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PubMed1981

Evidence for secondary hyperparathyroidism in the osteomalacia associated with chronic liver disease.

Previous reports have suggested that secondary hyperparathyroidism is extremely uncommon in hepatic osteomalacia. This, together with other findings, has led to suggestions that in chronic liver disease there may be selective resistance of bone to vitamin D or a specific bone mineralization defect unrelated to Vitamin D. To examine these possibilities, twenty-five patients with chronic liver disease have been studied by bone biopsy, serum calcium and inorganic phosphate, plasma 25-hydroxyvitamin D, plasma immunoreactive parathormone (iPTH), fasting urine cAMP, fasting renal tubular maximal reabsorptive capacity for phosphate (TmP/GFR) and fine grain hand x-rays. Nine of the patients had osteomalacia on bone biopsy, eight of these had subnormal levels of plasma 25-hydroxyvitamin D and the other had a borderline result. Based on the consensus of all the tests, five of these had evidence of secondary hyperparathyroidism. Plasma iPTH was higher in patients with osteomalacia than in patients without osteomalacia (P less than 0.01) or controls (P less than 0.01). Urine cAMP was higher in patients with osteomalacia than in patients without osteomalacia (P less than 0.001) or controls (P less than 0.01). TmP/GFR was significantly lower in patients with osteomalacia than in controls (P less than 0.05) but not significantly different from patients without osteomalacia. The findings of this study indicate that hyperparathyroidism occurs in a substantial proportion of patients with the osteomalacia of chronic liver disease. Moreover, osteomalacia in chronic liver disease is clearly related to reduced levels of plasma 25-hydroxyvitamin D. We conclude that hepatic osteomalacia is a vitamin D deficiency state and there is no need to suggest an unusual aetiology.

25-Hydroxyvitamin D 2↗
PubMed1995

Osteomalacia associated with adult Fanconi's syndrome: clinical and diagnostic features.

OBJECTIVE: Osteomalacia associated with adult acquired Fanconi's syndrome is thought to result from hypophosphataemia and relative 1,25-dihydroxyvitamin D deficiency. We have followed the clinical and diagnostic features of patients with osteomalacia associated with adult Fanconi's syndrome, with particular emphasis on their responses to treatment with calcium, phosphate and vitamin D. DESIGN: Retrospective Mayo Clinic case-note review from 1975 to 1994 and prospective follow-up study, combined with literature review. PATIENTS: Eleven patients (7 male, 4 female) were identified who satisfied criteria for diagnosis of osteomalacia and adult Fanconi's syndrome. Twenty-five additional patients were identified in a literature review from 1954 to the present. METHODS: Clinical history and physical examination, serum and urine bone and mineral parameter, X-ray radiography and iliac crest bone histomorphometry. RESULTS: All patients presented with typical symptoms of osteomalacia, including lower extremity or low back bone pain, and all had fractures, pseudofractures, and/or bone demineralization on X-ray radiography. Osteomalacia and Fanconi's syndrome were diagnosed concurrently in 10 patients, whereas osteomalacia preceded diagnosis of Fanconi's syndrome by 5 years in one patient. Pre-treatment bone biopsies in 9 of the 11 patients demonstrated increased osteoid surface, volume and width. In the one patient labelled with tetracycline prior to biopsy, mineralization lag time was prolonged at 111 days (normal 19.2 +/- 1.0 days). Hypophosphataemia, inappropriately low 1,25-dihydroxyvitamin D levels, renal insufficiency, and chronic acidosis due to bicarbonate leak and uraemia, contributed to the osteomalacia in these patients. Secondary hyperparathyroidism was present in two patients. Eight of the 11 patients with osteomalacia associated with Fanconi's syndrome had monoclonal disorders, including multiple myeloma or lymphoma, many of them manifest by light-chain proteinuria. Over a mean patient follow-up period of 46 months (range 1-239 months), patients responded symptomatically to calcium, phosphate, and vitamin D replacement typically within 1-6 months. In 8 patients in whom follow-up data were available, post-treatment serum phosphate and 1,25-dihydroxyvitamin D levels improved in the setting of stable mild renal insufficiency; only one patient developed end-stage renal failure after 20 years, suggesting that these patients do not invariably progress rapidly to renal failure. CONCLUSIONS: Regardless of the underlying cause, osteomalacia associated with adult acquired Fanconi's syndrome appears to respond well to calcium, phosphate, and vitamin D replacement. These patients do not appear to necessarily require 1,25-dihydroxyvitamin D replacement.

