Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the pathophysiology of bone disorder after gastrectomy, 320 patients and 40 Wistar male rats were used. Clinically, patients who had received gastrectomy 1-15 years previously, were examined for skeletal symptoms, serum biochemistry, microdensitometry of second metacarpal bone, and 20 of them were then studied in a calcium infusion test. Using microdensitometry, abnormality of bone metabolism was observed in 38% of the patients. In severe cases, a significant decrease of serum Ca. and increase of alkaline phosphatase were observed (p less than 0.05), 65% complained of joint pain. In the calcium infusion test, severe cases showed a low urinary excretion of Ca, like osteomalacia, and unlike osteoporosis. Experimentally, body weight & amount of food intake decreased and fatty diarrhea was observed in rats after total gastrectomy. Skeletal changes including thinning of the cortex, loss of medullary trabeculation & decrease of bone ash and biochemical changes such as low serum Ca. 25(OH)D3, 24, 25(OH)2D3 and high iPTH levels were observed. Also the bone formation rate was lower than control as detected by tetracycline double labelling method. As low food intake & fatty diarrhea after gastrectomy which result in Ca. & vit. D insufficiency may be the major etiology of bone disorder.
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PMID:[Bone disorder after gastrectomy--clinical & experimental studies]. 226 41

A 59-year-old male presented with systemic mastocytosis with extensive skeletal involvement resulting in vertebral compression fractures and bone pain. Histomorphometric analysis of bone revealed increased mast cells, elevated static parameters of bone resorption, and low bone formation. Serum calcium, phosphorus, and alkaline phosphatase were normal; however, serum 1,25-dihydroxyvitamin D3 and osteocalcin levels were low. Histamine levels in plasma and urine were elevated. Following therapy with ketotifen, the patient had resolution of bone pain along with decreased flushing and pruritus. Elevated plasma and urine histamine levels normalized, as did 1,25-dihydroxyvitamin D3 and osteocalcin levels. Indices of low bone formation improved on therapy. Eroded surfaces improved but remained elevated. This case is the first demonstration that bone symptoms and histomorphometric change in systemic mastocytosis are reversed with inhibition of mast cell degranulation. The role of mast cells and their products in bone metabolism is poorly understood, but the therapy of bone disease in systemic mastocytosis should include inhibition of the release of mast cell products along with the use of histamine antagonist.
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PMID:Inhibition of mediator release in systemic mastocytosis is associated with reversal of bone changes. 227 Jul 75

Twenty obligate carriers of infantile hypophosphatasia (HOPS), a severe autosomal recessive metabolic bone disorder, were studied and compared with 36 controls. Decreased serum alkaline phosphatase activity and increased urinary phosphoethanolamine excretion were confirmed in the HOPS carriers. Relative hyperphosphatemia was documented for the first time in the carriers. Logistic regression analysis was used to develop models for the diagnosis of and screening for HOPS carriers in the high-risk population of Manitoba Mennonites. Models based on serum alkaline phosphatase activity and on serum phosphate levels with or without urinary phosphoethanolamine excretion were used for diagnostic purposes. A model based on serum alkaline phosphatase activity and on the serum phosphate level was the most suitable for screening.
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PMID:Hyperphosphatemia in infantile hypophosphatasia: implications for carrier diagnosis and screening. 230 98

