Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three of seven Arctic fox kits, Alopex lagopus, trapped on St. Paul Island, Alaska, had evidence of rickets and hyperparathyroidism. Radiographic, morphologic and histologic examination confirmed the diagnosis. The disease was presumed to be a juvenile-onset disease due to calcium-deficient intake following weaning. The possibility of insufficient exposure to sunlight could not be determined. No other abnormalities (e.g., genitourinary) were found. Skeletal involvement was quite varied. All growth plates exhibited columnar hyperplasia compatible with rickets, while the metaphyses showed decreased trabeculation and cortical thinning compatible with osteodystrophia fibrosa. One fox had bilateral metaphyseal fractures through this osteodystrophic bone.
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PMID:Juvenile rickets and hyperparathyroidism in the Arctic fox. 52 28

Studied were mass disease outbreaks on eight farms in calves intensively fed concentrate mixtures that were rich in phosphorus compounds. Clinically, there were selling and deformations of the joints with pains. The tarsal and carpal joints were chiefly involved. Kyphosis of the backbone, spastic paresis of the posterior part of the body as well as tetaniform spasms in the initial stage of the disease were also observed. Morphologically, the diseased animals manifested erosions and thinning of the joint cartilage, tearing of the Achilles tendon, and increased amounts of the joint fluid. The histologic study revealed edema of the cartilage cells, disorders in the structure of the hyalin cartilage, formation of cavities, and broadening of the lumen of the Haversian canals. In most cases the blood serum presented hyperphosphatemia (up to 15.67 mg% inorganic P) and relative or absolute hypocalcemia (up to 4.47 mg% Ca). On the farm both hypocalcemia and hypophosphatemia were observed. Good prophylactic results were obtained through correct Ca:P ratios in the diet that contained calcium additives as well as by the injection of vitamin D solutions, etc. It is believed that these cases should be referred to a distinctive form of rickets of a characteristic clinical course' the inadequate Ca:P ratios in the rations playing the main etiologic role. Subsidiary causes are probably vitamin D deficiency, restricted movement of the animals, and mechanical traumata caused by the animal's own bodyweight.
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PMID:[Study of disorders in calcium and phosphorus metabolism in the intensive fattening of young cattle]. 125 54

Two young siblings had a syndrome of growth retardation, severe rickets, anemia, renal insufficiency, and renal tubular dysfunction, the last including acidosis, aminoaciduria, and polyuria. There was moderate psychomotor developmental delay. Neither child had cystinosis. Renal biopsy in the older child revealed severe glomerular abnormalities, with capillary wall thickening reminiscent of the hemolytic-uremic syndrome. The proximal convoluted tubules were lined with short, cuboidal cells containing mildly abnormal mitochondria. There was also thinning of brush border microvilli and basolateral infoldings, perhaps as the result of regressive changes, and interstitial fibrous tissue was moderately increased. The etiology of the tubular and glomerular changes is uncertain. We believe these patients represent a previously unreported hereditary syndrome sharing certain clinical features with severe nephropathic cystinosis.
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PMID:A familial syndrome of growth retardation, severe Fanconi-type renal disease and glomerular changes--a new entity? 372 23

Cement kiln dust (CKD) samples of which have been reported to stimulate growth in cattle and sheep, was fed to weanling pigs in a 42-d experiment. CKD at levels of 1.5 and 3.0% was added to a corn-soybean meal-oats-whey-type diet containing inadequate amounts of Ca (.4% of the diet) to provide final dietary Ca levels of .85 and 1.3%. A diet containing 3% limestone (1.3% dietary Ca) served as a positive control. Body weight gain was depressed by 3.0% CKD, and histopathological lesions of the humerus, not typical of nutritional secondary hyperparathyroidism or rickets, were observed. The lesions detected were osteonecrosis, thinning of the cortex and reduction in the width of the epiphyseal cartilage. Width of the proximal epiphyseal plate and cortical index of the humerus (width of cortex divided by total diameter at narrowest point of diaphysis) were smaller in pigs fed 3% CKD than in pigs fed 3% limestone. CKD contained 2.3% A1, 15 ppm Cd and 110 ppm Pb, providing 690, .45 and 3.3 ppm of A1, Cd and Pb, respectively, in the diet containing 3% CKD. Kidney, liver and bone ash concentrations of these three minerals were not increased by CKD, and typical toxicity signs were absent. It is concluded that CKD may contain one or more factors that interfere with normal bone metabolism in growing pigs when the diet contains 3.0% CKD.
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PMID:Bone lesions in growing swine fed 3% cement kiln dust as a source of calcium. 708 4