Adult↗
PubMed1986

Pathogenesis of osteomalacia in chronic renal failure and its relationship to vitamin D.

Considerable confusion arises in defining osteomalacia in the presence of renal disease. There are no radiographic or biochemical features which satisfactorily identify all patients with osteomalacia. Histological definitions need to distinguish increased amounts of osteoid due to defective mineralisation from that due to increased bone turnover, both of which may coexist in chronic renal failure. The pathogenesis of osteomalacia in renal failure is multifactorial and not always due to defective metabolism of vitamin D. Deficient production of 25-hydroxyvitamin D may occur because of nutritional privation or urinary losses in the nephrotic syndrome, but these are rare causes of osteomalacia in patients on haemodialysis treatment. It is not clear to what extent defective production of calcitriol, characteristic of end-stage chronic renal failure is causally related to osteomalacia, in part due to uncertainties as to whether vitamin D acts directly on bone to promote mineralisation or whether its effects are mediated indirectly by modulating calcium and phosphate transport at other sites. Following the institution of renal replacement therapy, the incidence of osteomalacia varies markedly between renal units due to the skeletal retention of aluminium caused by the contamination of dialysis fluid or by the chronic ingestion of aluminium-containing phosphate binding agents. This form of osteomalacia is associated with a high risk of fracture, probably more related to depressed bone formation than to the presence of osteomalacia. Rarer causes of osteomalacia include parathyroidectomy and calcium and phosphate deficiency.

Aluminum↗
PubMed1987

Aluminium-related osteomalacia: response to reverse osmosis water treatment.

It is generally accepted that aluminium induces osteomalacia in chronic hemodialysis patients by binding to the calcification front, thereby inhibiting mineralization of osteoid. Because this form of osteomalacia is vitamin D resistant, the condition has often been assumed to be irreversible, although promising results have been achieved recently by using a chelating agent for removal of aluminium from the skeleton. In this paper we present four chronic hemodialysis patients with aluminium toxicity and histologic osteomalacia in whom the mineralization defect greatly regressed after the use of reverse osmosis treated-water for dialysis, but without further treatment. In three other patients, also with aluminium toxicity and histologic osteomalacia, similarly treated, the histological severity of the osteomalacia remained static. Those patients in whom bone mineralization status improved developed hyperparathyroidism after reverse osmosis water-treatment, whereas the static patients remained euparathyroid. The results suggest that resolution of aluminium related osteomalacia may occur with reduction in dialysis fluid aluminium, and that parathyroid hormone plays a role in the healing of aluminium related osteomalacia. The therapeutic implications are twofold: attempts to remove all traces of hyperparathyroidism may be detrimental to the bone mineralization status; and stimulation of the parathyroid glands by means of a mild reduction in dialysis fluid calcium may be of value in the management of those cases with persistent osteomalacia and low bone turnover.

Adult↗
PubMed1980

Hypophosphatemic osteomalacia: association with prostatic carcinoma.

Hypophosphatemic osteomalacia that remits after resection of a coexisting tumor has been described in 35 patients. Because the associated neoplasms have been of mesenchymal origin, it has been inferred that this tumor-induced osteomalacia syndrome is uniquely related to tumours of this derivation. However, in the present investigation we studied subjects with coincident hypophosphatemia and prostatic carcinoma to ascertain whether this endodermal malignancy causes the tumor-induced osteomalacia syndrome. The hypophosphatemic patients had renal phosphate wasting, gastrointestinal malabsorption of calcium and phosphate, and negative phosphate balance. Moreover, bone biopsies showed histomorphologic changes indicative of osteomalacia. Although widespread metastases precluded establishing the diagnosis of tumor-induced osteomalacia by resection of the tumor, a series of studied excluded alternate causes for the osteomalacia. Further, affected subjects had a normal serum concentration of 25-hydroxyvitamin D, 28.0 +/- 8.3 ng/mL, and serum 1,25-dihydroxyvitamin D levels were low, 15.0 +/- 1.0 pg/mL, characteristic of the tumor-induced osteomalacia syndrome. Thus, prostatic carcinoma, although an endodermal malignancy, may cause the tumor-induced osteomalacia syndrome.

Aged↗
PubMed2000

Use of quantitative ultrasonography in differentiating osteomalacia from osteoporosis: preliminary study.