The histological features of thalassemic bone are imperfectly known, and the roles of bone marrow hyperactivity, iron overload or vitamin D deficiency in the pathogenesis of the disease are not clearly identified. In this study we examined iliac crest biopsies from 17 transfusion-dependent children with homozygous beta-thalassemia and severe radiological skeletal thalassemic changes, including widening of medullary spaces and osteoporosis. Rachitic lesions were not observed. Serum ferritin concentrations were increased in all but one subject. Iron deposits were histochemically detected in bone marrow, at the marrow-bone interface, along cement lines and mineralizing perimeters. Minor changes were present in trabecular bone, and osteomalacia was absent. By contrast, cortical bone exhibited severe changes including fissures and focal mineralization defects. Plasma 25-hydroxyvitamin D (25(OH)D) concentrations measured during the winter (December-May, 6.5 +/- 4.9 ng/ml, mean +/- SD, n = 6) and during the summer (June-November, 13.8 +/- 8.4 ng/ml, n = 9) did not differ from those of age-matched children living in the same country. Seven patients had moderate hypocalcemia but no biological signs suggestive of vitamin D deficiency: all had normal alkaline phosphatase activity, normal or slightly elevated plasma phosphate, only two had low plasma 25(OH)D concentrations and two others supranormal values of plasma immunoreactive parathyroid hormone. These results show that iron overload and vitamin D deficiency do not seem to play an important role in the pathogenesis of thalassemic bone disease, which is characterized by cortical lesions probably related to marrow hyperactivity.
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PMID:Bone disease in children with homozygous beta-thalassemia. 230 56

Inadequate vitamin D intake is an important cofactor in clinical and experimental bone disease induced by chronic cadmium exposure. The interaction was investigated by culture of rat osteoblastic osteosarcoma cells (ROS 17/2.8) in a serum-free medium with equimolar concentrations of cadmium chloride and 1 alpha,25-(OH)2 vitamin D3. After addition of cadmium alone to culture medium, the unstimulated secretion of osteocalcin and cellular alkaline phosphatase activity were inhibited at 10 pM, and of DNA synthesis and proline incorporation into collagen at 500 nM. In the presence of equimolar amounts of cadmium and 1 alpha,25-(OH)2 vitamin D3, all four responses paralleled those of 1 alpha,25-(OH)2 vitamin D3 alone up to the inhibitory concentration of 500 nM cadmium. Neither 10 nM 1 alpha,25-(OH)2 vitamin D3 nor 1 microM cadmium induced synthesis of metallothionein in these cells indicating that the protective effect of D3 was not related to the induction of a metallothionein-like protein in ROS 17/2.8 cells. In the presence or absence of D3, cadmium inhibited osteoblastic function at concentrations below the whole-organ concentration of cadmium in bone as reported in experimental and clinical cadmium-induced osteotoxicity. The extreme sensitivity of ROS 17/2.8 cells to cadmium may relate to the absence of metallothionein synthesis.
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PMID:Toxicity of cadmium to rat osteosarcoma cells (ROS 17/2.8): protective effect of 1 alpha,25-dihydroxyvitamin D3. 231 24

Alkaline phosphatase, osteocalcin and hydroxyproline levels were evaluated in patients with the following conditions: primary hyperparathyroidism, renal dialysis, hyperthyroidism, Cushing's syndrome, long term corticosteroid therapy, Paget's disease, osteoblastic metastases, osteolytic or mixed metastases, and nutritional osteomalacia. In all cases the levels of the three substances were increased, with the following exceptions: a) in endogenous or exogenous hypercortisolism states osteocalcin level was reduced and those of alkaline phosphatase and hydroxyproline were unchanged; and b) in blastic or lytic metastases osteocalcin level was unchanged. In general, alkaline phosphatase and hydroxyproline levels had a higher sensitivity than those of osteocalcin in structural bone disease (Paget's disease, blastic or lytic metastases), whereas the converse was true for endocrine bone disease (the remaining conditions except osteomalacia, which is mixed, both structural and endocrine; in this syndrome, the three substances showed the same sensitivity.
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PMID:[Different behavior of bone turnover markers in endocrine (extrinsic) and structural (intrinsic) osteopathies]. 234 91

