Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Hyperthyroidism was diagnosed in 131 cats during a 3 1/2-year period. The cats ranged in age from 6 to 20 years; there was no breed or sex predilection. The most frequent clinical signs included weight loss, polyphagia, increased activity, polydipsia, polyuria, and vomiting. Common serum biochemical abnormalities included high values for alkaline phosphatase activity (75%), lactate dehydrogenase activity (66%), aspartate transaminase activity (66%), and alanine transaminase activity (54%). Electrocardiographic changes included tachycardia (greater than or equal to 240 beats/min) and increased R-wave amplitude in lead II (greater than or equal to 0.9 mV) in 66% and 29% of the 131 cats, respectively. Thoracic radiography in 82 cats revealed cardiomegaly in 40 (49%) of these cats; 16 cats with congestive heart failure also had pulmonary edema or pleural effusion. In 5 cats with markedly increased fecal volume, mean 48-hour fecal fat content was significantly greater than normal, with daily fat excretion 2 to 15 times the upper limit of normal. Base-line serum thyroxine concentrations were increased above normal range in all cats, whereas triiodothyronine concentrations were increased in 127 (97%) of the 131 cats. In 11 cats tested, mean thyroxine concentration did not increase significantly after thyroid-stimulating hormone administration. Mean 24-hour percentage of thyroid radioiodine uptake in 32 hyperthyroid cats was significantly higher (39.1%) than normal (9.2%). Thyroid scans, performed on 126 cats, showed enlargement and increased radionuclide accumulation in 1 thyroid lobe in 36 (29%) and both lobes in 90 (71%) of the cats.
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PMID:Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. 687 10

Impairment of calcium metabolism and low bone density have been found in hypothyroid adults. We investigated the effect of thyroid replacement therapy on calcium metabolism and bone mineralization in congenital hypothyroid (CH) infants and children. One hundred and 16 Caucasian CH consecutive patients were studied and were grouped according to their age: 23 patients at diagnosis, 20 at 3 mo, 24 at 6 mo, 25 at 12 mo and 24 at 36 mo. Thyroid replacement therapy was started at an initial dose of 6-8 micrograms/kg/day of L-thyroxine, and then decreased progressively. Calcium, phosphorus, magnesium, alkaline phosphatase (AP), parathyroid hormone (PTH) and osteocalcin (BGP) were measured as calcium metabolism indices. Bone mineral content (BMC) was measured at the mid-portion of the right radius AP, PTH and BGP concentrations were significantly higher in subjects at 3 mo of age (p < 0.05). This rise coincided with the end of the period of maximum dosage of L-thyroxine. Mild asymptomatic hypercalcemia was observed in 20 patients. All the other indices did not differ between age groups. BMC values and BMC annual increment were not different from those calculated for age-matched controls. We found that L-thyroxine replacement therapy does not alter bone mineralization of CH infants and children. Only a transitory increase of osteoblastic function was observed after the first few months of therapy.
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PMID:Bone mineral metabolism and thyroid replacement therapy in congenital hypothyroid infants and young children. 756 Aug 9

To examine whether suppressive doses of thyroxine have any adverse effects on bone, we evaluated various bone metabolic markers (lectin-precipitated alkaline phosphatase, osteocalcin, carboxyl-terminal region of type I collagen propeptide, tartrate-resistant alkaline phosphatase, and urinary excretion of hydroxyproline and pyridinium crosslinks), incidence of vertebral deformity, total body and regional (lumbar spine and radius) bone mineral densities (BMDs), and rates of bone loss in 24 late postmenopausal (more than 5 years after menopause) women who were treated with levothyroxine (L-T4) after total thyroidectomy for differentiated carcinoma. Depending on the clinical records, including serum TSH levels measured by immunoradiometric assay, these patients were divided into two groups. One group of patients was given suppressive doses of L-T4 (TSH < 0.1 mU/L, n = 12) and the other group was given nonsuppressive doses of L-T4 (TSH > 0.1 mU/L, n = 12). There was no difference in bone metabolic markers and incidence of vertebral deformity between the groups. In patients with TSH suppression, Z-scores of BMDs calculated from age-matched healthy women (n = 179, aged 55 to 80) were nearly in the zero range of values (0.077 at total body, 0.228 at lumbar spine, and -0.117 at trabecular region of lumbar spine). The rate of bone loss in TSH-suppressed patients (-0.849 +/- 0.605%/year) was not significantly different from that of nonsuppressed patients (-0.669 +/- 0.659). These prospective and cross-sectional data suggest that long-term levothyroxine therapy using suppressive doses has no significant adverse effects on bone.
Thyroid 1995 Feb
PMID:Suppressive doses of thyroxine do not accelerate age-related bone loss in late postmenopausal women. 778 27