The aim of this work was to use ultrasonographic technology to differentiate osteoporosis from osteomalacia on the basis of different patterns of the graphic trace. Three patients with osteomalacia and three with osteoporosis, all with the same lumbar spine bone mineral density, were studied. The velocity of the ultrasound beam in bone was measured by a DBM Sonic 1,200/I densitometer at the proximal phalanges of the hands in all the patients. The ultrasound beam velocity was measured when the first peak of the waveform reached a predetermined minimum amplitude value (amplitude-dependent speed of sound) as well as at the lowest point prior to the first and second peaks, before they reached the predetermined minimum amplitude value (first and second minimum speeds of sound). The graphic traces were further analyzed by Fourier analysis, and both the main frequency (f0) and the width of the peak centered in the f0 (full width at half maximum) were measured. The first and second minimum speeds of sound were significantly lower in the patients with osteomalacia than in the osteoporosis group. The first minimum speed of sound was 2,169 +/- 73 m/s in osteoporosis and 1,983 +/- 61 m/s in osteomalacia (P < 0.0001); the second minimum peak speed of sound was 1,895 +/-59 m/s in osteoporosis and 1,748 +/- 38 m/s in osteomalacia (P < 0.0001). The f0 was similar in the two groups (osteoporosis, 0.85 +/- 0.14 MHz; osteomalacia, 0.9 +/- 0.22 MHz; P = 0.72), and the full width at half maximum was significantly higher in the osteomalacia patients (0.52 +/- 0.14 MHz) than in the osteoporosis patients (0.37 +/- 0.15 MHz) (P = 0.022). This study confirms that ultrasonography is a promising, noninvasive method that could be used to differentiate osteoporosis from osteomalacia, but further studies should be carried out before this method can be introduced into clinical practice.

Diagnosis, Differential↗
PubMed2000

Cadmium induces osteomalacia mediated by proximal tubular atrophy and disturbances of phosphate reabsorption. A study of 11 autopsies.

Osteomalacia of cadmium (Cd) poisoning (Itai-Itai disease) is induced by renal tubular dysfunction; however, the precise pathological changes and mechanisms have not been adequately elucidated. Of the 25 inhabitants in a Cd-polluted area who developed chronic tubular proteinuria, 22 individuals died over a 16-year period. Autopsies were performed in 11 cases and osteomalacia was detected in 9 cases (mean age at death 82.2 +/- 7.8 years; 1 man and 8 women). Histologically, osteomalacia occurred coincidentally with diffuse atrophy of the proximal tubules, moderate thickening of the tubular basement membrane and mild interstitial fibrosis in the renal cortex. Ultrastructurally, mitochondria in the proximal tubules were decreased in number and showed abnormal structure, while membrane enzymes, such as 5'-nucleotidase and ALPase, were still well preserved in their brush border. Glomeruli and distal tubules were minimally damaged. Severity of osteomalacia correlated with the damage of the proximal tubules as well as reduced serum calcium (Ca), serum Ca x phosphorus (P) and hematocrit, increased urine beta2-microglobulin, lysozymes, N-acetyl-b-D-glucosaminidase, retinol binding protein, creatinine, and reduced percent tubular reabsorption of phosphate. Multiple regression analysis showed that among these factors, serum Ca x P was an independent factor for predicting the severity of osteomalacia. Our findings suggest that osteomalacia by Cd poisoning causes degenerative changes in the proximal tubules, especially in mitochondria, which might affect the disturbance of the intracellular active transport energy system for calcium and phosphorus, resulting in osteomalacia.

5'-Nucleotidase↗
PubMed1990

Detection of osteomalacia in British Asians: a comparison of clinical score with biochemical measurements.