The significance of alkaline phosphatase (AP) elevation with otherwise normal transaminase and bilirubin values remains unclear. We evaluated the clinical outcome of hospitalized patients with an "isolated" AP elevation. Eighty-seven inpatients with isolated AP elevation were identified during February 1984 and followed for 1 year. Forty-five of 87 patients had normalization of AP during the follow-up period, usually within 1-3 months. The most common diagnoses in this group were congestive heart failure in nine, benign bone disease in six, and treatable malignancy in three patients. Twelve patients had no apparent explanation for the transient rise of AP. Persistent AP elevations were noted in 42 patients--14 of whom had terminal malignancies. Clinically obvious life-threatening diagnoses were made in 24 of the patients with persistent AP elevation. The etiology of AP elevation remained enigmatic in seven patients: two died, four are stable during 1 1/2-3 years of follow-up, and one patient was found to have metastatic carcinoma 17 months later. If the initial AP was greater than 1 1/2 times normal, there was a higher likelihood of persistent elevation (68% vs. 41%, p less than 0.05). Isolated elevations of AP in inpatients may be associated with a variety of medical illnesses and often normalize within months. If the AP elevation is persistent, there is usually a clinically obvious diagnosis. A reasonable approach to such patients is a careful history, physical exam, and routine lab studies to detect obvious diagnoses, followed by repeat enzyme determination at 1-3 months.
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PMID:"Isolated" elevation of alkaline phosphatase: significance in hospitalized patients. 239 49

We analyzed transiliac bone biopsy specimens obtained after tetracycline double labeling from 24 patients with aluminum-related bone disease who had undergone long-term hemodialysis. The specimens were selected by the following criteria: Al deposits at the mineralization fronts, a dramatic reduction in double-labeled surfaces, reflecting a low mineralization rate, and a significant increase in osteoid volume and osteoid surfaces. The bone formation rate at the tissue level and at the basic multicellular unit level was decreased in all patients. Seventeen biopsy specimens (group 1) showed morphologic and dynamic evidence of osteomalacia, as defined by an increase in the osteoid seam thickness and a decreased mineralization rate. In one specimen from group 1, thickened osteoid seams were present only in a small part of the specimen. In seven specimens (group 2), the osteoid seam thickness index was normal, indicating "aplastic bone." Two specimens from group 2, however, showed morphologic and dynamic evidence of focal osteomalacia either in trabecular or in cortical bone. Specimens from group 2 patients differed from those in group 1 in their significantly lower values of osteoid volume and lower levels of serum alkaline phosphatase and parathyroid hormone. These data show that the absence of significant increase in osteoid seam thickness and the focal distribution of thickened osteoid seams in patients with Al overload and low rate of bone formation reflect the marked reduction of bone matrix formation at the cellular level. It is suggested that low parathyroid activity might play a role in the reduction of bone matrix formation.
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PMID:Low rate of bone formation with or without histologic appearance of osteomalacia in patients with aluminum intoxication. 241 May 22

We have determined the activity of alkaline phosphatase in chorionic villous tissue obtained in the first trimester of pregnancy, in order to obtain the normal range of values as a prerequisite for application to the prenatal diagnosis of the rare bone disease hypophosphatasia. The activities found were a combination of intestinal and liver/bone/kidney types; traces of placental type were present in only one sample.
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PMID:Activities of alkaline phosphatase in first trimester chorion biopsy tissue. 241 34

Clinical and biochemical features of transient hyperphosphatasemia of infancy and early childhood are reviewed in 21 patients we have studied and in a further 93 cases reported in the literature. The diagnosis is suggested by the finding of an increased activity of alkaline phosphatase (EC 3.1.3.1) in plasma, typically more than fivefold the adult upper reference limit, in a child under five years of age, without evidence of liver or bone disease. The condition is confirmed by the presence of a characteristic pattern of alkaline phosphatase isoenzymes and by the normalization of the enzyme's activity in plasma within approximately three months. The etiology of the condition and possible mechanisms of the enzyme increase are discussed.
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PMID:Transient hyperphosphatasemia of infancy and early childhood: clinical and biochemical features of 21 cases and literature review. 243 76


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