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The concept of risk in the field of avitaminoses is very important and useful for the practitioner, who should consider two aspects: a) risk factors, which could be individual (physiological, pathological and psychological) and extra-individual (alimentary, environmental, etc.); b) subjects with an elevated risk of avitaminosis (childhood, old age, pregnancy, etc.). In these subjects the risk can be a generical one, when there is an elevated requirement for all vitamins (nursing women, sportmen, etc.) or a specific one, when there is a high requirement only for a single vitamin (osteomalacia, some professional diseases, use of oral contraceptives) or a vew of them (alcoholism, diabetes, etc.). On the basis of this kind of knowledge it is easy for the practitioner to estimate which vitamins are necessary for each subject or for a group of subjects in physiological or in pathological conditions. For example, there is an elevated risk of apyridoxinosis in old age (acalciferolosis in aged women), of athiaminosis and apyridoxinosis in diabetes, of apyridoxinosis in oral contraceptives users, of axeroftolosis in hyperthyroidism, of athiaminosis, apyridoxinosis, aniacinosis and anascorbosis in alcoholics. In the second chapter the concept of the latency period in avitaminosis is illustrated. This period corresponds to the interval between the moment when deficiency stimulus starts operating and the moment when its effect, that is the picture of avitaminosis, appears. The latency time is not measurable, on account of the difficulties in establishing the onset of the deficiency stimulus; generally it is very long and is followed by the period of biochemical symptomatology and subsequently by the one of clinical symptomatology. Each of these three phases can be further divided in several steps, which have summarized in a Table. The last chapter is dedicated to the classification of avitaminoses. From the etiopathogenetic point of view avitaminoses can be due to: a) deficiency of introduction (alimentary level)); b) deficiency of absorption (enteric level); c) deficiency of utilization (tissue level). From the clinical point of view avitaminoses can be distinguished in deficiency with: a) a complete clinical symptomatology (scurvy, beriberi, pellagra, rickets, osteomalacia, xerophthalmia, hemeralopia); b) an incomplete clinical symptomatology (mono- or oligo-symptomatic or partial clinical picture); c) a biochemical symptomatology only (subclinic or clinically asymptomatic picture).
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PMID:[Vitaminology for practitioners. II. Avitaminoses, risk, latency period, classification]. 58 76

Adult-onset osteomalacia with multiple renal tubular defects and generalized aminoaciduria is uncommon, and where familial it is characteristically an autosomal recessive disorder. This paper describes a kindred in which the syndrome has appeared in four successive generations, apparently inherited in a dominant manner, and possibly associated with diabetes mellitus. The proposita had hypophosphataemia, renal glycosuria, proteinuria and generalized aminoaciduria, and at the age of 22 developed symptoms of osteomalacia which responded to treatment with oral phosphate. Her father had been similarly affected: renal glycosuria was first noted when he was 24, and 12 years later he developed diabetes mellitus from which he died. One sister, aged 31, has renal glycosuria, aminoaciduria and hypophosphataemia without bone disease. In the three preceding generations at least seven other individuals had crippling bone disease and profound muscle weakness of early adult onset; in four, preterminal polydipsia was recorded, and others had renal glycosuria or diabetes mellitus. Three of the five children in the latest generation have slight proteinuria but not other detectable abnormality. The possible association between these renal tubular defects and diabetes mellitus is discussed.
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PMID:Hypophosphataemic osteomalacia and Fanconi syndrome of adult onset with dominant inheritance. Possible relationship with diabetes mellitus. 94 41

Histomorphometric examination and histological observation of femoral bone were performed on long-standing neonatal streptozotocin-induced diabetic rats (n2STZ, n5STZ) as a human model of non-insulin-dependent diabetes mellitus. The growth and strength of femurs decreased in the STZ diabetic rats. Histomorphometric parameters such as cortical bone thickness, number of metaphysical trabeculae and percent trabecular volume of metaphysical area all significantly decreased in the STZ diabetic rats. There were no significant differences in parameters between the n2STZ and n5STZ diabetic rats. Histological findings demonstrated no significant change in the number of osteoclasts in femur nor change corresponding to osteomalacia. Bone absorption in the STZ diabetic rats appeared unchanged. The plasma calcium level did not change in the STZ diabetic rats, although their plasma phosphate or A1-p levels increased. Circulating 24, 25 (OH)2D3 was significantly lower in the STZ diabetic rats than the controls. However, 25 (OH) D3 or biologically active 1, 25 (OH)2D3 was not different between the controls and STZ diabetic rats. Osteopenia is thus present in the femurs of long-standing neonatal STZ diabetic rats, due in part to abnormal vitamin D metabolism.
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PMID:Alterations in femoral bone histomorphometry and vitamin D metabolism in neonatal streptozotocin-induced diabetic rat. 133 71