1. In a prospective study of 160 Asian outpatients, plasma calcium, phosphate, alkaline phosphatase, 25-hydroxyvitamin D and parathyroid hormone were compared with a clinical score to determine which measurements singly or in combination were most useful in the detection of osteomalacia. 2. Bone biopsies were performed in 45 of 48 patients considered to be at risk of osteomalacia. Of the 39 quantifiable bone biopsies, nine showed unequivocal osteomalacia, 13 were judged to be borderline and 17 biopsies were normal. 3. The clinical score was highly sensitive, identifying eight of nine patients with osteomalacia, but not specific, six of 17 normal patients having an abnormal score. 4. Plasma parathyroid hormone was the best single biochemical test for identifying osteomalacia. By using a discriminant function based on parathyroid hormone and alkaline phosphatase, it was possible to classify 96% cases correctly; a discriminant function utilizing calcium, phosphate and alkaline phosphatase was successful in 85% of cases. It was not possible to discriminate between histological groups on the basis of plasma 25-hydroxy-vitamin D values. 5. We confirm that the clinical score is a useful and inexpensive screening test for osteomalacia in British Asians. In those patients with an abnormal score we suggest that parathyroid hormone and alkaline phosphatase are measured. Where both parathyroid hormone and alkaline phosphatase are high, in the absence of hypercalcaemia, histological osteomalacia is extremely likely.

Adult↗
PubMed1976

The use of high calcium dialysate in the treatment of renal osteomalacia.

Four chronic haemodialysis patients suffering from osteomalacia were treated by increasing their dialysate calcium concentration from 1-40 to 2-15 mM/I. Bone biopsies were taken before and after 22 weeks of this treatment and a further biopsy was taken in one patient after 52 weeks. Symptomatic cure occurred in one patient with mild osteomalacia and some improvement osteomalacia and hyperparathyroidism. Bone biopsies showed slight improvement in the patient with mild osteomalacia after 22 weeks, and considerable improvement after 25 weeks. In the patient with mixed histology, the osteitis fibrosa subsided and the osteomalacia became a little worse after 22 weeks. There was no histologic improvement in the two patients with severe osteomalacia after 22 weeks. It is concluded that high calcium dialysis is not an effective treatment for renal osteomalacia.

Aged↗
PubMed1982

Value of plasma calcium, phosphate, and alkaline phosphatase measurements in the diagnosis of histological osteomalacia.

Plasma calcium and phosphate concentrations and alkaline phosphatase activities were examined retrospectively in 50 patients with histologically proven osteomalacia and 50 age- and sex-matched control subjects with normal bone histology. An abnormal plasma alkaline phosphatase activity was more useful than an abnormal plasma calcium or phosphate concentration in distinguishing between normal and osteomalacic subjects, producing a false-negative rate of 14% and a false-positive rate of 8%. False-negative and false-positive rates of 10% and 8% respectively were obtained when the presence of an abnormality in any one of the three biochemical measurements was used as a predictor of histological osteomalacia. When discriminant analysis was applied to plasma calcium, phosphate and alkaline phosphatase together a false-negative rate of 12% and a false-positive rate of 0% was obtained.Sixty-two patients in whom a diagnosis of osteomalacia was suspected were investigated prospectively, using both single biochemical abnormalities and the classification functions derived from the discriminant analysis of all three biochemical measurements to predict the presence or absence of histological osteomalacia. Plasma alkaline phosphatase activity gave false-negative and false-positive rates of 10% and 32% respectively but was a more reliable predictor of abnormal bone histology than were plasma calcium or plasma phosphate concentrations or the presence of an abnormality in any one of the three measurements. Discriminant analysis using plasma calcium, phosphate and alkaline phosphatase together produced a false-negative rate of 16% and a false-positive rate of 10%. We conclude that plasma alkaline phosphatase activity is the best single routine biochemical screening test for osteomalacia, although a high false-positive rate may occur. Direct discriminant analysis of plasma calcium, phosphate and alkaline phosphatase together provides a more sensitive method of detecting histological osteomalacia which should be useful in determining the prevalence of osteomalacia within high-risk populations.

Adolescent↗
PubMed1982

Osteomalacia in fractures of the proximal femur.

The occurrence of osteomalacia was studied in 58 hip fracture patients who were admitted to the University Central Hospital of Kuopio for operative treatment. Findings indicating osteomalacia were frequent in the series. Hypocalcaemia was found in 70 per cent and an increase in serum alkaline phosphatase in 22 per cent of the patients. Urinary calcium excretion was decreased in 45 per cent and urinary hydroxyproline excretion was increased in 70 per cent of the cases. The serum levels of 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D were significantly decreased in the patients compared with the controls. Histomorphometric analysis revealed no difference in the amount of trabecular bone in the patients compared with the controls, but the amount of osteoid and resorption surfaces was increased in the patients. Histological osteomalacia was found in 12 out of 50 patients (24 per cent). In 10 of these 12 cases the diagnosis of osteomalacia was supported by biochemical changes. There was only one patient, a 29-year-old man with glutein enteropathy who had an evident reason for osteomalacia. The most obvious cause of osteomalacia was the lack of vitamin D due to a deficient diet and lack of exposure to sunlight. The conclusion drawn was that osteoporosis was the main cause and osteomalacia was an important aggravating factor in the bone fragility in these hip fracture patients.