Because of the previous controversial findings in studies of bone mineral density in patients with hyperthyroidism with older methodologies, we assessed bone mineral density in 15 Japanese patients with Graves' disease (8 males and 7 females) before and after treatment using dual energy X-ray absorptiometry (DEXA). Bone mineral density of the lumbar vertebrae and the femur, and thyroid function, and several metabolic parameters were measured before treatment and again after patients achieved a euthyroid state following treatment with methimazole for 4 to 20 months (mean 10.6 months). The bone mineral density of patients was calculated as the percentage of the mean value (%BMD) in an age- and sex-matched control group, and correlations between the changes in bone mineral density and metabolic parameters before and after treatment were investigated. The %BMD of vertebrae in patients with Graves' disease before treatment was 89.7% of that found in the normal population. When patients became euthyroid after treatment, %BMD increased significantly to 94.9%, although it still remained below the control level. TSH receptor antibody, osteocalcin, and alkaline phosphatase were elevated before treatment, but decreased significantly after treatment. The change between pre- and posttreatment TSH receptor antibody was negatively correlated with the change in bone mineral density. In conclusion, these findings suggest that bone mineral density is decreased in patients with Graves' disease and that successful treatment of hyperthyroidism results in a significant increase in bone mineral density within a short period of time. Furthermore, TSH receptor antibody is a useful marker of changes in bone metabolism in this group of patients.
Thyroid 1994
PMID:Change in bone mineral density in patients with hyperthyroidism after attainment of euthyroidism by dual energy X-ray absorptiometry. 791 94

Thyroid hormone (T3) and retinoic acid (RA) are essential for normal vertebrate development and are known to coregulate several genes. Early development is predominantly retinoic acid sensitive, yet thyroid hormone receptor-alpha (T3R alpha) is expressed along with retinoic acid receptors (RAR)-alpha, -beta, and -gamma. To determine the role of unliganded T3R alpha in early development and on RA-stimulated neural development, we used homologous recombination techniques to inactivate both T3R alpha gene alleles in mouse embryonic stem (ES) cells. Loss of both T3R alpha alleles resulted in an increase in basal and RA-induced expression of the endogenous RA-responsive genes, RAR beta and alkaline phosphatase, which demonstrates that T3R alpha has an inhibitory effect on the RA response. A similar magnitude of T3R inhibition of the RA response was seen in transient transfection assays of RA response elements in both ES and assays of RA response elements in both ES and JEG cells. Cotransfection experiments were used to demonstrate that inhibition of the RA response could be mediated by T3R alpha 1. The addition of T3R alpha 1, but not the T3R alpha variant c-erbA alpha 2, to T3R alpha-null ES cells restored the inhibitory effect on RA-induced gene expression. RA-stimulated neural differentiation was seen in the wild-type, but not in T3R alpha-null ES, cells, consistent with reports of abnormal neural development as a consequence of premature RA stimulation. Our results demonstrate that the early expression of unliganded T3R alpha functions to modulate the RA response and RA-stimulated neural differentiation.
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PMID:Thyroid hormone receptor-alpha inhibits retinoic acid-responsive gene expression and modulates retinoic acid-stimulated neural differentiation in mouse embryonic stem cells. 793 90