CAPD is considered a risk factor for low turnover bone disease. This was previously attributed to aluminum accumulation. We evaluated by biochemical and histomorphometric parameters (including double tetracycline labelling), 26 patients maintained on CAPD for 12-14 months. Three (11.5%) showed mild hyperparathyroidism, 5 (19.2%) osteitis fibrosa, 3 (11.5%) mixed forms, 4 (15%) osteomalacia and 11 (42.3%) adynamic bone disease. Only one patient with diabetes mellitus showed an aluminum stained bone surface > 10%. Intact PTH serum levels were lower in LTBD (133.2 +/- 128 vs 468.2 +/- 451 pg/ml; p < 0.05). We also evaluated prospectively 11 patients who underwent a bone biopsy at start of dialysis and after 12 months of CAPD treatment. Bone biopsies pre CAPD demonstrated normal-high bone turnover disease in 8/11 (72.7%) and low turnover bone disease in 3/11 (27%). In the follow-up biopsies, 2 patients showed osteitis fibrosa and other two mild forms. Low turnover bone disease was found in 7 patients (3 osteomalacia and 4 adynamic bone disease). We conclude that the predominant bone lesion in our CAPD patients is low turnover bone disease, predominantly adynamic forms, and aluminum does not seem to play a role on its genesis. Low intact PTH serum levels may be a predictor of low turnover bone disease.
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PMID:Low turnover bone disease is the more common form of bone disease in CAPD patients. 136 27

Follow-up of a previously reported family with dominantly inherited adult onset hypophosphatemic osteomalacia with Fanconi syndrome and diabetes mellitus has shown that both the proposita and her affected sister have developed renal glomerular failure. We describe the evolution of renal failure in this family and discuss the possible mechanisms involved. The development of renal tubular acidosis in this condition further impairs renal function and we suggest that correction of systemic acidosis might improve renal function and prevent further decline in these patients.
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PMID:Renal failure in adult onset hypophosphatemic osteomalacia with Fanconi syndrome: a family study and review of the literature. 164 11

Renal transplantation is associated with several abnormalities of function and structure of the musculoskeletal system. Some of these skeletal problems result from incomplete resolution of abnormalities of bone and mineral metabolism present at the time of transplantation. In this regard, persistent hyperparathyroidism, diabetes mellitus type 1, and accumulation of beta 2-microglobulin may lead to residual skeletal effects despite excellent function of the allograft. Persistent hyperparathyroidism may accelerate bone loss and increase the risk for osteonecrosis, as well as cause hypercalcemia and hypophosphatemia; some patients with severe hyperparathyroidism require parathyroid surgery. Osteonecrosis is the most debilitating skeletal complication after transplantation and frequently requires surgical therapy. Although osteomalacia associated with aluminum overload generally resolves after transplantation, bone complications due to dialysis amyloidosis and diabetes mellitus type 1 often fail to improve. Alternatively, skeletal abnormalities can be acquired after transplantation. Most of the new derangements of bone and mineral metabolism are due to the immunosuppressive medications. Toxic effects of glucocorticoids on bone contribute to the pathogenesis of osteonecrosis, increase the risk for fractures by decreasing cancellous bone mass and synthesis of bone matrix, and dampen the linear growth response in pediatric recipients. Whether cyclosporine independently causes appreciable toxic effects on bone metabolism is not yet clear, but use of this drug increases the prevalence of gout and dental problems. Osteonecrosis, osteopenia, and short stature remain important skeletal complications in recipients of renal allografts. Therapeutic efforts should be directed toward alleviating pretransplant bone disease and attenuating bone loss after transplantation.
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PMID:Musculoskeletal complications after renal transplantation: pathogenesis and treatment. 129 May 51

The clinical relevance of regular serum aluminium monitoring in dialysis patients was investigated in a multicentre study by 6-monthly determination of the serum aluminium during 4 consecutive years. In a group totalling 1193 patients, a striking decrease of mean serum aluminium was observed the last 2 years of the study. This phenomenon was accompanied by a substantial reduction of the prescribed dose of aluminium hydroxide (Al(OH)3) and its partial replacement by calcium carbonate (CaCO3) and/or magnesium hydroxide (Mg(OH)2). Under this policy serum phosphate control remained satisfactory. In all the centres, water treatment was found to be adequate, yielding dialysate aluminium around 2 micrograms/l. Dialysis patients with clinically overt liver disease showed a significantly greater median serum aluminium concentration than that observed in a control dialysis population. Compared to the latter group, the median serum aluminium concentration of dialysis patients with diabetes mellitus did not differ significantly. Results further indicated that patients with biopsy-proven osteomalacia presented a significantly greater median serum aluminium compared to that of patients without osteomalacia. We demonstrated that a serum aluminium of 60 micrograms/l provides a relatively sensitive (82%) and specific (86%) index for the detection of aluminium-related bone disease (ARBD). Provided the aluminium determinations are performed by a qualified laboratory, serum monitoring in dialysis patients (a) allows the safer use of aluminium-containing phosphate binders, and (b) is of value in the diagnosis of overload/toxicity.
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PMID:Value of serum aluminium monitoring in dialysis patients: a multicentre study. 131 84