Aged↗
PubMedDate not supplied

The osteomalacias.

Osteomalacia is characterized by large osteoid seams and a preserved volume of bone trabeculae. The mineralization of newly formed bone requires adequate concentrations of calcium and phosphate: the Ca.P product has been regarded as a useful, empirical diagnostic test of osteomalacia. It decreases in patients with osteomalacia mainly because they have very low plasma phosphate levels. At present total body bone mineral and total body bone density can be directly measured by whole body absorptiometry, which indicates the lowest total mineral content of the skeleton which can increase quickly after adequate treatment. The main symptoms of osteomalacia are: bone pain; muscular weakness (commonly as pelvic girdle myopathy); Looser-Milkman pseudofractures or more often a pattern of generalized demineralization at X-ray. The main biochemical parameters in osteomalacia include: defective calcium absorption with hypocalcemia and hypocalciuria; defective intestinal phosphate absorption with hypophosphatemia; there is often increased renal phosphate clearance due to hypocalcemia and secondary hyperparathyroidism; elevated alkaline phosphatase and osteocalcin levels; high bone turnover confirmed by kinetic studies carried out with radiocalcium or 99mTc-MDP. An etiological classification of the osteomalacias includes: 1) nutritional osteomalacia: a) inadequate exposure to sunlight and/or insufficient vitamin D intake; b) defective intestinal absorption of vitamin D because of malabsorption syndromes (e.g. jejuno-ileal bypass for obesity).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcification, Physiologic↗
PubMed1983

Osteomalacia in patients with chronic renal failure before dialysis or transplantation.

The case records of 327 patients who underwent bone biopsy in late or terminal renal failure, before any form of dialysis or transplantation, were examined for clues to the aetiology of renal osteomalacia and its manifestations. Fifty four per cent of the biopsies showed pure osteitis fibrosa, 34 per cent osteomalacia with osteitis fibrosa and 12 per cent showed neither abnormality. Osteomalacia was strongly associated with chronic pyelonephritis and obstructive uropathy as primary renal disease. In two matched groups of 100 each, and within the major primary diseases, it was associated with acidosis, hypocalcaemia and normophosphataemia (as opposed to hyperphosphataemia). There was no association with known length or uraemia and only a weak and inconsistent relationship with severity of uraemia. In the few patients studied, there was no relationship between osteomalacia and serum 25-hydroxycholecalciferol level. In contrast to the state of patients treated by haemodialysis, osteomalacia in this undialysed group was manifested by a higher level of serum alkaline phosphatase than pure osteitis fibrosa, serum iPTH did not differ between the groups, there was no predominance of symptoms in one group, other than proximal myopathy which had a weak association with osteomalacia, and Looser zones were more common than complete fractures. Our study shows that osteomalacia has different manifestations, and probably different causes, before and after the start of haemodialysis. These two stages of renal failure should be clearly distinguished in reports of renal bone disease.

Acidosis↗
PubMed1999

Tumor-induced osteomalacia and symptomatic looser zones secondary to mesenchymal chondrosarcoma.

Tumor-induced osteomalacia is a rare clinical entity that is associated with soft-tissue or skeletal tumors. We present a case report of a patient with a chest wall mesenchymal chondrosarcoma who presented with bone pain. The patient had skeletal changes in the femoral neck and fibula consistent with osteomalacia and laboratory values suggesting phosphate diabetes. The patient was treated with tumor resection and phosphate supplementation with reversal of the signs and symptoms of osteomalacia. Tumor-induced osteomalacia is vitamin-D-resistant and often reversed by complete removal of the tumor. Most commonly, the causative tumors are of vascular, mesenchymal, or fibrous origin. The osteomalacia is associated with bone pain, muscle weakness, and radiographic changes. Tumor-induced humoral factors have been implicated in causing the osteomalacia, but the definite etiology has yet to be determined. Current treatment includes complete tumor resection and electrolyte supplementation.

Bone Neoplasms↗
PubMed1986

Reflex sympathetic dystrophy syndrome: an unusual mode of presentation of osteomalacia.