We monitored thyroid function in 75 peritoneal dialysis patients (55 +/- 15 years). A total of 20 (27%) were hypothyroid; 9 were diagnosed about the time of initiation of dialysis, and 11 prior to onset of renal failure. Thyroid function surveillance found an increase in serum thyrotropin (TSH) concentration to hypothyroid values in only one patient. On replacement therapy serum thyroxine was similar in euthyroid and hypothyroid patients (6.94 +/- 1.69 vs 6.52 +/- 1.65 micrograms/dL, respectively; p = 0.380), but TSH was higher in hypothyroid patients (5.61 +/- 5.67 vs 2.59 +/- 1.49 microU/mL, respectively; p = 0.001). Serum creatinine (8.6 +/- 3.1 vs 11.4 +/- 5.1 mg/dL, respectively; p = 0.049) and albumin concentrations (3.76 +/- 0.47 vs 3.33 +/- 0.71 g/dL, respectively; p = 0.006) were lower in hypothyroid than euthyroid patients. Hyperthyroid patients had higher serum triglyceride concentrations than euthyroid patients (306 +/- 176 vs 189 +/- 122 mg/dL, respectively; p = 0.013). Parathyroid hormone (PTH) was lower in hypothyroid than normothyroid patients (108 +/- 80 vs 261 +/- 265 pg/mL, respectively; p = 0.032). No differences were observed in serum calcium, phosphorus, and alkaline phosphatase. We conclude that hypothyroidism is common in peritoneal dialysis patients, usually antedates dialysis therapy, results in lower serum albumin and creatinine concentrations and higher serum triglyceride concentrations, is associated with lower serum PTH concentrations, and that thyroid function surveillance is not necessary in the absence of symptoms suggestive of hypothyroidism.
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PMID:Thyroid function surveillance in CAPD patients. 853 10

We studied 10 postmenopausal women with Hashimoto's hypothyroidism treated with varying doses of L-thyroxine replacement. Each patient received incremental doses of L-thyroxine sufficient to achieve subclinical hypothyroidism, euthyroidism, and subclinical hyperthyroidism as determined by normal total serum thyroxine levels (80-160 micrograms/L) and serum TSH concentrations greater than 3.5, 0.3-3.5, and less than 0.3 mU/L, respectively. Metabolic parameters of bone turnover (including serum bone Gla-protein, serum alkaline phosphatase, serum procollagen 1, and serum carboxytelopeptide) were assessed once steady state was achieved, and measurements were compared to 10 healthy controls matched for age and years since the menopause. Our findings suggest that overzealous thyroxine replacement producing subclinical hyperthyroidism may result in an increase in bone turnover as reflected by elevated serum carboxytelopeptide concentrations.
Thyroid 1996 Apr
PMID:Fine adjustments in thyroxine replacement and its effect on bone metabolism. 873 75

It is still uncertain whether bone mass and bone turnover are completely normalized after treatment of hyperthyroidism. The aim of the present investigation was to determine bone mass, bone turnover, body composition, and calcium homeostasis in former hyperthyroid patients who had been euthyroid for at least 4 years following combined medical therapy. Thirty-nine former hyperthyroid patients and 67 normal sex- and age-matched controls participated. Height, body weight, and body composition were similar in the two groups. All patients were euthyroid. However, serum FT3I (free T3-index) was reduced by 9% (p < 0.01) in the patients compared to controls, serum FT4I was normal, while serum TSH was nonsignificantly reduced by 39%. No significant differences were observed between patients and controls with respect to total or regional bone mineral content (BMC) or density (BMD). The former hyperthyroid patients had slightly higher serum calcium (2.35 +/- 0.06 vs. 2.32 +/- 0.07 mmol/L, p < 0.05) and lower serum phosphate (1.15 +/- 0.15 vs. 1.24 +/- 0.15 mmol/L, p < 0.01) than their controls. Renal excretion of calcium and serum levels of magnesium, 1,25-vitamin D and intact PTH were unchanged. Renal excretion of pyridinoline was increased by 30% (p < 0.05) in the patients, whereas the remaining resorptive markers, renal excretion of hydroxyproline and deoxypyridinoline and serum cross-linked carboxy-terminal teleopeptide of type I collagen (ICTP) were unaltered. Among the formative bone markers the average serum carboxy-terminal propeptide of human type I procollagen (PICP) level was 12% lower (p < 0.05) than in the control group, whereas serum levels of osteocalcin and total and bone alkaline phosphatase were normal. In conclusion, former hyperthyroid patients treated by combined medical therapy have normal bone mineral content and density in spite of minor variations in thyroid hormones and skeletal homeostasis.
Thyroid 1996 Jun
PMID:Bone mass, bone turnover, body composition, and calcium homeostasis in former hyperthyroid patients treated by combined medical therapy. 883 21