Hyperparathyroid bone disease is a common complication of end stage renal failure, particularly in patients on maintenance haemodialysis. Several studies have, however, shown a near absence of hyperparathyroid bone disease in diabetic patients who have been receiving haemodialysis for periods of up to 4 years. We have studied biochemical indices of mineral metabolism in 54 consecutive pre-dialysis patients with moderate to severe renal impairment. Deteriorating renal function was associated with developing hypocalcaemia and hyperphosphataemia. Hypocalcaemia was strongly related to increased severe alkaline phosphatase activity (p less than 0.001), suggesting the development of hyperparathyroidism. Five patients with hypocalcaemia and increased alkaline phosphatase were studied in detail. All had elevated serum concentrations of parathyroid hormone and histological signs of hyperparathyroidism on bone biopsy. Three of the patients had low serum 25 hydroxyvitamin D levels with associated osteomalacia, the other 2 patients were notable for their long duration of renal failure. In the long-term (greater than 4 years) we also observed the development of hyperparathyroidism in a small group of diabetic patients maintained on haemodialysis. We conclude that diabetic patients are not uniquely protected against renal osteodystrophy. Although the prevalence of hyperparathyroidism may be lower in diabetic patients than in those with other types of renal disease, the same factors which predispose to bone disease in non-diabetic patients (long duration of renal failure, low serum 25 hydroxyvitamin D and long periods on haemodialysis) also operate in the diabetic population.
Diabetes Res 1990 Aug
PMID:Hyperparathyroid bone disease in diabetic renal failure. 213 93

The basic prerequisite of treatment of diabetic osteopenias is perfect metabolic compensation of diabetes. Insulin administration is an advantage in this respect, as it enhances calcium absorption from the gut and reduces its urinary excretion. Conversely, oral antidiabetics interfere in a negative way with vitamin D metabolism and thus also calcium metabolism and mineralization of bone. The combination of calcium, small doses of vitamin D, NaF and exercise used in the treatment of diabetic osteoporoses leads in general to a significant rise of the calcium serum level, an insignificant rise of the phosphorus level and it reduces alkaline phosphatase activity. A certain disadvantage is the elevated urinary calcium excretion. The main drug in diabetic osteomalacia are usually large doses of vitamin D. The rise of the serum calcium level improves the metabolic compensation of diabetes in a linear fashion. Thiazide diuretics used to reduce excessive calciuria cause slight deterioration of the glucose tolerance but the compensation does not cause major difficulties.
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PMID:[Diabetic osteopathies. 6. Treatment and its pitfalls]. 213 68

Magnesium (Mg) makes up 0.5-1% of bone ash and is therefore not a trace element in the skeleton. Mg influences both mineral and matrix metabolism in bone by a combination of effects on hormones and other factors that regulate skeletal and mineral metabolism, and by direct effects on bone itself. The skeletal content of Mg is very variable both between and within species, and reported values range between 150 and 440 mmol/kg ash weight (AW). Dietary Mg has a direct influence and age an inverse influence on skeletal Mg content. It is unclear whether skeletal Mg content varies from region to region. In humans, reported values cluster around the 200 mmol/kg AW level, 30-40% lower than most rat data. Human iliac crest cortical bone has 10-20% less Mg per unit weight than iliac crest trabecular bone. Mg depletion adversely affects all phases of skeletal metabolism. In the rat, cessation of bone growth is noted with a decrease in both osteoblast and osteoblast activity, decreased bone formation, osteopenia, increased fragility and development of a form of 'aplastic bone disease'. The epiphyseal growth plate is thinned and the percent ash weight of the growth plate is increased, possibly due to enhanced crystallization of bone salt under conditions of Mg depletion. In contrast, in chicks and in rats with severe Mg deficiency, these 'antianabolic' effects are not observed but instead, predominant inhibition of bone resorption occurs with increased cortical thickness rather than osteopenia, and the occasional development of subperiosteal hyperplasia or of fibrous tumors of the periosteum. It is probable that this unusual response under conditions of severe Mg deficiency is in part an indirect effect secondary to a defect in secretion and/or skeletal responsiveness to parathyroid hormone (PTH) and vitamin D metabolites. Mg excess also has adverse biologic effects on bone. Crystallization of bone salt is severely impaired and an osteomalacia-like picture may be produced with decreased osteoblastic activity, widened growth plates, excessive osteoid seams and short, thickened bones. In some studies, especially in mice, Mg excess stimulates bone resorption, independently of PTH. The role of Mg deficiency and excess in human skeletal conditions requires more extensive investigation. Bone Mg is uniformly increased in renal insufficiency and may play a role in renal osteodystrophy since improvement has been noted in the osteomalacic component by normalizing the serum Mg. Decreased bone Mg has been reported in alcoholic patients, diabetes and in osteoporosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of magnesium on skeletal metabolism. 218 30


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