Up to the mid-1960s, beta-thalassemia was treated with blood transfusions as frequent as needed to keep symptoms under control and to prevent transfusional hemosiderosis. In the following years, high transfusion regimens and iron chelation therapy with desferrioxamine were used. Because of these different treatment modalities, skeletal findings in thalassemia have markedly changed. In the past, thalassemic patients treated with a low transfusion regimen and without chelation therapy developed osteopenia--with widened medullary spaces, cortical thinning and trabecular atrophy--secondary to chronic expansion of red marrow, due to increased erythropoietin response to chronic anemic hypoxia. Typical radiographic patterns in the skull included widened diploic space, atrophic-especially outer--tables and, in some patients, the "hair-on-end" pattern. As for the face, obliteration of the paranasal sinuses and the typical "rodent facies" were observed. In the ribs, bulbous expansion of the posterior and anterior segments and the "rib within a rib" patterns were observed. As for the spine, coarse trabecular arrangement was seen. The "cobweb" pattern was seen in the pelvis and finally the lack of the normal concave outline was observed in the long bones. In the patients treated with high transfusion regimens and iron chelation therapy over the last 30 years, both skull anomalies and disfigurement are less frequent. The skull is almost normal, with the exception of osteopenia and thickened diploic space in the frontal bone only; the paranasal sinuses are usually not obliterated. The hands and rib are normal, just like long bones, pelvis, scapulae and vertebral bodies. Nevertheless, in some adequately treated patients new skeletal features have been recently observed in the long bones, which are similar to those occurring in rickets and/or scurvy, and in the vertebral bodies, resembling platyspondylia. These abnormal features might be caused by several factors--i.e., marrow expansion, transfusion regimens, direct/indirect effects of desferrioxamine, iron load, endocrine abnormalities, deficiency of some minerals and finally dysvitaminoses. Nevertheless, osteopenia remains the main negative factor of thalassemia.
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PMID:[The evolutionary effects of therapy on the skeletal lesions in beta-thalassemia]. 819 Sep 18

Radiography of the hand often reflects the picture of generalized diseases, affecting both the muscolo-skeletal system and the others. Some of the most common hematologic disorders may be detected in roentgenograms of the hand, especially in the anemias, but also in plasma cell dyscrasias and proliferative malignant diseases (i.e., lymphomas and leukemias). On the basis of their experience, the authors have reviewed and discussed the radiographic "pattern" of the hand in several hematologic conditions (i.e., anemias; thalassemias; sickle-cell disease; lymphomas; multiple myeloma; etc.), and their pathogenesis. Radiographies of both the hands, in antero-posterior view, were performed using Kodak-Min R film; xeroradiography was performed--in the same projection--using Rank Xerox plate, developed always in "positive mode" in 125 Rank Xerox System, conditioned with contrast "D", for emphasizing osseous details. Recently, digital radiography--employing PCR system--has substituted xeroradiography, because of its well-known properties and diagnostic advantages: in this manner, changes in bone and soft tissue are demonstrated on the same image, with augmentation of diagnostic information, with reduced dose to patient. In our series, hand is always involved (100% of cases) in thalassemias: lesions are characterized by diffuse osteopenia (washed out melted appearance), with widening of bone marrow space, diaphyseal convex aspect of the long bones, thinning of the cortex, and cyst-like changes (rain drops). Lesions disappear completely after the hypertransfusion regimen (HTR). Following chelation therapy, lesions of the wrist and hand are similar to those described in rickets and/or scurvy. Sometimes, the hand is characteristically affected in sickle-cell disease--particularly in the so called hand-foot syndrome--as "cone-deformity". In multiple myeloma incidence of hand involvement is 2.9%: lesions reflect general abnormalities observed in other skeletal sites, and they consist in multiple well-circumscribed lytic lesions. In amyloidosis, poorly defined radiolucent areas may be discovered. In non-Hodgkin lymphoma, incidence of hand involvement is less frequent, approximately 0.2%: the radiographic pattern is aspecific (mottled lytic lesions), sometimes simulating multiple myeloma and/or leukemias. In hemophilia, swelling of soft tissues, around the interphalangeal joint, related to intra-articular and/or per-articular hematoma, is observed. The other conditions reflect general radiographic features of anemias, which are of three main types: 1. the over active marrow (i.e., polycythemia); 2. the infarction of bone (i.e., sickle-cell disease); 3. non-specific findings, resulting from chronic illness (delays of maturation; dwarfism; osteopenia; tendency to infection).
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PMID:[The hand in hematologic diseases]. 824 5

