were maintained within normal limits during tooth development by controlled phosphate supplementation. Because in acquired rickets the globules were seen at the developmental stage that the teeth had reached when the nutritional disturbance occurred, the fault in mineralisation is thought to be different from that in HVDRR teeth.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1977

Seizures and demineralization of the skull. A diagnostic presentation of rickets.

We present four infants with seizures, and one without seizures, in whom the diagnosis of rickets was first suggested because of a demineralized skull. A review of the skull films in all of our patients with rickets showed that 20 of 25 (80%) showed demineralization. Demineralization of the skull is a common and important feature of rickets. Furthermore, as demonstrated by our cases, it may be the first clue to the presence of rickets in certain infants.

Alveolar Process↗
PubMed1976

Rickets in low birth weight infants receiving total parenteral nutrition.

Development of rickets in association with parenteral nutrition is described in four premature infants having gestational ages of 26-31 wk. In the first two infants there was a documented deficiency of vitamin D, but in the second two adequate supplementation was achieved. Vitamin D, whose primary action is to facilitate intestinal absorption of calcium, may also be a hormone of prime necessity in infant bone formation. Conversion of precursor cholecalciferol to the active form of hormone, 1,25-DHCC, requires intermediate hydroxylation by the liver. The premature infant liver may be deficient in its ability to carry out this step of metabolism, and in normal intrauterine existence the fetus may receive 1,25-DHCC, the active metabolite, from the mother. Calcium intake in these infants was far below that achieved by fetuses of comparable age in utero, even though in excess of that provided by usual premature infant oral formulas. Although calcium deficiency has not been incriminated as a cause of rickets in the past, it is possible that in very tiny premature infants rapid growth requirements lead to a relative calcium deficiency which may be manifested as uncalcified osteoid. Until the mechanism of the formation of rickets in small premature infants is clarified it is recommended that supplemental calcium and vitamin D be given to all premature infants receiving parenteral nutrition, and that periodic x-rays be obtained to detect the development of rickets.

Calcium↗
PubMed1991

Rickets in Nigerian children: a consequence of calcium malnutrition.

Eleven Nigerian children with clinically and radiologically proven rickets were assessed biochemically. The children had low or low normal concentrations of total and corrected calcium, and elevated plasma alkaline phosphatase (ALP) activity, but normal plasma phosphate concentrations. Their serum 25-hydroxyvitamin D (25-OHD) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) concentrations were not significantly different from those in controls, but the ratio of 1,25-(OH)2D to 25-OHD was significantly greater than that in controls. Parathyroid hormone (PTH) concentrations were greater in rachitic children, and there was a significant correlation between 1,25-(OH)2D and PTH concentrations. Osteocalcin concentrations in rachitic children were not significantly different from those in controls, but they were markedly elevated in the three patients with the highest 1,25-(OH)2D and PTH concentrations. One child, from whom a sample of bone (from a corrective osteotomy) was available for histological examination, showed markedly thickened osteoid seams, characteristic of rickets. All the rachitic children had a calcium intake of less than 150 mg daily. Treatment of these rachitic children with calcium gluconate (1 g/d) led to clinical, radiological, and biochemical healing of rickets. We conclude that rickets in Nigerian children is not due to vitamin D deficiency, but to a lack of calcium. This observation has implications regarding the pathogenesis, treatment, and prevention of rickets/osteomalacia in Nigeria and possibly other African and tropical countries.

Alkaline Phosphatase↗
PubMed1991

Bone mineral density of the spine and radius shaft in children with X-linked hypophosphatemic rickets (XLH).

X-linked hypophosphatemic rickets (XLH) is characterized by inadequate skeletal mineralization. The bone mineral density (BMD) of the radius shaft and the lumbar spine was determined in 13 children with XLH. Ten patients were on treatment, whereas three patients had discontinued treatment 20-32 months prior to this study. Two of them had radiological evidence of rickets. The radius shaft BMD was significantly diminished: Z score was -1.33 +/- 0.89 (P less than 0.001), while the BMD of lumbar spine was significantly augmented (Z score +1.95 +/- 1.17, P less than 0.001). A positive correlation was found between the Z scores for the BMD of the radius shaft and spine. The two patients with overt rickets had lower radius shaft BMD values and a lesser increment of BMD of the spine. The BMD deficit of cortical bone may be related to the lack of efficacy of the treatment and/or to an intrinsic defect of the bone on this disease. On the other hand, the augmented BMD of the lumbar spine might reflect the overabundance of partially mineralized osteoid. The determination of the BMD of the radius shaft by SPA was a sensitive method for detecting abnormalities of the bone mass in XLH patients under treatment without radiological signs of rickets.

Absorptiometry, Photon↗