Untreated hyperthyroidism is characterized by increased bone turnover with loss of bone and bone mineral. The aim of the present investigation was to evaluate the reversibility of these changes by measuring bone mass, bone turnover, and calcium homeostasis in surgically treated former hyperthyroid patients who had been euthyroid for at least 6 years. Sixty euthyroid former hyperthyroid patients and 94 normal sex- and age-matched controls participated. Heights and body weights and composition were similar in the two groups. In the thyroxine substituted patients (n = 27) both serum T4 and serum free T4-index (S-FT4I) were increased (p < 0.001) compared to the normal controls as well as the nonsubstituted patients. In the nonsubstituted patients. In the nonsubstituted patients (n = 33), serum TSH was increased (p < 0.001) compared to the normal controls. No significant differences were observed between substituted and nonsubstituted patients and normal controls with respect to serum T3, serum free T3-index (S-FT3I), or regional or total bone mineral content (BMC) and density (BMD) values. Serum levels of calcium, phosphate, magnesium, intact PTH, and renal excretion of calcium were unchanged. However, serum levels of 1,25-dihydroxy- and 25-hydroxyvitamin D were reduced. Urinary excretion of hydroxyproline was increased by 16% (p < 0.05), but serum cross-linked carboxy-terminal teleopeptide of type I collagen (ICTP) was decreased by 11% (p < 0.01). Urinary excretion of collagen cross-links was normal. Serum levels of osteocalcin, carboxy-terminal propeptide of human type I procollagen (PICP), and total and bone alkaline phosphatase were all normal. In conclusion, surgically treated former hyperthyroid patients have normal bone mass, bone turnover, and calcium homeostasis in spite of minor variations in thyroid hormones and vitamin D metabolites.
Thyroid 1996 Jun
PMID:Bone mass, bone turnover, calcium homeostasis, and body composition in surgically and radioiodine-treated former hyperthyroid patients. 883 22

The mechanism of action of thyroid hormones on bone is poorly understood. Thyroid hormones may act on bone cells either indirectly by increasing secretion of growth hormone (GH) and insulin-like growth factor-1 (IGF-1), or directly by influencing target genes via specific nuclear receptors. The presence of thyroid hormone receptors (TRs) has been demonstrated in human and rodent osteoblast-like cells and cell lines and recently in osteoclasts derived from an osteoclastoma in vitro. However, their presence in human bone in situ has not been reported. We have used specific polyclonal antibodies to TR-alpha 1, -alpha 2, and -beta 1 to investigate the expression of these receptors in sections of human osteophytes and heterotopic bone. Osteoblasts and osteoclasts were identified by alkaline phosphatase (ALP) and tartrate-resistant acid phosphatase (TRAP), respectively, whereas chondrocytes were identified morphologically. At sites of endochondral and intramembranous bone formation, TR-beta 1 and the splice variant -alpha 2 were widely expressed by proliferating, mature, and hypertrophic chondrocytes and also in cells within the fibrous tissue and at the bone forming surfaces, respectively. They were also detected in osteoblasts, osteoclasts, and a few osteocytes at sites of bone remodeling. In contrast, TR-alpha 1 was the least expressed and was present mainly in osteoblasts at remodeling sites and in a few mature and undifferentiated chondrocytes. Our results show, for the first time, the presence and distribution of TRs in human bone in situ and suggest that the skeletal actions of thyroid hormones may be mediated via these receptors. Further studies are required to define the role of the individual receptor isoforms in bone metabolism.
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PMID:The expression of thyroid hormone receptors in human bone. 926 88


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