We evaluated the radiological, biochemical and growth hormone (GH)/insulin-like growth factor-I (IGF-I) changes in 10 children with severe protein-energy malnutrition (PEM) who had rachitic manifestations (group 1), 10 children with severe PEM without clinical signs of rickets (group 2), and 10 children with normal body weight-for-length and -age, suffering from vitamin-D-deficiency with signs of florid rickets (group 3) and 10 normal age-matched children (group 4). Serum calcium (Ca2+), phosphorus (PO4), and albumin concentrations were markedly decreased in the two groups with PEM. Malnourished children with rickets had significantly higher serum alkaline phosphatase (ALP) concentrations compared to the malnourished group without rachitic manifestations. Radiological evaluation of the two groups who had rachitic manifestations revealed demineralization of long bones, thinning of the bony cortex, increased formation of osteoid tissue, and metaphyseal changes including cupping, fraying, and flaring. The incidence of these radiological findings did not differ among the well-nourished and the malnourished groups with clinical signs of rickets. However, the incidence of fracture of the shaft was higher (40 per cent) in the malnourished group compared to the well-nourished group (10 per cent) with rickets. In the malnourished group without clinical evidence of rickets, demineralization and cortical thinning was detected in 40 per cent without significant metaphyseal changes. Basal concentrations of GH and peak GH response to clonidine were significantly elevated and IGF-I concentrations were significantly depressed in the malnourished groups v. the other two groups. There were no significant differences in the fasting and the clonidine provoked GH levels or IGF-I concentrations between the rachitic children (group 3) and the normal children. These data suggest that in rachitic children there is not a major role for circulating GH (and by implication IGF-I) on bone mineralization. However, during malnutrition decreased IGF-I production can slow or stop epiphyseal growth and might contribute to the demineralization of the cortex of long bones.
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PMID:Radiological, biochemical, and hormonal changes in malnourished children with rachitic manifestations. 882 Jun 18

Vitamin D is synthesized in skin through a reaction mediated by sunlight, and it is metabolized to 25-hydroxyvitamin D, in liver, and in 1,25-dihydroxyvitamin D, in kidney. This last reaction has a tight feedback mechanism. 1,25-dihydroxyvitamin D is the active hormone, and its actions are mediated mainly by nuclear receptors. Its major functions are in calcium metabolism and bone mass maintenance. Hypovitaminosis D, as a disease in adult people, manifests itself with hypocalcemia and secondary hyperparathyroidism with subsequent loss of trabecular bone, thinning of cortical bone, and, eventually, a higher risk of fractures. Hypovitaminosis D is a very common condition in Europe, Africa, North America and some South American countries, such as Chile and Argentina. Measurement of serum total 25-hydroxyvitamin D concentration is the gold standard to diagnose vitamin D deficiency. Serum concentrations below 50 nmol/L are associated with an increase in parathyroid hormone concentration, and bone loss. Risk factors for vitamin D deficiency, like poor sunlight exposition, aging skin and factors that interfere with normal vitamin D metabolism, are well established. Oral vitamin D supplementation, an easy and inexpensive treatment, is needed to treat this illness.
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PMID:[Vitamin D deficiency in adults: to better understand a new presentation of an old disease]. 1662 72

1. In all age groups the effects of ammonium chloride administration were found to be strikingly dependent upon the calcium intake. 2. Dogs receiving an adequate calcium diet and ammonium chloride showed less decalcification than those receiving a low calcium diet with or without ammonium chloride. 3. In the younger groups the added effect of ammonium chloride to calcium-low diet brought out more striking changes than a low calcium diet alone. 4. When the decalcification was less severe-in the oldest dogs on the low calcium diet with or without ammonium chloride, and in the younger dogs on an adequate calcium intake with ammonium chloride -generalized thinning of the bones without marrow fibrosis resulted (osteoporosis). 5. When the decalcification was rapid and severe-in the youngest dogs on low calcium diet, particularly with ammonium chloride- generalized decalcification and secondary marrow fibrosis resulted (ostitis fibrosa). 6. Generalized ostitis fibrosa is a rather inclusive term and may be applied to the histologic picture which results when clinical or experimental decalcification is rapid, and therefore leads to extensive marrow fibrosis. 7. The special underlying causes of the decalcification may incidentally contribute features to modify the generalized osteoporosis or ostitis fibrosa as in rickets and in von Recklinghausen's disease.
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PMID:AMMONIUM CHLORIDE DECALCIFICATION, AS MODIFIED BY CALCIUM INTAKE: THE RELATION BETWEEN GENERALIZED OSTEOPOROSIS AND OSTITIS FIBROSA. 1987 Jan 5

Introduction. Nutritional deficiencies are rarely reported in developed countries. We report a child of Pakistani origin brought up in Dubai who developed skeletal manifestations of scurvy due to peculiar dietary habits. Case Presentation. A 4.5 year old boy presented with pain and swelling of multiple joints for three months and inability to walk for two months. Dietary history was significant for exclusive meat intake for the preceding two years. On examination the child's height and weight were below the 5th percentile for his age. He was pale and tachycardic. There was significant swelling and tenderness over the wrist, knee and ankle joints, along with painful restriction of motion. Basic blood workup was unremarkable except for anemia. However, X-rays showed delayed bone age, severe osteopenia of the long bones, epiphyseal separation, cortical thinning and dense zone of provisional calcification, suggesting a radiological diagnosis of scurvy. The child was started on vitamin C replacement therapy. Over the following two months, the pain and swelling substantially reduced and the child became able to walk. Repeat X-rays showed improvement in the bony abnormalities. Conclusion. Although scurvy is not a very commonly encountered entity in the modern era, inappropriate dietary intake can lead to skeletal abnormalities which may be confused with rickets. A high index of suspicion is thus required for prompt diagnosis of scurvy in patients with bone and joint symptoms.
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PMID:Skeletal manifestations of scurvy: a case report from dubai. 2325 26


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