We report 2 patients with reflex sympathetic dystrophy syndrome (RSDS) associated with renal tubular osteomalacia. In both patients, RSDS was the presenting manifestation. Treatment of the underlying condition with calcitriol resulted in healing in both patients. These cases prompted us to undertake a retrospective study of 24 consecutive patients with osteomalacia (6 of renal tubular origin, 18 related to vitamin D deficiency), and of 259 consecutive patients with RSDS. Among those with osteomalacia, radiologic lesions strongly suggestive of RSDS were found in 5 patients (21%), 4 of whom had renal tubular defects, and only 1 had vitamin D deficiency. In the group with RSDS, 1 patient (0.4%) was found to have osteomalacia of renal tubular origin. Thus, radiologic findings suggestive of RSDS are frequent in patients with osteomalacia, especially that of renal tubular origin. On rare occasions, the full-blown clinical picture of RSDS may obscure the diagnosis of osteomalacia.

Aged↗
PubMed1979

[The frequency of adult anticonvulsant osteomalacia in relation to duration of therapy and dosage of anticonvulsants (author's transl)].

Of 837 epileptics over 16 years of age treated with mono- or combined hydantoin therapy 20.3% showed radiographic signs of anticonvulsant osteomalacia. With the exception of the patients with severe disturbances of the skeletal system no positive correlation was found with duration of therapy. The percentage of moderate bone changes was the highest in the patients treated for 1 to 2 years; the percentage of severe bone changes in the group treated over 10 years. The rate of osteomalacia correlated with the total dose of hydantoin, phenobarbital, or primidone; the correlation with the dose per year was even more evident. The risk of osteomalacia rose distinctly with doses over 3000 equivalent units/year. The patients with combined hydantoin-barbiturate treatment showed a higher risk than those treated with phenytoin alone. The rate of osteomalacia was the highest in the patients aged under 20 years and over 50 years. Males showed a relatively higher rate of osteomalacia than females, they were treated however with a higher dose per year. The chemical parameters blood alkaline phosphatase and 25-hydroxycholecalciferol corresponded to the radiographic signs, whereas calcium and anorganic phosphate showed no correlation. Early routine radiologic and chemical control especially of the epileptic patients with high risk of osteomalacia should be routinely performed in future.

Adult↗
PubMed2004

Lack of association between vitamin D receptor gene polymorphism (BsmI) and osteomalacia.

Vitamin D receptor (VDR) gene polymorphism has been reported to be a determinant of bone formation and intestinal calcium absorption. We carried out this study to assess the role of VDR gene polymorphism in the pathogenesis of osteomalacia. We investigated BsmI polymorphisms in the gene encoding the 1,25 dihydroxyvitamin D receptor in 38 patients with osteomalacia and 31 healthy controls, along with examination of serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, and 25 hydroxyvitamin D levels. VDR allelic variants were: BB, 31.6%; Bb, 44.7%; and bb, 23.7% in the osteomalacia patients and BB, 19.4%; Bb, 61.3%; and bb, 19.4% in the controls. Although heterozygotes (Bb) were more frequent than other genotypes in both groups, the BB genotype was found to be more prevalent in osteomalacia than in controls. There was no statistical relationship between VDR genotype and osteomalacia. It is concluded that, in this small group of patients, there was no relationship between VDR allelic polymorphisms and osteomalacia.

Adult↗
PubMed1980

1,25(OH)2D3 is not the only D metabolite involved in the pathogenesis of osteomalacia.

Three patients are described in whom there was no simple correlation between plasma 1,25(OH)2D3 concentration and the occurrence of osteomalacia. One patient had severe osteomalacia with high plasma 1,25(OH)2D3 and normal mineral ion product; the second had a normal mineral ion product and no evidence of osteomalacia even though plasma 1,25(OH)2D3 was undetectable; and the third had osteomalacia, low plasma 1,25(OH)2D3 and a reduced mineral ion product. In considering these data in the light of presently available information, it is concluded that osteomalacia can occur as a consequence of a lack of a vitamin D metabolite other than 1,25(OH)2D3, or a consequence of a reduced mineral ion product, but not as a consequence of 1,25(OH)2D3 lack if the mineral ion product is normally maintained and other D metabolites are present. However, a deficiency of 1,25(OH)2D3 normally leads to a reduction in the mineral ion product hence 1,25(OH)2D3 deficiency may play a role in the development of certain forms of osteomalacia.

Adult↗